< 11 %; ■». -h- * & x A _»*n -»■* ■ r- -* •_ „y y—■. ~-«V ^ e** •”• -■ •» — ■ ~~ '--V i: . 'JVETERINARY OBSTETRICS AND GENITAL DISEASES (THERIOGENOLOGY) VETERINARY OBSTETRICS AND GENITAL DISEASES (THERIOGEN OLOG Y) * by Stephen J. Roberts DVM, MS Professor Emeritus, Department of Medicine, Obstetrics and Surgery, New York State College of Veterinary Medicine, Cornell University, Ithaca, New York 14853 Published by the Author Woodstock, Vermont 05091 1986 Distributed by David and Charles Inc. North Pomfret, Vermont 05053 Lithographed by Edwards Brothers, Inc. Ann Arbor, Michigan 48104 *(Term proposed by D. Bartlett and others to indicate all aspects of veterinary obstetrics, genital diseases and animal reproduction; “therio” = animal or beast and “gen” = coming into being from Greek medical terminology.)First Edition March 1956 Second Edition 1971 Third Edition 1986 Copyright 1956, 1971, 1986 by Stephen J. Roberts Lithographed in the United States by Edwards Brothers, Inc. Ann Arbor, MichiganDedicated to BeejayCONTRIBUTING AUTHORS Chapter XVII Infertility in the Bitch and Queen Donald H. Lein, DVM, Ph.D. Assistant Director Veterinary Diagnostic Laboratory, Associate Professor, Dept, of Pathology and Dept, of Clinical Sciences, New York State College of Veterinary Medicine, Cornell University, Ithaca, N.Y. Chapter XIX Artificial Insemination Robert H. Foote, Ph.D. Jacob Gould Shurman Professor of Animal Physiology, Dept, of Animal Sciences, New York State College of Agriculture and Life Sciences, Cornell University, Ithaca, N.Y. Chapter XX Embryo Transfer Maarten Drost, DVM, Professor of Reproduction, Department of Reproduction, Col- lege of Veterinary Medicine, University of Florida, Gainesville, Fla.CONTENTS PART I—OBSTETRICS Page INTRODUCTION.............................................................. 1 CHAPTER I—OBSTETRICAL ANATOMY The Pelvic Bones and Ligaments................................. 3 The Ovaries and Female Genital Tract........................... 5 Embryology of the Female Reproductive Tract.................... 12 CHAPTER II—EXAMINATIONS FOR PREGNANCY Pregnancy Diagnosis in the Cow................................. 14 External Indications............................................ 14 Rectal and Vaginal Examination ................................. 15 Differential Diagnosis.......................................... 22 Pregnancy Diagnosis in the Mare...................................... 24 Rectal and Vaginal Examination ................................. 25 Biologic Tests.................................................. 30 Pregnancy Diagnosis in the Ewe....................................... 31 Pregnancy Diagnosis in the Sow ...................................... 32 Pregnancy Diagnosis in the Bitch and Queen........................... 32 CHAPTER III—GESTATION PERIOD—EMBRYOLOGY, FETAL MEMBRANES AND PLACENTA—TERATOLOGY Periods of the Embryo and Fetus...................................... 38 The Development of the Nervous, Digestive, Circulatory Systems. 39 The Development of the Urogenital System............................. 41 The Fetal Membranes.................................................. 41 The Placenta......................................................... 44 The Umbilical Cord................................................... 48 Anomalies of Development, Teratology ................................ 51 Inherited Anomalies............................................. 52 Noninherited Anomalies.......................................... 68 CHAPTER IV—PHYSIOLOGY OF THE GESTATION PERIOD Shape and Location of the Pregnant Uterus ........................... 93 Position of the Fetus in the Uterus.................................. 94 Number of Fetuses in the Uterus...................................... 94 Twinning and Multiple Births in Unipara......................... 95 Immunogenetics.................................................. 96 Freemartins..................................................... 97 Sex Parity.......................................................... 102 Bacterial Flora of the Pregnant Uterus.............................. 103 viiVETERINARY OBSTETRICS viii Length of Pregnancy........................................................ 104 Hormonal Control of Gestation.............................................. 107 Duration and Rate of Reproduction.......................................... 110 Abnormalities in Fertilization and Gestation......................... Ill The Mammary Gland and Lactation...................................... 113 CHAPTER V—DISEASES AND ACCIDENTS DURING THE GESTATION PERIOD Abortion................................................................. 123 Abortion in Cattle....................................................... 125 Abortion in Horses ..................................................... 162 Abortion in Swine........................................................ 180 Abortion in Sheep and Goats.............................................. 192 Abortion in Dogs......................................................... 206 Abortion in Cats ........................................................ 210 Mummification of the Fetus............................................... 213 Fetal Maceration......................................................... 218 Prevention of Conception and Induction of Abortion....................... 220 Extra-uterine “Pregnancies” and Fetuses.................................. 222 Dropsy of the Fetal Membranes and Fetus.................................. 223 Abdominal Hernias Resulting in Hysterocele............................... 228 Torsion of the Uterus ................................................... 230 Vagino-cervical Prolapse................................................. 233 Paraplegia of Pregnancy.................................................. 240 Miscellaneous Accidents During Pregnancy................................. 242 CHAPTER VI—PARTURITION Symptoms of Approaching Parturition........................................ 245 The Initiation of Parturition.............................................. 247 The Induction of Parturition............................................... 248 Stages of Parturition...................................................... 251 Involution of the Uterus................................................... 256 Artificial Interferences in Normal Parturition............................. 259 Diseases and Care of the Newborn ................................... 262 Care of the Postpartum Dam ......................................... 272 CHAPTER VII—THE CAUSES OF DYSTOCIA Incidence ........................................................... 277 Basic Causes of Dystocia............................................. 277 Immediate Causes of Dystocia......................................... 282 Common Forms of Dystocia in Domestic Animals.................... 283 CHAPTER VIII—PROCEDURES PRELIMINARY TO THE HANDLING OF DYSTOCIA History of the Case.................................................... 287 General Examination.................................................... 287 Specific Examination and Restraint..................................... 287 Prognosis.............................................................. 290 Obstetrical Equipment and Anesthesia................................... 290CONTENTS ix CHAPTER IX—OBSTETRICAL OPERATIONS FOR RELIEVING DYSTOCIA Mutation............................................................... 298 Forced Extraction...................................................... 301 Fetotomy............................................................... 307 Cesarean Section and Hysterectomy...................................... 314 CHAPTER X—DIAGNOSIS AND TREATMENT OF THE VARIOUS TYPES OF DYSTOCIA Pathological Presentations, Positions, and Postures of the Fetus. 326 Abnormal Size of the Fetus, Monsters, or Twinning...................... 333 Uterine Displacements, Including Uterine Torsion....................... 337 Obstruction or Stenosis of the Birth Canal............................. 344 Uterine Inertia........................................................ 347 Postmortem Changes in the Fetus ....................................... 349 CHAPTER XI—INJURIES AND DISEASES OF THE PUERPERAL PERIOD Postpartum Hemorrhage.................................................. 353 Lacerations and Contusions of the Birth Canal and Adjacent Structures........................................................... 354 Rupture of the Uterus, Vagina, and Perineum ........................... 357 Prolapse of the Abdominal or Pelvic Viscera, Including Uterine Prolapse............................................................. 360 Metabolic Diseases of the Postparturient Period........................ 368 Postparturient Infections and Diseases................................. 373 Retained Placenta.................................................. 373 Septic Metritis.................................................... 384 Infections of the Cervix, Vagina, and Vulva ........................... 390 Postpartum Paraplegia...........................•................ 393 PART II—GENITAL DISEASES CHAPTER XII—PHYSIOLOGY OF REPRODUCTION (FEMALE) Reproductive Hormones.................................................. 398 Anterior Pituitary Hormones......................................... 399 Posterior Pituitary Hormones........................................ 402 Ovarian Hormones.................................................... 403 Other Reproductive Hormones......................................... 406 Other Endocrine Glands.............................................. 408 Puberty................................................................. 409 The Estrous Cycle....................................................... 411 Coition................................................................. 415 Oogenesis (Ovogenesis) ................................................. 417 Ovulation............................................................... 419 Fertilization and Transport of the Ovum, Sperm and Zygote............... 422 Reproductive Table...................................................... 427X VETERINARY OBSTETRICS CHAPTER XIII—INFERTILITY IN THE COW Reproductive Physiology............................................. 434 Infectious Diseases ................................................ 447 Trichomoniasis.................................................. 447 Vibriosis (Campylobacteriosis).................................. 456 Brucellosis..................................................... 467 Granular Venereal Disease....................................... 468 Infectious Pustular Vulvovaginitis.............................. 474 Miscellaneous Infections of the Bovine Female Genital Tract..... 475 Hormonal Disturbances Resulting in Infertility...................... 478 Cystic Ovaries or Nymphomania................................... 478 Failure of Estrum or Anestrum................................... 495 Miscellaneous Conditions........................................ 511 Nutritional Causes.................................................. 514 Congenital or Hereditary Causes .................................... 520 Other Pathological Causes—Ovary, Oviduct, Uterus, Cervix, Vagina, and Vulva................................................. 533 The “Repeat Breeder” Cow............................................ 559 Postpartum Period................................................... 572 Management Problems ................................................ 575 CHAPTER XIV—INFERTILITY IN THE MARE Reproductive Physiology............................................. 582 Irregularities of the Estrous Cycle and Anestrum.................... 588 Nutrition and Infertility........................................... 598 Genital Infections.................................................. 599 Other Infectious Diseases of the Genital Organs..................... 618 Miscellaneous Pathological Factors.................................. 619 Evaluation of a Mare for Fertility ................................. 623 “Repeat Breeders”................................................... 625 Breeding Farm or Stud Management.................................... 627 CHAPTER XV—INFERTILITY IN THE SOW Reproductive Physiology............................................. 636 Anatomical, Congenital, and Genetic Abnormalities of the Genital Tract..................................................... 642 Pathologic Lesions or Diseases of the Reproductive System........... 643 Infections of the Genital Tract..................................... 643 Hormonal or Endocrine Disturbances.................................. 644 “Repeat Breeders”................................................... 647 Nutritional Deficiencies............................................ 647 Reproductive Management in Swine Herds.............................. 648 CHAPTER XVI—INFERTILITY IN THE EWE AND DOE Infertility in Ewes................................................. 654 Reproductive Physiology......................................... 654 Pathology of the Ovine Reproductive System...................... 660 Infections of the Genital Tract................................. 661 Nutrition and Fertility......................................... 662 Fertilization and Embryonic Deaths.............................. 663 Infertility in Does ................................................ 669 Reproductive Physiology......................................... 669 Pathology of the Caprine Reproductive System ................... 671CONTENTS xi CHAPTER XVII—INFERTILITY AND REPRODUCTIVE DISEASES IN BITCHES AND QUEENS (by D. H. Lein) Reproductive Physiology of the Bitch................................. 675 Reproductive Physiology of the Queen................................. 698 Anatomic and Congenital Defects, Intersexes................................ 709 Nutritional Aspects ....................................................... 711 Hormonal Disturbances—Anestrus, Ovarian Cysts, Hypothyroidism and Others ............................................... 712 Pathology of the Genital Tract............................................. 718 Developmental Anomalies and Cystic Embryological Remnants .... 718 Neoplasia.............................................................. 721 Infections of the Genital Tract........................................ 728 Specific Infections............................................... 728 Miscellaneous Infections.......................................... 732 Cystic Hyperplasia, Endometritis, Metritis and Pyometra................ 734 Miscellaneous Disorders of the Genital Tract........................... 740 Subinvolution of Placental Sites.................................. 742 Breeding Soundness Examination............................................. 745 CHAPTER XVIII—INFERTILITY IN MALE ANIMALS (ANDROLOGY) Anatomy and Embryology of the Male Reproductive Tract................ 752, 759 Physiology of the Male..................................................... 760 Frequency of Service....................................................... 774 Coital Injuries ........................................................... 775 Vices of the Male Animal................................................... 776 Nutrition and Infertility.................................................. 782 Hormonal Causes of Infertility............................................. 784 Forms of Infertility in the Male........................................... 786 Reduced Sex Drive...................................................... 786 Inability to Copulate or Complete Coitus .............................. 786 Incapacity or Reduced Capacity to Fertilize............................ 813 With Normal Semen Production...................................... 813 With Defective or Abnormal Semen Production, Testicular Hypoplasia, Degeneration and Orchitis........................... 815 Hereditary or Congenital Sperm Cell Defects, Male Intersexes and Cryptorchidism.............................. 818 Acquired Testicular Pathology or Degeneration and Testicular Neoplasms........................................ 826 Pathological or Functional Disturbances of the Epididymis, Vas Deferens and Accessory Glands................................... 841 Diagnosis of Infertility in the Male and Evaluation of Breeding Soundness....................................................... 857 Semen Collection........................................................... 861 Semen Examination and Fertility Assessment................................. 872 CHAPTER XIX—ARTIFICIAL INSEMINATION (by R. H. Foote) History.................................................................... 894 Advantages and Disadvantages............................................... 895 Artificial Insemination of Cattle.......................................... 896 Handling and Extending of Semen........................................ 897 Frozen Semen .......................................................... 900 Shipping Semen, and Insemination of the Cow ........................... 904 Artificial Insemination in the Horse....................................... 911xii VETERINARY OBSTETRICS Artificial Insemination of Swine................................. 916 Artificial Insemination of Sheep and Goats.................. 920 Artificial Insemination of Dogs ................................. 923 Artificial Insemination of Cats.................................. 925 Artificial Insemination of Other Species......................... 926 CHAPTER XX—EMBRYO TRANSFER (by M. Drost) History.......................................................... 927 Embryo Transfer in Cattle........................................ 927 Embryo Transfer in Horses........................................ 934 Embryo Transfer in Sheep and Goats .............................. 935 Embryo Transfer in Pigs.......................................... 937 Embryo Transfer in Dogs and Cats................................. 938 ADDENDUM—CURRENT (1983-1985) SELECTED SUPPLEMENTAL REFERENCES (By Chapter)............................................ 942 INDEX................................................................ 955TABLES Number Page 1. Approximate Diameters of the Female Bony Pelvis.......................... 5 2. Undifferentiated Genital Structures in the Embryo and Their Adult Male and Female Counterparts....................................................... 12 3. Size and Characteristics of the Bovine Fetus and Uterus During Pregnancy . . 19 4. Size and Characteristics of the Equine Fetus and Uterus During Pregnancy .. 27 5. The Diploid Chromosome Number of Domestic Animals....................... 51 6. Sex Ratios in Domestic Animals.......................................... 102 7. Duration of Pregnancy in Animals............................................ 105 8. Composition of Milk in Domestic Animals................................. 117 9. Summary of Causes of Abortion in Cattle.............................. 127 10. Summary of Causes of Abortion in Horses.............................. 163 11. Summary of Causes of Abortion in Swine............................... 180 12. Summary of Causes of Abortion in Sheep and Goats ........................... 193 13a. Summary of Causes of Abortion in Dogs................................. 207 13b. Summary of Causes of Abortion in Cats................................. 211 14. The Differential Diagnosis between Hydrallantois and Hydramnios in Cattle 225 15. Relative Incidence of Fetal Monstrosities................................... 335 16. Developmental States in the Maturation of the Ovum...................... 418 17. The Reproductive Cycle of Domestic Animals.............................. 427 18. Cultural Characteristics of Common Vibrios.................................. 457 19. Summary of Reports of the Manual Removal of the Corpus Luteum in Nonpregnant Cows............................................................. 505 xiiiXIV VETERINARY OBSTETRICS Number Page 20. Incidence of Gross Lesions of the Uterine Tubes.......................... 535 21. A Frequency Distribution Graph of the Monthly Percentage of Ovulation in Mares......................................................................583 22. Outline of Spermatogenesis in the Bull, Boar and Ram...................... 765 23. Semen Characteristics in Domestic Animals................................. 772 24. An Approximate Guide to the Frequency of Service and the Number of Females Allotted to Male Domestic Animals................................. 775 25. Summary of Reports on the Comparative Incidence of Testicular Tumors in Dogs...................................................................... 835 26. Sperm Cell Concentration and Semen Color in Bulls and Rams................ 874 27. Superovulation Treatments in the Cow...................................... 928FIGURES Number Page 1. Pelvices of Domestic Animals........................................... 4 2. Nonpregnant Uterus of the Cow.......................................... 7 3. Uterus of the Cow...................................................... 7 4. Genital Organs of the Mare............................................. 7 5. Nonpregnant Uterus of the Mare......................................... 7 6. Bovine Ovaries ........................................................... 8 7. Equine Ovary.............................................................. 8 8. Equine Ovaries............................................................ 8 9. Porcine Ovaries........................................................... 8 10. Genital Organs of the Sow................................................. 10 11. Uterus of a Cow 60 to 70 Days Pregnant.................................. 17 12. Twin, Bicomual Bovine Pregnancy......................................... 17 13. Uterus of a Cow 60 to 70 Days Pregnant.................................. 18 14. Two-Months-Old Bovine Fetus in Its Membranes.............................. 18 15. Uterus of a Mare 60 Days Pregnant......................................... 28 16. Diagram of the Fetal Blood Circulation.................................... 40 17. Placentome of the Ewe..................................................... 45 18. Placentome of the Cow..................................................... 45 19. Normal Placenta of a Cow................................................ 46 20. Adventitious Bovine Placentae............................................. 46 21. Zonary Canine Placenta ................................................... 46 xvXVI VETERINARY OBSTETRICS Number Page 22. Diagramatic Modification of Grosser’s Classification of the Placenta of Domestic Animals (after Bjorkman)......................................... 47 23. Brachycephalic Hereford Dwarfs............................................ 54 24. Spastic Syndrome, “Stretches,” in a Holstein Cow.......................... 55 25. Syndactyly in a Holstein Calf............................................. 55 26. Spastic Paresis in a Holstein Calf........................................ 55 27. Congenital Dropsy and Anasarca in an Aborted Ayrshire Fetus............... 55 28. Congenital Dropsy or Edema in an Ayrshire Calf............................ 56 29. Cerebral Hernia in an Overtime Holstein Fetus ...................... 56 30. Skulls of a Normal Calf and One with a Cerebral Hernia.................... 56 31. “Bulldog,” Achondroplastic Ayrshire Fetus................................. 57 32. Hypotrichosis Congenita in a Guernsey Calf................................ 57 33. Guernsey Fetus with Adenohypophysial Hypoplasia .......................... 57 34. Epitheliogenesis Imperfecta in a Pig...................................... 58 35. False Masculine Porcine Hermaphrodite..................................... 73 36. False Masculine Bovine Hermaphrodite...................................... 74 37. False Masculine Equine Hermaphrodite...................................... 74 38. Diphallus or Double Penis in a Bull....................................... 75 39. Hydrocephalus in a Feline Fetus .......................................... 76 40. Anasarca or Edema of a Canine Fetus....................................... 76 41. Cyclopia or Cebocephalus in a Holstein Calf............................... 77 42. Skulls of Normal and Cebocephalic Calves.................................. 77 43. A Bovine Schistosomus Reflexus Monster.................................... 78 44. A Bovine Perosomus Elumbis Monster........................................ 79 45. A Bovine Perosomus Horridus Monster ...................................... 79 46. A Porcine Double Monster.................................................. 79FIGURES xvii Number P'dgc 47. Amorphus Globosus on a Cow’s Placenta................................... 80 48. Yolk Sac Remnant on a Mare’s Placenta................................... 80 49. A Bovine Amorphus Globosus................................................ 80 50. A Holocardius Bovine Monster.............................................. 80 51. A Parasitic Limb Attached to a Calf..................................... 81 52. Ectopia Cordis in a Calf................................................ 81 53. An Ovine Monster........................................................ 81 54. Amelia in a Jersey Calf................................................... 82 55. A Freemartin Genital Tract................................................ 98 56. Clinical Diagnosis of a Freemartin........................................ 98 57. XX and XY White Blood Cells from a Chimeric Bull, Cotwin to a Freemartin................................................................ 99 58. Udder and Subcutaneous Edema in a Heifer................................. 114 59. Embryonic Death of One of Twin 35-Day Zygotes............................ 137 60. Fetal Resorption 60 Days Postconception.................................. 137 61. Pustular Vulvovaginitis in a Heifer Due to 1BR-IPV Virus............ 138 62. Nodular Chronic Lesions of the Fetal Liver in Epizootic Bovine Abortion . . . 139 63. Aspergillus fumigatus Mold on the Skin of an Aborted 7-Month Bovine Fetus 146 64. Aspergillus fumigatus Mold Infection of the Equine Fetal Placenta........ 147 65. Chronic Ergot Poisoning of a Pregnant Jersey Cow......................... 147 66. Torsion of the Umbilical Cord of a Bovine Fetal Cadaver Undergoing Early Mummification............................................................ 147 67. Lesions of the Liver and Lung from an Aborted Equine Fetus with Herpesvirus Infection ................................................... 167 68. Intranuclear Inclusion Body in an Equine Fetus Aborted Due to Herpesvirus 167 69. Torsion of the Umbilical Cord Causing Death and Abortion of an Equine Fetus.................................................................... 168xviii VETERINARY OBSTETRICS Number Page 70. Toxoplasma gondii Abortion in Ewes: Toxoplasma Bodies in the Fetal Cotyledon.............................................................. 168 71. Mummification of Twin Bovine Fetuses................................... 214 72. Removal by Cesarean Section of a 7-Month Bovine Mummified Fetus........ 214 73. Mummification of a Bovine Fetus Due to Displacement of the Umbilical Cord....................................................................214 74. Porcine Fetal Death and Mummification.................................. 215 75. Maceration of a 4-Month-Old Bovine Fetus............................... 218 76. Bones of a 6-Month-Old Macerated Bovine Fetus in the Uterus.......... 218 77. Hydrops Allantois in a Jersey Cow...................................... 224 78. Rupture of the Prepubic Tendon in a Cow................................ 224 79. Impending Rupture of the Prepubic Tendon in a Mare..................... 229 80. Rupture of the Prepubic Tendon in a Mare............................... 229 81. A Massive Hematoma Cranial and Dorsal to the Bovine Udder, Resembling a Rupture of the Prepubic Tendon....................................... 229 82. Prolapse of the Vagina in a Heifer..................................... 235 83. Prolapse of Vagina, Including the Bladder, in a Cow.................... 235 84. Prolapse of the Vagina, Cervix and Rectum in a Cow..................... 235 85. A Technique for the Control of Chronic Prolapse of the Vagina.......... 239 86. Normal and Abnormal Presentations, Positions and Postures in Bovine and Equine Births.......................................................... 284 87. Bovine and Equine Obstetrical Instruments.............................. 292 88. Procedures Followed in Mutation of Deviated Fetal Extremities.......... 302 89. Dystocia Due to a Tranverse Presentation in a Bitch.................... 327 90. Normal Dorso-Pubic Position of an Equine Fetus Late in Gestation....... 327 91. Ascites and Anasarca in a Bovine Fetus................................. 334 92. An Anasarcous Bovine Fetus............................................. 335FIGURES xix Number Page 93a. Diagram of a Normal and Twisted Bovine Uterus and Vagina................... 339 93b. The Schaffer Method for Correction of Uterine Torsion...................... 339 94. Bilateral Peroneal Nerve Injury and Paralysis.............................. 356 95. Rupture of the Gastrocnemius Muscle........................................ 357 96. Rupture of the Rectum, Vagina and Perineum of a Mare....................... 358 97. Transverse Rupture of an Isolated Uterine Horn Containing Canine Fetuses . . 358 98. Uterine Prolapse in a Hereford Cow......................................... 362 99. 100. Surgical Technique for Amputation of a Prolapsed Uterus in a Cow .... 366 101. Dislocation of the Sacroiliac Articulation in a Cow....................... 395 102. Diagram of the Neuroendocrine Control of Reproduction in Female Animals 400 103. Heifer in Standing Estrum ................................................ 411 104. Normal Genital Tract of a Heifer in Estrum............................... 411 105. Granular Venereal Disease in a Heifer.................................... 469 106. Bovine Genital Tuberculosis............................................... 473 107. Cysts of the Bovine Ovary................................................ 479 108. Cystic Ovaries (Follicular Cysts) in a Cow............................... 479 109. A Central Luteal Cyst in a Bovine Ovary.................................. 479 110. Bovine Luteal Cysts Associated with Superovulation....................... 480 111. A Bovine Cystic Corpus Luteum............................................. 480 112. A Chronic Cystic Ovary Associated with a Unilateral Mucometra............. 484 113. Cystic Endometrial Glands Caused by Cystic Ovaries........................ 486 114. A “Sterility Hump” in a Cow Associated with Chronic Cystic Ovaries....... 486 115. A Steer-Like Appearance of a Cow with Chronic Cystic Ovaries.............. 486 116. Anestrus Associated with Segmental Aplasia of the Bovine Uterus, Mucometra, Mucocervix and a Retained Corpus Luteum....................... 496XX VETERINARY OBSTETRICS Number Page 117. Congenital Absence of Endometrial Glands in a Heifer with Anestrus and a Retained Corpus Luteum.................................................... 496 118. Bilateral Total Hypoplasia of the Ovaries in a 3-Year Holstein Cow....... 510 119. A “Smooth” Inactive Ovary Seen Bilaterally in Debilitated, Anestrous Heifers or Cows........................................................... 511 120. Uterus Didelphys with Unilateral Cystic Dilation of the Left Cervix and Mucometra of the Left Uterine Horn........................................ 522 121. White Heifer Disease with a Marked Aplasia of the Vagina, Cervix and Uterus.....................................................................523 122. Segmental Aplasia of the Cervix with Secondary Hydrometra in a Heifer. . . . 523 123. Double External Os of the Cervix Due to the Persistence of the Median Wall of the Paramesonephric Ducts ............................................. 524 124. White Heifer Disease with an Imperforate Hymen Causing Mucovagina, Mucocervix and Mucometra.................................................. 524 125. Uterus Unicornis in a Cow........................................‘....... 524 126. Uterus Unicornis with a Cystic Apex Containing Bodies of Inspissated Mucus......................................................................525 127. Segmental Aplasia of the Base of the Right Horn Resulting in an Accumulation of Inspissated Mucus......................................... 525 128. Segmental Aplasia of Both Uterine Horns and Cervix in a Heifer.......... 526 129. Cystic Gartner’s or Mesonephric Ducts in the Floor of the Vagina.......... 529 130. Bilateral Granulosa Cell Tumors of the Ovaries in a Cow................... 534 131. Bilateral Hydrosalpinges with Adhesions Around the Left Ovary............. 534 132. Ovarian Adhesions and Hydrosalpinx in a Cow............................... 536 133. Intramucosal Cysts or Cysts of the Diverticula of the Bovine Oviduct...... 536 134. Some Common Instruments Used in the Treatment of Infertility in the Cow and Mare.................................................................. 542 135. Chronic Postpartum Metritis and Pyometra Due to Inspissated Necrotic Cotyledons and Caruncles.................................................. 546 136. Extensive Perimetritis and Ovaritis with Adhesions Following a Severe Metritis After an 8-Month Abortion....................................... 548FIGURES xxi Number Page 137. Abscess of the Uterine Wall............................................. 548 138. Ectropion of the External Cervical Os................................... 549 139. Lymphosarcoma of the Bovine Uterus...................................... 549 140. Adenocarcinoma of the Bovine Uterus ................................... 550 141. Atresia of the Internal Os of the Bovine Cervix Secondary to an Acute Cervicitis ............................................................ 553 142. A Horizontally-Tipped Abnormal Vulva Causing Pneumovagina in a Cow . . . 553 143. Carcinomas of the Vulva of a Cow....................................... 554 144. An Anomaly or Wattle Present on the Vulva of a Heifer.................. 554 145. Ovaries of a 5-Month-Old Equine Fetus.................................. 599 146. Appearance of the Perineal Region of a Mare with Pneumovagina.......... 600 147. Coital Vesicular Exanthema or Genital Horse Pox in a Mare.............. 618 148. Granulosa Cell Tumor of the Mare’s Ovary............................... 619 149. Squamous Cell Carcinoma of the Vulva of a Mare......................... 619 150. Persistent Hymen in a Filly ........................................... 623 151. Parovarian Cysts in a Ewe.............................................. 660 152. Pyometra in a Bitch.................................................... 719 153. Segmental Aplasia of the Uterine Homs with Mucometra in a Bitch........ 719 154. Segmental Aplasia of the Right Horn with Mucometra in a Queen ...... 719 155. Uterus Unicornis in a Bitch............................................ 719 156. Cystic Ovaries from a Bitch............................................ 720 157. Cystadenoma of a Feline Ovary.......................................... 720 158. Granulosa Cell Tumor of a Canine Ovary................................. 721 159. The Genital Organs of the Bull......................................... 754 160. The Urogenital System of the Boar...................................... 755 161. The Uterus Masculinus in a Bull........................................ 756xxii VETERINARY OBSTETRICS Number Page 162. Diagram of the Neuroendocrine Control of Reproduction in the Male Animal 761 163. Diagram of the Ultrastructure of the Sperm Cell.......................... 767 164. Diphallus in a Bull...................................................... 794 165. A Spiral or Corkscrew Deviation of the Penis of an Angus Bull............ 795 166. A Ventral or “Rainbow” Deviation of the Penis of a Hereford Bull ........ 796 167. A Persistent Frenulum, A Cause of Deviation of the Bovine Penis.......... 796 168. Tearing of the Prepuce from its Attachment to the Gians Penis in a Bull .... 797 169. A Chronic Abscess Causing Severe Phimosis in a Bull...................... 797 170. Transmissible Fibropapilloma of the Penis in a Young Bull................ 799 171. Squamous Cell Carcinoma of the Penis and Sheath in a Stallion............ 799 172. Chronic Prolapse and Stenosis of the Preputial Orifice of a Santa Gertrudis Bull...................................................................... 801 173. Chronic Granular Venereal Disease Lesions of the Bovine Penis and Sheath 803 174. Dislocated Hip in a Jersey Bull........................................ 804 175. Spastic Syndrome or “Stretches” in a 8-Year-Old Holstein Bull............ 804 176. Bilateral Testicular Hypoplasia in a Fat 3-Year-Old Angus Bull........... 816 177. Bilateral Testicular Hypoplasia in a 2-Year-Old Holstein Bull............ 816 178. Abnormal Acrosomes or Knobbed Spermatozoa in a Sterile Bull.......... 816 179. Lack of Intact Sperm Cells and Coiled Tails in a Sterile Guernsey Bull.. 816 180. Abnormal Attachment of the Cremaster Muscle to the Left Testis Causing a Nearly Horizontal Position of the Testis High in the Scrotum............. 823 181. Left Inguinal Hernia in a Bull........................................... 823 182. Scrotal Dermatitis and Edema in a Bull Secondary to Chorioptic Mange .... 827 183. Varicoceles of the Spermatic Vein in a Ram............................... 828 184. Acute Orchitis of the Right Testis in a Holstein Bull.................... 830 185. Acute Orchitis and Periorchitis Secondary to a C. pyogenes Infection.... 830FIGURES xxiii Number Page 186. Longitudinal Section of a Normal Bovine Testis.......................... 831 187. Testis with Advanced Testicular Degeneration, Fibrosis and Calcification. . . . 831 188. Advanced Testicular Degeneration, Fibrosis and Atrophy.................. 831 189. Sperm Granuloma and Fibrosis of the Tail of the Epididymis in a Ram Due to the R.E.O. Agent...................................................... 831 190. Edema of the Scrotum Associated with Equine Infectious Anemia............ 832 191. Interstitial Cell Tumors of a Bovine Testis.............................. 833 192. Sertoli Cell Tumor of a Bovine Testis.................................... 833 193. Testicular Abscesses in a 3-Month-Old Calf............................... 834 194. Segmental Aplasia of the Ductus Deferens with Dilation of the Ampulla with Semen in a Bull.......................................................... 844 195. Aplasia of the Right Ampulla, Ductus Deferens and Seminal Vesicle in a Bull..................................................................... 844 196. Seminovesiculitis in a Bull.............................................. 848 197. Ejaculates Containing Pus from a Bull with Seminovesiculitis............. 848 198. Normal Bovine Spermatozoa................................................ 879 199. “Primary” Spermatozoan Abnormalities..................................... 880 200. “Secondary” Spermatozoan Abnormalities................................... 881 201. Miscellaneous Cells Found in Semen ...................................... 882 202. Normal Bovine Spermatozoa................................................ 883 203. Normal Canine Spermatozoa ............................................... 883 204. Proximal Protoplasmic Droplets in Bull Spermatozoa....................... 883 205. Coiled Tails and Middlepieces in an Infertile Guernsey Bull ............. 883 206. Diagrams of Normal Bovine Embryos........................................ 931CHARTS Number Page I. Pregnancy Wastage in Domestic Animals................................... 126 Ila. Hormones Used Effectively for the Induction of Parturition............. 249 b. Condition of the Fetus and Maternal Endometrium and Response to Hormonal Induction of Parturition in the Cow.............................. 249 III. A Schematic Summary of Endocrine, Behavioral, Cytological and Mucosal Changes during the Canine Estrous Cycle................................... 677 IV. A Schematic Representation of Endocrine Changes Occurring during the Nonpregnant Canine Ovarian Cycle.......................................... 681 V. Events of Canine Pregnancy Timed in Relation to LH Peak and Fertile Matings...................................................................684 VI. A Schematic Representation of Endocrine Changes during the Canine Estrous Cycle, Pregnancy and Lactation and Their Relation to Time of Breeding, Pregnancy Diagnosis and Gestation Length.................................. 685 VII. Antinidatory Injectable Estrogen Treatments for Mismated Bitches........ 692 VIII. A Schematic Representation of Endocrine Changes during Estrous Cycles, Pregnancy or Pseudopregnancy in Queens.................................... 701 IX. Induction of Estrus in Queens by PMSG.................................. 706 XXIVPREFACE This third edition has engendered in the author a sense of enormous humility and gratitude. Humility in the re- alization of the great efforts, expenditures, honesty, study and research of innumerable persons who have contrib- uted to all aspects of this broad interdisciplinary subject of reproduction an animals and man. The number and breadth of the selected references reviewed by the author has been an enriching experience and attests to the will- ingness of those in this field to share and advance the accumulated and new knowledge. As one of my former professors remarked, “Everything I know has been built on research and knowledge of other persons.” This current field of reproduction has a strong heritage going back over 60 years to studies by W. L. Williams, Nils Lagerlof, E. C. Amoroso, F. Benesch, C. G. Hart- man, A. S. Parkes and L. E. Casida. In more recent times the tradition of excellence has been carried on by: K. McEntee, M. G. Fincher, R. Zemjanis, Wm. Han- sel, H. H. Cole, P. T. Cupps, L. E. McDonald, O. J. Ginther, G. H. Arthur, M. Vandeplassche, J. Hughes, W. B. Pickett, R. H. Foote, W. R. Allen, D. A. Mor- row, E. S. E. Hafez, L. Ball, E. L. Squires, M. Drost, and many others to whom we all owe a sincere and con- tinuing debt. In this third edition the author is pleased to be able to include the reviews and insights of his colleagues, Don- ald H. Lein, R. H. Foote and M. Drost who have con- tributed Chapters XVII, XIX and XX on Infertility in Bitches and Queens, Artificial Insemination, and Em- bryo Transfer, respectively. With my retirement from Cornell University in 1972 and entering a busy general practice with my brother James F. Roberts in Wood- stock, Vermont, it was impossible to keep fully abreast with the progress and literature within these three fields so graciously and competently reviewed by these con- tributing authors. For the rest of the text the author takes full respon- sibility for its’ shortcomings in English grammar and ex- position. His primary concern was the organizing, doc- umenting and abstracting of new and pertinent knowledge and fitting it into the framework of his first and second editions. “The printed word is not the truth nailed down, it is the author.”* At the suggestion of my professional colleagues, the author has removed nearly all individual names of researchers and reviewers from the text and replaced them with reference numbers. He hopes this will improve the readibility of the text without detracting from the importance of the individuals’ contribution. This third edition was a challenge and a goal that nearly overwhelmed the author by the enormous increase in published material. Fortunately his health and eyes have remained excellent due to his wife’s food, ministrations and understanding that have enabled him to spend the many hours of necessary reading, filing and writing. The author has purposely not tried to simplify, elim- inate controversial material, or omit any phase of the subject that concerns itself with veterinary obstetrics or genital diseases of domestic animals. This book was written for veterinary undergraduates and those practi- tioners who are still students. The layman was not con- sidered, as to do so would make the text less satisfactory for its intended readers. The author has stressed diag- nosis and physiology throughout the text because he feels these phases are of greatest concern for veterinarians. An accurate diagnosis often requires an extensive knowl- edge of the field and of all the possible conditions that may be responsible for certain symptoms. As Bertillon, the famous French detective said, “One can only see what one observes, and one observes only things which are already in the mind.” Students might prefer a streamlin- ing of information such as befits a core course. But each case in practice is different and a breadth of specific knowledge, skill and the art of its applications are es- sential. This text would not have been possible without access over the years to the outstanding Flower Veterinary Li- brary at Cornell and its skilled, pleasant and cooperative librarians. The author must also extend his appreciation to Dr. Kenneth McEntee, his respected colleague, who was a source of knowledge in reproductive pathology, *From Fischer, M. FI., Professor of Physiology, University of Cin- cinnati. XXVXXVI VETERINARY OBSTETRICS and also a source of illustrative material both of which were freely offered. My brother Jim and his wife, Dot, must be thanked for graciously and at a sacrifice allow- ing him extended “sabbatics” to work uninterruptedly at the New York State College of Veterinary Medicine at Cornell in the winters of 1981-1982 and 1982-1983. Ms. Joyce Reyna deserves grateful recognition for her sec- retarial services and help, as does his printer of the past 30 years, Edwards Bros., Inc., Ann Arbor, Michigan. My past 10 years in veterinary practice in Woodstock, Vermont, has been very rewarding in personal satisfac- tion and in the realization of the many facets necessary to provide a needed service “out where the action is.” It has given me great moments of pleasure and gratifi- cation to combine my “ivory tower” knowledge and as- sociations with practical on the farm and in the office transmittal and application of this knowledge. This in- terface is the ultimate area where veterinary knowledge serves animals and man. I am grateful to have lived and worked in the veterinary profession during what may have been the “golden age” of veterinary medicine and sci- entific progress. It has been inspiring, fascinating and challenging to keep abreast of many of these advances. However it has also provided rewarding satisfaction and opportunities for service. Woodstock, Vermont S. J. Roberts January, 1986Part I INTRODUCTION Veterinary obstetrics has in the past been defined as that branch of surgery dealing with the oversight of the female animal during pregnancy and parturition. How- ever, with our increased knowledge of genital diseases of female and male animals, the study of veterinary ob- stetrics has expanded to include the latter highly impor- tant field. The livestock industry depends upon repro- duction. Any disease or pathological condition causing sterility or infertility in our domestic animals, whether it be a sporadic or enzootic condition, must be the con- cern of veterinary practitioners. The recent introduction and rapid growth of artificial insemination, and its in- herent problems, require the modem veterinarian, es- pecially in cattle practice, to be well acquainted with this field of obstetrics. The fields of reproductive physiol- ogy, endocrinology, immunology, nutrition, genetics, embryology, teratology, anatomy, virology, bacteriol- ogy, pathology, surgery, and medicine, all supply im- portant necessary links in our chain of obstetrical knowl- edge. In the broad interdisciplinary field of veterinary obstetrics and genital diseases, as in any clinical field of study, the advances made in the basic sciences must be studied, considered, and applied. For the veterinarian entering practice the importance of this field of obstetrical and genital disease cannot be overestimated. The figures from the large New York State Veterinary College Ambulatory Clinic, in which 85 to 90 percent of the animals treated are dairy cattle, show that about 25 to 30 percent of the cases treated were obstetrical or dealt with the reproductive system. These include such common conditions as dystocia, retained placenta, pregnancy examination, sterility examination and treatment, abortion, metritis, blood testing, vacci- nating for brucellosis and other abortion diseases and the treatment of many other genital conditions. From a purely business viewpoint, the volume of obstetrical work in a large animal or small animal practice is considerable. One must realize that the average layman or farmer places an undue amount of importance and significance on the successful handling of obstetrical cases and breeding problems. The young or inexperienced veterinarian may make or ruin his chances for success with a certain farmer or in a certain territory by the way in which he handles a single obstetrical case or problem. 1Chapter I FEMALE GENITAL ANATOMY AND EMBRYOLOGY The bony and ligamentous structures comprising the pelvis are of particular interest in obstetrics. The bony pelvis is composed of the sacrum, the first to third cau- dal vertebrae and the two ossa coxarum, each formed by the ilium, ischium and pubis. The sacrum is composed of five fused vertebrae in the cow. It is somewhat triangular in form with the base articulating cranially with the last lumbar vertebra and caudally with the first caudal vertebra. The ventral face of the sacrum is smooth and concave. The dorsal surface exhibits the sacral spine. The wing of the sacrum artic- ulates or fuses with the ilium laterally as the sacroiliac joint. In older animals the first caudal vertebra may fuse with the sacrum in the horse, cow and pig. The ilium is irregularly triangular in shape. The broad, flat, dorsal part of the ilium is called the wing. The me- dial portion of the wing is called the tuber sacrale and its ventral medial aspect articulates with the sacrum. The external portion of the wing of the ilium is called the tuber coxae, hip bone, or “hook” bone. Dorsally the wing of the ilium in the horse, cow, sheep and pig is concave, providing attachment for the gluteal and back muscles. Ventrally the wing is convex. In the dog and cat the wing of the ilium is rotated laterally so it lies nearly par- allel to spinal column. The narrow, ventral part of the ilium is called the body. This bone fuses ventrally with the ischium and pubis at the acetabulum. Its medial or pelvic surface is smooth and is grooved for the obturator vessels and nerve. The ischium forms the caudal part of the ventral floor of the pelvis. Its dorsal surface is smooth and rather con- cave. The caudal border of the ischium slopes inward and forward to join with the opposite ischium to form the ischiatic arch. The caudal lateral portion of these bones is called the ischiatic tuberosity or “pin” bone. The is- chiatic tuberosity in the pig is largely cartilaginous in nature and the symphysis does not undergo complete an- kylosis until 6 or 7 years of age. The cranial border of the ischium forms the caudal margin of the obturator fo- ramen. Dorsally the ischium bears the ischiatic spine, cranial and caudal to which are the greater and lesser sciatic notches respectively. These notches become fo- raminh when the sacrosciatic ligament completes their boundaries. The ischiatic spines are prominent in the sow and cow. Medially the ischium and pubis fuse to form the pelvic symphysis. In the cow and ewe the portion of the pelvic floor formed by the two ischia is deeply con- cave from side to side. The pubis is the smallest of the three bones of the os coxae and forms the cranial portion of the pelvic floor. The dorsal or pelvic surface is smooth and usually con- cave in females, while in males it may be convex. Oc- casionally in the young cow a sharp tuberosity projecting into the pelvic canal is present on the cranial portion of the pubic symphysis. This prominence may rarely cause contusion or even laceration of the birth canal during a difficult birth. The cranial medial border of the pubic bone provides attachment for the prepubic tendon. The caudal border forms the cranial border of the obturator foramen. The acetabulum is formed by the fusion of the ilium, ischium, and pubis. These bones form a cotyloid cavity lodging the head of the femur. The acetabulum consists of articular and non-articular portions. The acetabular notch is made into a foramen by the transverse ligament and transmits the accessory ligament to the head of the femur in the horse. The ligament of the femoral head is a short, strong band between the head of the femur and the acetabulum. There are three, single or paired, pelvic ligaments that maintain the relationship of the pelvis to the spinal col- umn. (1) The dorsal and lateral sacroiliac ligaments, which are attached to the medial wing of the ilium and lateral portion of the sacrum and the summits of the sa- cral spines. This articulation is very firm and rigid and is further maintained and supported by the sacrosciatic ligament and prepubic tendon. (2) The sacrosciatic lig- ament is an extensive quadrilateral aponeurosis that completes the lateral wall of the pelvic cavity. The lig- ament extends from the lateral border of the sacrum and the transverse processes of the first two caudal vertebrae to the ischiatic spine and tuber ischii. It furnishes at- tachment for the large gluteal muscles and the vulva. In the dog this ligament, called the sacrotuberous ligament, 34 VETERINARY OBSTETRICS Figure 1. Pelves of the domestic animals.ANATOMY 5 is a narrow strong band extending from the caudal part of the lateral margin of the sacrum to the tuber ischii. (3) The prepubic tendon is essentially the tendon of in- sertion of the rectus abdominis muscle. It is attached strongly to the cranial border of the pubic bones. The pelvic cavity is somewhat cone-shaped, with the base of the cone located cranially. This base is formed by the bony pelvis. The pelvic inlet is roughly oval in shape in all species, with the largest diameter being sacro- pubic. The size of the pelvic inlet varies greatly within a species due to breed, age and size. The sow and cow have the most elliptical pelvic inlets; while the mare and some dogs have nearly round inlets. (See Figure 1) The approximate diameters of pelves of domestic animals are given in Table 1. Table 1. Approximate Diameters of the Female Bony Pelvis Species Sacro-pubic cm Iliac cm Mare 20.3-25.4 19.0-24.1 Cow 19.0-24.1 14.6-19.0 Sheep 7.6-10.8 5.7- 8.9 Sow 9.5-15.2 6.3-10.2 Bitch 3.3- 6.3 2.8- 5.7 In our larger domestic animals the cross section of the fetal chest or hips may be greater in diameter than the maternal pelvic inlet but birth is possible by the dis- placement and realigning of the fetal parts at the time of parturition. The caudal portion of the pelvic cavity is smaller than the cranial portion formed by the bony pel- vis but the caudal portion at the time of parturition di- lates markedly to allow the passage of the fetus. This ability to dilate is brought about by the relaxation of the pelvic ligaments, especially the sacrosciatic ligament. This relaxation in the cow is an obvious indication of ap- proaching parturition. The pelvis of the male domestic animal differs from the female in a number of definite points. The diameter of the pelvic inlet is smaller in the male and the ischiatic arch is usually narrower. The pelvic cavity is smaller and less roomy than in the female. The obturator foramen is smaller in the male. The cranial floor of the pelvis is more apt to be convex in the male while it is usually concave in the female. The bones of the pelvis are thicker and heavier in the male. The pelvis of the male castrated at an early age resembles that of the female. These dif- ferences are most noticeable in the larger domestic an- imals. The comparative differences, other than size, between the pelves of the various animals should be noted. In the mare the transverse or iliac and sacro-pubic diameters are nearly alike, making the pelvic inlet almost spheri- cal. The coxal tuberosities are large and prominent and the wings of the ilia are nearly perpendicular to the long axis of the body. In the cow the ischial tuberosities are prominent and high. The ilia and coxal tuberosities are smaller than in the mare. The pelvic inlet is more el- liptical than in the mare. The pelvis of the ewe is similar to the cow in the shape of the inlet but the wings of the ilia are more nearly parallel to each other and the tubera ischii are relatively much smaller. In the sow the pelvic inlet is long and narrow. The wings of the ilia are not prominent and large, as in the cow and mare. The sym- physis pubis in the sow is thicker and does not undergo complete ankylosis. The tubera ischii are not completely ossified. In the bitch the wings of the ilia are small and nearly parallel with the median plane. The ischium has a twisted appearance, since the caudal part is nearly hor- izontal. The pelvis of the queen is similar to that of the bitch but has a relatively larger obturator foramen. The coxo-femoral articulation is a ball-and-socket joint with the head of the femur fitting into the acetabular fossa made deeper by the cotyloid ligament. This is a fibrous band circling the acetabular fossa. The transverse ace- tabular ligament crosses the acetabular notch. The lig- ament of the femoral head extends from the subpubic groove in the acetabulum to the head of the femur and is intra-articular. In occasional cases this ligament may be small or absent. The increased frequency of hip joint or coxo-femoral dislocation in the cow is due to the shallowness of the acetabulum, lack of bulky muscle around the joint, the small, or occasionally absent, ligament of the femoral head, absence of the accessory ligament present in the mare, the awkward gait, excessive relaxation of the pel- vic ligaments in advanced pregnancy and with cystic ovaries, and the large size and weight of the abdomen in advanced pregnancy, twin pregnancy and hydrops of the fetal membranes. The Ovaries and Female Genital Tract The generative organs of the female consist of the ovaries and the tubular portion of the reproductive tract including the oviducts or uterine tubes, uterus, cervix and the cranial portion of the vagina arising from the primitive Mullerian or paramesonephric ducts. The vulva, vestibule and the caudal portion of the vagina develop from the urogenital sinus. The ovaries consist of a stroma or network of con-6 VETERINARY OBSTETRICS nective tissue and blood vessels surrounded by a cov- ering of peritoneum except at the attached border or hilus where the vessels and nerves enter. Within the ovary are interstitial cells, primitive ova, developing or secondary ova or follicles, maturing or mature Graafian follicles, atretic or degenerating follicles, and developing, mature or degenerating corpora lutea. The ovary is supported and attached by the portion of broad ligament called the mesovarium dorsally and laterally and by the proper lig- ament of the ovary medially. Ovaries increase in size as the animal becomes older. The blood supply to the ovary is from the ovarian artery. Varying degrees of anasto- moses between the ovarian and uterine arteries as well as the close apposition of the tortuous ovarian artery and the utero-ovarian vein in most domestic animals, except the mare, result in a local venoarterial pathway for pros- taglandins from the endometrium to induce luteolysis.2,8 The nerve supply is the autonomic nerves from the ovar- ian plexus that arises from the renal and aortic plex- 7 12 r uses. ’ In the cow the ovaries are oval in shape and vary in size from 1.3 to 5 cm. in length, 1.3 to 3.2 cm. in width and 0.6 to 1.9 cm. in thickness. The right ovary is usu- ally slightly larger than the left, since it is physiologi- cally more active. Ovarian weight varies from 5 to 15 gm. per ovary with the average weight of both ovaries in cattle of all ages being 19.5 gm.6 The size of the ovary varies depending upon the structures present either cor- pora lutea or follicles. The bovine ovaries are located on the cranial border of the broad ligament, occasionally under it, on the ventral lateral floor of the pelvis near, on, or slightly cranial to the pelvic inlet and slightly cra- nial and lateral to the internal os of the cervix. The pocket formed by the proper ligament of the ovary and the me- sovarium is called the ovarian bursa. In the dog the me- sosalpinx forms the bursa. The mature Graafian follicle is usually about 1.0 to 2.0 cm. in diameter and smooth, convex, thin-walled, and fluctuates on palpation. The corpus luteum is usually about 1.9 to 3.2 cm. in diam- eter and may comprise up to three-quarters of the size of the ovary. The corpus luteum of pregnancy and the mature corpus luteum of the estrous cycle weigh from 3 to 9 gms. or an average of 5 to 6.5 gm. Its consistency is liver-like. It is usually, but not always, irregular in outline with a protrusion or crown that may be variable in size, from 0.5 to 1.5 cm. in diameter extending 0.5 to 1.0 cm. above the surface of the ovary. About 3 to 5 days after ovulation the corpus luteum can be recognized by rectal palpation. About three days before the next ovulation the corpus luteum begins to regress in size, gradually atrophies and is replaced by connective tissue, the corpus albicans. The corpus albicans replacing the corpus luteum of pregnancy is large, 2 to 5 mm., and persists indefinitely. These structures tend to make old cows’ ovaries feel quite fibrous and roughened. The po- sition of the ovary in the cow varies with the stage of pregnancy or with the size and contents of the uterus. During pregnancy the ovary tends to be drawn down- ward and forward into the abdominal cavity. In older, pluriparous cows the ovaries and non-pregnant uterus often lie over the brim of the pelvis on the caudal floor of the abdominal cavity. Usually by the fourth or fifth month of pregnancy the ovaries are drawn forward out of reach of the hand on rectal palpation. (See Figures 2, 3 and 6). In the mare the ovaries are bean-shaped and vary in size from 4 to 8 cm. in length, 3 to 6 cm. in width and 3 to 5 cm. in thickness and weigh 30 to 90 gm. They are suspended in the abdominal cavity by the mesovari- um or cranial portion of the broad ligament. The ovaries are 5 to 7.5 cm. dorso-lateral to the uterine horns and joined to them by the proper ligaments. A few or several developing follicles 1.3 to 6.3 cm. in diameter may be present in one or both ovaries. Occasionally follicles may reach a size of 7.5 to 10.0 cm. in which case the ovary is temporarily greatly enlarged. The corpus luteum in the mare is about 2 to 3 cm. in diameter within the substance of the ovary. It can be palpated several days after ovu- lation as a small protrusion in the region of the ovulation fossa and for about 7 days as a pear-shaped structure, liver-like in consistency. It does not project above the surface of the ovary because of the dense, thick tunica albuginea investing the ovary of the mare. The free bor- der or concave portion of the ovary in the mare is spoken of as the ovulation fossa. (See Figures 4, 5 and 7). In the ewe the ovaries are almond-shaped, about 1.3 to 1.9 cm. long resembling those in the cow. In the sow the ovaries are oval in shape about 4 to 5 cm. long, weighing 3.5 to 12 gm., but in maturity having a mulberry-like appearance due to multiple fol- licles, and/or corpora lutea. Porcine ovarian follicles are normally about 7 to 8 mm. and corpora lutea about 12 to 15 mm. in diameter. The location of the ovaries in gilts is approximately the same as in the cow. Due to the long broad ligament, the location of the ovaries in the abdominal cavity in older sows is variable. The sow’s ovaries are almost completely covered in the ovarian bursae by the mesosalpinx. In the bitch and queen the ovaries are oval in shape, 1.0 to 3 cm. in length, 0.7 to 1.25 cm. in width and 0.5 to 0.75 cm. in thickness and firmly fastened just beneath the third and fourth lumbar vertebrae, 1 to 4 cm. caudal to the corresponding kidney. The ovaries are concealed in the ovarian bursae which have a 0.6 to 2.0 cm. slit-ANATOMY 7 Figure 2. Nonpregnant uterus of the cow, cranial aspect. 1. Cervix, 2. Body of uterus, 3. Horn of uterus, 4. Uterine tube, 5. Ovaries, 6. Ovarian ventricle, 7. Corpus luteum, 8. Intercomual ligament, 9. Rectum. Figure 4. Genital tract of the mare. 1. Vulvar lips, 2. Clitoris, 3. Vestibule, 4. Urethral orifice, 5. Vulvovaginal fold, 6. Vagina, 7. Frenulum, 8. Cervix, 9. Body of uterus, 10. Homs of uterus, 11. Mesometrium, 12. Uterine tube in mesosalpinx, 13. Fimbria of uter- ine tube, 14. Ovary. Figure 3. Uterus of cow, dorsal aspect. 1. Ovarian bursa, 2. Ovary, 3. Corpus luteum, 4. Follicle, 5. Corpus albicans, 6. Uterine tube, 7. Uterine hom, 8. Uterine body, 9. Cervix, 10. Vagina. Figure 5. Nonpregnant uterus in the mare. 1. Uterine horns, 2. Uter- ine body, 3. Ovaries, 4. Uterine tube, 5. Rectum.8 VETERINARY OBSTETRICS Figure 6. Bovine Ovaries—The right ovary contains 2 corpora lutea and an atretic follicle. Left ovary is small since a double ovulation occurred in the right ovary about 6 days ago. like opening medially.5 The wall of the ovarian bursa in the bitch usually contains fat. The ovary in the bitch and queen, like that of the sow may be mulberry-like in ap- pearance due to multiple follicles or corpora lutea. The corpora lutea contain no pigment. In the queen, the ovaries are similar to the bitch but are suspended more ventrally in the abdominal cavity. The ovarian bursa contains no fat. The tubular genital tract develops from the primitive paramesonephric (Mullerian) duct system. These prim- itive ducts, two in number, unite caudally in the region of the vagina, cervix and body of the uterus to form a long tube with various constructions that is modified in structure and function to protect the developing fetus. Figure 8. Ovaries of a mare bisected—Note pear-shaped follicles with narrow portion toward the ovulation fossa. The uterine tube or oviducts are about 20 to 30 cm. long and about 1.5 to 3.0 mm. in diameter in the mare and cow. They are tortuous, wiry and hard, feeling nearly cartilaginous when rolled between the fingers. They may be imbedded in fat in the mesosalpinx, a portion of the broad ligament supporting the uterine tube. The oviducts or uterine tubes are difficult to palpate on rectal exam- ination. Bimanual vaginal and rectal examination often is of assistance in palpating the uterine tube. Another technique in the cow is to slip several fingers into the ovarian bursa or ventricle and palpate the uterine tube between them and the thumb. The distal or caudal, short segment, 1 to 3 cm. in length, attached to the tip of the uterine horn is called the isthmus; while the major por- tion of the uterine tube from the isthmus to the infun- inti if f immi ! 111 • 11111111111 1" 1 « I o 1 'i a Ik 1 c Figure 7. Equine Ovary—The corpus luteum is protruding into the ovulation fossa. Note depression over CL due to loss of follicular fluid at the time of ovulation about 48 hours ago. Figure 9. Ovaries of a sow—Note mature corpora lutea and small follicles.ANATOMY 9 dibulum is called the ampulla. The diameter of the uter- ine tube at the ovarian end becomes larger, 4 to 8 mm. and the uterine tube becomes funnel-shaped, the infun- dibulum. From this funnel-shaped end of the uterine tube arises the fimbriated portion of the tube. This has a par- tial attachment to the lateral side of the ovary and to the proper ligament of the ovary medially. The uterine end of the uterine tube in the bitch and mare opens into the uterine lumen through a small slit on a mound or papilla. In the cow and ewe there is a marked flexure at the tran- sition of the isthmus with the elongated curving end of the uterine horn. The latter has a very narrow lumen. In the sow and bitch the mucosa of the uterine tube projects into the uterine lumen as folds well-supplied with blood.10,11 The uterine tube of the sow is 15 to 18 cm. long; that of the bitch and queen is 4 to 9 cm. long and has a slightly tortuous course around nearly the entire circumference of the ovarian bursa. The blood supply of the uterine tube is from the uterine and ovarian arteries. The nerve supply is the same as that of the uterus and ovary. The uterus is a muscular membranous structure de- signed for the reception of the fertilized ovum, for the nutrition and protection of the fetus, and for the initial stage of its expulsion at parturition. The form of the uterus in animals varies with the degree of fusion of the para- mesonephric ducts. The endometrium of the uterus in domestic animals is the only structure that can form suf- ficient placental attachment to result in normal devel- opment of the embryo and fetus. In uniparous animals the placenta lies against the cervix, while in multiparous animals the placenta does not touch the cervix. The mus- cular coat of the uterus is composed of smooth muscle in circular and longitudinal layers. The uterus receives its blood supply from the uterine artery, the ovarian ar- tery and a branch of the urogenital artery. Nerve supply to the uterus consists of sympathetic fibers from the lum- bar and lower thoracic region forming the uterine and pelvic plexuses. Nerve filaments from these plexuses supply the uterus, cervix, and proximal portion of the tubes. Parasympathetic fibers originate from the first to third sacral nerves and reach the plexus by way of the pelvic nerves or nervi erigentes. In the cow the uterus is comuate in shape, with the two uterine horns leaving the internal os of the cervix at an acute angle and lying nearly parallel to each other. The “uterine body” or proximal portion of the fused uterine horns with a single lumen is about 2.5 to 4 cm. long. Depending on the age and breed of the cow the horns are 20 to 40 cm. long and from 1.25 to 5 cm. in diameter in the nonpregnant state. The horns are joined by the dorsad and ventral intercomual ligaments for about one-half their length. The uterus is located either on the floor of the pelvis, on the pelvic brim, or most com- monly in parous cows over the brim on the caudal floor of the abdominal cavity. The uterus is usually dorsal or lateral to the bladder and is attached dorso-laterally by the broad ligament and the mesometrium. During preg- nancy the uterus enlarges greatly and becomes located further cranially and ventrally in the abdominal cavity. In the mare the nonpregnant uterus is cruciform or T- shaped with the horns perpendicular to the body of the uterus. The body is about equal in size to each horn, 15 to 20 cm. long, 4 to 7.5 cm. wide and 2 to 5 cm. thick. The uterus is suspended in the pelvic and abdominal cav- ities dorsal to the bladder by the broad ligaments. In the mare these ligaments are attached dorsally to the sub- lumbar region. The uterine horns in the mare lie ventral to the intercomual ligament. Unless gravid, the uterus usually does not lie on the floor of the pelvic or abdom- inal cavities. In the ewe the uterus is shaped like that of the cow and located similarly. Each horn is 10 to 12 cm. long. In the sow the uterine body is about 5 cm. long with long tortuous horns that are freely movable because of the long broad ligaments. In pregnant animals the horns may be 1.2 to 1.8 m. long.15 In the nulliparous medium-sized bitch and queen the uterus has a short body, 1 to 3 cm. long with straight horns 12 to 15 cm. long and 0.5 to 1.0 cm. in diameter that diverge at an acute angle toward the poles of each kidney. Suspended from the sublumbar region by the broad ligaments, the uterus lies entirely within the ab- dominal cavity. The cervix (cervix uteri) is a tubular sphincter muscle between the vagina and uterus. Its wall is harder, thicker, and more rigid than are the walls of either the uterus or the vagina. This is more noticeable in uniparous than in multiparous animals. The blood and nerve supply are the same as those of the uterus and vagina with the excep- tion of the ovarian artery. The cervix in the cow is about 5 to 10 cm. in length by 1.5 to 7 cm. in diameter, the larger of the measure- ments occurring in pluriparous animals. In some Brah- man or Brahman-cross, pluriparous cows the cervical di- mensions may greatly exceed these averages. The cervix is located caudal to the uterus either in the pelvic cavity, on the pelvic brim, or in the abdominal cavity. During pregnancy the cervix is drawn forward into the abdom- inal cavity. The cervix of the cow is composed of 3 to 5 muscular fibrous transverse annular folds that have an almost cartilaginous consistency. The external os of the cervix does not protrude into the vagina, although pro- lapsed cervical rings in pluriparous cows may present10 VETERINARY OBSTETRICS such an appearance. The cervix of the cow is difficult if not impossible to dilate manually. It dilates slightly during estrum. The cervix of the mare is 5 to 7.5 cm. long and 2.5 to 5 cm. in diameter. It is suspended in the pelvic cavity caudal to the uterus and is characterized by numerous small low longitudinal folds of mucous membrane. The caudal os of the cervix extends into the vagina 2.5 to 5 cm. carrying with it a frenulum of vaginal mucous mem- brane below the external os. The cervix of the mare is relaxed, soft and easily dilated during estrus and tightly constricted and firm during diestrus. The cervix of the ewe is about 2.5 to 5 cm. long and is similar to that of the cow. Its external os is located in the cranial ventral portion of the vagina and is partially covered by a projecting “hood” of mucosa.3 The cervix of the sow, bitch and queen is poorly de- fined, being characterized by a thickened wall with transverse folds. The sow’s cervix is about 10 to 20 cm. long and is directly continuous with the vagina (See Fig- ure 10). The cervix or neck of the uterus in the bitch is very short, 0.5 to 1 cm. in length and caudally the cervix projects into the vagina. The vagina is a muscular membranous structure lying mostly retroperitoneally in the pelvic cavity dorsal to the bladder. It acts as a copulatory organ and as a passage for the fetus at the time of parturition. The vagina is capable of great dilation. Its caudal extremity is just cra- nial to the urethral opening in the region of the hymen or vaginovestibular junction. This junction is character- ized in the mare, cow and sow by a slight constriction and annular folds.12 A degree of persistence of the hy- men, where in the embryo the paramesonephric ducts join the urogenital sinus, may occasionally occur. This may vary from a thin vertical central band to a com- pletely imperforate structure. About 10 to 15 percent of heifers have hymenal remnants. These usually disappear after copulation or parturition. Prominent hymenal folds are present in the mare. A true hymen is lacking in the bitch and queen. The blood and nerve supply of the va- gina arises from branches of the urogenital artery and autonomic nerves from the pelvic plexus. It is sur- rounded by loose connective tissue and varying amounts of fat. The vagina of the cow is about 25 to 30 cm. long in the nonpregnant animal. The recto-genital pouch of peri- toneum extends caudally about 12 cm. on the dorsal cra- nial surface and 5 cm. on the ventral cranial surface of the vagina. On the ventral floor of the vagina beneath the mucosa and running the length of the vagina, the two Gartner’s ducts 0.25 cm. in diameter, remnants of the primitive mesonephric (Wolffian) ducts, are frequently Figure 10. Genital organs of the sow. 1. Ovarian Bursa, 2. Ovary, 3. Uterine horn, 4. Uterine body, 5. Cervix, 6. Vagina, 7. Vestibule, 8. Clitoris. present. Cysts of these structures may occasionally be observed. The vagina of the mare is about 18 to 28 cm. long and 10 to 13 cm. in diameter when dilated. Most of the vagina, except a small dorsal cranial portion, is retro- peritoneal. Mesonephric duct remnants are only occa- sionally present. The vagina of the ewe is 7.5 to 10 cm. long and sim- ilar to the cow’s vagina. The vagina of the sow is 7.5 to 11.5 cm. long. It is small in diameter with a thick muscular coat. Meso- nephric ducts are occasionally present. The vagina in the bitch is long, 10 to 14 cm. and narrow, 1.5 cm. The muscular coat is thick, and me- sonephric ducts are usually absent. A large dorsal me- dian postcervical fold blends caudally into lesser dorsal longitudinal folds. The configuration of this fold and the lateral and ventral vaginal walls, when viewed through a speculum, simulates the external uterine ostium. This configuration of the vagina and vaginal portion of the cervix prevents or makes difficult, intrauterine cannu- lation.13 However, if the cervix is relaxed introductionANATOMY 11 of fluid into the cranial portion of the vagina propels the fluid through the cervix and into the uterus. In the queen the vestibule and vagina are the same length. The vestibule, located between the vulva and the va- gina, and the vulva comprised of the two labia, the dor- sal and ventral commissures and the clitoris, form the caudal termination of the genital tract. These two struc- tures do not arise from the primitive paramesonephric ducts but rather from the ventral portion of the primitive cloaca. The ventral commissure of the vulva is pendu- lous and always lies ventral and caudal to the ischiatic arch.12 The urethra opens into the cranial ventral portion of the vestibule. The vestibule has several circular or sphincter-like muscles that close the genital canal to the outside. These muscles are attached to the perineal body and the sphincter muscle of the anus and the caudal and last sacral vertebrae. Thus during parturition the vesti- bule acts as the point of attachment for the entire genital tract to contract upon when expelling the fetus. The cli- toris is about 3 to 6 cm. long in the larger animals, but practically all of it is hidden in tissues between the vulva and the ischiatic arch. In the mare, bitch and sow the glans of the clitoris is well-developed and lies in a true fossa. The vulvar lips normally come together evenly, do not gape, and vulvar opening normally lies at a 90° angle to the pelvic floor. The vestibule and vulva are supplied with blood from the urogenital and the external and internal pudendal arteries and have the same auto- nomic innervation as the vagina. They are well-supplied by the sensory nerve fibers of the pudendal and caudal rectal nerves. The vulva and vestibule are the only re- productive organs of the female well-innervated by sen- sory nerve fibers. The vestibule of the cow is about 10 to 12.5 cm. long on the ventral floor and 7.5 to 10 cm. long on the dorsal wall. Beneath the urethral orifice is the suburethral di- verticulum, which is about 2.5 to 4 cm. long. The ex- ternal visible portion of the clitoris in the cow is small in size. The major vestibular or Bartholin’s glands, are two in number, one on each side, located in the con- strictor muscles of the vestibule. They are about 1.5 to 3 cm. in diameter. These glands in the cow each open by a single duct in the lateral wall of the vestibule about 2.5 cm. caudal to the vagina.14 The vestibule of the mare is similar in size to that of the cow. Eight or 10 ducts from the minor vestibular glands open through its dorso-lateral wall. The external visible portion of the glans of the clitoris of the mare is large and prominent, 2.5 to 5 cm. long and 2 to 2.5 cm. wide. It is composed of erectile tissue similar to the penis. The clitoral fossa and sinuses of the mare are homo- logues of the preputial folds, and fossa glandis of the stallion. The clitoral sinuses are 3 in number with the central sinus being the largest, located on the dorsal as- pect of the glans clitoridis. The narrow openings of these sinuses are hard to detect unless the clitoris is partially extruded and held downward thus drawing them clear of the thin fold which separates the clitoral fossa from the vestibule.16 Contractions of the vestibular and vulvar sphincter muscles elevates the clitoris and protrudes it between the vulvar lips. This is called “winking.” The vestibule and vulva in the ewe are similar to that of the cow, but the suburethral diverticulum is very small. Minor, but not major, vestibular glands are present. The vestibule is about 2.5 to 3 cm. long. The clitoris is short, with the glans concealed in a fossa. The vestibule in the sow is fairly long, about 7 to 9 cm. The labia are thick. The minor vestibular glands are variable in number. The clitoris is located about 2 cm. cranial to the ventral commissure. On either side of the cranial portion of the floor of the vestibule there is a cul- de-sac. The vulva in the bitch and queen has thick labia. The vestibule is 2.5 to 5 cm. long. The urethral orifice opens on the urethral tubercle, which is elevated above the floor of the vestibule. There are small depressions on either side of the urethral orifice. Minor vestibular glands are present in the bitch but not in the queen which has two major vestibular glands. The clitoris in the bitch has a small, 0.6 cm. long by 0.2 cm. diameter, pointed glans and lies in a fossa. The dorsal commissure of the vulva is 8 to 9 cm. below the anus. The anatomy of the perineal region of the cow and mare has been well-described.9 References 1. Benesch, F. (1957) Lehrenbuch Der Tierarztlichen Geburtshilfe und Gynakologie. Urban and Schwarzenberg, Wien-Innsbruck, Austria. 2. Del Campo, C. H. and Ginther, O. J. (1974) Arteries and Veins of Uterus and Ovaries in Dogs and Cats, Am. J. Vet. Res. 35, 3, 409. 3. Dun, R. B. (1955) The Cervix of the Ewe, Austral. Vet. Jour. 31, 101. 4. Engel, H. N. and St. Clair, L. E. (1981) Diseases of Swine, 5th Ed., Edited by Leman, A. D., Iowa State Univ. Press, Ames, Iowa. 5. Evans, H. E. and Christensen, G. C. (1979) Miller’s Anatomy of the Dog, 2nd Ed., W. B. Saunders Co., Philadelphia. 6. Foley, R. C., Black, D. L., Black, W. G., Damon, R. A., Howe, G. R. (1964) Ovarian and Luteal Tissue Weights in Relation to Age, Breed and Live Weight in Nonpregnant and Pregnant Heif- ers and Cows with Normal Reproductive Histories, J. An. Sci., 23, 3, 752. 7. Getty, R. (1975) Sisson and Grossman’s The Anatomy of the Domestic Animals, 5th Ed., W. B. Saunders Co., Philadelphia.12 VETERINARY OBSTETRICS 8. Ginther, O. J. and Del Campo, C. H. (1974) Vascular Anatomy of the Uterus and Ovaries and the Unilateral Luteolytic Effect of the Uterus: Cattle, Am. J. Vet. Res. 35, 2, 193. 9. Habel, R. E. (1966) The Topographic Anatomy of the Muscles, Nerves and Arteries of the Bovine Female Perineum, Amer. J. Anat. 119, 1, 79. 10. Hafez, E. S. E. and Blandau, R. J. (1969) The Mammalian Ovi- duct, Univ. of Chicago Press, Chicago, 111. 11. Hook, S. J. and Hafez, E. S. E. (1968) A Comparative Study of the Mammalian Uterotubal Junction, J. Morphol. 125, 2, 159. 12. Nickel, R., Schummer, A., Seiferle, E. and Sack, W. O. (1973) The Viscera of Domestic Animals, Springer-Verlag, N.Y.C. 13. Pineda, M. H., Kainer, R. A. and Faulkner, L. C. (1973) Dorsal Median Postcervical Fold in the Canine Vagina. Am. J. Vet. Res. 34, 12, 1487. 14. Reutner, T. F. and Morgan, B. B. (1948) A Study of the Bovine Vestibular Gland, Anat. Rec., 101, 2, 193. 15. Sack, W. O. (1982) Essentials of Pig Anatomy and Horowitz/ Kramer Atlas of Musculoskeletal Anatomy of the Pig, Vet. Text- books, Ithaca, N.Y. 16. Simpson, D. J. and Eaton-Evans, W. E. (1978) Sites of CEM Infection, Vet. Res. 102, 488. 17. Sisson and Grossman’s The Anatomy of Domestic Animals, 5th Ed., Ed. by R. Getty, W. B. Saunders Co., Philadelphia. 18. Swenson, M. J. (1977) Duke’s Physiology of Domestic Animals, 9th Ed., Cornell Univ. Press, Ithaca, N.Y. EMBRYOLOGY OF THE FEMALE REPRODUCTIVE TRACT The urogenital system is formed mainly from meso- dermal tissue that in the early embryonic period forms the nephric and genital regions. The ovaries develop from the undifferentiated gonads that form late in the embry- onic period in the genital or gonadal ridge located be- tween the dorsal mesentery and the mesonephros. The primordial germ cells from the wall of the yolk sac in the region of the hind gut have migrated into the gonads by the early fetal period. The surface epithelium of the female gonad gives rise to cortical cords that contain primitive germ cells, later called oogonia. The surround- ing epithelial cells from the surface epithelium form the follicular cells. Thus secondary cortical cords are char- acteristic of the early female gonad. The ovaries remain in the abdominal cavity suspended by the mesovarial portion of the broad ligaments. In both the male and female during the embryonic pe- riod, two pairs of genital ducts are formed that enter the cloaca, the mesonephric (Wolffian) tubules and ducts and the paramesonephric (Mullerian) ducts. The mesoneph- ric duct development is described in the section on em- bryology of the male reproductive tract. The parame- sonephric ducts arise as longitudinal invaginations of the coelomic epithelium in the same region as the meso- nephric tubules and ducts. The cranial portion of the paramesonephric ducts differentiate in the female to form the uterine tubes while the caudal portions of the ducts unite or fuse to form the uterus, cervix and the cranial two-thirds or more of the vagina. The septum initially present between the two ducts in the caudal region dis- appears early in the fetal period. The caudal one-third or less of the vagina is formed by evaginations from the wall of the urogenital sinus. The hymenal region and annular folds are formed by the junction of the fused paramesonephric ducts and the urogenital sinus. In the male the paramesonephric ducts degenerate but portions may persist as remnants, the appendix testis, near the head of the epididymis, and the uterus masculinus be- Table 2. Undifferentiated Genital Structures in the Embryo and Their Adult Male and Female Counterparts Embryological Structure Adult Female Adult Male Gonad Ovary Testis Mesentery Mesovarium Mesorchium Gubemaculum Round ligament of the uterus and proper ligament of the ovary Proper ligament of the testis Paramesonephric duct (Mullerian duct) Uterine tubes Uterus Cervix Vagina (cranial portion) Appendix testis Uterus masculinus Mesonephric tubules and duct Epoophoron Efferent ducts (Wolffian duct and body) Paroophoron (Parovarian or mesonephric duct or cysts) (Gartner’s) ducts Epididymis Ductus (vas) deferens (ductuli aber- rantes, appendix epididymis, paradidymis) Genital tubercle Clitoris Penis Genital folds Vestibule Penile urethra Genital swellings Vulva ScrotumANATOMY 13 tween the ampullae near the prostate gland. Portions of the mesonephric tubules and ducts may persist as rem- nants in the female forming the epoophoron on the cra- nial pole of the ovary, the paroophoron or parovarian cysts, and (Gartner’s) ducts in the vaginal floor. (See Table 2). Early in the fetal period the external undifferentiated genitalia become modified so the genital tubercle forms the clitoris, the genital folds, failing to unite as in the male, become the vestibule and the genital swellings en- large to form the vulvar lips. References 1. Arey, L. B. (1954) Developmental Anatomy, 6th Ed., W. B. Saunders Co., Philadelphia, Pa. 2. Langman, J. (1963) Medical Embryology, Williams and Wilkins Co., Baltimore, Md. 3. Miller, R. I. and Campbell, R. S. F. (1978) Anatomy and Pa- thology of the Bovine Ovary and Oviduct, Vet. Bull. 48, 9, 737- 753. 4. Evans, H. E. and Christensen, G. C. (1979) Millers’ Anatomy of the Dog, 2nd Ed., W. B. Saunders Co., Philadelphia, Pa. 5. Patten, B. M. (1948) Embryology of the Pig, 3rd Ed., The Blak- iston Co., Philadelphia, Pa.Chapter II EXAMINATIONS FOR PREGNANCY An accurate, early diagnosis of pregnancy (cyesiog- nosis) in the cow, mare and sow has become essential for a successful, profitable breeding program. In recent years the owners of sheep and goats are recognizing the benefits of the early diagnosis of pregnancy. These ben- efits in the above herds of animals include a prompt as- sessment of the breeding efficiency of females, males or semen, and the management to maintain an acceptable parturition interval or to reduce the economically costly interval from parturition to conception. Pregnancy di- agnosis increases the percentage of pregnant animals in a herd by the prompt treatment or culling of nonpregnant animals. An accurate pregnancy diagnosis is necessary in female animals bred, or possibly bred, either natu- rally or by artificial insemination prior to treatment for suspected failure of estrus. Most effective treatments would usually cause the expulsion of the conceptus in pregnant animals. Pregnancy Diagnosis in the Cow External or presumptive indications for pregnancy in- clude: (1) Service by a bull or artificial insemination— This information may not be known either through error, lack of records, lack of observation or accidental breed- ing. (2) Cessation of the estrous cycle and periods—This is a moderately accurate means of diagnosis of preg- nancy if the herdsman observes animals closely. It is not infallible since the herdsman may not see the signs of estrus or the animal may not exhibit signs of estrus (“si- lent” heats). About 15 to 30 percent of cattle not ob- served in estrus after service were not pregnant when examined rectally several months later.-’5'35 After conception early embryonic death occurred in an estimated 10 to 25 percent of cattle based on the analysis of milk progesterone studies.7,33,34 Also uterine pathol- ogy such as pyometra and ovarian pathology such as cysts may occasionally cause cessation of estrous cycles in serviced but nonpregnant cows. Conversely 3 to 6 percent of pregnant cows, especially the first trimester of gestation, may occasionally exhibit signs of estrus.891131 As in mares this estrus during pregnancy was apparently associated with follicular growth. (3) Radioimmunoassays (RIA) and enzyme im- munoassays for determining progesterone levels in blood plasma and milk have been developed in recent years and have proven helpful in monitoring the repro- ductive status, including pregnancy of cows. When the time of the prior estrus and breeding is known samples may be taken 21 to 23 days later. Milk samples are eas- ier to obtain than blood samples and potassium dichro- mate can be added to milk samples as a preservative be- fore shipping or long term storage.— 14,15,29,263,32 Based on rectal palpation at 40 to 60 days after ser- vice, these tests for progesterone levels have proven to be 65 to 85 percent accurate for predicting pregnancy at 3 weeks post-service.6,15,176,18,24,42 At this time a pregnant cow has a functional corpus luteum and a high level of milk and blood progesterone. When progesterone con- centrations are low indicative of estrus and the absence of a functional corpus luteum and pregnancy, these tests have proven to be 94 to 100 percent accurate. An enzyme immunoassay that may be an alternative to the radioimmunoassay for milk progesterone analysis for pregnancy diagnosis in cows has recently been de- scribed.263 This test is simple, reliable and practical and with further refinement could replace the radioimmu- noassay. Each laboratory performing progesterone assays fol- lows different procedures and thus different diagnostic levels of progesterone are reported. Progesterone is closely associated with the butter fat in milk so milk with high butter fat content will have a higher progesterone level than low fat milk. Thus procedures for sampling and interpretations of test results recommended by each lab- oratory should be followed.14,28,29,32,42 The inaccuracies or high percentage (15 to 20) of false positive results of this test limits its value as a diagnostic test for pregnancy. Further confirmation of pregnancy by manual examination per rectum at a later date is indi- cated. Causes for this high incidence of error include: prior service of the cow at a time other than estrus; per- 14PREGNANCY DIAGNOSIS 15 sistence of the corpus luteum due to pyometra, presence of a luteal cyst, a sampling error, or possibly most fre- quently, early embryonic death from 15 to 50 days post- service. This test cannot detect failure of fertilization or early embryonic death prior to 10 to 14 days of preg- nancy. When milk progesterone from cows of unknown pregnancy status was determined at three 7-day inter- vals, 97 percent of 88 pregnant cows and 98 percent of 83 non-pregnant cows were diagnosed correctly.28 Manual rectal palpation of the genital tract of a cow by a skilled veterinarian at 20 to 23 days after service to detect the presence or absence of a functional corpus luteum or follicle, the turgidity of the uterine horns and the presence or absence of a clear or bloody vaginal mu- cus is equal to or more accurate than the progesterone assay in the detection of either pregnancy or the absence of pregnancy. (4) The presence or absence of postestrous bleed- ing—“Menstruation” from the cow’s vulva 24 to 48 hours after service is believed by some herdsmen to indicate conception. Careful studies have indicated that about 50 to 60 percent of cows and 75 to 85 percent of heifers exhibited some bleeding after estrus. There is no rela- tionship between postestrous bleeding and conception.19 (5) Changes in the udder size of heifers and the size of the abdomen in advanced stages of pregnancy— In heifers increased development of the udder is no- ticeable about 4 months of gestation. In pluriparous cows enlargement and edema of the udder only occurs the last few weeks or month of gestation. Increased size of the abdomen is quite variable depending on the parity of the gestation. Young cows exhibit increased abdominal size after the sixth month of gestation and older cows after the seventh month of gestation. Progressive relaxation of the pelvic ligaments becomes evident the last month of gestation as does relaxation and edema of the vulva. Similar, but lesser, signs of relaxation of pelvic liga- ments and edema and relaxation of the vulva may occur in cows with cystic ovaries. (6) Ballottement of the fetus or observation of fetal movements after the sixth month of pregnancy. Occa- sionally in some thin animals where the fetus lies close to the abdominal wall, ballottement may be done as early as the fifth month of gestation. In fat animals this may not be possible until the eighth month of pregnancy. De- pending upon the size of the fetus, the condition of the cow and the size and degree of fullness of the abdomen, the fetus can be ballotted in 5 percent or less of pregnant dairy cows at 5 months of gestation, 10 to 50 per cent at 6 months, 70 to 80 per cent at 7 months, 80 to 90 percent at 8 months and over 90 per cent at 9 months. Abdominal ballottement of the fetus is easy in the cow because of the relaxed, flaccid abdominal walls. The fist is pushed in an intermittent manner in a dorsal medial direction deeply into the lower right abdominal wall. If the fetus is ballotted, it is felt as a large, hard, solid object suspended or floating in the softer structures of the abdomen, such as the uterus, uterine contents and the abdominal viscera. The more advanced the pregnancy or the larger the fetus, the more dorsally in the right flank region the fetus may be ballotted. (7) Auscultation of the fetal heart may be per- formed from the sixth to seventh month of pregnancy to term only with great difficulty due to the thick abdom- inal walls and viscera and the difficulty of obtaining a sufficiently quiet location. Fetal electrocardiography has been used to study the fetal heart and as an aid in the diagnosis of twin pregnancy and fetal mummification after the fifth month of pregnancy in cows.22,23,38 (8) Ultrasonography or the use of ultrasound to detect pregnancy has only recently been developed to detect pregnancy in cattlela,25a'b (see Pregnancy Diag- nosis in the Mare). Further research and improvement of the technique is necessary. Early pregnancy diagnosis with ultrasonography is more difficult in the cow be- cause of the elongated rather than the oval blastodermic vesicle present in the mare, bitch and queen. Presently errors in diagnosis, especially in detecting nonpregnant cows, are too great for routine use of this technique when compared with the accuracy and lower costs of rectal palpation for pregnancy. Internal indications of pregnancy in the cow The rectal palpation of the uterus, ovaries, and uterine vessels is the most practical and accurate, as well as the earliest means of accurately diagnosing pregnancy in the cow. Prior to the actual rectal examination, the breeding history of the cow should be studied, including the date of the last calving, the dates and number of services, and information on any pathologic or disease condition pre- viously affecting the reproductive organs. Complete breeding and reproductive records are very helpful for an accurate and rapid pregnancy or sterility examination of a cow or herd. Unfortunately many herds, especially range beef herds, do not have this information.20 If a herd is to be examined it is helpful if someone is available to record notes on the results of the examina- tion. The operator should wear proper protective cloth- ing, consisting of rubber boots, a pair of clean, short- sleeved coveralls, or rubber pants, and a short-sleeved cloth jacket, and a thin rubber surgical, or disposable plastic glove and obstetrical sleeve. The sharp sealed edges of the plastic sleeve and glove often irritate and lacerate the rectal mucosa and anal skin. The glove and sleeve16 VETERINARY OBSTETRICS is essential to protect the examiner’s arm from chafing, infection, feces, and odor. It also protects the cow’s rec- tum from irritation due to the examiner’s hair and fin- gernails. No rings, especially rings with settings, should be worn on the examinating hand. The fingernails should be short. Either hand may be used for the examination, but if many examinations are to be made it is usually desirable to use the stronger arm. Many prefer to do ex- aminations with the left arm, so that the right is free for writing and for the manipulation of instruments or pi- pettes. The cow should be fastened or held securely to prevent forward or lateral motion. If many cows are to be examined it is helpful for an assistant to hold the tail away from the examiner’s arm. Caution should be ex- ercised when examining cows near posts or other ob- structions that might cause the examiner injury if the cow moved suddenly. Cows seldom kick when being ex- amined rectally but an excitable cow may occasionally kick backwards and injure the operator. When beef or range cows are in a chute a bar should be placed behind the cow above the hocks. Applying a nose lead or forc- ing the cow’s tail dorsally and cranially in a firm manner may be necessary to restrain certain cows. The arm should be well-lubricated with a non-irritat- ing agent. The fingers and the hand are inserted into the rectum in the form of a cone. They are advanced into the rectum beyond the organ or structure to be palpated. Do not introduce the hand and arm a short distance into the rectum and push the rectum forward, thus stretching and irritating the rectal wall. With the arm well-inserted, bring a portion of the rectum caudally as a fold upon the hand and arm, thereby giving more freedom to the hand and producing greater relaxation of the rectum. It is usu- ally necessary to remove most of the fecal material from the rectum before a thorough examination can be made. This can be done by raking the feces from the rectum with the hand, palm uppermost, or by stimulating peri- staltic contractions and defecation by massaging the rec- tal wall just anterior to the anus and by allowing some air to enter the rectum. In the older, larger dairy cows one can leave the arm and hand in the rectum when a peristaltic wave is passed backward. However, in heifers and small beef cattle such a practice occasionally results in a laceration of the mucosa or even the rectal wall. In some cases, particularly where cattle have been on lush pasture and the feces are thin and loose, the rectal mu- cosa is easily irritated and the cow will suck air into the rectum, making examination nearly impossible through the dilated, tense rectal walls. Stimulating peristalsis, as mentioned above, will result in evacuation of the air. This may be aided and hastened by hooking the fingers cranially into a peristaltic contraction ring and pulling it gently caudally. The cow’s back should not be pinched down, since this tends to fill the rectum with air. Ex- aminations of certain cows under epidural anesthesia may be desirable, however, ballooning of the rectum with air is a complication of this technique. All rectal examina- tions should be done with care, gentleness, and patience to avoid traumatizing the mucosa, rupturing the rectum, or irritating the anus. The presence of free blood, or a fresh blood clot, in amounts of 15 to 30 ml. or more, not mixed with the feces, is highly indicative of a rectal rupture. If a rupture of the rectum occurs in the cow, examinations should cease immediately. Supportive treatment with penicillin and streptomycin, tetracyclines or sulfonamides and atropine are indicated. If the cow is not valuable, im- mediate slaughter may be indicated. If recovery follows rectal trauma with perforation, adhesions of the rectum to the genital tract, occasionally associated with ab- scesses, may occur. A regular routine for examining the female genital tract should be developed and followed at each examination so no structure or portion of the tract will be overlooked. In making a rectal examination the hand is introduced cranial to the pelvic inlet or bony pelvis and is passed or swept from one side downward, across, and up the other side. If no structure is palpated the uterus is in the pelvic cavity. Usually the cervix or uterus is palpated on the brim of the pelvis in older cows. The hard, firm cer- vix is relatively easily located on the floor of the pelvis or cranial to it. The uterine cornua can be palpated in nonpregnant cows or in early pregnancy. The ovaries may be palpated lateral and slightly cranial to the cervix. As pregnancy develops they are drawn forward, especially the ovary corresponding to the horn containing the fetus, until by the fourth to sixth month of pregnancy they are out of reach. The uterus may be located laterally in the pelvic cavity if held there by a full bladder or a short broad ligament. The normal non-pregnant uterus in the heifer and pluriparous cow vary greatly in size. The uterus is normally soft, pliable and relaxed with a slight amount of tonicity in early pregnancy. A completely flaccid atonic uterus is characteristic of true anestrus and chronic cystic ovarian disease. At the time of estrus or following vig- orous massage the uterus may become quite erect and turgid. In late estrum and early diestrum, 1 to 2 days after ovulation, the uterus may be thick-walled and edematous. Often about 20, 40 or 60 days post-concep- tion the uterus may be quite tonic with a normal corpus luteum and an occasional follicle in the ovary. The technique for manual retraction of the nonpreg- nant or one- to three-month pregnant bovine uterus into the pelvic cavity from the abdominal cavity to facilitatePREGNANCY DIAGNOSIS 17 its examination may be helpful.-’3 This involves caudal traction on the cervix, then further caudal traction on the ventral intercomual ligament. The cranial border of the broad ligament medial to the ovary may also be re- tracted. In particularly difficult cases the application of Knowles cervical forceps to the external cervical os will aid retraction of the uterus. The ovary may be grasped and slid between the middle and third fingers and held there while it is carefully palpated by the thumb and in- dex finger. Taking into consideration a number of factors includ- ing the age of the cow, rectal examination to diagnose pregnancy can be made quite accurately from about 35 days after conception. It is easier to detect early preg- nancy in heifers than in cows. After 45 to 55 days of gestation, pregnancy diagnosis is usually easy for the ex- perienced veterinarian. An accurate early pregnancy di- agnosis is an important, economic necessity for the pro- gressive cattle owner. Veterinarians should be cognizant of the fact that the incidence of death of the early zygote, embryo and fetus in cows is highest during the earlier stages of gestation and declines rapidly after 60 to 90 days of gesta- tion.5,21'33 Early embryonic deaths occur whether rectal palpation of the uterus and its contents of fluids, membranes or amniotic vesicle, for confirmation of early pregnancy is performed or not. Recent studies on early pregnancy di- agnosis using assays of progesterone in milk 21 to 23 days after service and continuing for 75 days have dem- Figure 11. Uterus of a cow. 60 to 70 days pregnant. Figure 12. Twin, bicomual bovine pregnancy, 60 days pregnant. Note CL in each ovary and lymphocytomas in the vagina. (Courtesy K. McEntee) onstrated an incidence of early embryonic deaths of 7.2 to 14.5 percent in cows not subject to early rectal pal- pations of the uterus. These embryonic deaths were con- firmed by a late return to estrus 28 to 60 days after ser- vice and rectal examinations at 55 to 75 days.7,21’33,34 Vigorous, intense and prolonged rectal examinations for early pregnancy diagnosis, especially between 30 and 50 days of gestation, by certain, inexperienced exam- iners can result in an increased incidence of embryonic death and a return to estrus usually within 30 days but occasionally not until 50 to 90 days later.1'3’4'27’40 Pal- pation of the amniotic vesicle and slipping of the mem- branes were potentially more damaging to the develop- ing embryo than palpation for the enlargement of the gravid uterine horn by fetal fluids or “fluctuance.” The incidence of embryonic deaths were 4 to 9 percent in cows examined per rectum at 30 to 45 days of gestation compared to 2.5 to 4 percent when examinations were performed after 40 to 45 days of gestation.1 3 27 33 34 Since the “natural” embryonic death rate may be augmented by early pregnancy diagnosis per rectum, it behooves veterinarians to be particularly gentle and careful if early diagnostic examinations are made and possibly to reex- amine and reconfirm the pregnancy diagnosis after 55 to 60 days of gestation. As mentioned earlier under the use of progesterone18 VETERINARY OBSTETRICS Figure 13. Uterus of cow 60 to 70 days pregnant. Note CL in the left ovary and large follicle in the right ovary. assays for diagnosing pregnancy, rectal examinations of the cow’s genital tract by a skilled veterinarian 19 to 23 days after service would be equally as accurate, about 75 to 90 percent, in assessing pregnancy at such an early date. If the cow failed to conceive estrus signs should be detectable including an erect, tonic uterus, an invo- luted, firm, small corpus luteum, a developing follicle, about 1 cm. in diameter, or a depression on the ovary where ovulation occurred. A vaginal examination by speculum should reveal the presence of an excess of clear, stringy mucus, possibly tinged with blood if ovulation has occurred, associated with a moderately hyperemic vaginal mucosa and a slightly relaxed external cervical os. If the cow conceived 19 to 23 days before the rectal examination one should detect a mature functional cor- Figure 14. Sixty-day-old bovine fetus in the amniotic sac within the chorioallantoic membranes. Note beginning development of the co- teledons. (Courtesy K. McEntee) pus luteum, the absence of a maturing or ovulated fol- licle, and a uterus that is somewhat flaccid and lacking the tone of a uterus under the influence of estrogens. A vaginal examination will reveal a pale mucous mem- brane, a closed cervical os and only a small amount of tenacious, thick mucus. The definite or certain signs of pregnancy in the cow as determined by a rectal examination are: (1) The pal- pation of the enlarged horn containing the fluctuating placental fluids from 30 to 90 days of gestation. (2) The careful, very gentle palpation of the amniotic vesicle in early pregnancy from 30 to 50 days. (3) The slipping of the fetal membranes including the allantois chorion and its blood vessels upon gentle pinching of the uterus with the thumb and forefinger in early pregnancy from 40 to 90 days. (4) The palpation or ballottement of the fetus in the enlarged uterus containing fetal membranes and placental fluids after about 80 days. (5) The palpation of the placentomes after 100 days and (6) The palpation of the enlarged, thin-walled, ‘‘whirring” uterine arteries after 90 days of gestation. Less definite signs of pregnancy include the increase in size of the uterus and a thinning and distension of its walls, its location in the abdominal cavity, the location, size and persistence of the corpus luteum and vaginal changes. Uterine changes during pregnancy: During early pregnancy, the uterine horns, especially the horn con- taining the embryo or fetus, increase in size due to the distention of the horn by the amniotic vesicle, placental fluids, the membranes, and the conceptus. This increase in the diameter of the uterine horns is characterized by a thinning of the uterine wall and a fluid, watery, “alive” fluctuating feeling on palpation of the uterine horn. The uterine horns have a fair amount of tone due to their tenseness and distention. From 40 to 90 days of preg- nancy, the uterus feels somewhat like a thick rubber bal- loon nearly filled with water. The approximate size of the hom containing the fetus during the first 5 months of pregnancy is given in Table 3. Since the size of the fetus is small during the early stages of pregnancy the amount of fluid in the uterine hom largely determines its size or diameter. The volume of fluid increases rapidly the first 5 months of pregnancy but increases more slowly after the fifth or sixth month (Table 3). In cattle there is a marked increase in the allantoic fluid volume between 40 and 75 days and 6-1/2 and 7-1/2 months of gestation and a marked rise in amniotic fluid volume between 3-1/2 and 4 months of gestation that is not reflected in the total volumes of placental fluids given in Table 3.2 The size of the amniotic vesicle varies as noted in Table 3. The amniotic vesicle is spherical in outline upTable 3. Size and Characteristics of the Bovine Fetus and Uterus during Pregnancy* Days of Gestation Diameter of the Flom Containing the Fetus Amount of Fetal Fluid Diameter of the Amniotic Vesicle Length of the Fetus (C-R) Weight of the Fetus Diameter of the Placentomes Diameter of the Uterine Artery Fetal and Placental Characteristics 30 2-4 cm 30-60 ml 1.0 cm (pea size) .8-1 cm ■ 3-. 5 gm Head and limb buds recognizable, placenta not attached. 40 3-6 cm 75-100 ml 2.5-3.0 cm (size of plum) 1.75-2.5 cm 1-1.5 gm 50 5-7 cm 90-200 ml 3.5-5.0 cm (1-1/2—2") 3.5-5.5 cm 3-6 gm 60 6-9 cm 200-450 ml 6-7.5 cm 6-8 cm (mouse size) 8-30 gm Claw buds and small scrotum recognizable, palate and sternum closed, placenta attached and lens- sized cotyledons present. 70 7-10 cm 350-650 ml 7-10 cm 25-100 gm 0.5-0.75 cm 80 9-12 cm 500-800 ml 8-13 cm 120-200 gm 0.5-1.0 cm 90 10-13 cm 750-1400 ml 13-17 cm (rat size) *200-400 gm 1-1.5 cm (size of dime) 0.3-0.5 cm Hair on lips, chin and eyelids, scrotum present. 120 12.5-18 cm 2000-3500 ml 22-32 cm (small cat size) 1000-2000 gm 1.5-2.5 cm (size of quarter) 0.5-0.8 cm Fine hair on eyebrows, claws developed and yellow-colored, epithelial plaques present on amnion, horn pits present. 150 18-23 cm 4000-5000 ml 30-45 cm (large cat size) 3000-4000 gm 2.5-4 cm (size of 1/2 dollar) 0.6-1.0 cm Hair on eyebrows and lips, testes in the scrotum, teats developing. 180 4000-7500 ml 40-60 cm 5-10 Kg. 4-5 cm 0.9-1.25 cm Hair on inside of ear and around the horn pits, tip of tail and muzzle. 210 6300-10,000 ml 55-75 cm 8-18 Kg. 5-7.5 cm 1.25-1.5 cm Hair on metatarsal, metacarpal and phalangeal region of extremities and beginning on the back, long hair on tip of tail. 240 8000-12,000 ml 60-85 cm 15-25 Kg. 6-9 cm 1.25-1.7 cm Fine short hair all over the body. Incisor teeth not erupted. 270 12,000-20,000 ml 70-100 cm 20-50 Kg. 8-12 cm 1.5-1.9 cm Hair coat complete and long, fetus large, incisor teeth erupted. * Richter & Goetze, Fraser, Bongso and Basrur, Swett, Matthews and Fohrman, Gier and Marion, Zemjanis, Arthur, Winters, Green, Comstock, Ball, Evans and Sack and Eley etal. These are all approximate figures as there is much individual variation especially between heifers and cows. PREGNANCY DIAGNOSIS20 VETERINARY OBSTETRICS to about 40 days, at which time it becomes oval. The palpation of the amniotic vesicle in the free most dis- tended portion of the horn at 30 to 65 days of pregnancy is helpful in diagnosis because of its fairly tense spher- ical to ovoid shape. If the vesicle is not palpable or is small or collapsed the embryo may have died and is ma- cerating. If the operator is experienced, skillful and gentle early embryonic death may be detected at 30 to 40 days of gestation by palpation of the amniotic vesicle.3,36 These embryos are probably resorbed. Palpation of the am- niotic vesicle should be performed very carefully and gently to avoid damaging or rupturing it or the heart or other friable organs of the embryo. The fingers and thumb gently palpate the gravid horn and as they are moved slowly back and forth the vesicle can be felt to slip be- tween them. If such an examination cannot be done skill- fully and gently it is best to omit it as it is not necessary for an accurate pregnancy diagnosis. Slipping of the fetal membranes is another aid to early pregnancy diagnosis in the cow that is best per- formed from 35 to 90 days of gestation. Prior to 40 days of gestation slipping of the fetal membranes is difficult to detect because the membranes are thin and fragile. The technique consists of gently picking up and pinching or compressing either hom of the uterus and feeling the fetal membranes, the allantois chorion and its vessels slip between the thumb and the fingers before the uterine wall escapes from between the fingers.3-’13 The entire hom may be grasped and let slip through the fingers so that the connective tissue band and allantoic vessels on the lesser curvature of the uterus, which are three to four times thicker than the chorioallantoic membrane, can be palpated. Excessive or rough pinching of the uterus, par- ticularly over the amniotic vesicle is to be avoided, to prevent damage to the embryo or fetus. This technique of slipping the membranes is especially valuable in the differential diagnosis of pregnancy from uterine diseases characterized by fluids causing uterine distention, such as pyometra or mucometra. Location of the pregnant uterus in older cows, since the uterus in the nonpregnant state lies on or over the brim of the pelvis, the pregnant uterus is found in the abdominal cavity as early as at the time of conception to the second to third month of pregnancy. In all ages of cattle the uterus lies on the floor of the abdominal cavity after the fourth month of pregnancy. In uteri that hang forward in the abdominal cavity the allantoic fluid tends to gravitate to the apices or pendant portions of the uterus frequently out of reach of the operator unless he retracts the uterus into or towards the pelvic cavity. In heifers or young cows 2 to 3 months pregnant, the uterus often lies in the pelvic cavity and the hom containing the fetus exhibits a typical dorsal bulging or terracing because of its location. By the fifth to sixth month of pregnancy in all cows the uterus is drawn well-forward and downward in the abdominal cavity so that in some cases only the cervix and uterine vessels can be palpated per rectum. By the sixth to seventh month the fetus be- comes large enough so that it can again be palpated on rectal examination in nearly all cows: and by the eighth or ninth month the fetus may, in a few cows, actually extend caudally so that the nose and feet are resting in the pelvic cavity. As the uterus drops forward into the abdominal cavity during pregnancy the mesometrium stretches and thickens and the ovaries are also drawn ventrally and cranially. The ovaries can usually be pal- pated through the fourth month of gestation and occa- sionally during the fifth month. During the latter month the ovary on the side of the uterine hom containing the fetus is usually drawn out of reach of the hand in the rectum. Fetal size and characteristics at various stages of pregnancy: The statistics of bovine fetal, length, and weight have been recorded by a number of authors. The average fig- ures and records given by these workers are noted in Table 3. The author estimates that the fetus may be pal- pated per rectum in over 95 percent of cows at 3 to 4 months of gestation, about 40 to 70 percent of cows at 5 and 6 months of gestation, about 80 percent of cows at 7 months and about 95 percent or more of the cows at 8 to 9 months of gestation. Palpation of the fetus be- fore 60 to 70 days of gestation is not possible because of the tense, distended amniotic vesicle and the small size of the embryo or the fetus. Between 70 to 120 days fetal crown-to-nose or head size measurements are 1.5 cm. at 70 days, 5.5 cm. at 90 days and 9.0 cm. at 220 days.3 The larger and deeper the abdomen of the cow and the longer the mesometrium the greater the difficulty in pal- pating the fetus per rectum during midgestation. Thus in heifers the fetus can often be palpated per rectum the entire gestation period. If the fetus cannot be felt, preg- nancy diagnosis is based on the position of the uterus, the size of the uterine arteries, the palpation of the pla- centomes and the slipping of the fetal membranes. After the sixth month of pregnancy one can elicit or cause fetal movements by pinching the claws, grasping and pulling a fetal leg, pinching the eyeballs, or grasping the nose of the fetus either through the rectal or vaginal wall. The latter is possible only during the last month or so of preg- nancy. If the bovine fetus can be secured and measured an approximation of its age, especially up to 6 months of age, as thereafter there is too much variation between breeds, may be obtained by doubling the crown-rumpPREGNANCY DIAGNOSIS 21 length in inches and taking the square root of the result which is equal to the months of gestation.4 Palpation of placentomes Although the placentomes are forming by 60 to 70 days of pregnancy, they seldom can be palpated as definite structures until 75 to 80 days. At this time they can be palpated in the uterine wall at the level of the intercomual ligaments of the horn con- taining the fetus as ovoid thickened areas. They increase in size as the fetus develops (see Table 3). Inexperienced examiners may mistake a placentome for the ovary be- tween 110 and 180 days of gestation. In general the pla- centomes in the middle of the horn containing the fetus and nearest the attachment of the middle uterine artery are larger than those placentomes in the cervical or api- cal end of the horn or in the opposite nongravid horn. Thus the largest placentomes from the fifth month of pregnancy to term are usually out of reach of the rectal hand. The development and enlargement of the uterine artery is closely associated with the size of the fetus and the duration of pregnancy. The artery supplying the greatest amount of blood to the uterus is the uterine ar- tery. Palpation of changes that occur in the size of this artery and the character of its pulse are of diagnostic value. The uterine artery arises from the internal iliac artery close to its origin at the aorta. In the nonpregnant cow it curves caudally in the broad ligament over the dorsal part of the shaft of the ilium into the pelvic cavity and then downward and forward over the pelvic brim to enter the concave aspect of the uterine horn near its cen- ter. As pregnancy progresses the artery is pulled more cranially as the uterus drops forward in the abdominal cavity until in the latter half of pregnancy it may be lo- cated 5 to 10 cm. cranial to the shaft of the ileum. One should not confuse the internal iliac artery which is se- curely fastened by fascia to the shaft of the ileum with the uterine artery in the broad ligament which is movable for a distance of 10 to 15 cm. In heifers a change in the size of this artery to the horn containing the fetus may be noted as early as 60 to 75 days of pregnancy, when it may be 0.15 to 0.3 cm. in diameter. In older cows the change in size of the middle uterine artery to the horn containing the fetus can be noted at 90 days, when the artery is about 0.3 to 0.45 cm. in diameter. The ap- proximate size of the artery at different stages of ges- tation are noted in Table 3. The uterine artery to the nongravid hom also enlarges but the changes are not so great as those in the artery to the gravid hom and they occur later. With the enlargement of the artery the ar- terial wall becomes thinner, so that instead of feeling a pulsation in the artery a characteristic “whirr,” “thrill” or fremitus is felt. This is first recognized at about 80 to 120 days of pregnancy, but the time may be variable. By the fourth to fifth month of pregnancy it is always palpable. If the uterine artery is pressed too tightly this fremitus may stop, so that only a pulsation is felt. In advanced pregnancy this artery, when palpated lightly, feels much like a stream of water surging intermittently through a thin rubber hose. Aneurysms producing lo- calized fremitus of the uterine artery in the cow may rarely be present. This change in the size of the artery and the character of the pulse is helpful in diagnosing pregnancy about the fifth and sixth months, when the uterus is forward in the abdominal cavity and the fetus cannot be palpated. It is of value and aid in determining the stage of pregnancy. If both uterine arteries are equally enlarged, twin bicomual pregnancy should be suspected. The characteristic fremitus of the pulse is often of value in determining whether or not a normal pregnancy with a viable fetus is present. Determining the stage of gestation up to 120 days by rectal palpation when the date of service is unknown is quite precise, to within a few to 10 days but as gestation progresses it becomes less precise due to individual and breed variations in the size of the uterus and fetus. The horn of the pregnant bovine uterus not con- taining the fetus may vary greatly in size. In most bo- vine pregnancies a portion or usually all of the non-gravid horn takes part in the placental attachments. There is a progressive enlargement of the nongravid hom, its uter- ine artery, and placentomes but these changes are not as great as those of the gravid hom. In possibly 10 to 20 percent of cows, some or most of the caruncles and coty- ledons in the nongravid hom fail to develop normally or may be absent, in which case this horn is smaller than normal or even is nonfunctional. As a result an excessive burden may be placed on the gravid hom, with an hy- pertrophy of the placentomes causing them to become 15 cm. in diameter in some cases. Examination of the ovaries. The ovary may be gently grasped between the first and second or second and third fingers and palpated with the thumb. The ovary follow- ing ovulation develops a corpus luteum at the site of the ruptured follicle. If fertilization and development of the ovum and embryo proceed normally this corpus luteum persists throughout pregnancy in the cow. The corpus luteum of pregnancy, or corpus luteum verum, is slightly larger, 2.46 cm. in diameter and 6.5 gms. in weight, than the corpus luteum of the estrous cycle, 2.3 cm. and 5.7 gms., respectively. These small differences are of no diagnostic value.10 However, as pregnancy pro- gresses the corpus luteum tends to develop a darker golden-brown color and its projection above the surface of the ovary is less prominent due to a heavy layer of epithelium and stroma that covers it. It remains essen- tially the same size until near parturition.22 VETERINARY OBSTETRICS With few exceptions the corpus luteum of pregnancy is on the ovary corresponding with the horn of the uterus containing the fetus. Less than 1 percent of the corpora lutea of pregnancy were in the ovary opposite the horn containing the fetus.-2,53,12 Thus, more than 99 percent of cows have the corpus luteum of pregnancy on the ovary corresponding to the horn containing the fetus. The pos- sible reasons for the presence of the corpus luteum being on the ovary opposite the horn containing the fetus might include: (1) External migration of the ovum across the peritoneal cavity. This is highly unlikely. (2) Internal or transuterine migration of the early embryo through the uterine body, which is rare in the cow.32b (3) Regression of the corpus luteum of pregnancy and the development of another corpus luteum on the opposite ovary. This has been observed by the author during the first trimester of pregnancy in 3 cows. If a rectal examination of a cow 20 to 24 days after service reveals a normal corpus luteum on one ovary and no signs of estrum, the examiner can be reasonably sure that conception has taken place. These early diagnoses are about 80 to 90 percent accurate. This can be con- firmed on re-examination at 40 to 50 days by the pres- ence of the corpus luteum in the same site on the same ovary with typical changes occurring in the gravid uter- ine hom. The manual removal of a bovine corpus luteum of pregnancy or the administration of a prostaglandin the first 5 months of gestation will invariably result in abor- tion. Vaginal changes during pregnancy as determined by examination with a vaginal speculum and light or man- ually may be of some diagnostic value but are of only secondary importance to the uterine changes. During pregnancy the vagina usually develops a pale, dry, sticky mucous membrane similar to that observed in diestrum. The external os of the cervix is closed and pale. Since milk or serum progesterone levels and vaginal electrical resistance correlate closely, a commercially-produced instrument to measure the latter as an estrus-detection aid may be of value for early pregnancy diagnosis.243 In about 60 to 70 percent of the cows the cervical seal which forms after conception increases in size until it protrudes or covers the external os and is visible and palpable be- tween 40 to 120 days of pregnancy. In the rest of the cattle it is present in the cervical canal but does not be- come visible. The seal is a translucent, whitish mucus that is very tough, adhesive, and tenacious. This seal may remain after the fetus has died in such diseases as mummification of the fetus and trichomoniasis with fetal maceration. Occasionally there may be a normal preg- nancy with a cervicitis of the external os and a purulent vaginitis. In such an instance, the cervical canal and in- ternal os have a normal cervical seal present. There is in rare cases a condition characterized by a cervical seal of large proportions called mucocervix. This is noted by a cervix with a diameter of 7.5 to 10 cm. filled with tenacious mucus and accompanied by a persistent corpus luteum or luteal cyst and a failure of estrum. Just prior to parturition and abortion the normal cervical seal breaks down and is discharged in strings. The vaginal mucous membrane becomes more moist and hyperemic, and the cervix relaxes and dilates. Thus a vaginal examination is of value in diagnosing impending abortion or partu- rition. Passing a catheter or insemination pipette through the sealed cervix in a pregnant cow may introduce in- fection into the uterus and cause the death of the fetus the release of prostaglandin and subsequent abortion. In advanced pregnancy a manual examination of the vagina frequently reveals the presence of a portion of the uterus and fetus in the pelvic cavity dorsal or lateral to the va- gina. The cervix is pulled forward by the weight of the gravid uterus causing a lengthening of the vaginal cav- ity. Biologic tests for the diagnosis of pregnancy in the cow have been reported but are not as accurate as the rectal diagnosis of pregnancy by a competent veterinar- ian. Presently the only practical biologic test for preg- nancy in the cow is the radioimmunoassay (RIA) test for determining the levels of progesterone, produced by a functional corpus luteum, in the milk or blood plasma as described previously. Differential Diagnosis in Pregnancy Examinations Anatomically there is no reason for confusing a preg- nant uterus with such structures as the bladder, the pen- dulous left kidney or the rumen. Careful rectal exam- ination, consideration of the anatomical structure and relationships of these organs and their consistency, will prevent erroneous diagnoses. Tumors may be confused with pregnancy in the cow if a careful examination is not performed. The tumors most commonly confused with pregnancy are lympho- cytoma, granulosa cell tumor of the ovary, and fat ne- crosis in the mesentery. Other tumors of the uterus or genital tract of the cow such as leiomyomas and fibro- mas that might be confused with pregnancy are rare. Mummification of the bovine fetus characterized by the death of the fetus from 3 to 8 months of gestation, failure of abortion, absence of estrum or parturition, ab- sorption of the fetal and placental fluids, contraction and thickening of the uterine walls, resorption of the placen- tomes, and the presence of the hard, firm fetus andPREGNANCY DIAGNOSIS 23 membranes in the closely applied uterine horn lying deep in the abdominal cavity may be confused with preg- nancy. The history of apparent conception but failure of udder development, failure of an increase in the size of the abdomen or fetus, and failure of parturition should cause the examiner to suspect the presence of this con- dition. On rectal examination the uterus is usually drawn forward into the abdominal cavity and may require cau- dal traction on the cervix or lifting of the ventral ab- dominal wall to bring it within reach of the rectal hand. The typical “whirring” or fremitus in a enlarged uterine artery is absent. If palpable, the ovary on the side of the horn containing the fetus has a corpus luteum of preg- nancy. Mummification of the fetus has not been asso- ciated with rectal palpation of the uterus for pregnancy diagnosis even when the examinations have been vig- orous and prolonged. Pyometra or accumulation of pus, from 200 to 20,000 ml. in amount, in the uterus is characterized by failure of estrum and may be confused with pregnancy. Pyom- etra may occur either postpartum or post-service. In most cases pyometra follows a retained placenta and postpar- tum metritis, in which case there is frequently an inter- mittent discharge of pus from the vagina. In trichomo- niasis or other infections early pregnancy may occur and the fetus may be killed by the organisms. The fetus and fetal membranes then macerate with pyometra resulting. In these cases the cervical seal may remain intact in the cervix for long periods. In pyometra the uterine walls are usually thick and heavy and lack tone. The fluid in the uterus may be watery, syrup-like or viscous. The uterine horns are usually unequal in size as in pregnancy. The pus tends to gravitate and collect in the pendant por- tion of the horns and there is no dorsal bulging of the horn as in often palpated during early pregnancy. The fetus or placentomes cannot be palpated and the fetal membranes cannot be slipped. The uterine arteries are usually contracted and the fremitus is absent. If the di- agnosis is uncertain, reexamination in one to two months is indicated. In normal pregnancy progressive develop- ment of the fetus and uterus occurs, whereas in pyometra the condition remains essentially the same. As in mum- mification of the fetus the corpus luteum remains in the ovary. Maceration of the fetus exhibits signs similar to those of pyometra with the exception that death of the fetus after the fourth month of pregnancy results in the pres- ence of fetal bones in the uterus causing crepitation when palpated. Occasionally the cervical seal breaks down and a vaginal discharge is observed. Mucometra or hydrometra may occur secondarily to an imperforate hymen, in the defective horn of a cow with uterus unicornis, in other anomalies of the devel- opment of uterus, cervix, or vagina, segmental aplasia, and in long-standing cases of cystic ovaries causing a cystic degeneration of the uterine wall. This condition is variable in its manifestation. Anomalies of the devel- opment of the paramesonephric duct system may not be characterized by failure of estrum, whereas in cystic ovaries failure of estrum is common. The mucus varies in consistency from a thin, watery secretion seen in cys- tic degeneration of the uterine wall, to a heavy mucus secretion in heifers with imperforate hymens, to a gummy and inspissated type of mucus that might be confused with a mummified fetus in certain defects including seg- mental aplasia of the uterine horn. The uterine wall in most of these conditions is fairly thin but in cystic de- generation of the uterine wall it may be so extremely thin that it is difficult to palpate. These conditions differ from pregnancy based on the history; and on rectal exami- nation by a failure to “slip” or feel fetal membranes, by the absence of the fetus and placentomes, lack of frem- itus or increase in size of the uterine artery, and a failure of the progressive development of the uterus as in a nor- mal pregnancy. Embryonic or early fetal death with abortion or possible absorption. Death of the embryo or fetus prior to 70 to 90 days of gestation may be followed by im- mediate or occasionally delayed abortion.4 In early preg- nancy the fetal membranes may continue to grow and develop for several weeks after fetal death before show- ing degenerative changes. Thus a positive diagnosis of fetal death and absorption can only be made late in the absorbtive process when the signs of pregnancy do not correspond with the breeding history, a diminished amount of fetal fluids are in the uterus, the membranes feel col- lapsed and wrinkled upon slipping between the fingers and thumb, the amniotic vesicle may be atonic and flac- cid or be absent, and the uterine wall is thick and some- what contracted. These cases when detected or suspected should be brought to the attention of the owner so that he can watch the cow closely for a recurrence of the estrous cycle or if this is not observed the cow can be reexamined two to four weeks later. Probably in most of these cases, expulsion or abortion of the degenerated partially macerated embryo and its membranes occurs and is unobserved. Careful rectal examination may reveal abnormalities or pathology of the pregnant uterus and fetus in such conditions as hydrops amnii and allantois, fetal mon- sters, twins, torsion of the uterus, adhesions of the preg- nant uterus to other abdominal structures, rupture of the uterus with an extra-uterine fetus, metritis characterized by lack of tone of the uterus and gaseous crepitation within the uterus that occasionally precedes bacterial abortion. The diagnosis of twins may be based on the findings24 VETERINARY OBSTETRICS of equal enlargement of both uterine horns or uterine ar- teries, the presence of two amniotic vesicles, or the pres- ence of two fetuses—usually one in each horn, but oc- casionally two in one horn. In most cases there are two corpora lutea, usually one on each ovary, as bicomual twins are by far more common than unicomual twins. Dizygotic bovine twins are much more common than monozygotic twins. There is ample evidence to indicate that in the dairy cow the right ovary is slightly more active.-5*’12'13 About 60 percent of pregnancies occur in the right horn and 40 percent in the left horn. In beef cattle these percentages are more nearly equal.12 PREGNANCY DIAGNOSIS IN THE MARE The external indications of pregnancy in the mare are similar to those in the cow. Since the breeding sea- son for most mares is short, early and accurate preg- nancy diagnosis is essential in a good breeding program. Following service the mare should be teased regularly by a stallion or an aggressive, or testosterone-primed gelding every one to two days to determine the end of estrum, and continuing for 18 to 21, and even to 40 days to determine if conception has apparently occurred. It is not unusual for up to 10 to 15 percent of pregnant mares to exhibit some or all the signs of estrum, especially the first several months of gestation.20 50 These signs are usually weak and short, lasting for only one or two days. They are probably due to developing ovarian follicles that regularly occur in mares the first 90 days of ges- tation. Other mares may show no signs of estrum after breeding and yet have failed to conceive. Post-estrual bleeding as seen in cattle after estrum does not occur in the mare. Diagnosis of pregnancy in the mare based on an in- crease in the size of the abdomen is hazardous even though most mares in advanced pregnancy show a marked in- crease in the size and a characteristic shape of the ab- domen. The pregnant mare’s abdomen after the fifth to sixth month of pregnancy is usually pear-shaped with the greatest width in the ventral third. In fat mares or mares fed large amounts of roughage the abdomen is large but round with the greatest width in the middle third. The last month of pregnancy the mammary glands begin to enlarge. Distention of the teats with colostrum occurs the last 3 to 4 days of gestation and in most mares “waxing” of the teats due to the expression of colostrum occurs 4 to 48 hours before foaling. This may be absent or in a few mares may occur for three to ten days before foal- ing. Edema of the abdomen just anterior to the udder may occur in advanced pregnancy. Relaxation of the pel- vic ligaments occurs in late gestation but is not as evi- dent in the mare as in the diary cow. Ballottement of the fetus in the mare in advanced pregnancy is difficult due to the thick abdominal wall and because the mare will tense the abdomen. Ballotte- ment in the mare, however, is occasionally possible on either or both sides of the abdomen. Fetal movements may be observed through the abdominal wall the last months of pregnancy especially after the mare has in- gested cold water. Prior to parturition the vulva becomes enlarged, flaccid, and edematous. Plasma and milk progesterone values, determined by radioimmunoassay techniques, as in the cow, have been shown to be helpful in determining the reproductive status of mares, including the stages of the estrous cycle and the diagnosis of early pregnancy. However several days are usually required for transporting and laboratory procedures on the samples. Progesterone levels are prob- ably more reliable than behavioral patterns toward a teaser stallion in assessing ovarian activity in certain mares. This test would be of value for bred mares when no stal- lion was available for teasing or for mares exhibiting poor estrous behavior. Plasma samples from all mares were more easily obtained and processed than milk samples from lactating mares and produced equally accurate re- sults. In a limited study over 90 percent accuracy was obtained in the diagnosis of pregnancy by the presence of high levels of plasma progesterone 16 to 17 days after bred mares went out of estrus. These diagnoses were later confirmed by rectal palpation. Low levels of plasma pro- gesterone indicated non-pregnancy and the presence of estrus at this time.24b’29 Persistence of the corpus luteum without pregnancy is not uncommon in the mare and could cause an occasional inaccurate early pregnancy diagnoses when large numbers of mares are examined.—24b'28,29 Ultrasonography or ultrasonic echography of the genital organs of the mare shows definite promise of being very useful in the detection of early preg- nancy. 8b34b-40'44ab-49bc56a57a Although this technique in- volving the use of a rectal probe or transducer, requires further study and refinement and the equipment is very costly ($13,000 to $28,000) (see footnotes 1-5), re- search has shown that pregnancy diagnosis for the pres- ence of a chorionic vesicle or conceptus may be per- (1) ADR-Advanced Diagnostic Research, 734 W. Alameda Dr., Tempe, Ariz., 85282; (2) ATL-Advanced Technology Laboratories, 13208 Northrup Way, Bellevue, Wa., 98007; (3) Bion Corporation, 7000 N. Broadway, Bldg 1, Suite 105, Denver, Colo., 80221; (4) Fischer Ultrasound (‘Vetscan’) 10516 United Parkway, Schiller Park, 111.,. 60176; (5) Westmed, 801 Dexter Ave, North Seattle, Wa., 98109.8bPREGNANCY DIAGNOSIS 25 formed without damage to the embryo with an accuracy of over 95 percent from 15 to 50 days of gestation. Re- peated examinations at 5 to 10 or more day intervals greatly reduces the possibility of error as the size of the normal viable vesicle grows at a steady rate from about 1.5 to 2 cm. in diameter at 15 days of gestation to 2.75 cm. at 20 days, to 3.25 cm. at 25 days, 3.6 cm. at 30 days, 4.45 cm. at 35 days, 6.0 cm. at 40 days and 8.85 cm. (range 7-10 cm.) at 50 days. The viable embryo increases in size from about 1 cm to 3.5 cm from ges- tation day 15 to 50.34b'49c,56a In early pregnancy diagnosis errors may be due to scanning near the tip of the uterine horn and locating an ovarian follicle or in older mares finding an endometrial cyst or enlarged lymphatic la- cunae in the uterus.34b,56a In one study49c 11 of 67 mares (16.4%) had a resorption or death of the embryo between 15 and 50 days of gestation. This ultrasound instrument has also proven valuable in the detection of twin em- bryos early in gestation when treatment is best accom- plished. 34b,56a Presently many veterinarians are using this instrument on horse farms in England, France and the U.S. Further controlled studies are indicated to assess its value and possible harmful effects, which presently are negligible, and to obtain needed data on the incidence and fate of early twin embryos and early embryonic deaths in mares. Fetal pulses are visible at 24 days. Ultrasound is useful in the diagnosis of pregnancy and fetal moni- toring in dogs, cats, sheep, cattle and goats as well as the mare.43b The accuracy of an ultrasonic pregnancy detector with the transducer applied to the external abdomen of the mare was unsatisfactory.49b'57a Fetal electrocardiography has been found to have some technical limitations for the diagnosis of early pregnancy and twinning. Further studies will be neces- sary if this technique is to become practical.12 27'33'34 Internal examination for pregnancy in the mare. Before the internal examination for pregnancy in the mare is performed, a good breeding history should be obtained if possible. The foaling and breeding dates, dates of es- trum, the frequency and efficiency of teasing before and after breeding, and knowledge of the regularity of the mare in her estrual cycles and past foalings are helpful. The rectal diagnosis of pregnancy in the mare by an experienced veterinarian is presently one of the earliest and most accurate methods available. In performing a rectal examination of a mare the same equipment, dress, and mode of procedure is used as for examinations of the cow, with the following exceptions. Restraint is more essential in mares. Since most horses are more accus- tomed to being handled on the left or near-side, the au- thor prefers to perform rectal examinations with the right arm and make the initial anal penetration while standing lateral to the left hip of the mare. Thus both the operator and the man on the twitch or halter are on the same side of the mare. Many mares require the application of a nose twitch to control and make them stand quietly and prevent them from kicking the operator. Some veteri- narians have the mare’s tail forced firmly dorsally and cranially over the sacrum as a further form of restraint. Certain excitable mares that object to restraint must be handled gently and quietly if a rectal is to be performed. Often these mares may be examined by having only a foreleg elevated. In some mares tranquilization or even sedation may be required as well as application of a twitch. If breeding hobbles are used to restrain a mare, kicking is prevented but the hocks may be raised suddenly and injure the operator if he is standing too close to the rear quarters. A mare can be examined in stocks, around a stall partition, or by being backed up to a manger or several bales of hay or straw. If a mare is in stocks, the rear rope or board should be low so that if the mare drops her hind quarters suddenly the examiner’s arm will not be injured. It may be desirable to bandage the mare’s tail and have it held upward and to one side by an as- sistant so the long tail hair does not irritate the anus and rectum at the time the arm is inserted and the tail does not become soiled. A bland, nonirritating lubricant should be used on the arm. The rectum of the mare is drier than that of the cow and the operator’s arm requires frequent liberal lubrication. The author favors a bucket of soapy water made with bland soap and applied to the arm with a sponge. Nonirritating obstetrical lubricants such as K- Y Jelly or a low-cost lubricant of 500 grams of Na car- boxymethyl cellulose (Hercules) mixed with 8 gallons of water and 100 ml of chlorhexidine (Novalsan) as used at the Univ. of California57b are also satisfactory. The preparation of this latter lubricant requires careful con- trol of temperature and mixing procedures. The peri- staltic waves in the mare are stronger than in a cow. The hand and arm should be withdrawn from the rectum when a peristaltic contraction occurs. Trauma to the rectum is more easily produced than in the cow and has more se- rious and sometimes fatal consequences because of the mare’s increased susceptibility to peritonitis. Lacerations of the rectum have become a serious malpractice prob- lem not limited to younger inexperienced veterinarians. Of 54 cases of rectal tears over 90 percent resulted in the death of the horse. Of a total of 720 equine mal- practice cases from 1968 to 1981 these rectal lacerations represented 13.4 percent.50 The need for prompt vigor- ous surgical treatment of such tears of the rectum is im- perative.571’ Even with such treatment the prognosis is guarded to poor. Rectal examinations should therefore26 VETERINARY OBSTETRICS be made with quiet restraint, care, and gentleness. Daily or every other day palpation of the mare’s genital tract and ovaries during estrus, especially by inexperienced operators to detect a mature follicle and predict the time of ovulation, caused a delayed and lowered conception rate.56 After entering the rectum of the mare and locating the bony pelvis, it is easier to locate one of the ovaries, until with more experience the uterus can be readily found. The distinct fibrous bean-shaped ovary, 4 to 8 cm. long by 3 to 5 cm., in thickness is located about 10 to 20 cm. cranial to the shaft of the ilium and about 5 to 10 cm. below the lumbar vertebrae in the nonpregnant mare or mare in early pregnancy. The operator who uses his right hand can more readily locate the left ovary of the mare and vice versa. After locating one ovary the hand is passed down the proper ligament of the ovary to the uterus. The uterus is cupped in the hand between the fingers and thumb and palpation of the cranial border, ventral, and dorsal portions of the nonpregnant or early pregnant uterine horns, the opposite ligament and the opposite ovary is performed. The nonpregnant completely-involuted uterus during estrus or/anestrus is pliable, soft, flat, and rather flaccid, 4 to 7 cm. wide and 2 to 5 cm., thick. In the maiden or young mare the nonpregnant uterus is sus- pended above the floor of the pelvis and abdomen. In older mares, especially the first month after foaling, the uterus may be located more ventrally and be hanging cranial to the pelvis in the abdominal cavity. In circum- stances where the uterus was located well-forward and downward in the abdominal cavity, traction on the broad ligament, or bimanual examination, with the other hand in the vagina grasping and exerting traction on the cer- vix, could be helpful.20 Uterine changes during pregnancy. A presumptive diagnosis of pregnancy may be made at 18 to 22 days after service by the absence of signs of estrus in a mare with a normal behavioral pattern. On rectal palpation at this time the uterus is firm and tubular, the cervix is also contracted and firm, and 1 or 2 follicles of small to me- dium size may be present in the ovaries. Possibly a thin- ning of the uterine wall usually near the bifurcation over the conceptus often can be palpated. The accuracy of rectal palpation at this time varied from 80 to 93 per- cent.5'26,35,48,52 These signs, together with those revealed by a speculum, of a pale rather dry vaginal mucosa and a closed, nonedematous external cervical os are highly indicative of pregnancy. Confirmation of this presump- tive diagnosis should be performed by rectal palpation, and/or biologic tests for pregnancy at 30 to 45 and 90 days after service. In most mares rectal palpation of the uterus to diag- nose pregnancy can be performed by an experienced op- erator with accuracy from 30 to 40 days of gestation. Diagnosis usually is easier for the less experienced vet- erinarian from 40 to 50 days of pregnancy. Pregnancy diagnosis is easier in maiden mares or primigravidae, and barren, nonfoaling mares than in mares conceiving on foal estrum when the uterus has not completely in- voluted. Highly skilled veterinarians may accurately di- agnose pregnancy as early as 20 to 30 days of gestation. Care must be used not to injure the embryo, the cho- rionic or blastodermic vesicle or the rectum. Careful repeated early pregnancy examinations by rec- tal palpation of the uterus were not detrimental to fer- tility by causing an increased abortion rate.7-30,56,57 The rectal examination for the diagnosis of early pregnancy in mares consists mainly of gentle palpation of the oval chorionic vesicle in a localized area of the uterine horn and doesn’t involve the procedures of direct palpation of the amniotic vesicle and manual slipping of the mem- branes as practiced in the cow. This may account for the much lower incidence of embryonic damage after rectal palpation in the mare. It is often desirable to reexamine the mare once or twice at 60 to 120 days of gestation to make certain embryonic death and resorption did not oc- cur. In the mare, as in the cow, early embryonic deaths are not uncommon with an incidence of 2 to 20 percent or greater between early pregnancy diagnosis and 110 days of gestation.1142 46 60 A survey of 100 equine practition- ers revealed that 5 to 6 percent of mares abort after hav- ing been diagnosed pregnant early in gestation.31 Early embryonic deaths with absorptions or probably abortions from 25 to 30 days of gestation was reported in mares on a low plane of nutrition.53 In a preliminary study us- ing ultrasound to diagnose pregnancy and early equine embryonic deaths from 20 to 50 days of gestation, em- bryonic deaths occurred at all intervals with peaks around 20 and 35 days.563 The cause of the deaths was not de- termined. “Spurious” conceptions may follow a normal service in a healthy cycling mare in which further estrous cycles are not exhibited on regular teasing, and on rectal examination at a later date the mare is not pregnant. Some of these are undoubtedly due to early embryonic death, resorption, unobserved abortion or persistence of the corpus luteum. In a few instances one of a pair of twin embryos in mares may die early, the dead embryo and its membranes may undergo maceration and absorption of mummification and the normal embryo survives to term. The thickness and tone of the uterine wall increases slightly in both pregnant and nonpregnant mares from days 10 to 16 after the onset of the estrum. From dayTable 4. Size and Characteristics of the Equine Fetus and Uterus During Pregnancy* Diameter Days of Gestation Size and Shape of the Chorionic Vesicle Amount of Fetal Fluids in ml. of the Horn Containing the Fetus Weight of the Fetus Length of the Fetus (C-R) Fetal and Placental Characteristics 16 2-4.0 cm. Bantam’s egg (round) 0.32 cm. 20 2.5-4.5 cm. Small Hen’s egg (slightly oval) 0.66 cm. 25 2.5-4.5 cm. Small Hen’s egg (slightly oval) 30-40 0.6-0.85 cm. 30 2.5-5.0 cm. Hen’s egg (oval) 40-50 4-1/2-5 cm. 0.2 gm. 0.9-1.0 cm. Eye, mouth and limb buds visible, chorionic vesicle present only in the uterine horn. 35 3.5-6.5 cm. Goose’ egg (oval) 60-90 4.5-6.5 cm. 0.8 gm. 1.5-2.0 cm. 40 4.5-7.5 cm. Small orange (oval) 100-150 7-8.5 cm. 1.6 gm. 2.5-4.0 cm. Eyelids and pinnae have appeared. 45 6-10 cm. Large orange (oval) 150-200 7.5-10 cm. 3.0-4.0 gm. 2.6-4.5 cm. 50 12 x 7.5 cm. Small melon (oval) 200-350 8.3-10 cm. 5.5-6.5 gm. 3.0-6.0 cm. 60 13.3 x 8.9 cm. Melon (oval) 300-500 8.9-10 cm. 10-20 gm. 4-7.5 cm. Lips, nostrils, and beginning development of feet observed, eyelid partially closed. Placenta not attached but beginning to go into the body of uterus. 90 14 x 23 cm. Football (oval) 1200-3000 12.5-15 cm. 100-180 gm. 10-14 cm. Villi of placenta present but without firm attachment, mammary nipples and hoofs visible, body and horn of uterus both involved and enlarged. 120 3000-4000 700-1000 gm. 15-25 cm. External genitalia formed but scrotum is empty, placenta attached, ergots and orbital areas prominent. 150 5000-8000 1500-3000 gm. 25-37 cm. May or may not have fine hair on orbital arch and tip of tail, prepuce not yet developed. 180 6000-10,000 3-5 Kg. 35-60 cm. Hair on lips, orbital arch, nose, eyelashes and fine hair on mane. 210 6000-10,000 7-10 Kg. 55-70 cm. Hair on lips, nose, eyebrow, eyelids, edge of ear, tip of tail, back and mane. 240 6000-12,000 12-18 Kg. 60-80 cm. Hair on mane and tail, back and distal portion of extremities. 270 8000-12,000 20-27 Kg. 80-90 cm. Short fine hair over entire body. 300 10,000-20,000 25-40 Kg. 70-130 cm. Body completely covered with short hair, prepuce developed, hair in mane and tail increased. 330 10,000-20,000 30-50 Kg. 100-150 cm. Complete hair coat and hair coat gets its final color, testes descend. *lc, 4, 9, 10, 18, 20, 21, 23b, 36, 44b, 52, 54, 55, 59, 60. to PREGNANCY DIAGNOSIS28 VETERINARY OBSTETRICS 16 to 21 there is a 3-fold increase in thickness in the uterine wall in pregnant mares while in nonpregnant mares the thickness of the uterine wall declines to a low point at the onset of the next estrum. The tone of the uterine wall follows the same pattern, with a definite increase in the tone of the uterine wall of both the pregnant and nonpregnant mares to day 16 followed by a decline in tone in nonpregnant mares to a soft flaccid state about one day before the next estrum. In pregnant mares the uterine tone continues to increase after day 16 with the uterine horn becoming round and tubular about 5 days later 7-26'35'43'44a’b-52 Palpation of the chorionic or blastodermic vesicle. During early pregnancy a portion of the uterine horn en- larges. (See Table 4). The earliest this can ordinarily be detected is 20 to 30 days. This enlargement is charac- terized by a circumscribed, ventral bulge or distention and thinning of the uterine horn just to the right or left of the center or bifurcation of the horns. The enlarge- ment of the uterus produced by the ovoid conceptus in mares is localized and not diffuse as it is in the cow that has an elongated blastodermic vesicle. Rarely the em- bryo and its membranes may develop more laterally in either horn or in the body of the uterus. The spherical bulge or swelling is caused by the chorionic or blasto- dermic vesicle in early gestation and later by the oval chorioallantoic vesicle containing the enclosed amniotic sac and embryo, the vitelline or yolk sac and the allan- toic sac. From 3 to 6 weeks the vitelline or yolk sac is large and the amniotic cavity around the embryo is small. The allantoic cavity grows rapidly from 5 to 7 weeks of gestation when it contains much fluid.22,55 This chorionic vesicle at first is oval and then as it enlarges it assumes a more ovoid, tubular or sausage-shaped outline and ex- tends into the body of the uterus about 60 to 90 days of gestation. The uterine wall during this early stage of pregnancy is more tubular in shape, has a more tonic, firm consistency, and is thinner, especially over the ven- tral bulge. As in the cow these changes are primarily due to the localized distension of the uterine horn and body with fetal membranes and fluid, imparting the feeling of heavy, water-filled rubber balloon. By 60 to 70 days the chorioallantoic vesicle is so large it is difficult to delineate its extent and the early uterine tonus is less evident. Slipping of the fetal membranes is not performed in the mare because it is difficult, possibly damaging to the embryo and not necessary because the discrete, localized oval area of the uterus occupied by the conceptus in early pregnancy readily differentiates pregnancy from pyometra or mucometra. The thicker, more tonic, equine rectal wall also makes this technique hazardous. Palpation of the changes in the size of the horn and body containing the fetus has been outlined in Table 4. Since the size of the round and later oval chorionic or chorioallantoic vesicle is closely correlated with the size of the uterine horn, the diagnosis and duration of early pregnancy may be ascertained. The pregnant uterus in the mare is usually suspended above or on the level of the floor of the pelvis until the third to fourth month of gestation, when it drops enough to rest on the abdominal floor and the ventral surface of the uterus can’t be palpated. In older mares it may rest there by the third month. If the mare is more than 3 months pregnant it will be difficult or impossible to re- tract the uterus, due to its weight; whereas if the mare is not pregnant the uterus can be retracted and palpated. By the fifth to sixth month of pregnancy the uterus is well-forward in the abdominal cavity and the broad lig- ament is under definite tension. The ovary may be 20 to 25 cm. below the lumbar vertabrae and is moved with difficulty because of the stretching of the mesovarium. Palpation of the fetus through the rectal wall can usually be performed from 90 to 120 days of gestation when the fetus feels like a small, heavy, submerged but floating object as the hand by a patting motion ballots it. It is usually possible in most mares to palpate the fetus per rectum from the third month throughout the rest of the gestation period. The size and weight of the equine fetus during the various stages of pregnancy are noted in Table 4. In a few deep-bodied older mares palpation of the fetus may be difficult from the fifth to seventh month of gestation. In these mares the location of the uterus, the position of the ovaries, and the palpation ofPREGNANCY DIAGNOSIS 29 the enlarged, whirring uterine artery will aid or confirm a diagnosis of pregnancy. The ovaries of the mare during early pregnancy, differing from the cow, are of no value in determining the uterine horn containing the fetus. The corpus luteum is only palpable for a few days to a week after ovulation before it is covered by the dense fibrous ovarian tunic. A number of reports indicate that the incidence of ovu- lation may be slightly higher from the left ovary, 51 to 60 percent. The early embryo, up to 30 or possibly more days of gestation can migrate within the uterus resulting in slightly more pregnancies, up to 60 percent, in the right hom.-'3,8'13'25,38 The gestation period can be divided into four periods based on the changes that occur in the ovaries.19 The first period, from ovulation to 40 days, is characterized by the presence of a single corpus luteum of pregnancy and a number of various-sized follicles on both ovaries. Great follicular activity occurs between 17 and 30 days after conception and before the secretion of gonadotropin by the endometrial cups.6,19'52 The second period, from 40 to 150 days, is characterized by marked ovarian activity many follicles over 1 cm. in diameter and the formation of accessory corpora lutea. Ovulation occurs during this period.3 Usually 3 to 5 or more accessory corpora lutea are present in each ovary. This ovarian activity with fol- licle and corpora lutea formation is probably caused by the high FSH and LH levels in the mare and not the high PMSG secreted by the endometrial cups from 40 to 120 days of gestation. Mares’ ovaries apparently are unre- sponsive to PMSG (pregnant mare serum gonadotropin). The third period, from 150 to 210 days, is characterized by a regression of the corpora lutea and the absence of large follicles. The fourth period from 210 days to foal- ing no corpora lutea or follicles are present. During these latter two periods, gestation is maintained by steroid hor- mones produced in the placenta.47 The vaginal examination as an aid in pregnancy di- agnosis may be helpful but is not as accurate as the rec- tal examination of the uterus. By 30 days of pregnancy the normal equine vagina and cervix, on examination with a speculum, are very white and pale. They are more white and pale than at any time during the estrual cycle and resembles a mare’s vagina in anestrus during the winter months. The mucous membrane is very dry, sticky, and gummy. There is less tendency for the vagina to balloon when the speculum is inserted than during the estrual cycle. More gummy mucus is present on the mucous membrane of the vagina during pregnancy than during the anestrous period. About 75 percent of pregnant mares show these characteristic vaginal changes.20 The other pregnant mares may show a more hyperemic or con- gested mucous membrane with less mucus. In rare cases a vaginitis with a mucopurulent exudate may be seen. The cervix in pregnant mares is usually tightly closed and small with a puckered external os. It is usually pulled downward and to one side. The external os of the cervix usually becomes covered with gummy, sticky mucus. In advanced pregnancy it may be easier to palpate the fetus through the vagina than through the rectum, as the mare objects less to the vaginal examination. Differential diagnosis in pregnancy examinations should be considered by the inexperienced examiner. Occasionally a large endometrial cyst or lymph lacuna of the uterine wall may be mistaken for early pregnancy. From 70 to 110 days a distended bladder may be con- fused with pregnancy. Pneumovagina or a uterus filled with air might be mistaken for pregnancy. From 90 to 120 days an enlarged or distended right colon or pelvic flexure of the colon might rarely be confused with a pregnant uterus. Pyometra and mucometra associated with endometritis and focal cystic degeneration of the endo- metrium are occasionally found in the mare. The uterine wall and the fluid contents of the uterus may be heavy and thick. Tumors of the uterus and ovaries are uncom- mon in the mare. Mummification of a single fetus has not been observed in the mare. Fetal maceration is also uncommon. Double ovulation occurs in 18 to 25 percent of mares and twin pregnancies are quite commonly diagnosed. But the incidence of twin births is low, 0.5 percent, due to embryonic or fetal death and abortion of possible of one, or more often, both fetuses.4,38 Twin embryos may be detected early, 21 to 25 days, by the palpation of two chorioallantoic vesicles or ventral bulges, often with one in each horn. If both vesicles lie close together produc- ing a ventral bulge of the hom 10 to 30 percent greater in size than that of a single pregnancy, diagnosis is dif- ficult, especially after 60 days.35 Later, twin fetuses might be palpated and both uterine arteries might be enlarged. Embryonic deaths in mares may be diagnosed at 35 to 45 days or more of gestation by a loss of fluid and tone in the chorioallantoic vesicle and a marked reduc- tion in the size of the ventral bulge. These affected mares may not return to estrum and a regular estrous cycle for 40 to 80 days or more because of the presence of en- dometrial cups and the elevated secretion of PMSG.1,2,53 Douching the uterus with 500 ml. of warm saline or an injection of 10-15 mg. of prostaglandin (PGf2a) or a prostaglandin analogue if performed before 40 days of gestation, usually results in a return to estrus within a few days in these mares. If early embryonic death is sus- pected, repeated examinations per rectum may be needed to confirm it.30 VETERINARY OBSTETRICS The Biologic Tests for Pregnancy in the Mare The tests are practical and nearly as accurate as preg- nancy diagnosis per rectum. They are particularly indi- cated in highly nervous or vicious mares and small pon- ies in which rectal examinations would be highly dangerous for the operator or impossible because of the size of the animal. Veterinarians not experienced in the techniques of pregnancy diagnosis per rectum frequently employ these tests. The gonadotropic hormone, present at high levels during the early stages of the equine ges- tation period, is the principal hormone utilized for preg- nancy testing. The gonadotropic hormone (pregnant mare serum gonadotropin (PMSG) or equine chorionic gonado- tropin, (ECG) from the endometrial cups in pregnant mares is first found in mare serum from 38 to 42 days of gestation. It reaches its maximum levels between 50 and 80 days and then gradually declines and is absent after 120 to 150 days. Ten ml. of blood should be drawn from the mare’s jugular vein into a sterile tube. After clotting and separation of the serum at room tempera- ture, the serum should be removed and refrigerated. Ov- erheating of the sample should be avoided. This test may be conducted with accuracy from 40 to 120 days of preg- nancy. Tests before 40 days and after 120 days of ges- tation in the mare may be inaccurate due to the low level of circulating gonadotropins in the plasma. The hemagglutination-inhibition test is highly accu- rate, over 90 percent, in mares.14,32,41,49 The hemagglu- tination inhibition test utilizes the principle that PMS go- nadotropins inhibit the agglutination of horse erythrocytes coated with PMS gonadotropin in the presence of PMS gonadotropin antiserum. This test, the Mare Immuno- logical Pregnancy (MIP) test is sold commercially in the U.S. by Diamond Laboratories, Des Moines, Iowa. A recently developed radioreceptor assay test22b and the possible commercial development of an ELISA test563 for the presence of PMSG or ECG may be more accurate than the MIP test at 35 to 45 days to 100 to 150 days of gestation. Further studies should be conducted on these promising tests even though the former requires care- fully controlled laboratory techniques. The tests for gonadotropic hormone in pregnant mare serum are based on the development of endometrial cups in the region of the junction of the horn containing the embryo and the body of the uterus at about 30 to 40 days of gestation. These endometrial outgrowths are closely invested by the chorioallantois. The endometrial cups enlarge and fill with a mucoprotein secretion very rich in gonadotropic hormone the amount of which parallels levels in the blood.15-18 At 40, 80 and 150 days of ges- tation the total gonadotropic secretory activity in the cups and in the plasma of the mare were 21,000 I.U. and 0.1 to 6.0 I.U./ml.; 73,000 I.U. and 6 to 296 I.U./ml.; and 42,000 I.U. and less than 0.5 to 106 I.U./ml., respec- tively. The equine gonadotropin produced in the endo- metrial cups is formed by the apocrine glandlike cells from the early chorionic girdle. The endometrial cups and their associated structures begin to show very early desquamation and regression at about 80 days of ges- tation and have completely desquamated by 100 to 120 days21 but the high levels in the plasma of PMSG may require more time to completely disappear. When a mare is carrying a mule fetus the MIP test is not accurate because the equine gonadotropin concen- tration of her serum is about one-tenth that associated with a horse fetus.16 Ponies have as much as 8 times the concentration of gonadotropin as the draft breeds.17 This might be a breed difference or due to a dilution factor. Mares with a twin pregnancy of 52 to 72 days duration usually had twice the level of gonadotropin in their plasma than mares carrying single fetuses.45 This difference was apparently due to a double set of endometrial cups in mares carrying twins. Ovarian activity was not corre- lated to gonadotropin levels in the blood. Gonadotropins are not found in the urine of pregnant mares as they are in women. False negative reactions may occur due to taking semm from mares at 35 to 38 days and from 110 to 150 days of gestation when the level of serum gonadotropin may be very low in some mares. False positive reactions in mares may be due to early embryonic deaths that may occur in 5 to 10 percent of mares between 40 and 120 days of gestation and in which PMSG is continued to be secreted by the endometrial cups.41 Because of these oc- casional false positive results when testing for equine go- nadotropin, some owners rely on the rectal examination or ultrasonography by a skilled veterinary examiner for the most accurate determination of pregnancy in mares. Pregnant mares in which spontaneous or induced em- bryonic deaths occur after 40 days of gestation, when endometrial cups secreting PMSG are present, enter a pseudopregnant or infertile period that persists until the endometrial cups have sloughed or desquamated and lev- els of PMSG have disappeared from the blood plasma at about 120 or more days after conception. Thorough- bred mares during this period are in anestrus and have small firm inactive ovaries while pony mares have ir- regular frequent but anovulatory estrus periods charac- terized by follicular activity and apparent premature lu- teinization of the follicles. Repeated douching of the uterus or injections of prostaglandins to cause involution of the corpora lutea failed to produce estrus, ovulation and con- ception in these mares.1,2 Other tests for gonodotropin in the plasma of maresPREGNANCY DIAGNOSIS 31 include the Ascheim-Zondek or immature rat test, the Friedman modification of the A.Z. test or rabbit test, the male frog or toad test and the direct latex agglutination test. These tests are more difficult, costly and give slower results than the convenient, practical, rapid, cheaper hemagglutination-inhibition or MIP test.43 The Cole-Hart modification of the A.Z. test or “mouse” test is currently considered to be more accurate than the M.I.P. test or manual pregnancy test in mares for insurance purposes in Australia.3911 The Cuboni and other tests for detecting the pres- ence of estrogenic hormone in the urine of pregnant mares are accurate when applied from 120 to 250 days of pregnancy.43 These tests have not proven practical be- cause horse owners want the results of pregnancy testing much earlier than 120 days of gestation. Pregnancy Diagnosis in the Ewe and Doe Pregnancy diagnosis in the ewe and doe has been based primarily on post-conception clinical observations of changes in the animal similar to those occurring in the cow and mare, such as: service by a male and cessation of the estrous cycle. The use of a marking harness on the ram with different colored chalk used every 2 to 3 weeks and keeping of breeding records with ewe iden- tification is desirable.8,12'17 In a well-managed flock over 90 percent of the ewes were marked and apparently bred but 20 percent failed to lamb so embryonic death losses probably occur. In advanced pregnancy there is an in- crease in the size of the abdomen and udder. The latter is most evident in primipara. During gestation up to 20 to 30 percent of pregnant ewes exhibit an estrous period of about 18 hours’ duration one or more times. These periods were most common during early pregnancy but also occurred even in the late stages of gestation.8,22 Ninety-four percent of ewes failing to return to estrus by 21 days after service were pregnant but matings must be closely supervised and observations recorded.8,17 In the ewe and doe one can occasionally observe fetal movements in advanced pregnancy and ballot the fetus on the right side from 3-1/2 to 4 months of pregnancy to term. The latter is most readily accomplished in thin fine-wool breeds by placing them on their rump on a crate and ballotting of the lower abdomen.7,15,18,21 A radiographic diagnosis of single or possibly twin pregnancy can be made in 90 percent of ewes and does from 75 to 90 days of gestation to term but it is rather expensive.7,17 The use of the fetal electrocardiogram as reported in horses and cattle has not proven practical for pregnancy diagnosis in sheep and does.717 The use of an ultrasonic Doppler instrument by rectal insertion or application to the abdomen was over 90 percent accurate in the detec- tion of pregnancy in ewes and does from 65 to 135 days of gestation.—,4,7.9,loa.iob,12.13,17 j^ese £)0ppier instru- ments detect movements of the fetus, blood in the heart and the pulse in the large vessels of the fetus. The ac- curacy in detecting twins was about 50 to 60 percent. Using an ultrasonic device similar to that used in swine had an accuracy of 80 to 90 percent in does and ewes pregnant more than 65 days.la (See Pregnancy Diagnosis in the Mare) A direct method of palpation of the uterus with the fingers through a small abdominal incision in the in- guinal region between 5 to 8 weeks of gestation was de- scribed.8 Progesterone levels in blood plasma, milk or milk fat may be used in ewes and does, especially the latter for pregnancy diagnosis. Blood or milk samples taken at 16 to 21 days and 32 to 35 days after mating in ewes and 21 days in does are analyzed by radioim- munoassay. Progesterone levels in blood and milk fat were more accurate for pregnancy diagnosis in does than milk levels.10 High levels of progesterone indicate preg- nancy and low levels nonpregnancy. The results are about 90 or more percent accurate when correlated with lamb- ing of kidding.—,7,12,14,17,20 A bimanual rectal probe-abdominal palpation technique for ewes has been described and illustrated that is over 90 percent accurate by 65 to 70 days post- breeding. It is simple, easy and practical. Thin and re- laxes ewes are easier to examine than fat or straining ewes. This technique was quite accurate in diagnosing single or twin fetuses.5,6,19 However, careful manipula- tion of the rectal probe is essential to avoid injury. Oc- casional abortions and deaths due to laceration of the rectum have been reported. Skilled operators produced very few rectal perforations but rectal abrasion and bruising are common, especially in nonpregnant ewes. This rectal abdominal palpation technique has been eval- uated in does and is accurate8 but the possibility of abor- tions and deaths occasionally produced by this procedure limits its usefulness.13 Laparoscopy or peritoneoscopy with an instrument inserted through the upper right flank area is an alternative to the laparotomy procedure.3,11 The technique of vaginal biopsy after 40 days of ges- tation was over 90 percent accurate for pregnancy di- agnosis but was of no value in determining twinning. Its accuracy in detecting non-pregnant ewes was about 80 percent. This technique required a laboratory and a skilled person to examine the slides prepared from the biopsy of the vaginal mucosa.12,16 A variety of other techniques to determine pregnancy in ewes and does have been evaluated, such as palpation of the caudal uterine artery per vaginum, assay of blood levels of estrogen and others but they are either unsat-32 VETERINARY OBSTETRICS isfactory, unreliable, too expensive or too time consum- •__7,12,17 mg. About 10 to 20 percent of the embryos in sheep, es- pecially with double ovulation, will undergo transuterine migration from one horn to the other. Sixty-two percent of single ovulations in ewes and 56 percent of multiple ovulation occurred on the right ovary.1 Ovine fetal crown- rump length at various stages of gestation are as follows: 30 days, 1.5 cm.; 60 days, 5.0 cm.; 90 days, 15 cm.; 120 days, 27 cm.; and 150 days, 50 cm. Pregnancy Diagnosis in the Sow Clinical observations may be used to diagnose preg- nancy in sows as in ewes, cows and mares. Although the incidence of ovulation from each ovary may vary in sows, transuterine migration and placement of embryos results in nearly an equal number of fetuses in both uter- ine horns.3,13 Rectal examinations and palpation of the uterine artery for diagnosing pregnancy can be performed in most sows and large gilts with an accuracy of over 90 percent after 40 or more days of gestation. Diagnosis was based on the size, tone and fremitus in the uterine artery compared to the external iliac artery. The tone of the cervix was also considered.1,8 Testing blood plasma for elevated estrone levels by radioimmunoassay be- tween 20 to 30 days after service could be used as a pregnancy test in sows and gilts.—,2,61013b This elevated estrogen level produced by the blastocysts in the uterus, was first detectable at 15 days after service and resulted in the maternal recognition of pregnancy and persistence of the corpora lutea. Laparoscopy techniques have also been used in sows and gilts for a highly accurate diag- nosis of early pregnancy.16 Ultrasonography or ultrasonic amplitude depth or fetal pulse analysis, despite the initial cost of the equip- ment, is rapidly becoming the method of choice for pregnancy diagnosis in swine. A number of commercial companies are selling these solid-state machines utilizing a transducer probe placed on the lower abdomen or flank region of the female just lateral to the nipples and caudal to the navel and directed toward the uterus. A water sol- uble gel or com oil is placed on the tip of the probe before placing it on the skin to improve contact. This test has proven to be over 90 percent accurate between 30 and 90 days of gestation in both pregnant and non- pregnant sows or gilts. The test is rapid and safe and restraint is minimal.-3,5,9 Amniotic and allantoic fluids are largely responsible for the positive acoustical pat- terns. The allantoic fluid increases rapidly from day 23 to day 65 and amniotic fluid from day 30 to day 80 of gestation. The proportion of conceptus volume, fluids vs. fetus, declines rapidly after 90 days coinciding with rapid fetal growth resulting in a decline in the reliability of this method (amplitude-depth) after 90 days of ges- tation. The fetal-pulse ultrasonic analysis is over 90 per- cent accurate after 55 days of gestation.5 The vaginal biopsy technique for early pregnancy di- agnosis in sows or gilts is over 90 percent accurate from 20 to 90 days after service. A special biopsy instrument is inserted into the vagina when the females are eating and a portion of the vaginal epithelium is recovered. Fro- zen, unstained tissue sections or stained tissue sections are examined under a microscope. A pregnant animal has four or fewer layers of epithelial cells with no in- terpapillary pegs. While a nonpregnant female has a many layered vaginal epithelium with abundant interpapillary pegs.-4,5,7,15 The fetal crown-rump length of swine fetuses at var- ious stages of gestation is: 30 days, 1.8 to 2.5 cm.; 60 days, 8 to 11 cm.; 90 days, 17 to 23 cm. and at farrow- ing, 23 to 29 cm.14 Pregnancy Diagnosis in the Bitch and Queen During pregnancy in the bitch there is usually a marked progressive increase in abdominal size from 35 days to term due to the deposition of fat and the increase in size and weight of the uterus. The teats between 35 to 45 days of gestation become enlarged and turgid. After 45 days they soften and become still larger. The mammary glands become enlarged and edematous from 50 to 55 days of pregnancy. Since these changes are even pres- ent, but usually less apparent, in non-pregnant bitches following estrum due to the pseudopregnant state, one must be cautious in diagnosing pregnancy on the basis of the above signs. Pseudopregnancy in the bitch extends for approximately the same period of time as gestation and may be followed by lactation if suckling is allowed. In dogs abdominal distention may also result from as- cites, splenic enlargement, abdominal tumors, pyome- tra, or other causes. Palpation of the uterus through the abdominal wall is one of the best and earliest methods of diagnosing early pregnancy in the bitch.- The ease with which this is done will depend on a number of factors such as: the tem- perament of the bitch, size of the dog, the stage of ges- tation, the number of fetuses in the uterus, and the de- gree of obesity.- At 18 to 21 days the embryos and their chorioallantoic vesicles produce a series of round swell- ings about 1.25 cm. in diameter in the uterine horns which frequently may be difficult to palpate at this time throughPREGNANCY DIAGNOSIS 33 the abdominal wall. From 28 to 32 days of pregnancy these round ping-pong ball-like swellings in the uterus are about 1.5 to 3.5 cm. in diameter and are usually readily palpable. After 30 days it is difficult to palpate the pregnant uterus since the swellings increase in size, elongate, become confluent, lose their tenseness and come to rest on the abdominal floor. In some cases abdominal enlargement is noticeable. At 40 days of gestation these uterine swellings are 5.4 x 8.1 cm. in pregnant bitches.5 It is easier to palpate the caudal portions of the uterus. Fecal material in the colon should not be confused with pregnancy. From 45 to 55 days of pregnancy the size of the uterine horns and fetuses increase rapidly. The cau- dal fetuses are about 7.5 cm. long in medium-sized bitches and may be palpated in thin bitches with a thin, relaxed abdominal wall. The horn, since it is greatly distended and elongated, is usually bent in the middle at the liver. The apical portion of the horn is bent caudal and lies lateral and dorsal to the cervical portion of the horn. From 55 to 63 days the size of the fetuses are such that they can readily be detected. Rectal palpation with the finger with the forequarters elevated often is successful if pal- pation through the abdominal wall is difficult. The crown- rump length of the canine fetus at various stages of ges- tation is: 21 days, 0.7 to 1.0 cm.; 30 days, 1.5 to 1.6 cm.; 40 days, 6.3 to 7.8 cm.; 50 days, 11 to 12 cm. and 60 days, 14 to 20 cm.612 Radiography is a helpful diagnostic aid in the bitch and queen especially late in pregnancy since fetal bones calcify during the last 20 days of gestation.710 With care- ful technique and experience the introduction of air, 200 to 800 ml., depending on the size of the bitch, into the abdominal cavity producing pneumoperitoneum, may help delineate the swellings in the uterus as early as 30 to 35 days of pregnancy. In the feline fetus the radius and ulna at 41 days and the tibia, fibula, ilium, ischium and oc- cipital bones at 43 days, metacarpals and metatarsals at 49 days, and the entire skeleton at 55 days is calcified and can be visualized radiographically.1,3'4 Radiographs prior to 25 days in bitch and queen should be avoided because teratologic effects may be produced in the em- bryos. In the queen palpation of the implantation sites in the uterus through the thin abdominal wall is easier than in the bitch and possible from 14 to 25 days but best ac- complished from 17 to 21 days of gestation when these sites are about 1 to 1.5 cm. in size and firm. The fingers and thumb are placed together through the abdomen be- neath the transverse lumbar vertebrae. Slowly draw these ventrally feeling first the rectum and then the uterus. After this period the uterus enlarges rapidly, becomes much softer and doughy and is difficult to palpate. By 45 days of gestation the abdomen has become enlarged in queens carrying four or more fetuses. This manual examination should be done carefully and gently at all stages of ges- tation to prevent possible death and abortion of the em- bryos or fetuses. Between days 45 and term, the fetus, especially the head, can be palpated. Ultrasonography or ultrasound techniques have been utilized in pregnancy diagnosis in the bitch and queen from about 30 days of gestation to term.13 It may also be used to detect fetal life in conditions in which ra- diography and auscultation of the fetal heart are difficult or not definitive. Further studies are needed to develop and make more practical this technique. Presently the cost of the equipment is nearly prohibitive. (See Preg- nancy Diagnosis in the Mare.) Laparoscopy has been developed and used for preg- nancy diagnosis in the bitch and queen. It is accurate in early gestation from about day 15 to term.3,8 Biologic tests for pregnancy diagnosis are not avail- able in the bitch and queen. Vaginal cytology is also unreliable.3,10 General References la. Arthur, G. H. (1975) Veterinary Reproduction and Obstetrics, 4th Ed., Lea & Febiger, Philadelphia. _lb. Evans, H. E. and Sack, W. O. (1973) Prenatal Development of Domestic and Laboratory Mammals: Growth Curves, External Features and Selected References, Anat., Histol., Embryol., 2, 11-45. 2. Fraser, A. F. (1971) Tables of Data on Livestock Reproduction, Williams Wilkins Co., Baltimore, Baillier Tindall, London. 3a. Hunter, R. H. F. (1980) Physiology and Technology of Repro- duction in Female Domestic Animals, Academic Press, N.Y.C., London. 3b. Jochle, W. (1980) Early Pregnancy Tests and Their Accuracy (Mare, Cow, Sow, Ewe), An. Reprod. Rept. 3, 16, 56 (Denville, N.J.). 4. Richter, J. and Gotze, R. (1960) Tiergeburtshilfe, 2nd Ed., Paul Parey, Berlin and Hamburg, W. Germany. 5. Zemjanis, R. (1970) Diagnostic and Therapeutic Techniques in Animal Reproduction, Williams and Wilkins Comp., Baltimore. Pregnancy Diagnosis in Cattle la. Abbitt, B., Ball, L., Kitto, P. G., Sitzman, C. G., Wilgenburg, B., Raim, L. W. and Seidel, G. E. Jr. (1978) The Effect of Three Methods of Palpation for Pregnancy. Diagnosis per Rec- tum on Embryonic and Fetal Attrition in Cows, JAVMA 173, 8, 973. lb. Archibong, M S. and Diehl, J. R. (1962) Evaluation of an Ul- trasonic Amplitude Depth Analysis Technique for Pregnancy Diagnosis in the Cow, Amer. J. Vet. Res. 43, 4, 711. 2. Arthur, G. H. (1957) Some Notes on the Quantities of Fetal Fluids in Ruminants, Brit. Vet. J. 113, 17. 3. Ball, L. (1980) Pregnancy Diagnosis in the Cow, in Current34 VETERINARY OBSTETRICS Therapy in Theriogenology edited by Morrow, D. A., W. B. Saunders Comp., Philadelphia, London, Toronto 229-235. 4. Ball, L. and Carroll, E. J. (1963) Induction of Fetal Death in Cattle by Manual Rupture of the Amniotic Vesicle, JAVMA 142, 373. 5a. Belling, T. H. Jr. (1964) Dairy Herd Reproductive Health Pro- gram: Part IV Discussion of Clinical Observations and Treat- ment, Vet. Med. 59, 5, 177. 5b. Bongso, T. A. and Basrur, P. K. (1976) Fetal Fluids in Cattle, Can. Vet. J. 17, 38-41. 6. Booth, J. M. (Milk Marketing Board, Worcester, England) (1979) Milk Progesterone Testing: Application to Herd Management, J. Dairy Sci. 62, 1829. 7. Bulman, D. C. and Lamming, G. E. (1979) The Use of Milk Progesterone Analysis in the Study of Oestrus Detection, Herd Fertility and Embryonic Mortality in Dairy Cows, Brit. Vet. J. 135, 559. 8. Donald, H. P. (1943) Heat During Pregnancy in Dairy Cows, Vet. Rec. 55, 297. 9. Donoho, H. R. and Rickard, H. E. (1955) The Occurrence of Estrus During Pregnancy in Several Holstein Herds, J. Dairy Sci. 38, 6, 602. 10a. Edwards, M. J. (1962) Weights of Cyclic and Pregnancy Cor- pora Lutea of Dairy Cows, J. of Reprod. and Fert. 4, 93. 10b. Eley, R. M., Thatcher, W. W., Fuller, W. B., Wilcox, C. J., Becker, R. B., Head, H. H. and Adkinson, R. W. (1978) De- velopment of the Conceptus in the Bovine, J. Dairy Sci. 61, 467. 11. Erb, R. E. and Morrison, R. A. (1958) Estrus after Conception in a Herd of Holstein Friesian Cattle, J. Dairy Sci. 41, 2, 267. 12. Erdheim, M. (1942) The Incidence of Right and Left Horn Preg- nancies in Dairy and Beef Cattle, JAVMA 100, 781, 343. 13. Fincher, M. J. (1942) Methods of Increasing Fertility in Do- mestic Animals, Transact, of the Amer. Soc. for the Study of Sterility, 1. 14. Foote, R. H. (1979) Hormones in Milk That May Reflect Re- productive Changes, Animal Reproduction, BARC Sympos. 3, H. Hawk Editor, Allenheld, Osmun, Montclair. 15. Foote, R. H., Oltenacu, E. A. B., Kummerfeld, H. L., Smith, R. D., Riek, P. M., and Braun, R. K. (1979) Milk Progesterone as a Diagnostic Aid, Brit. Vet. J. 135, 550. 16. Foote, R. H., Smith, R. K., Oltenacu, E. A. B., Braun, R. K. and Reimers, T. J. (1980) Milk Progesterone Assays as Part of a Reproductive Management Program for Dairy Cattle Proc 9th Intemat. Congr. on An. Reprod. and A.I., Madrid, Spain. 17a. Gier, H. T. and Marion, G. B. (1960) Prenatal Growth Mea- surements of the Bovine, J. Dairy Sci. 43, 6, 865. 17b. Gowan, E. W., Etches, R. J., Bryden, C. and King, G. J. (1982) Factors Affecting Accuracy of Pregnancy Diagnosis in Cattle, J. Dairy Sci., 65, 1294. 18. Hoffman, B., Hamburger, R., Gunzler, O., Komdorfer, L. and Lohoff, H. (1974) Determination of Progesterone in Milk Ap- plied for Pregnancy Diagnosis in the Cow, Theriog. 2, 1-2, 21. 19. Kanagawa, H., Too, K., Kawata, K. (1966) Fetal Electrocar- diogram in Dairy Cattle. IV Diagnostic Application for Fetal Mummification, Jap. J. Vet. Res. 14, 3 and 4, 114. 20. Koger, L. M. (1960) Routine Pregnancy Examination in Beef Cattle Practice, JAVMA 136, 3, 130. 21. Kummerfeld, H. L., Oltenacu, E. A. B. and Foote, R. H. (1978) Embryonic Mortality in Dairy Cows Estimated by Nonreturns to Service, Estrus and Cyclic Milk Progesterone Patterns, J. Dairy Sci. 61, 12, 1773. 22. Larks, S. D., Holm, L. W. and Parker, H. R. (1960) A New Technique for the Demonstration of the Fetal Electrocardiogram in the Large Domestic Animal (Cattle, Sheep, Horse), Cor. Vet. 50, 4, 1959. 23. Lindahl, I. L., Reynolds, P. J. and Allman, K. E. (1968) Fetal Electrocardiograms in Dairy Cattle, J. An. Sci. 27, 5, 1412. 24a. McCaughey, W. J. (1982) Diagnostic Use of Vaginal Electrical Resistance in Cows, Abstr. Vet. Med./Sm. An. Clin., Feb. 1982, 170 (Vet. Res. Comm. 5, 1, Sept. 1981). 24b. Mather, E. C. (1977) Milk Steroid Studies and Their Use in Fertility Examination, Proc. Ann. Meeting Soc. for Theriog., St. Paul, Minn., p. 143. 25a. Mitchell, D. (1973) Detection of Foetal Circulation in the Mare and Cow by Doppler Ultrasound. Vet. Rec. 93, 365. 25b. Momont, Harry (1980) Ultrasound Detection of Pregnancy in Ruminants, Proc. Ann. Meeting Soc. for Theriog., Omaha, Neb., 209. 26a. Nakao, T., Sugihashi, A., Ishibshi, Y., Tosa, E., Nakagawa, Y., Yato, H., Nomura, T., Ohe, T., Ishimi, S., Takahashi, H., Koiwa, M., Tsunoda, N., and Kawata, K., (1982) Use of Milk Progesterone Enzyme Immunoassay for Early Pregnancy Di- agnosis in Cows, Theriog. 18, 3, 267. 26b. Nielsen, F. (1949) Sterility in Cattle, Proc. 14th Intemat. Vet. Congress, Vol III Section 4 (c), 105. 27. Paisley, L. G., Mickelsen, W. D. and Frost, O. L. (1978) A Survey of the Incidence of Prenatal Mortality in Cattle Follow- ing Pregnancy Diagnosis by Rectal Examination, Theriog. 9, 6, 481. 28. Pennington, J. A., Spahr, S. L. and Lodge, J. R. (1976) Milk Progesterone During the Cow’s Reproductive Cycle, Abstr. J. An. Sci. 42, 5, 1361. 29. Pennington, J. A., Spahr, S. L. and Lodge, J. R. (1981) Influ- ences on Progesterone Concentration in Bovine Milk, J. Dairy Sci. 64, 259. 30. Perkins, J. R., Olds, D. and Seath, D. M. (1954) A Study of 1000 Bovine Genitalia, J. Dairy Sci. 37, 10, 1158. 31. Rahlmann, D. F. and Mead, S. W. (1958) False Heat During Pregnancy, Hoard’s Dairyman, Sept. 883. 32a. Reimers, T. J., Smith, R. D. and Foote, R. H. (1980) Milk Progesterone Testing to Determine Reproductive Status of Cows, Intemat. Congr. on Dis. of Cattle, Tel-Aviv. 32b. Rowson, L. E. A., Lawson, R. A. S. and Moor, R. M. (1971) Production of Twins in Cattle by Egg Transfer, J. Reprod. Fert., 25, 261-268. 33. Shemesh, M., Ayalon, N., Shalev, E., Nerya, A., Schindler, H. and Milguir, F. (1978) Milk Progesterone Measurement in Dairy Cows, Theriog. 9, 4. 34. Smith, R. D., Braun, R. K., Oltenacu, E. A. B. and Foote, R. H. (1981) The Use of Milk Progesterone to Monitor Reproduc- tive Status in New York Dairy Herds, J. Dairy Sci. 64, Suppl. I, 163. 35. Spaulding, R. W., Everett, R. W., Foote, R. H. (1975) Fertility in N.Y. Artificially Inseminated Holstein Herds in Dairy Herd Improvement, J. Dairy Sci. 58, 718. 36. Studer, E. (1969) Early Pregnancy Diagnosis and Fetal Death, Vet. Med. 64, 7, 613. 37. Swett, N. W., Matthews, C. A. and Fohrman, M. H. (1948) Development of the Fetus in the Dairy Cow, U.S.D.A. Tech. Bull. 964, Washington, D.C. 38. Too, K., Kanagawa, H., and Kawata, K. (1965) Fetal Electro- cardiogram in Dairy Cattle, I Fundamental Studies, Jap. J. Vet. Res. 13, 3, 71.PREGNANCY DIAGNOSIS 35 39. Trimberger, G. W. (1941) Menstruation Frequency and Its Re- lation to Conception in Dairy Cattle, J. Dairy Sci. 24, 819. 40. Vaillancourt, D., Bierschwal, C. J., Ogwu, D., Elmore, R. G., Martin, C. E., Sharp, A. J. and Youngquist, R. S. (1979) Cor- relation Between Pregnancy Diagnosis by Membrane Slip and Embryonic Mortality, JAVMA 175, 5, 466. 41. Winters, L. M., Green, W. W. and Comstock, R. E. (1942) The Prenatal Development of the Bovine, Tech. Bull. 151 Agr. Exp. Stat. Univ. of Minn., St. Paul, Minn. 42. Zaied, A. A., Bierschwal, C. J., Elmore, R. G., Youngquist, R. S., Sharp, A. J. and Garverick, A. J. (1979) Concentrations of Progesterone in Milk as a Monitor of Early Pregnancy Di- agnosis in Dairy Cows, Theriog., 12, 1, 3. 43. Zemjanis, R. (1978) Production, Reproduction, Veterinarian, The Bov. Pract. 13, 57. Pregnancy Diagnosis in Mares 1. Allen, W. E. (1978) Some Observations on Pseudopregnancy in Mares, Brit. Vet. J. 134, 263. 2. Allen, W. E. (1979) Abnormalities in the Oestrus Cycle in the Mare, Vet. Rec. 104, 166. 3. Amoroso, E. C. and Rowlands, I. W. (1948) Ovarian Activity in the Pregnant Mare, Nature 161, 355. 4. Arthur, G. H. (1958) An Analysis of the Reproductive Function of Mares Based on Postmortem Examination, Vet. Rec. 70, 682. 5. Back, D. J., Pickett, B. W., Voss, J. L. and Seidel, G. E. Jr. (1974) Observations on the Sexual Behavior of Nonlactating Mares, JAVMA 165, 717-720. 6. Bain, A. M. (1967) The Ovaries of the Mare During Early Preg- nancy, Vet. Rec. 80, 6, 229. 7. Bain, A. M. (1967) The Manual Diagnosis of Pregnancy in the Thoroughbred Mare, N.Z. Vet. Jour. 15, 12, 227. 8a. Bain, A. M. and Howey, W. P. (1975) Ovulation and Trans- uterine Migration of the Conceptus in Thoroughbred Mares, J. Reprod. Feit., Suppl. 23, 541. 8b. Barton, K. (1982) Diagnostic Ultrasound, Eq. Vet. Data, 3, 16, 241-256. 9. Benesch, F. (1952) Lehrbuch der Tierarzlichen Geburtshilfe and Gynakologie, Urban and Schwarzenberg, Wien-Innsbruck, Aus- tria. 10. Bergin, W. C., Gier, H. T., Frey, R. A. and Marion, G. B. (1967) Developmental Horizons and Measurements Useful for Age Determination of Equine Embryos and Fetuses, Proc. Amer. Assoc. Equine Pract., New Orleans, La., 179. 11. Britton, J. W. (1947) Clinical Studies on Early Equine Abor- tion, Cor. Vet. 37, 1, 14. 12. Buss, D. D., Asbury, A. C., Chevalier, L. (1980) Limitations in Equine Electrocardiography, JAVMA 177, 2, 173-176. 13. Butterfield, R. M. and Matthews, R. G. (1979) Ovulation and the Movement of the Conceptus in the First 35 Days of Preg- nancy in Thoroughbred Mares, J. Reprod. Fert. Suppl. 27, 447. 14. Chak, R. and Bruss, M. (1968) The M.I.P. Test for the Di- agnosis of Pregnancy in Mares, Proc. 14th Ann. Conv. A.A.E.P., Phila., 53. 15. Clegg, M. T., Boda, J. M., Cole, H. H. (1954) The Endometri- al Cups and Allantochorionic Pouches in the Mare with Em- phasis on the Source of Equine Gonadotrophin, Endocrin, 54, 448. 16. Clegg, M. T., Cole, H. H., Howard, C. B. and Pigon, H. (1962) The Influence of Fetal Genotype on Equine Gonadotrophin Se- cretion, J. of Endocrin, 25, 245. 17. Cole, H. H. (1938) High Gonadotropic Hormone Concentration in Pregnant Ponies, Proc. Soc. Exp. Biol., N.Y., 38, 193. 18. Cole, H. H. and Cupps, P. T. (1977) Reproduction in Domestic Animals, 3rd Ed., Academic Press, N.Y.C. and London. 19. Cole, H. H., Howell, C. E. and Hart, G. H. (1931) The Changes Occurring in the Ovary of the Mare During Pregnancy, Anat. Rec. 49, 3, 199. 20. Dimock, W. W. (1947) Early Clinical Examination of Mares for Pregnancy, Ken. Agr. Exp. Stat., Univ. of Ken. Circular 61. 21. Douglas, R. H. and Ginther, O. J. (1975) Development of the Equine Fetus and Placenta, J. Reprod. Fert., Suppl. 23, 503. 22a. Ewart, J. C. (1897) Critical Period in the Development of the Horse, Adam and Charles Black, London. 22b. Fay, J. E. and Douglas, R. H. (1982) The Use of Radioreceptor Assay for the Detection of Pregnancy in the Mare, Theriog. 18, 4, 431. 23a. Fink, H. and Frie, A. (1966) A Rapid Direct Reading Latex Agglutination Pregnancy Test, Obst. and Gynec. 28, 5, 660. 23b. Ginther, O. J. (1979) Reproductive Biology of the Mare, Cross Plaines, Wise. 24a. Graham, M. A. and Kalish, P. E. (1966) A Comparison of a New Latex Agglutination Pregnancy Test with an Established Latex Agglutination-Inhibition Test, Tech. Bull of Registry of Med. Techn. 36, 12, 306. 24b. Gunther, J. O., Foley, C. W., Garverick, H. A. and Plotka, E. D. (1980) Comparison of Milk and Blood Plasma Progesterone Concentrations in Cycling and Pregnant Mares, J. An. Sci. 51, 5, 1131. 25. Hancock, J. L. (1948) Notes on Oestrus, Ovulation and Preg- nancy in the Mare, Vet. Rec. 60, 679. 26. Hillman, R. B. (1976) Equine Breeding Techniques, Equine Short Course Notes, N.Y.S. College of Veterinary Medicine, Ithaca, N.Y. 27. Holmes, J. R. and Darke, P. G. G. (1968) Fetal Electrocar- diography in the Mare, Vet. Rec. 82, 651. 28. Holtan, D. W., Nett, T. M., Estergreen, V. L. Jr. (1975) Plasma Progestins in Pregnant, Postpartum and Cycling Mares, J. An. Sci. 40, 251-259. 29. Hunt, B., Lein, D. H. and Foote, R. H. (1978) Monitoring of Plasma and Milk Progesterone for Evaluation of Post Partum Estrous Cycles and Early Pregnancy in Mares, JAVMA 172, 11, 1298. 30. Irwin, C.F.P. (1975) Early Pregnancy Testing and Its Relation- ship to Abortion, J. Reprod. Fert., Suppl. 23, 485-488. 31. Jackson, R. S. (1968) Preliminary Report on a Survey of Causes of Equine Infertility, A.A.E.P. Newsletter, 2, 29. 32. Jeffcott, L. B., Atherton, J. G. and Mingay, J. (1969) Equine Pregnancy Diagnosis, A Comparison of Two Methods for the Detection of Gonadotropin in Serum, Vet. Rec. 84, 80. 33. Kanagawa, H., Too, K., Kawata, K., Ogaraski, Y., Sano, S. (1967) Fetal Electrocardiogram at Late Gestational States in Horses, Jap. Jour. Vet. Res. 15, 1, 15. 34a. Larks, S. D., Holm, L. W. and Parkes, H. R. (1960) A New Technique for the Demonstration of the Fetal Electrocardiogram in the Large Domestic Animal, Cor. Vet. 50, 4, 459. 34b. Layton, G. E. (1982), Paris, Ky., Personal Communication. 35. Lyall, W. L. (1972) The 21-Day Pregnancy Examination, Proc. 18th Ann. Conv. A.A.E.P., San Francisco, 483. 36. Marrable, A. W. and Flood, P. F. (1975) Embryological Studies on the Dartmoor Pony During the First Third of Gestation, J. Reprod. Fert. Suppl. 23, 499.36 VETERINARY OBSTETRICS 37. Mitchell, D. (1973) Detection of Foetal Circulation in the Mare and Cow by Doppler Ultrasound, Vet. Rec. 93, 365. 38. Osborne, V. E. (1960) An Analysis of the Pattern of Ovulation as it Occurs in the Annual Reproductive Cycle of the Mare in Australia, Austral. Vet. Jour. 42, 149. 39a. Osborne, V. E. (1975) Factors Influencing Foaling Percentages in Australian Mares, J. Reprod. Fert., Suppl. 23, 477-483. 39b. Osborne, V. E. (1982) Personal Communication. 40. Palmer, E. and Driancourt, M. A. (1980) Use of Ultrasonic Echography in Equine Gynecology, Theriog. 13, 3, 203. 41. Parker, W. G., Sullivan, J. J. and Larson, L. L. (1975) Com- parison of the Methods of Rectal Palpation and Haemagglutin- ation-Inhibition Assay for Diagnoses of Pregnancy in Mares, J. Reprod. Fert. Suppl. 23, 489-493. 42. Patterson, A. W., Jr. (1965) Personal Communication. 43a. Rantanen, N. W. (1982) Personal Communication. 43b. Rantanen, N. W., Torbeck, R. L., and DuMond, S. S. (1982) Early Pregnancy Diagnosis in the Mare Using Transrectal Ul- trasound Scanning Techniques: A Preliminary Report., Eq. Vet. Sci. 2, 1, 27. 43c. Roberts, S. J. (1971) Veterinary Obstetrics and Genital Diseases (2nd Ed.), Woodstock, Vt., p. 30. 44a. Roberts, S. J. (1980) Gestation and Pregnancy Diagnosis in the Mare in Current Therapy in Theriogenology edited by Morrow, D. A., W. B. Saunders Comp., Philadelphia, London, Toronto, pp. 736-753. 44b. Rossdale, P. O. and Ricketts, S. W. (1980) Equine Stud Farm Medicine, 2nd Ed., Lea and Febiger, Philadelphia. 45. Rowlands, I. W. (1949) Serum Gonadotrophin and Ovarian Ac- tivity in the Mare, J. of Endocrin. 6, 184. 46. Sager, F. (1963) Personal Communication. 47. Short, R. V. (1965) Recent Advances in Equine Reproductive Physiology, Proc. Brit. Eq. Vet. Assoc. 48. Solomon, W. J. (1971) Rectal Examination of the Cervix and Its Significance in Early Pregnancy Evaluation of the Mare. Proc. 17th Ann. Conv. A.A.E.P. pp. 73-80. 49a. Solomon, W. J. and Hoff, G. (1969) An Immunologic Preg- nancy Test for Mares, JAVMA 155, 1, 42. 49b. Squires, E. L., Pickett, B. W., Shideler, R. K., and Voss, J. L. (1981) Detection of Pregnancy Using Ultrasound, Proc. 27th Ann. Conv. A.A.E.P., New Orleans, La., 206. 49c. Squires, E. L. and Villahoe, M. (1982) Detection of Pregnancy with Ultrasound, Ann. Conf. AVMA, Salt Lake City, Utah (abstr.). 50. Stauffer, V. D. (1981) Equine Rectal Tears—A Malpractice Problem, JAVMA 117, 8, 798. 51. Terqui, M. and Palmer, E. (1979) Oestrogen Pattern During Early Pregnancy in the Mare, J. Reprod. Fert. Suppl. 27, 441-446. 52. Van Niekerk, C. H. (1965) Early Clinical Diagnosis of Preg- nancy in Mares, J.S. Afr. Vet. Med. Assoc. 36, 1, 53. 53. Van Niekerk, C. H. (1965) Early Embryonic Resorption in Mares, J.S. Afr. Vet. Med. Assoc. 36, 1, 61. 54. Van Niekerk, C. H. (1965) The Early Diagnosis of Pregnancy, the Development of the Fetal Membranes and Nidation in the Mare, J.S. Afr. Vet. Med. Assoc. 36, 4, 483. 55. Van Niekerk, C. H. and Allen, W. R. (1975) Early Embryonic Development in the Horse, J. Reprod. Fert. Suppl. 23, 495. 56a. Villahoe, M. D. (1982) Pregnancy Diagnosis by Ultrasound in the Mare, Lecture Dec. at Cornell Univ. based on studies at the Colorado State Univ., Reproduction Laboratory—Data to be further compiled and presented at the A.A.E.P. Convention 1983, In Press. 56b. Voss, J. L., Pickett, B. W., Back, D. G. and Burwash, L. D. (1975) Effect of Rectal Palpation on Pregnancy Rate of Non- lactating Normally Cycling Mares, J. An. Sci. 41, 3, 829. 57a. Wallace, A. K., Voelkel, S. A., Thompson, D. L. and Godke, R. A. (1981) Use of the New Ultrasonic Pregnancy Detector on Gestating and Open Mares, Abstr. J. of An. Sci. 53, Suppl 1, 60. 57b. Witherspoon, D. M. (1977) Exploration of the Abdominal Cav- ity by Digital Manipulation. Proc. 23rd Ann. Conv. A.A.E.P., 15 (Comments by Proctor, D. L., Meagher, D. M. and Vaughn, J. T.). 57c. Wohanka, K. (1961) Untersuchungen Der Ursachen Des Ver- fohlens, 4th Intemat. Vet. Congr. on An. Reproduction, The Hague. 58. Wormstrand, A. (1969) Immunological Pregnancy Diagnosis in the Mare, Acta Vet. Scand. 10, 299. 59. Zietzschmann, O. and Krolling, O. (1955) Lehrbuch Der En- twicklungsgeschichte Der Haustiere, Paul Parey, Berlin and Hamburg, Germany. 60. Zemjanis, R. (1961) Pregnancy Diagnosis in the Mare, JAVMA 139, 5, 543. Pregnancy Diagnosis in Ewes and Does la. Bon Durant, R. H. (1980) Pregnancy Diagnosis in Sheep and Goats: Field Tests with an Ultrasound Unit, Calif. Vet. 34, 26- 28. lb. Casida, L. E., Woody, C. O. and Pope, A. L. (1966) Inequality in Function of the Right and Left Ovaries and Uterine Homs of the Ewe, J. An. Sci. 25, 4, 1169. lc. deMontigny, G., Millerioux, P., Jeanguyot, N., Humblot, P. and Thibier, M. (1982) Milk Fat Progesterone Concentrations in Goats and Early Pregnancy Diagnosis, Theriog. 17, 4, 423. 2. Ford, E. J. H., Clark, J. W. and Gallup, A. L. (1963) Detection of Fetal Numbers in Sheep by Means of X-rays, Vet. Rec. 75, 958. 3. Harrison, R. M. and Wildt, D. E. (1980) Animal Laparoscopy, Williams and Wilkins, Baltimore, Maryland. 4. Hulet, C. V. (1969) Pregnancy Diagnosis in the Ewe Using an Ultrasound Doppler Instrument, J. An. Sci. 28, 1, 44. 5. Hulet, C. V. (1972) A Rectal Abdominal Palpation Technique for Diagnosing Pregnancy in the Ewe, J. An. Sci. 35, 4, 819. 6. Hulet, C. V. (1973) Determining Fetal Numbers in Pregnant Ewes, J. An. Sci. 36, 2, 325. 7. Hunter, R. H. F. (1980) Physiology and Technology of Repro- duction in Female Animals, Academic Press, N.Y.C., London, pp. 298-301. 8. Lamond, D. R. (1963) Diagnosis of Early Pregnancy in the Ewe, Austral. Vet. Jour. 38, 192. 9. Lane, S. F. and Lewis, P. E. (1981) Detection of Pregnancy in Ewes with the Ultrasonic “Scanopreg,” J. An. Sci. 52, 3, 463. 10a. Lindahl, I. L. (1969) Pregnancy Diagnosis in Dairy Goats Using Ultrasonic Doppler Instruments, J. Dairy Sci. 52, 4, 529. 10b. Lindahl, I. L. (1976) Pregnancy Diagnosis in Ewes by Ultra- sonic Scanning, J. An. Sci. 43, 6, 1135. 11. Megale, F. (1967) Endoscopic Photography of Ruminants, Vet. Med. Sm. An. Clin. 62, 555. 12. Memon, M. A. and Ott, R. S. (1980) Methods of Pregnancy Diagnosis in Sheep and Goats, Cor. Vet. 70, 226-231. 13. Ott, R. S., Braun, W. F., Lock, T. F., Memon, M. A. and Stowwater, J. L. (1981) A Comparison of Intrarectal DopplerPREGNANCY DIAGNOSIS 37 and Rectal Abdominal Palpation for Pregnancy Testing in Goats, JAVMA 178, 7, 730. 14. Pennington, J. A., Hoffman, W. F., Schultz, L. H. and Con- sidine, D. J. (1982) Use of Milk Progesterone for Pregnancy Diagnosis in Dairy Goats, (Abstr.) J. Dairy Sci. 63, Suppl. 1, p. 95; J. Dairy Sci., 65, 10, 2011. 15. Pratt, M. S. and Hopkins, P. S. (1975) The Diagnosis of Preg- nancy in Sheep by Abdominal Palpation, Austral. Vet. J. 51, 378. 16. Richardson, C. (1972) Diagnosis of Pregnancy in the Ewe by Vaginal Biopsy, Brit. Vet. J. 128, 316. 17. Richardson, C. (1972) Pregnancy Diagnosis in the Ewe: A Re- view, Vet. Rec. 90, 264. 18. Smith, M. C. (1980) Pregnancy Diagnosis in the Doe, Current Therapy in Theriogenology, Edited by Morrow, D. A., W. B. Saunders Co., Philadelphia, 975-977. 19. Tyrell, R. N. and Plant, J. W. (1979) Rectal Damage in Ewes Following Pregnancy Diagnosis by Rectal-Abdominal Palpa- tion, J. An. Sci. 48, 2, 348. 20. Shemesh, M., Ayalon, N. and Lindner, H. R. (1973) Early Pregnancy Diagnosis Based Upon Plasma Progesterone Levels in the Cow and Ewe, J. An. Sci. 36, 4, 726. 21. West, D. M. (1980) Pregnancy Diagnosis in the Ewe, Current Therapy in Theriogenology, edited by Morrow, D. A., W. B. Saunders Co., Philadelphia, 900. Pregnancy Diagnosis in Sows la. Balke, J. M. E. and Elmore, R. G. (1982) Pregnancy Diagnosis in Swine: A Comparison of the Technique of Rectal Palpation and Ultrasound, Theriog. 17, 3, 231-236. lb. Cameron, R. D. A. (1977) Pregnancy Diagnosis in the Sow by Rectal Examination, Austral. Vet. J. 53, 432. 2. Cupps, P. T., Briggs, J. R., Hintz, H. F. and Heitman, H. Jr. (1966) Pregnancy Diagnosis in the Sow, J. An. Sci. 25, 3, 646. 3. Dhindsa, D. S. and Dzuik, P. H. (1965) Time of Embryonal Migration in Pigs with One Ovary, J. An. Sci. 24, 3, 916. 4. Diehl, J. R. and Day, B. N. (1973) Utilization of Frozen Sec- tions with Vaginal Biopsy Technique for Early Pregnancy Di- agnosis in Swine, J. An. Sci. 37, 1, 114. 5a. Diehl, J. R. (1980) Pregnancy Diagnostic Methods for the Sow, in Current Therapy in Theriogenology, edited by Morrow, D. A., W. B. Saunders Co., Philadelphia, London, 1057-1064. 5b. Fraser, A. F. and Robertson, J. G. (1968) Pregnancy Diagnosis and Detection of Foetal Life in Sheep and Pigs by an Ultrasonic Method, Brit. Vet. Jour. 124, 239. 6. Guthrie, H. D. and Deaver, D. R. (1979) Estrone Concentration in the Peripheral Plasma of Pregnant and Non-Pregnant Gilts, Theriog. 11, 4, 321. 7. Herman, J. (1966) Pregnancy Diagnosis in Sows by Means of Vaginal Biopsy, Vlaams. Diergeneesk. Tijdschr. 35, 2, 81. 8. Huchzermeyer, F. and Plonait, H. (1960) Pregnancy Diagnosis in Swine by Rectal Examination, Tierarztl. Umschau 15, 399. 9. Lindahl, I. L., Totsch, J. P., Martin, P. A. and Dzuik, P. J. (1975) Early Diagnosis of Pregnancy in Sows by Ultrasonic Amplitude-Depth Analysis J. An. Sci. 40, 2, 220. 10. Lunaas, T. (1963) The Estrogens of the Sow in Early Preg- nancy: Accumulation of Estrone in the Allantoic Fluid, J. of Endocrinol. 26, 401. 11. Mather, E. C., Diehl, J. R. and Tumbleson, M. E. (1970) Preg- nancy Diagnosis in Swine Utilizing the Vaginal Biopsy Tech- nique, JAVMA 157, 1522. 12. Morton, D. B. and Rankin, J. E. F. (1969) The Histology of the Vaginal Epithelium of the Sow and Its Use in Pregnancy Diagnosis, Vet. Rec. 84, 658. 13a. Nalbandov, A. V. (1958) Reproductive Physiology, 1st Ed., W. H. Freeman Co., San Francisco. 13b. Stoner, C. S., Geisert, R. D., Bazer, F. W. and Thatcher, W. W. (1981) Characterization of Estrogen Patterns in Early Preg- nant Gilts, J. An. Sci. 53, Suppl. 1, 598, 370 abstr. 14. Ullrey, D. E., Sprague, J. I., Becker, D. E. and Miller, E. R. (1965) Growth of the Swine Fetus, J. An. Sci. 24, 3, 711. 15. Walker, D. (1967) Diagnosis of Pregnancy in Pigs by Exami- nation of Vaginal Mucosae, Vet. Rec. 81, 25, 648. 16. Wildt, D. E., Spencer, J. L. and Dukelow, W. R. (1974) Lapa- roscopy for Reproductive Study in Swine, Abstr. J. An. Sci. 39, 1, 229. Pregnancy Diagnosis in the Bitch and Queen la. Allen, W. E. and Meredith, M. J. (1981) Detection of Pregnancy in the Bitch, J. of Sm. An. Pract. 22, 609-622. lb. Boyd, J. S. (1971) The Radiographic Identification of the Var- ious Stages of Pregnancy in the Domestic Cat, J. Sm. Animal Pract., 12, 501. 2. Cartee, R. E. (1980) Ultrasonography Finds its Nitch in Veteri- nary Medicine, DVM, 11, 4, 32. 3. Colby, E. D. (1980) Pregnancy Diagnosis in the Cat, Current Therapy in Theriogenology, edited by Morrow, D. A., W. B. Saunders Co., Philadelphia, London, 436, 437. 4. Colby, E. D. and Stein, B. S. (1982) The Genital System, Feline Medicine and Surgery, 3rd Ed., Amer. Vet. Public, Inc., Santa Barbara, Cal. 5. Evans, H. E. (1967) Personal Communication. 6. Evans, H. E. and Sack, W. O. (1973) Prenatal Development of Domestic and Laboratory Mammals, Growth Curves, External Features and Selected References, Anat. Histol. Embryol. 2, 11- 45. 7. Fraser, A. F. and Robertson, J. G. (1968) Pregnancy Diagnosis and Detection of Foetal Life by an Ultrasonic Method, Brit. Vet. Jour. 124, 2, 39. 8. Harrison, R. M. and Wildt, D. E. (1980) Animal Laparoscopy, Williams and Wilkins, Baltimore, Maryland. 9. Helper, L. C. (1970) Diagnosis of Pregnancy in the Bitch with an Ultrasonic Doppler Instrument, JAVMA 156, 1, 60. 10. Sokolowski, J. H. (1980) Pregnancy Diagnosis in the Bitch, in Current Therapy in Theriogenology, edited by Morrow, D. A., W. B. Saunders Co., Philadelphia, London, 593-595. 11. Wildt, D. E., Kenney, G. M. and Seager, S. W. J. (1977) La- paroscopy for Direct Observation of Internal Organs of the Do- mestic Cat and Dog, Amer. J. Vet. Res. 38, 1429. 12. Zietzschmann, O., and Krolling, O. (1955) Lehrbuch de En- twicklungsgeschichte der Haustiere, 2nd Ed., Paul Parey, Berlin und Hamburg.Chapter III GESTATION PERIOD—EMBRYOLOGY, FETAL MEMBRANES AND PLACENTA—TERATOLOGY The gestation or pregnancy period is the period from fertilization or conception, to parturition or the birth of the young. During this period single cells divide and de- velop into highly organized individuals. This antenatal period is the least understood and probably one of the most important periods of life. There is a separate and distinct physiology of the fetus and placenta that is being intensively studied. The mortality rate of the ovum, em- bryo, or fetus during this period is much greater than for any other period of equal length after birth. Because they are usually unrecognized, early deaths of the fertilized ovum, or the early embryo, with resulting resorption or abortion, are often considered as sterility or infertility. The expulsion of a dead embryo or fetus that has reached recognizable size is called an abortion. The expulsion of a live fetus is called a birth. Until birth has occurred the viable bovine or equine fetus should not be called a calf or foal. The antenatal bovine individual or fetus, not a “calf,” is present in the uterus and may be ballotted through the abdominal or rectal wall. Dead fetuses, not “calves,” may be aborted, or expelled at term. Calves are only bom alive and the term “bom dead” is im- proper. Through common usage the fetuses expelled dead at parturition in swine and some other species are called stillbirths. Those bom before the end of the normal ges- tation period are spoken of as premature calves, foals, pups and etc. The gestation period can roughly be divided into two parts, based on the size of the individual and the devel- opment of its tissues and organs. These two periods in the gestation period of the cow are:64 The period of the early embryo, ovum or blastula—Presently the des- ignation of the period of ovum or blastula has been dropped because as soon as fertilization occurs embryo- genesis begins. Unfertilized ova die within a few hours after ovulation. This period of about 10 to 12 days in the cow extends from the time of fertilization, that usu- ally occurs within a few hours after ovulation, to the development of the zygote’s primitive fetal membranes in the uterus. The size of the ovum in domestic animals, not including the zona pellucida or granulosa cells, is about 120 to 180 microns at the time of fertilization and the shedding of the second polar body. During this pe- riod, division or cleavage of the fertilized ovum pro- gresses in the region of the ampullary—isthmic junction of the uterine tube to the morula stage characterized by the inner and outer cell masses totalling about 16 to 32 cells. The morula enters the uterus on day 3 after fer- tilization in the sow and days 4 to 6 in the other domestic animals. By 8 to 11 days after fertilization the zona pel- lucida has fragmented and a blastocyst has formed com- posed of the embryoblast or inner cell mass and troph- oblast or outer cell mass and fluid, probably absorbed from the uterine cavity. By 11 days in the ewe and 12 days in the cow the blastocyst is about 1 and 1.5 mm. in diameter, respectively. Elongation of the blastocyst has not yet occurred. During this period defective em- bryos die and are absorbed. The corpus luteum is de- veloping and producing progesterone, a hormone nec- essary for the growth and preparation of the endometrium, so a favorable environment for the embryo will be pres- ent in the uterus. (See Chapter 20 on Embryo Transfer.) Period of the embryo and organogenesis—This pe- riod extends from 12 to 15 days to about 45 days of gestation in the cow, 11 to about 34 days in the ewe and probably about 12 to 55 to 60 days in the mare. During this period the major tissues, organs and systems of the body are formed and changes in body shape occur so that by the end of this period the species of the embryo is readily recognizable. This usually coincides with the development of the eyelids.54 Starting at 12 days of ges- tation in the ewe and 14 days in the cow the trophoblast elongates very rapidly so by 14 days in the ewe and 17 days in the cow it is 10 cm. to 30 cm. in length, re- spectively and maternal recognition of pregnancy oc- curs. By 18 to 19 days of gestation in the cow the tro- phoblast may extend into the opposite horn.33-41’52 In the sow during this same period, 13 to 17 days, the length- ening of the trophoblast and the migrating and position- ing of embryos in the uterus occurs. By 24 days of ges- tation the trophoblasts in the sow are about 24 cm. long.13 In the mare, bitch and queen the trophoblast or blasto- 38GESTATION PERIOD—EMBRYOLOGY, TERATOLOGY 39 dermic vesicle does not elongate but remains oval during this period causing a localized enlargement in the uterus helpful in early pregnancy diagnosis. In the cow the am- nion is completely formed and closed and somites are forming by 20 days of gestation, by 22 days the heart is crudely formed and beating, by 25 days the neural tube is closed and 25 somites are present, the allantois is well developed, anterior limb buds are formed and eye and brain development are well advanced. In the cow, as in other animals, attachment of the fetal membranes is a gradual process that begins with the for- mation of the first villi about 30 days of gestation and progresses to a primitive attachment of the chorioallan- tois to the endometrium in the caruncular areas about 33 to 36 days of gestation.32,33 In the ewe attachment begins at about 17 to 20 days and is well-developed by about 28 to 30 days.19 While in the mare, attachment is de- layed until 70 to 90 days when villi develop on the cho- rion and project into crypts in the endometrium.8 In do- mestic animals the term attachment is preferred to the term implantation or nidation. Implantation refers to the process in humans and rodents where the zygote erodes, penetrates and implants itself within the endometrium. Up until the time of the well-developed attachment of the chorion to the endometrium the nourishment of the early embryo is provided by the secretion of the uterine glands called “uterine milk,” a yellowish or whitish, thick, opaque secretion, grossly resembling, and occasionally mistaken for, a purulent exudate. During this period nearly all of the more severe ter- atologic defects or anomalies of development occur. Also during this period the embryo may die, be expelled un- noticed at the next estrum, or become macerated and ab- sorbed without external signs. The period of the fetus and fetal growth. This pe- riod extends from about 34 days of gestation in the ewe and bitch, 45 days in cows and 55 days in the mare to parturition. During this period minor details in the dif- ferentiation of organs, tissues, and systems occur along with the growth and maturation of the antenatal individ- ual. Changes in the bovine fetus from 70 days to par- turition are not radical. During this period caruncles and cotyledons develop and enlarge to supply nutrition to the fetus in the cow and ewe. The increase in size of the fetus is a geometric-like curve, with the weight of the bovine and equine fetus increasing very rapidly the last two to three months of gestation.8,22,24,27 From 210 to 270 days the increase in weight of the bovine fetus is equal to three times the increase from the time of fertilization to 210 days. The prenatal development of the ovine and bovine zygote have been carefully described.18,31,58,64 The em- bryology of swine has been reviewed.6 Recent valuable information on embryology in horses and dogs, has been provided.8,22,25,27 Embryology Embryology is the study of the physiological devel- opment and growth of the antenatal individual. Tera- tology is the division of embryology and pathology deal- ing with abnormal development and malformations of the antenatal individual. Teratologic studies are of value because they constitute important available records of in- jury and arrested or pathologic development of the em- bryo or fetus. These studies explain the nature of some of the teratologic abnormalities in the fetus that fre- quently result in dystocia as well as other defects of the reproductive and other body systems. The embryology of importance in obstetrics, excluding that relating to the male and female reproductive systems which are dis- cussed in detail elsewhere, is as follows: The nervous system. The hypophysis or pituitary gland is an important endocrine gland. It is composed of the anterior, intermediate, and posterior lobes. The former and latter are of greatest significance. The posterior lobe arises embryologically as a downward extension of the floor of the diencephalon, a portion of the primitive brain. The deep portion of Rathke’s pocket loses its original connection with the stomodeal ectoderm and becomes closely applied to the infundibulum and forms the an- terior lobe. Thus the posterior lobe of the hypophysis arises from neural tissue and the anterior lobe from ec- todermal tissue. Teratologic defects or arrests in devel- opment of the nervous system may result in such con- ditions as: ankyloses, hydrocephalus, hypoplasia of the cerebellum, cerebral hernia, cyclopia, lack of optic tis- sue, and persistence of the anterior neuropore with fail- ure of facial bones to fuse (Schistocephalus bifidus).7 The digestive system. This system is of little impor- tance in obstetrical studies in animals. Arrested devel- opment at the terminal portion of the digestive system may result in atresia ani or the lack of a rectum. Oc- casionally a common cloaca is observed in the female or atresia ani is made less acute by the rectum emptying its contents into the vulva. Anomalous development of the gut may result in atresia coli. In the mouth region arrested development may result in a cleft palate or per- sistence of epithelial linings of the pharyngeal pouches, as seen by pharyngeal cysts in dogs. The circulatory system. The heart, arising from the fusion of the primitive endocardial tubes, develops ini- tially in the neck region caudal to the gill clefts or pha-40 VETERINARY OBSTETRICS ryngeal arches and then descends into and is enclosed by the chest in the bovine embryo around the fifth to sixth week of gestation. If this fails to occur the con- dition of ectopia cordis results. When the heart de- scends, the aortic arches descend also and carry with them the laryngeal nerves. The left aortic arch persists and the right aortic arch disappears. In dogs and cattle and rarely in other animals, the right aortic arch persists and the left disappears. In these instances, if the left ductus ar- teriosus is present, a chronic stenosis of the esophagus occurs as it passes over the base of the heart. It is com- pressed between the trachea, the aorta, the ligamentum or ductus arteriosus, and the base of the heart. The fetal venous circulation of blood consists largely of “arterial” blood rich in oxygen and nutrients coming from the placenta into the umbilical vein of the fetus. This vein passes through the umbilicus into the liver of the fetus where it anastomoses with the portal vein. In the fetal liver in most animals including the dog, cow, and sheep there is a direct shunt, called the ductus ven- osus, from the umbilical vein to the posterior vena cava. The blood that enters the portal veins goes through the liver tissue and into the posterior vena cava by means of hepatic veins. From the posterior vena cava, the blood then enters the right atrium where about 50 percent of it is immediately shunted through the foramen ovale into the left atrium.20 The remainder passes into the right ventricle and is pumped into the pulmonary artery, where again a large portion of the blood is shunted through the short ductus arteriosus into the aorta. A small amount goes through the pulmonary artery into the lungs as only a small blood supply is needed since the lungs are not functional in the fetus. Blood from the lungs is returned to the left atrium by the pulmonary veins. Blood that comes through the foramen ovale is mixed in the left atrium with blood from the pulmonary veins, passes to the left ventricle, and is pumped into the aorta and thence through the arteries to the various organs and tissues of the body. The aorta carries blood caudally to the rear quarters and in the region of the last lumbar vertebrae the two large umbilical arteries arise that carry largely “venous” blood down on either side of the bladder through the umbilicus to the placenta where waste products and carbon dioxide can be exchanged for nutrients and ox- ygen. More than 50 percent of the fetal cardiac output goes to the placenta.20 In the fetal lamb at 130 days of gestation 48 percent of the blood volume was in the pla- centa; at near term about 26 percent of the blood volume was in the placenta.5,6 The effect of allowing the cord to remain intact for a short time after birth to increase the blood volume in the newborn is evident. Hemoglobin values and red blood cell numbers in the fetus are much higher than in the adult. These values rapidly drop to normal after birth. Fetal hemoglobin apparently has a greater affinity for oxygen and releases it more slowly than does hemoglobin in the adult. The fetus has a high heart rate, about twice that of a young animal, promoting a high cardiac output per unit of body weight necessary Figure 16. Diagram of fetal blood circulation (arrows indicate the direction of the blood flow).GESTATION PERIOD—EMBRYOLOGY, TERATOLOGY 41 to compensate for the low oxygen content of the fetal blood.5,6 Marked changes occur in the fetal circulatory system at the time of birth.20,29 The umbilical cord ruptures. The umbilical vein present in the umbilical stump apparently closes due to a smooth muscle effect. The remnant of this vessel from the umbilicus to the liver becomes in later life the round ligament of the liver. The ductus ven- osus is apparently closed by a smooth muscle sphincter within 30 minutes to several hours after separation of the umbilical cord. In later life it becomes the ligamentum venosus in the substance of the liver. The liver then has the entire volume of portal blood going through its lob- ules instead of about one-third the volume. The foramen ovale closes mechanically within 5 to 20 minutes after birth by the closing of its lumen with the thin fold of tissue lying in close apposition to the foramen. This thin membrane or valve is maintained by an increase in blood pressure in the left atrium over the right. Finally after a year or more a complete septum is formed, the ductus arteriosus is closed by the contraction of its smooth mus- cle within 4 to 5 minutes after birth. This closure is ap- parently associated with an increased supply of oxygen in the blood of the newborn. The ductus arteriosus atro- phies and eventually becomes the ligamentum arter- iosum. The umbilical arteries are stretched at the time the cord is broken and they contract into the abdominal cavity and are closed by smooth muscle contraction. These are similarly affected by an increased oxygen level in the blood. The umbilical arteries later become the round or lateral ligaments of the bladder. Concomitant with these changes after separation of the fetus from the placenta at birth is a marked rise in arterial blood pressure.5,6 De- fects in cardiac development are occasionally seen in an- imals, especially calves, dogs and pigs, where they may be associated with weakness, hypoxia, signs of circula- tory failure, and death soon after birth. The urinary system. This system is formed mainly from mesodermal tissue. The earliest or most primitive urinary or excretory organ in the embryo is the prone- phros with two pronephric ducts, one on each side in the body wall dorsal to the peritoneum. This organ soon de- generates, to be succeeded by the mesonephros or Wolf- fian body. This structure, using the earlier pronephric ducts now called mesonephric or Wolffian ducts opens into the common cloaca. Later in the development of domestic animals the mesonephros degenerates and the metanephros or true kidney develops more caudally as an outpocketing of the mesonephric ducts. These ducts become the ureters, which open into the bladder. This latter structure opens caudally by the urethra into the am- niotic cavity and cranially by the urachus into the allan- toic cavity. During most of the late development of the fetus, urinary wastes are discharged principally into the allantoic cavity and little passes through the urethra into the amniotic cavity. Occasionally in domestic animals anomalies of the urinary system are observed, with poly- cystic kidneys or dilations or stenoses of the ureter. In rare cases a horse-shoe kidney, ren arcuatus, in which both kidneys are joined, is observed. This condition is noted more frequently in fetal monsters. The embryol- ogy of the genital system of the male and female animals are discussed separately in chapters relating to the anat- omy of the genital tract. The physiology of the fetus is a fascinating study. It has been shown that contractions of the heart and cir- culation of the blood through the vessels occurs early in the embryonic period. During this period respiratory movements are present. Although they may occur inter- mittently at first, they become more frequent and occur continually during the period of the fetus. The principal carbohydrate circulating in the ovine, caprine, equine, porcine and bovine fetuses is fructose produced by the placental tissues while in the canine and feline fetuses it is glucose.36 Fructose does not pass through the placenta into the dam’s circulation. The fetus starts swallowing late in the embryonic or early in the fetal period. Un- doubtedly large amounts of amniotic fluid are swallowed and absorbed. Some of the waste products are stored in thr rectum and colon as part of the meconium. This swallowing reflex of the fetus may be associated with maintaining the proper amounts of amniotic fluid. In fe- tal monsters, where defects of the cranial portion of the fetus or alimentary canal are present, hydrops amnii often occurs. Fetal movements begin early, at 90 days in the mare, and are more or less continuous in the form of paddling movements of the limbs and moving of the head and neck.30 If these movements do not occur or are markedly restricted, ankyloses with such abnormalities as wry neck or ankylosed limbs may result. The Fetal Membranes and Placenta The fetal or extra-embryonic membranes serve as pro- tection, a means of transmitting nutrients from the dam to the fetus, in caring for fetal waste products and syn- thesis of enzymes and hormones. The latter are neces- sary for the maintenance of pregnancy in most domestic animals. The fetal membranes are discarded at the time of parturition. The fetal membranes consist of the prim- itive yolk sac, the amnion, the allantois and the tropho- blast or chorion which when combined with the allantois42 VETERINARY OBSTETRICS forms the chorioallantois. The trophoblast is the most important single tissue of the fetal membranes and pla- centa as it has functions of absorbing, transmitting and handling nutritive and waste products. It has an erosive action on the endometrium mediating the attachment of the blastocyst; and it has a regulating function by being the site of the synthesis of enzymes and hormones. The needs of the embryo and fetus are supplied and cared for as follows: water, oxygen, and nutrients are taken from the maternal structures as the uterus and, after placental attachment has occurred, the maternal blood and carried to the developing embryo and fetus by the yolk sac, the amniotic chorion and the chorioallantois. The first two structures develop early in the life of the embryo of do- mestic animals and only function a short period of sev- eral weeks until the chorioallantois develops. Waste products from the embryo and fetus such as carbon diox- ide and urea are eliminated by the same structures. The allantoic cavity stores much waste material from the fetal kidneys. The large intestine and rectum of the fetus store waste products from the digestive tract as meconium. The amnionic cavity may play an early role in the care of some waste products. The fetal fluids permit the growth and movement of the fetus by distending the uterine lu- men. Protection of the embryo and fetus is performed principally by the amnion, although the allantois, uterus, and maternal body assist in this function. Heat and im- munity to early diseases of the newborn are supplied by the mother’s body. These immune bodies in domes- tic animals are mainly supplied by the colostrum. The fetal membranes and placentae have been well-de- scribed '■•2’1?'2'8'9'16'19'23'24'36 The respiratory form of the disease is very common; the abortigenic form is less common. The neurologic form which occasionally fol- lows the respiratory or abortigenic forms is uncommon or rare. The disease may be introduced into a farm by infected foals or horses and by infective material carried by persons, dogs, foxes, or carrion birds. This virus is quite resistant and may survive 7 to 42 days or more in dry stable surroundings.14 Following a natural infection the horse may spread the virus for 3 to 4 weeks. This virus, as other herpesviruses, may persist or be latent in certain tissues of “carrier” animals for long periods of time. Stress probably plays a role in releasing this virus and causing an exacerbation of the disease. Equine her- pesvirus I is only naturally pathogenic for horses. It can be adapted and grown in suckling hamsters and in cul- tures of kidney tissue cells from a number of animal spe- cies. Recent studies19,24’36'37'39 on respiratory and aborti- genic strains or subtypes of equine herpesvirus (EHV) I using restriction endonucleases to analyse the DNA of the virus have shown them to be dissimilar. Based on this and clinical, serological and laboratory observed dif- ferences in the strains24'36,37'39 it was suggested that fur- ther studies on the various subtypes and vaccine effec- tiveness are indicated. The clinical signs of rhinopneumonitis are those of a mild, febrile respiratory disease usually observed in young horses 4 to 8 months of age in the fall and early winter months. The incubation period is 2 to 3 days. The body temperature is elevated to 102 to 104° F. A serous rhini- tis with congestion of the nasal mucosa and conjunctiva occurs often associated with coughing, inappetence, and depression. A leucopenia usually is present. In about 7 to 10 days, the febrile period ends and a mucopurulent rhinitis, “the snots,” develops which, along with a cough, lasts for several weeks or longer. The disease can occur in any age of horse at any time of the year. The virus is highly infectious and contagious and is spread mainly by inhalation or droplet infection or occasionally by ingestion. In older mares this disease may frequently be so mild as to be unrecognized. The incubation period for abortion in natural infec- tions due to rhinopneumonitis virus or equine herpes- virus I is 20 to 30 days with a range of 14 to 120 days.13,36 Since evidence indicates that fetuses die soon after they are infected with herpesvirus I and are aborted, the long incubation period of this disease is intriguing. It has been shown that a viremia with the virus in the lymphocytes and monocytes2'3'4,21 may last for about 21 days. It has been hypothesized that the virus may reside in the cho- rion of the placenta for a time, as is possible with IBR virus in cattle, before infecting and rapidly killing the fetus.26 Thus abortions in mares on breeding farms often follow the outbreak of the respiratory disease in foals by several months.16 If the mare exhibits typical respiratory signs of the disease, abortions may follow apparent re- covery by several weeks or months. Fetal deaths and abortions seldom occur before 5 months of gestation and over 90 percent of the abortions occur from 8 to 11 months of gestation. Often foals infected in utero may be born alive but die within a few minutes to 4 days postpartum. Some workers consider this neonatal EHV I infection, associated with a high mortality rate from respiratory failure, a fourth form of the disease.5'10 Live foals in- fected with EHV I virus before birth often have an el- evated temperature, heart rate and respiratory rate, edema and congestion of the lungs and a leucopenia. Thus breeding practices largely determine the season or time when abortions occur; in Kentucky 90 percent of the abortions occurred from December through April. Immunity to herpesvirus (EHV) I, like other herpes- viruses, is relatively short lasting only a few months to a year and requiring frequent natural exposure or vac- cination to maintain protective antibody levels in the blood.1' 3 4 14 30 36 The degree of immunity and the num- ber of pregnant mares at the time of the outbreak deter- mine the abortion rate on a farm which may vary from 1 to 90 percent of a band of mares. Keeping the pregnant mares on a farm separated into small units well-isolated from other mares, horses, and young stock does much to reduce the spread and incidence of abortion in an out- break. In Kentucky 85 percent of the farms had 3 or fewer cases of virus abortion with an average abortion rate per farm per year of 2.5 percent, with a range of 1.6 to 6 percent. Abortions on a farm will occur over a period of 2 weeks to 3 months with 88 percent of the abortions occurring within 60 days of the first abortion. Data from Kentucky in 1963 indicated that this virus was present in 52 percent of aborted, infected fetuses and caused 26 percent of the total abortions in mares.16 The equine herpesvirus I causes the death of the fetus and no signs of impending abortion are observed. Re- tention of the placenta is uncommon. The mare is not traumatized unless a large fetus causes tearing of the tis- sues of the vulva or perineal region. Following viral abortions, mares usually conceive readily the next breed-DISEASES AND ACCIDENTS OF GESTATION 167 ing period unless secondary infections have oc- curred.1,2,8,16,33 Examination of the aborted fetus and membranes in this disease usually reveals a “fresh” nonautolyzed fetus, an edematous amnion, yellow amniotic fluid, a slightly yellow or icteric color of the fetal body tissues, straw- colored fluid in the thoracic cavity, interlobular edema and small hemorrhages in the lung, petechial and ec- chymotic hemorrhages in the epicardium, and small whitish-yellow, pinhead-sized foci of necrosis in the liver. On microscopic examination of stained liver, biie duct, lymph node, thymus, and bronchial cells, intranuclear inclusion bodies are frequently found. These latter signs in the fetus are of great diagnostic value. (See Figures 67 and 68.) The neurologic form of herpesvirus I may follow or occur with abortion in pregnant mares or after the onset of the respiratory form of the disease when EHV I in- vades the central nervous system producing dissemi- nated, necrotizing myelo- and meningo-encephalitis with vasculitis of the smaller vessels of the brain and spinal cord. The clinical signs vary from a mild ataxia to com- plete paralysis and death.25 In recent years this form of the disease has been reported widely in a number of states in the United States, Canada, Europe and Australia. Some of these reports described cases of epizootic outbreaks of the neurologic disease.10,23,27 A number of cases fol- lowed about 10 days after the vaccination of horses with a MLV herpesvirus I vaccine grown in a vero-monkey tissue cell line.20,28 Although this commercial product had undergone extensive trials prior to approval, it was with- drawn from the market because of its propensity to rarely produce neurologic disease. Treatment of this neurologic Figure 67. Liver and lung of an aborted 10-month equine fetus. Fe- tal death was due to equine herpesvirus I. Note small necrotic foci in the liver and edema of the lung. (Courtesy K. McEntee.) Figure 68. Intranuclear inclusion body in a liver cell of an equine fetus following herpesvirus abortion. (Courtesy K. McEntee.) syndrome is entirely by supportive therapy and deaths are common.35 There is no permanent immunity to viral rhinopneu- monitis or abortion. Many aborting mares apparently de- velop a fairly long immunity of one to two years. The respiratory form of the disease does not provide as long nor as good as an immunity as occurs following an abor- tion. Some horses may lose their immunity within 3 to 6 months after infection or vaccination but the disease is so common that most horses are frequently exposed and thus maintain a satisfactory immunity. Repeated fre- quent exposures to diseased horses or repeated vacci- nations with a vaccine increases the level of resistance. Strict isolation of mares on breeding farms without vac- cination is therefore likely to increase their susceptibil- ity. The complement fixation (CF) test or serum neutral- ization test can be used to determine antibody levels in the serum of horses following this viral respiratory dis- ease or abortion but it is not diagnostic. Antibodies per- sist for only a month or two up to one year even in abort- ing mares.3,14,16 This test is also of limited value in diagnosis since both CF positive and negative mares may abort or not abort when challenged by the equine her- pesvirus I. During and after a respiratory infection or exposure to virus from an abortion, there is a viremia persisting for up to 3 weeks in mares despite the coex- istence of virus neutralizing antibody in the blood.3 The vims is carried within the lymphocytes and the latter cells carry the virus throughout the body and to the placenta. It was shown that several “grades” of immunity existed depending upon the amount of antibody present at the site of infection in the nasopharynx. This immunity was a reflection of the level of virus neutralizing antibody in168 VETERINARY OBSTETRICS Figure 69. Torsion of the umbilical cord of a 7-month equine fetus resulting in abortion. the blood.2'3,4 12 30 Culture of the liver or lungs of freshly aborted fetuses on tissue culture medium often results in the recovery of the virus. The fluorescent antibody test applied to fetal tissues also is of great diagnostic value.34 Although many small horse farms with multiple equine activities experience a constant influx of “outside” horses and a constant exposure of broodmares to infection with EHV I virus, they seldom experience a serious epizootic outbreak of virus abortion. However, in controlling her- pesvirus I infection on a large breeding farm certain management procedures should be considered. Outside horses, especially from sales, should be carefully iso- lated for a month or more as virus may be shed from the respiratory tract and the horse appear clinically normal. Furthermore, if the addition to the farm is a mare in the Figure 70. Toxoplasma gondii abortion in a ewe. Note the white toxoplasma bodies in the maternal caruncles. latter half of gestation, isolation should be longer since the incubation period for abortion may be up to 4 months. Pregnant mares should be handled to avoid stress. Mares should be placed in small bands and not changed around. These bands should be kept separate from each other. Foals on nursing mares should be weaned early in a manner to avoid stress on the mare and to keep foals with the commonly occurring herpesvirus respiratory disease separated from the broodmares during the late fall and early winter. Pregnant mares in the last trimester of gestation should be kept from exposure to EHV I vi- rus during this critical period. Since vaccination does not protect all broodmares, management procedures to re- duce stress and prevent the spread of the disease should be instituted.-4'19 Since 1950 various vaccination procedures have been developed and discarded as better ones have superceded them. Initially a vaccine was prepared from equine fetal tissues.18 This killed vaccine which contained some red blood cells produced isoantibodies in some mares re- sulting in neonatal isoerythrolysis in their foals. The next vaccine was prepared from hamster tissues containing a live virulent virus that was injected intranasally.12,14,15 This product was not satisfactory for use on farms with a long breeding season as this vaccine produced a “con- trolled” or “planned” infection that could spread to other horses and it required that all horses on a farm be vac- cinated at the same time and “quarantined” for 3 to 4 weeks. In recent years two other vaccines have been devel- oped. One, a modified live virus (M.L.V.) vaccine that is given in two doses 4 to 8 weeks apart in pregnant mares after the second month of pregnancy and repeated every six months. Since immunity is rather short-lived repeated vaccinations are necessary to maintain high lev- els of antibody in the blood. This vaccine does not cause abortion or respiratory disease and does not spread to susceptible horses.1 The other vaccine is an inactivated EHV I vaccine with an added adjuvant that is recom- mended for use in pregnant mares at 5, 7 and 9 months of gestation to maintain a high level of protective anti- body.4 Both of these latter vaccines apparently provide a significant protection against abortion due to EHV I. However, a few vaccinated mares if stressed and/or ex- posed to a severe challenge with virulent virus may abort.-4,19 Of 8638 pregnant mares vaccinated from 1977 through 1980 with the inactivated vaccine, 1.6 per thou- sand aborted compared to 6.8 per thousand in 20,732 nonvaccinated mares.4,39 Of 233 abortions in vaccinated mares during a five year period a field strain EHV I was isolated from 93 fetuses. For this reason claims for its effectiveness in protecting pregnant mares from abortionDISEASES AND ACCIDENTS OF GESTATION 169 have been largely omitted. However, serological and clinical protection on two horse farms indicated the MLV vaccines probably are of value when used every 3 to 4 months.4,30 If an abortion due to EHV I occurs in a band of broodmares, prompt vaccination of all unvaccinated or susceptible mares is indicated to cause a rapid rise in levels of antibody in the blood. Adverse local reactions such as abscesses may rarely occur following the use of vaccines.4 One study indicated it was extremely difficult to eval- uate the efficacy of vaccines in preventing EHV I abor- tion because of the paucity of non-exposed mares, the lack of tests to measure residual protection and an in- complete understanding of the pathogenesis of the dis- ease.21 Further studies on the development of vaccines against the strains of EHV I, respiratory and fetal, are indicated.24,36,37,38,39 Since vaccination at present is not completely effec- tive in the control of abortion due to EHV I, sound man- agement procedures should be combined with vaccina- tion to control this disease. Equine viral arteritis (EVA) or epizootic cellulitis- pinkeye syndrome is caused by the arteritis virus, a to- gavirus, Bucyrus strain,2 that produces signs of severe general respiratory disease including abortion. These signs are closely related to the constant and characteristic ne- crotic lesions in the media of the small arteries produced by the arteritis virus and causing edema, hemorrhages, and infarcts. The disease is usually brought to a farm by an infected or convalescent horse. Outbreaks are pres- ently very infrequent in the U.S. The disease has been described in Europe.2 The virus is spread by droplet or aerosol infection and contracted in inhalation. Thus close contact between horses is necessary for the spread of this disease. The horse is apparently the only natural host of the disease. Since a carrier state can exist, spread of this disease at the time of coitus may occur.12 Clinical signs of the disease are often severe and should not be confused with the milder “shipping fever” type diseases of influenza or rhinopneumonitis.1’-’ ’ ’ 10 Horses of all ages may be affected. The incubation period of the disease is 3 to 9 days. The signs of the disease often include: an elevation of the body temperature to 103 to 106° F; leucopenia with panlymphopenia; conjunctivitis, lacrimation and occasionally keratitis, photophobia and palpebral edema; severe depression; a serous nasal dis- charge and congested nasal mucous membranes; an in- creased respiratory rate of 30 to 50 per minute, and oc- casionally dyspnea with a “heave line”; generalized weakness and stiffness; anorexia; a rapid loss of weight; and frequently colic and diarrhea. In a few horses edema of the limbs and/or the ventral abdominal wall develops. The course of the disease is 2 to 15 days. Deaths in nat- ural outbreaks are not common but experimentally in- fected old horses, pregnant mares, and weanlings may develop a severe illness with a 30 to 50 percent mortality due to pulmonary edema, pleural effusion, and second- ary cardiac disturbances. However, some natural cases of the disease may be so mild the signs of illness may pass unnoticed. Abortions are closely associated with the febrile and early convalescent period of the disease and occur 1 to 14 days after the onset of signs of illness. The mare fails to show signs of impending abortion. Abortion may oc- cur in up to 50 percent of the pregnant susceptible mares exposed to the virus.2,8,9 Some mares abort without ob- vious signs of clinical illness and some mares with def- inite signs of illness will not abort. Most abortions occur in mares from the fifth through tenth month of gestation. Retention of the placenta is uncommon in aborting mares. Some fetuses apparently die 2 to 4 days before abortion because autolytic changes are common in contrast to the freshly aborted fetuses associated with rhinopneumonitis virus (EHV-I) infection.- Postmortem fetal lesions in- clude petechial hemorrhages on the peritoneal and pleural surfaces, epicardium and endocardium, and pleural ef- fusions. These lesions indicated viral induced fetal death was followed by abortion. No inclusion bodies are found with this disease but the virus can be recovered from many fetal tissues including the liver and lungs.316 The virus can be grown on tissue cultures of horse and ham- ster kidney cells.3,15,16 Complement fixation and serum neutralization tests have been developed to detect anti- bodies.5 Following recovery a prolonged immunity to arteritis virus is probable. An attenuated live virus vaccine has been prepared that is an effective preventative.7,11,13 This has not yet become available commercially, because of the very limited occurrence of the disease. About 20 years after the severe epizootic outbreaks of viral arteritis on Standardbred farms in the Midwest, a serologic survey in 1972 revealed 55 percent of Standardbreds, 25 percent of a limited number of Saddle-breds and only 1.6 percent of Thoroughbred horses in the United States had positive titers for arteritis virus. An incidence of 2 to 5 percent positive titers were present in horses in England and Switzerland.12 Thus an apparent subclinical infection was present that conferred a lifetime immunity that resisted challenge with a virulent virus. However, it is evident that Thoroughbred horses in the U.S., England and Ja- pan because of a very low incidence of antibodies are at risk of a serious and widespread epizootic outbreak of viral arteritis should a virulent strain appear. Only 0.3 percent of 3772 horses tested by the National Veterinary170 VETERINARY OBSTETRICS Services Laboratory in 1978 and 1979 were seropositive for EVA.6 Proper segregation, isolation, and quarantine along with other sanitary procedures and with prompt vaccination, would be indicated in preventing the spread of this infection on a farm. Equine infectious anemia is occasionally character- ized by abortion in infected pregnant mares.-1,2 The pathogenesis of abortion due to equine infectious anemia virus has not been established and more study is indi- cated. Mycotic or fungal agents of the species Aspergillus fumigatus, the order Mucorales and Allescheria boy- dii, may cause sporadic abortions in mares. Occasional cases of yeast abortion due to Candida albicans1 or cryptococcus76 as well as rare cases of abortions due to histoplasma2 and coccidiomycosis due to Coccidiodes immitis have been reported.6 Mycotic agents may cause 5 to 10 percent of all abortions in mares in central Ken- tucky. Mycotic abortion has also been reported in Ger- many and England.1,3,4,5,7 The cause of the abortion is apparently a severely diseased necrotic, thickened allan- tois chorion which interferes with fetal nutrition and causes growth retardation and fetal death. (See Figure 64.) Mold may be cultured from the placenta, and occasionally the fetal organs such as liver, stomach, lungs and the fetal skin. It is likely that the mold is carried to the placenta in the blood stream from lesions in the wall of the in- testine or lungs. It may also be associated, as in cattle, with the ingestion or inhalation of mold spores from moldy hay or straw during pregnancy. Because of the excellent equine uterine defense mechanism, it seems very un- likely that mold introduced into the uterus at the time of copulation would remain viable for months and then in- fect the placenta. It is possible that fungi could invade the uterus and placenta through the cervix around the second month of pregnancy as described under bacterial causes of abortion. Mold abortions usually occur from the 4th to 11th month of gestation. Following abortion the mold infection does not persist in the uterus but ser- vice on the foal estrum should be avoided. Parasitic protozoan organisms including Trypano- some equiperdum causing dourine,12 Babesia equi and caballi causing piroplasmosis,8 Bedsonia spp,7 and Sarcocystis3 spp may occasionally or rarely produce abortion in mares. Dourine is transmitted almost entirely by sexual contact. It was first recognized in the U.S. in Illinois in 1885 by W. L. Williams in horses bred to a stallion shipped from France. By use of the complement- fixation test and destroying all reactors the disease has probably been eradicated from the last infected area in southwest U.S. This disease is discussed in more detail in a later chapter. Babesiasis or piroplasmosis may result in abortion in severely affected horses.1,6,8,10 This disease has been re- ported in South Africa and is endemic in many tropical countries. At present in the U.S. it is limited mainly to Florida. Signs of the disease closely resemble those of equine infectious anemia except icterus and hemoglo- binuria may also be present. The parasite is spread by bloodsucking ticks and it may be found, for diagnostic purposes, within the erythrocytes by proper staining techniques. In infected, aborted, premature or term fe- tuses or foals, icterus and anemia is present requiring differentiation from equine infectious anemia, rhino- pneumonitis virus abortion, neonatal isoerythrolysis, and leptospirosis.9,10 Abortion may be due to fetal or mater- nal stress with cortisol production. The fluorescent an- tibody technique may be helpful in detecting the parasite in the red blood cells of the fetus or foal.5 The comple- ment-fixation test on horse serum is highly specific for B. caballi infection and blood titers persist for 1 to 5 years.4 Therapy for mares with piroplasmosis is avail- able and effective.-9 Noninfectious Causes for Equine Abortion Chemicals, drugs and poisonous plants including: phenothiazine; thiabendazole; “Lentin”; purgatives, such as arecoline, aloes; Sudan or sorghum pastures,34,37 or- ganic phosphate insecticides and anthelmintics; ergot, locoweed (astragalus)223 and others have been reported as possibly causing abortions if given to or ingested by mares in advanced pregnancy. Iodine when fed greatly in excess of normal requirements to pregnant mares for a number of months caused hyperplastic thyroid glands, weak legs and premature birth of moribund foals.10 Such causes of sporadic abortions are often proposed but the scientific basis for these reports have not been ade- quately substantiated. If abortion should follow the administration or ingestion of these or other possibly toxic materials the attending veterinarian should obtain a care- ful history and have the fetus(es) necropsied and ex- amined carefully for the more common, known causes of abortion in horses. Hormonal causes of abortion in horses have re- ceived limited study. Estrogens in large doses over a long period regularly produces abortion in other species of animals. In mares evidence is lacking for an abortifacient effect of estro- gens. One report indicated that estrogen implants of 50 to 150 mg caused abortion in one of 3 mares.39 Further studies are indicated.DISEASES AND ACCIDENTS OF GESTATION 171 Oxytocin or pituitrin administered to pregnant mares prior to 310 days of gestation has not been proven to cause abortion. Oxytocin may induce parturition in mares after 345 days of gestation. Induction of equine partu- rition will be discussed in Chapter VI. When pregnant ponies were injected with human cho- ronic gonadotropin (HCG) at a dose level of 2000 I.U. every other day for 3 doses before 39 days of gestation, abortion resulted. Whereas pregnant ponies similarly in- jected from 40 to 97 days of gestation did not abort.1 Prostaglandin, PGF2a or one of its analogues, if in- jected in a single luteolytic dose before 38 days of ges- tation will regularly cause abortion within 2 to 5 days.14 36 A single large dose of P.G.F.2a injected into pony mares 70 to 300 days of gestation failed to cause abortion. When repeated doses of 2.5 mg. PGF2a were given at 12 to 24 hour intervals for an average of 3.7 doses all 13 mares aborted within 4 to 5 days, average 38+ hours.9 How- ever PMSG remained elevated after abortion in those mares having elevated levels before treatment. Although luteolysis occurred subsequent estrus and ovulation was erratic and generally occurred only after a prolonged in- terval in mares over 40 days pregnant at the time of treat- ment. In another trial about 1 mg/45 kg. (10 mg./lOOO lbs) PGF2a was given daily to 25 mares pregnant 100 to 245 days. Abortion occurred in 76 percent of the mares within 3 to 6 days and in the others the second through fourth week.14 Dystocia occurred in one mare. In an ex- periment with Equimate (fluprostenol-ICI) a single 250 (xg. injection produced abortions in 2 to 3 days in 7 of 8 mares pregnant 35 days.36 Repeated injections of a similar dose at 12 to 24 hour intervals was necessary to produce abortion at 70 days of gestation. The interval from abortion to first estrus averaged 11 days in mares aborted at 35 days of gestation and 35 to 45 or more days in those mares aborted at 70 days of gestation. None of the former and 75 percent of the latter had an anovula- tory estrus prior to an ovulatory estrus following abor- tion. Apparently if mares abort from 40 to 110 days of gestation when the endometrial cups are present, these structures must involute before normal reproductive cy- cling is reestablished. For these reasons breeding mares aborted after 40 days within the same year was very dif- ficult. A deficiency of progesterone has been suspected and diagnosed by veterinary practictioners as a cause of abortions from 1-1/2 to 8 months of gestation for the last 20 years based on clinical observations. The primary corpus luteum of pregnancy, along with secondary or accessory corpora lutea developing the first 60 to 90 days of gestation maintain pregnancy until the fourth to fifth month of pregnancy when the placenta, and probably the fetal gonads, produce sufficient steroids and progesto- gens to maintain pregnancy to term. After the third to fifth month of gestation the ovaries and corpora lutea involute and have no role in pregnancy maintenance. (See Chapter IV.) As mentioned previously, many veterinarians have re- ported an incidence of about 15 percent abortion rate in mares between pregnancy diagnosis at 40 days of ges- tation and term with two-thirds of that pregnancy loss between 40 and 150 days. Many of these early abortions occur without being seen, often in mares with a history of recurrent or “habitual” abortion. Since most of these aborted fetuses and placentas when examined are neg- ative for evidence of infection or teratologic defects it is logical to possibly suspect a hormonal cause for this high incidence of abortion. Whether a progesterone deficiency is actually a reason for abortion in the mare is still uncertain.15 However ex- ogenous supplemental progesterone produces no adverse effects, and has apparently resulted in many abortion- prone mares successfully completing their pregnancy. It has been demonstrated that about 3 to 4 ng/ml or more of progesterone in plasma is necessary to maintain preg- nancy.14'15’16,36 Daily injections of 200 mg. of progester- one in oil or weekly injections 1000 to 2000 mg. of res- positol progesterone resulted in plasma progesterone levels of 2 and 2.5 to 4.5 ng/ml, respectively in ovariectom- ized mares.15 In another study pregnant mares were given either 250 mg. progesterone-in-oil or respositol proges- terone intramuscularly on day 255 or 270 of gestation. Plasma progesterone levels peaked at 6.5 to 7.2 ng/ml in 6 hours and receded slowly to preinjection levels of 3.4 ng/ml 6 to 8 days later.8 These workers recom- mended injections of 250 mg progesterone in oil every 2 to 3 days or the same dose of repositol progesterone daily to maintain plasma levels of 1 to 2 ng/ml in pro- gesterone-deficient mares. Administering 22 and 44 mg. of allyl trenbolone or- ally daily or injecting 1000 mg of repositol progesterone every four days maintained pregnancy in nearly all mares in 3 groups of 8 mares each that were diagnosed preg- nant at 30 days of gestation and ovariectomized on days 34 and 35. All eight control mares, 7 of 8 mares given 500 mg. repositol progesterone every 4 days and 3 of 8 mares given 250 mg. of progesterone in oil every two days aborted 4 to 9 days after ovariectomy when the pro- gesterone levels in their blood plasma fell below 2 mg/ ml.36b It should be noted that these mares were ovariec- tomized before placental progestogens were produced. Since pregnant mares would be producing their own progestogens, the supplemental doses needed to main- tain pregnancy might well be somewhat lower than the172 VETERINARY OBSTETRICS above. Possibly they need not be as high 500 mg. pro- gesterone-in-oil given every 48 hours as recommended in a third study.12 When injections of progesterone are given regularly there is an accumulative effect on the maintenance of high plasma progesterone levels.12,16 Further detailed, long-term studies on possible proges- terone deficiencies in abortion-prone mares are indi- cated. The author has experienced three unusual, recent clin- ical cases to illustrate the value of supplemental proges- terone injections to prevent abortions in mares. One has been reported;333 the two others336 were very similar to the former. These were Thoroughbred mares 7 to 8 months pregnant. One had a history of being barren for several years and aborting twins the year previously. They were observed to suddenly be dripping milk from their udders and showing marked relaxation of their vulva and peri- neal region indicating impending abortion, possibly as- sociated with twinning. The mares were confined and placed on antibiotics and supplemental progesterone in- jections of 200 to 500 mg. of progesterone in oil daily for several days followed in one mare by 500 mg re- positol progesterone every 3 to 5 days for a month and in the other mare with 200 to 300 mg. of progesterone in oil daily for 14 days. After 10 days these mares were examined, the udder had involuted and the perineal re- gion was no longer relaxed and edematous. In one mare the vaginal mucus was blood-tinged but the cervix was tightly closed in all mares. Rectal examination revealed a live 7 to 8 month-old fetus in each mare. These mares were given 500 mg. of repositol progesterone intramus- cularly weekly until 330 days of gestation. These mares each delivered a live but small, 50-60 lb. foal together with a mummified, slightly macerated fetus enclosed in a necrotic, yellowish placenta. The mares and their foals recovered uneventfully. In the three cases impending abortion was “triggered” by the death of one fetus lo- cated in one hom based on the examination of the three placentas at birth. The normal placenta and fetus occu- pied the other hom and the body of the uterus. It ap- peared evident that the progesterone administered pre- vented the abortive process possibly occassioned by the release of cortisone or the release of prostaglandin by the dying fetus, the fetal membranes or endometrium. Possibly with the death of the fetus, the deficiency of placental progestagens from that “dead” placenta dropped the progestogen levels low enough to initiate expulsion of the fetuses or all three factors might have combined to initiate the near abortions. Studies of the blood levels of hormones in such cases would be most informative. A further observation on the value of progesterone in preventing abortion in the “abortion-prone,” nervous mare is that progesterone therapy in mares, stallions, cats and other animals apparently has a “tranquilizing” and calm- ing effect. This is most noticeable in pregnant animals the latter half of gestation. Thus progesterone therapy may minimize stressful influences that induce cortisone production in the pregnant animal. Excess cortisone levels induced by stress on the dams or by the exogenous injection of cortisone into pregnant mares requires further investigation. In other species of animals such as cows and ewes cortisone injections or stress particularly late in gestation readily induces abor- tion or premature birth. Hillman17 reviewed studies on the effect of cortisone (dexamethasone) in pregnant mares and concluded that induction of abortion early or birth late in gestation even with large daily doses of 10 to 80 mg usually failed. At 320 to 325 days of gestation mas- sive doses of 100 mg. of dexamethasone daily for 3 to 7 days were required to induce foaling. This may reflect the much higher threshold for hormonal effects required in mares compared to other domestic animals. Despite the above evidence of the lack of the effect of cortisone on pregnant mares, strong clinical evidence cited by Mitchell24 25 and Osborne29 and observed by the author32 and other practitioners would indicate that trans- portation, physical, nutritional or “emotional” stress in certain pregnant mares is definitely related to abortion at any stage of gestation. On horse farms where pregnant mares were used to collect urine as a sourse of estrogen, 87.3 percent of 237 abortions occurred between 90 to 150 days of gestation and 89 percent of these abortions occurred within 28 days after removing the mares from pasture and stabling them under stressful conditions.25 No infectious agents could be found in these fetuses. By instituting improved management practices the incidence of abortion could be greatly reduced. In another exper- iment 44 percent of 95 yearlings and two-year-old mares aborted between 30 and 160 days of gestation possibly due to immaturity, inadequate nutrition and physical stress24 as the fetuses on examination and culture failed to show any infectious agents. Besides the 5 abortions in 6 mares 4 to 5 months preg- nant subjected to stress in shipment from New Mexico to New York State cited in the second edition of this book, the author has observed a number of other similar occurrences. Most notable was a stakes-quality nervous Thoroughbred mare with a history of 8 abortions from 2 to 7 months of gestation over the prior 8 years. Culture and biopsy of the uterus were negative and no reason for the recurrent abortions was found. Before breeding she was vaccinated, wormed and had her teeth checked and feet trimmed. The mare conceived readily; was placed in a paddock on the farm with another old nonpregnantDISEASES AND ACCIDENTS OF GESTATION 173 mare for company and was not handled, treated, or re- moved from the paddock. Ten and one-half months later she delivered a live, normal foal. Osborne29 observed a 50 percent abortion rate in preg- nant mares at all stages of gestation when stressed in shipment to an abattoir where a postmortem survey on 5198 fetuses was performed. Early embryonic resorption was reported in many mares in South Africa that was apparently caused by a severe nutritional stress of the mares38 7 to 10 days after being placed on poor pasture at 18 days of gestation. Even in other species excessive stress or handling of normal pregnant females greatly de- creases the chance for survival of their offspring. Free- ranging female monkeys had a 2.7 percent incidence of stillbirths, caged monkeys a 15 percent and captured wild monkeys brought to the United States a 50 percent in- cidence of stillbirths.100 Modem practices of transpor- tation, changes in feeding and environment, thermal and physical stresses frequently imposed on pregnant mares may have a definite influence on the increased incidence of embryonic and fetal deaths and abortions recorded in recent years, especially in racing and show mares. Nutritional deficiencies as causes for abortion in mares have been reported.1314,19 Many early embryonic deaths occurred 7 to 10 days after the mares were placed on poor pasture at 18 days of gestation.19 A high incidence of abortion resulted at 3 to 5 months of gestation in mares 1 to 14 days after confinement in bams and the feeding of a poor ration together with a reduced water intake.13'14 These early embryonic and fetal deaths although asso- ciated with a lowered level of nutrition may have been due to other hormonal or physiological factors previ- ously discussed. There are no authoritative reports on abortions due to vitamin or mineral deficiencies in horses. Physical causes for abortion in mares The manual dilation of the cervix and the introduc- tion of several hundred mililiters of physiological saline, dilute Lugol’s solution or iodized oil readily produces abortion within 3 to 10 days in most mares. Occasionally a second treatment may be necessary.17'21 Purposely aborting mares the last 3 months of gestation is not rec- ommended because complications may arise due to the large size of the fetus. Natural service during early pregnancy, especially the first 3 months of gestation, is not uncommon due to increased ovarian follicular activity during this period. Abortions following natural matings during pregnancy are rare. Artificial insemination with intrauterine depo- sition of semen causes abortion during early pregnancy. Trauma or injury has been reported as a cause of abortion in mares. These reports are not well-docu- mented. Rough manipulation of the blastodermic or cho- rionic vesicle per rectum from 20 to 50 days of gestation should be avoided. Rectal palpation of the chorionic ves- icle for pregnancy diagnosis should be performed care- fully and gently to prevent injury. Frequent rectal pal- pation of 27 mares between 20 and 82 days of gestation caused no abortions.21 Only 2 of 6 mares aborted after 145 days of gestation when exposed to severe rectal and vaginal mechanical and thermal irritation. Thus a normal pregnant mare is relatively resistant to abortion produced by physical means. In twin pregnancy diagnosed prior to 30 days of gestation manual destruction of one blas- todermic vesicle permitted the other to develop nor- mally. 7,110,22 Severe stress produced by prolonged diffi- cult shipping, hard, sustained work, difficult and complicated operations, vigorous struggling and trauma during casting may cause abortion in mares as discussed previously. Placental insufficiency due to body pregnancies with little or no extension of the placenta into the uterine horns, adhesions or strictures limiting the size of the uterine lumen or access of the placenta to a portion of the uterine horns and extensive areas of chronic endometrial fibrosis may rarely cause abortion.20b Torsion or strangulation of the umbilical cord is responsible for about one-half to one percent of the equine fetal deaths and abortions from 150 to 300 days of ges- tation.1,5,20 The equine amniotic sac and fetus float free within the allantoic cavity except for the umbilical cord. The long, 55 cm. (range 30 to 95 cm.) umbilical cord in the normal foal has from 1 to 3 rotations.20 In occa- sional fetuses the cord becomes excessively twisted, sol- len and edematous (See Figure 69) or rarely becomes wrapped tightly around a fetal extremity closing the lu- men of the blood vessels between the placenta and the fetus. A long umbilical cord may be associated with is- chemic necrosis of the cervical pole of the chorioallan- tois.20 This appears to be accidental. Most of the exces- sive twisting and vascular occlusion occurs in the amniotic portion of the cord. Strangulation of the uterus by a li- poma or torsion of the uterus may rarely cause fetal death. Genetic or chromosomal and other causes of abortion Fetal anomalies as a possible cause for mid to full term equine abortion have been reported in about 1.3 percent of aborted equine fetuses from 1926 to 1947 in Kentucky.5 In a recent report from the same station the incidence had risen to 9.7 percent. The contracted foal syndrome was the most common anomaly at 3.8 per- cent.18 Further studies on the causes of these anomalies and their increased incidence is needed. Chromosomal174 VETERINARY OBSTETRICS defects of the equine zygote as in other animals (See abortion in cattle) may cause early embryonic deaths. These defects are favored by aging of the spermatozoa or ovum prior to fertilization which is highly possible in mares due to their long estrous period. A review and study of the cytogenetic basis of prenatal loss in the mare while inconclusive indicated the need for further stud- ies.3 Miscellaneous causes of abortion Twinning is the cause of 20 to 30 percent of all ob- served equine abortions.16,18,206 Double ovulations are re- ported in 4 to over 40 percent of estrous periods, es- pecially in a few mares prone to twinning.2'83,6,9'15 Double ovulations are most common in young and middle-aged mares and toward the end of the breeding season.9 Twin- ning is rare in ponies.8 Twinning in mares may be due to genetic factors. However, only 0.5 to 1.5 percent of mares give birth to twins.9,176 The mortality rate of equine twins greatly exceeds that in any other domestic animal. Most equine twin zygotes undergo early embryonic deaths.86,9 Certain mares, as cows, apparently produce twins more frequently than other mares;8b one mare ob- served by the author aborted twins in 4 of 9 gestation periods. About 60 to 80 percent of twin fetuses that sur- vive through the fourth month of gestation are aborted from 5 months to term with 72.6 percent from 8 months to term. Of 124 twin fetuses 31 were bom alive and only 18 or 14.5 percent survived to 2 weeks of age.9 A failure of the placental vessels of the allantois chorion of one twin to anatomose with the other, possibly because of the early physical distance between the two blastocysts together with a lack of sufficient placental area for ad- equate nutrition of one of the fetuses results in the death of that fetus and the abortion of both fetuses.6,9 Occa- sionally the larger twin may die and be aborted with the living smaller fetus. Occasionally mummification or maceration of the dead fetus will occur with its subse- quent explusion at a later date when the other fetus is aborted or bom at term. This unequal size of the pla- cental areas available for nutritional exchange probably accounts for the unequal size of most equine twin fetuses by growth retardation of the “malnourished” twin.9 Mares cannot increase the size of the uterus or placenta to ac- commodate twins. The differences in the size of the twin chorions may be due to the time of fertilization or im- plantation of the zygotes or the rates of growth of the placentae. This is often incorrectly diagnosed as super- fetation. Since it is probable that in the latter half of gestation in the mare progesterone necessary to maintain pregnancy is produced in the allantois chorion, it may be possible that abortion is due to a sudden drop in pro- gesterone levels or a rise in prostaglandins or both caused by the death of one fetus and its membranes (See pro- gesterone deficiency). Since twinning is the second most common cause of abortion1,9,16 various procedures have been attempted to avoid or prevent twin pregnancies, especially in the oc- casional twin-prone mare. These include: 1. Rectal examinations at daily or more frequent inter- vals are performed, especially in the twin-prone mare and, a) Breeding is only permitted when one mature fol- licle is present. Care must be used here because some- times a follicle develops rapidly late in estrus and ovu- lates, asynchronous ovulation. b) If two mature follicles are present then one may be tapped by an ovarian needle per vaginum. c) Wait until one follicle ovulates and then breed 12 to 18 hours later since the life of an unfertilized ovum is only about 10 to 12 hours. 2. In the future ultrasonography may aid in diagnosing double follicles and early twin pregnancy, 15 to 30 days of gestation. This equipment presently is very expen- sive. (See Pregnancy Diagnosis, Chapter II.) By ultra- sonography and rectal palpation twin pregnancy should be diagnosed if possible before 35 days of gestation. This may be difficult because the embryonic vesicles are small, may lie nearly together or one may be in the body of the uterus. If pregnancy is terminated after 38 days of ges- tation it is very difficult to get a mare to conceive that year because of the presence of the endometrial cups and the erratic estrous cycles, anovulatory estrous periods and the long time, usually 40 to 60 days or more before a normal ovulatory cycle occurs. If twin pregnancy is di- agnosed then one can: a) Douche the uterus, cause abortion and rebreed at the next estrous period which occurs normally within 10 days if the pregnancy is terminated before 35 days. b) Inject the usual single luteolytic dose of prostag- landin or its analogue to abort the embryos before 35 days with estrus occurring as in a). c) Destroy one embryo as early as possible, 20 to 35 days, usually by manual means. The other embryo often survives.7,116,22 The administration of progesterone and an antiprostaglandin such as butozolidin or flunixen meglumine (“Banamine”) before manually crushing one embryo might be indicated to prevent the loss of the remaining embryo. Further controlled trials are in- dicated. Ultrasonography for the early diagnosis of pregancy, <30 days, makes such experiments possi- ble. With the death of one embryo, both usually suc- cumbed if surgical intervention or aspiration is em- ployed.86DISEASES AND ACCIDENTS OF GESTATION 175 d) Allow the pregnancy to proceed. Most twin preg- nancies are lost by the death of one or both embryos or fetuses as described under progesterone deficiency in this Chapter. The mare with twins may be put on supplemental injections of progesterone and watched closely. If signs of udder development or perineal and vulvar relaxation occur immediately give large doses of progesterone for 10 to 14 days. This may prevent the twin abortion. At term a normal, usually small, single foal is bom along with a mummified, dead fe- tus. None of these procedures used to prevent or “treat” equine twin pregnancies is highly satisfactory in the han- dling of this common condition except the manual crush- ing of one chorionic vesicle early in gestation or the administration of progesterone late in gestation to pre- vent abortion. Both of these practices require further controlled investigation. Early embryonic deaths in horses have received little experimental study. Contagious equine metritis (CEM) due to Hemophilus equigenitalis is the only venereal disease causing early embryonic deaths in horses. Most recognized abortions in mares occur after 4 months of pregnancy. However, many unrecognized and unseen expulsions or abortions of embryos and fetuses probably occur from 8 days to 4 months of gestation. In the first few months of gestion maceration and partial or com- plete absorption of the dead conceptus may occur.176-19 Probably most of these macerating embryos are expelled after a variable period except in cases involving the death of only one of twin embryos with the other embryo re- maining viable.2,8b'14b'33b Many cases of early embryonic death, especially from 20 to 60 days of pregnancy, are erroneously diagnosed as failure of conception, “missed” or “silent” estrous pe- riods, “spurious” conceptions or pseudopregnancy.8 A mare with a “spurious” conception has been serviced by a stallion, apparently conceived, and failed to exhibit es- trus thereafter, even with a good “teasing” program. She exhibits normal vaginal signs of pregnancy but is not pregnant when examined rectally 30 to 50 days after ser- vice. This same condition of pseudopregnancy also oc- curs commonly in the bred or unbred mare due to a per- sistent corpus luteum.8 Recent studies based on embryo recovery in embryo transfer experiments show that about 80 percent of mares are pregnant at 8 days of gestation but at 35 days only about 65 percent are pregnant, a 15 to 20 percent loss of embryos.17c On well-managed farms with veterinary supervision of the mares, a 2 to 10 percent and occa- sionally up to 20 percent loss of embryos and fetuses is experienced between routine pregnancy diagnoses at 40 and again at 110 days of gestation.3-410 An incidence of 21 percent early embryonic death loss the second month of pregnancy in 573 foaling mares compared to only 2 percent loss in barren mares was reported.12 The inci- dence was highest in the mares conceiving on the foal estrum. The possible relationship between these early embryonic deaths and lactation was considered. Embry- onic deaths from 25 to 31 days of gestation associated with malnutrition was reported.19 On the basis of studies in other species, some of these losses in mares may be presumed to be due to genetic or chromosomal defects resulting in improper development of the embryo or fe- tus.3 One infertile stallion produced conceptions with twice the early embryonic death loss of other stallions.4 In- creased embryonic death loss may result from an ab- normal uterine environment in mares infected with Streptococcus zooepidemicus, klebsiella, pseudomonas or other bacteria. Bacterial infections are often associ- ated with improper closure of the genital tract due to poor conformation, lacerations and chronic scarring of the vulva resulting in pneumovagina, severe chronic lac- erations or scarring of the cervix, and cystic degenera- tion of the endometrium in older mares. Some mares may lack sufficient progesterone to maintain early pregnancy as discussed previously. Platt16 reported on factors influencing the incidence of abortion and noted that abortion rates, 21 percent, were higher in foaling mares conceiving from 7 to 21 days postpartum, compared to mares conceiving 22 to 42 days, 15.2 percent and over 42 days postpartum, 6.3 percent. The abortion rate of mares increased with increasing age, especially in mares over 18 years of age when it reached 28.6 percent. The incidence of abortion in brood mares barren for one year was 13.6 percent compared to 6.5 percent in mares that had foaled and conceived the same year. Abortion rates in mares covered by different stal- lions varied from 7.1 to 27.8 percent. Thus many factors can influence the incidence of abortion in mares. Further controlled, complete, competent studies on large num- bers of infertile and fertile mares, as has been done in cattle, are indicated. References on Equine Abortion General L Blood, D. C. and J. Henderson (1979) Veterinary Medicine, 5th Ed., Lea and Febiger, Philadelphia. 2. Gillespie, J. H. and Timoney, J. (1981) Hagan and Bruner’s In- fectious Diseases of Domestic animals, 7th Ed., Comstock Pub- lishing Co., Ithaca, N.Y. 3. Jennings, W. E. (1950) Twelve Years of Horse Breeding in the Army, JAVMA 116, 11, 874.176 VETERINARY OBSTETRICS 4. Roberts, S. J. (1971) Veterinary Obstetrics and Genital Diseases, 2nd Ed., Distributed by the author, Woodstock, Vt. Specific References Bacterial Infections 1. Allen, W. E. (1975) Ovarian Changes During Early Pregnancy in Pony Mares in Relation to PMSG Production., J. Reprod. Fert. Suppl. 23, 425. 2. Arnold, J. F. (1979) Problems Related to Pregnancy in Mares, Proc. 25th Ann. Conv. A.A.E.P., Miami Beach, Fla. 3. Aubaidi, J. M. (1969) Personal Communication and Thesis (1970) Bovine Mycoplasma, Cornell Univ., Ithaca, N.Y. 4. Bain, A. M. (1963) Common Bacterial Infections of Fetuses and Foals. Austral. Vet. Jour. 39, 413. 5. Benner, Ernest R., and Rhoades, H. E. (1966) Charlestown, W. Va. and Univ. of Illinois, Urbana, 111. Personal Communication. 6. Bryans, J. T. (1967) Personal Communication. 7. Cole, J. R. and Pursell, R. A. (1973) Serologic Incidence of Leptospirosis in Georgia Horses, Proc. 77th Ann. Mtg. U.S.A.H.A., St. Louis, Mo. 632-637. 8. Crane, C. S. (1956) A Report on Leptospirosis in a Herd of Shetland Ponies, JAVMA, 129, 260. 9. Dennis, S. M. (1980) Diagnosis of Equine Abortion, (A Re- view), Ann. Conv. AVMA, Washington, D.C. Contribution 21 Dept, of Path, Kansas Agr. Exp. Stat., Manhattan, Ks, 66506. 10. Denny, H. R. (1973) A Review of Brucellosis in the Horse, Eq. Vet. Jour. 5, 3. 11. Dimock, W. W., Edwards, P. R. and Bruner, D. W. (1947) Infections Observed in Equine Fetuses and Foals, Cor. Vet. 37, 2, 89. 12. Ellis, W. A., Bryson, D. G. and McFerran, J. B. (1976) Abor- tion Associated with Mixed Leptospira/Herpesvirus I Infection, Vet. Rec. 98, 218-219. 13a. Gibson, J. A. and Eaves, L. E. (1981) Isolation of Acineto- bacter calcoaceticus from an Aborted Equine Fetus., Austral. Vet. J. 57, 529. 13b. Gibson, J. A. et.al. (1982) Equine Abortion Associated with Enterobacter agglomerans, Eq. Vet. J. 14, 122. 13c. Hanson, L. E. (1982) Leptospirosis in Domestic Animals: The Public Health Perspective, JAVMA, 181, 12, 1505. 13d. Hults, C., and Murray, R. W. (1966) Rutland, Vermont. Per- sonal communication. 14. Jackson, R. S., Jones, E. E. and Clark, D. S. (1957) Abortion in Mares Associated with Leptospirosis, JAVMA, 131, 12, 564. 15. Kumar, S. and Gupta, B. K. (1972) Salmonella anatum from an Aborted Foal, Brit. Vet. Jour. 128, lxiv. 16. Lein, D. H. and Timoney, P. (1982) Personal communication. 17. Little, R. B., Beck, J. D. and McCahon, J. V. (1950) An Out- break of Bovine Leptospirosis in Pennsylvania, Vet. Med., 45, 3, 104. 18. Liu, I. K., Jang, S., Johnson, G. C., Knight, H. D. and Hawk- ins, D. (1977). Abortion Associated with Generalized Coryne- bacterium pseudotuberculosis Infection in a Mare, JAVMA, 170, 10, 1086-1087. 19. Mason, R. W., Brennan, R. G. and Corbould, A. (1980) Lis- teria monocytogenes Abortion in a Mare, Austral. Vet. J. 56, 613. 20. McCaughey, W. J. and Kerr, W. R. (1967) Abortion due to Brucellosis in a Thoroughbred Mare, Vet. Rec. 80, 186. 21. McNutt, S. H. and Murray, C. (1927) Bacterium abortum Iso- lated from the Fetus of an Aborting Mare, JAVMA, 65, 2, 215. 22. Mitchell, D. (1971) Early Fetal Death and a Serum Gonadotro- phin Test for Pregnancy in the Mare, Can. Vet. J. 12, 41-44. 23. Mitchell, D. and Allen, W. R. (1975) Observations on Repro- ductive Performance in the Yearling Mare, J. Reprod. Fert. Suppl. 23, 531-536. 24. Morse, E. V., Duncan, M. A., Page, E. A. and Fessler, J. F. (1976) Salmonellosis in Equidae: A Study of 23 Cases, Cor. Vet. 66, 198-213. 25. Morter, R. L., Herschler, R. C., Fessler, J. F. and Lavignette, A. (1964) Experimental Equine Leptospirosis (L. pomona), Proc. 68th Annual Meeting U.S.L.S.A., 147. 26. Osborne, V. E. (1975) Factors Influencing Foaling Percentages in Australian Mares, J. Reprod. Fert., Suppl. 23, 477-483. 27. Platt, H. (1973) Aetiological Aspects of Abortion in the Thor- oughbred Mare, J. Comp. Path. 83, 199-205. 28. Platt, H. (1975) Infection in the Horse Fetus, J. Reprod. Fert. Suppl. 23, 605-610. 29. Roberts, S. J. (1952) An Outbreak of Leptospirosis in Horses on a Small Farm, JAVMA, 121, 907, 237. 30. Smith, R. E., Williams, I. A. and Kingsbury, E. T. (1976) Ser- ologic Evidence of Equine Leptopirosis in the Northeast United States, Cor. Vet., 66, 105-109. 31. Swerczek, T. W. (1976) Pathology and Pathogenesis of Equine Fetal Diseases, Proc. 1976 Ann. Mtg. Soc. for Theriog. Lex- ington, Ky. 44-61 (Dept Vet. Sci., Ky. Agr. Exp. Stat., Univ. of Kentucky, Contrib. No. 76-4-156). 32. Swerczek, T. W. (1980). Early Fetal Death and Infectious Pla- cental Disease in the Mare, Proc. 26th Ann. Conv. A.A.E.P., Anaheim, Cal., 173-179. (See Arnold, 1979.) 33. Webb, R. F., Cockran, F. A., and Bryden, D. I. (1980) The Isolation of Pasteurella haemolytica from an Equine Fetus, Austral. Vet. J. 56, 610. Viral Infections EHV-I, Rhinopneumonitis Virus 1. Bass, E. P. (1978) Immunization with a Modified Live Virus Equine Rhinopneumonitis Vaccine, Proc. 24th Ann. Conv. A. A.E.P., St. Louis, Mo., 65-71. 2. Bryans, J. T. (1968) The Herpesvirus in Disease of the Horse, Proc. 14th Ann. Meeting A.A.E.P., Phila., 119. 3. Bryans, J. T. (1969) On Immunity to Disease Caused by Equine Herpesvirus I, Symposium on Immunity to Selected Equine Dis- eases, Lexington, Ky., JAVMA, 155, 2, Part 2, 295. 4a. Bryans, J. T. (1980) Application of Management Procedures and Prophylactic Immunization to the Control of Equine Rhino- pneumonitis, Proc. 26th Ann. Conv. A.A.E.P., Anaheim, Calif. 4b. Bryans, J. T. (1980) Herpesviral Diseases Affecting Reproduc- tion in the Horse, Vet. Clin, of N. Amer. 2, 2, 303-312, W. B. Saunders Co., Philadelphia. 5. Bryans, J. T., Swerczek, T. W., Darlington, R. W. and Crowe, M. W. (1977). Neonatal Foal Disease Associated with Perinatal Infection by Equine Herpesvirus I., J. Eq. Med. and Surg., 1, 1, 20-25. 6. Bruner, D. W. (1958) Personal Communication. 7. Carmichael, L. E. (1962) Personal Communication. 8. Comer, A. H., Mitchell, D., Meads, E. B., Girard, A., Greig,DISEASES AND ACCIDENTS OF GESTATION 177 A. S. and Mitchell, D. (1963) Equine Virus Abortion in Can- ada, Cor. Vet. 53, 1, 78 and 88. 9. Dimock, W. W., Edwards, P. R., and Bruner, D. W. (1942) Equine Virus Abortion, Kentucky Agr. Exp. Stat. Bulletin 426. 10. Dixon, F. J., Hartley, W. J., Hutchins, D. R., Lepherd, E. E., Feilen, C., Jones, R. F., Love, D. N., Sabine, M. and Wells, A. L. (1978) Perinatal Foal Mortality Associated with a Her- pesvirus. Austral. Vet. J. 54, 102-105. 11. Doll, E. R. (1954) History of Research on Equine Virus Abor- tion, Dept, of Animal Path., Kentucky Exp. Stat., Lexington, Ky. 12. Doll, E. R. (1961) Immunization against Viral Rhinopneumo- nitis of Horses with Live Virus Propagated in Hamsters, JAVMA, 139, 12, 1324. 13. Doll, E. R. and Bryans, J. T. (1962) Incubation Periods for Abortion in Equine Viral Rhinopneumonitis, JAVMA, 141, 3, 351. 14. Doll, E. R. and Bryans, J. T. (1962) Development of Comple- ment-Fixing and Virus Neutralizing Antibodies in Viral Rhi- nopneumonitis of Horses, Amer. J. of Vet. Res. 23, 95, 843. 15. Doll, E. R. and Bryans, J. T. (1963) A Planned Infection Pro- gram for Immunizing Mares Against Viral Rhinopneumonitis, Cor. Vet. 53, 2, 249. 16. Doll, E. R. and Bryans, J. T. (1963) Epizootiology of Equine Viral Rhinopneumonitis, JAVMA, 142, 1, 31. 17. Doll, E. R. and Kinter, J. H. (1954) A Comparative Study of Equine Abortion and Equine Influenza Viruses, Cor. Vet. 44, 3, 355. 18. Doll, E. R., Richards, M. G., Wallace, M. E. and Bryans, J. T. (1952) The Influence of an Equine Fetal Tissue Vaccine Upon Hemagglutination Activity of Mare Serums: Its Relation to He- molytic Icterus of Newborn Foals, Cor. Vet. 42, 495. 19. Eaglesome, M. D., Mitchell, D. and Henry, J. N. R. (1979) Control and Prevention of Equine Herpesvirus I Abortion, J. Reprod. Fert. Suppl. 27, 607-613. 20. Eugster, H. K. and Jones, L. P. (1977) Paralysis in Horses Fol- lowing Natural Infection or Vaccination with Equine Rhino- pneumonitis Virus. Texas Vet. Med. J. 39, 5, 15-16. 21. Gleeson, L. J. and Coggins, L. (1980) Response of Pregnant Mares to Equine Herpes I (EHV I), Cor. Vet. 70, 391-400. 22. Gleeson, L. J. and Studdert, M. J. (1977) Equine Herpesvi- ruses, Experimental Infection of a Fetus with Type 2, Austral. Vet. J. 53, 360-362. 23. Greenwood, R. E. S. and Simson, A. R. B. (1980) Clinical Report of a Paralytic Syndrome Affecting Stallions, Mares and Foals on a Thoroughbred Studfarm, Eq. Vet. J. 12, 2, 113— 117. 24. Homer, G. W. (1981) Serological Relationship Between Abor- tifacient and Respiratory Strains of Equine Herpes Virus Type I in New Zealand, N.Z. Vet. Jour. 29, 7-8. 25a. Jackson, T. A. and Kendrick, J. W. (1971) Paralysis of Horses Associated with Equine Herpesvirus I Infection, JAVMA, 158, 8, 1351-1357. 25b. Jackson, T. A., Osbum, B. I., Cordy, D. R. and Kendrick, J. W. (1977) Equine Herpesvirus I Infection of Horses: Studies on the Experimentally Induced Neurologic Disease, Amer. J. Vet. Res. 38, 6, 709-719. 26. Kendrick, J. W. (1969) Comments on Equine Herpesvirus In- fection (Equine Rhinopneumonitis) and Bovine Herpesvirus In- fection (Infectious Bovine Rhinotracheitis), JAVMA, 155, 2 (Part 2), 306. 27. Little, P. B. and Thorsen, J. (1976) Disseminated Necrotizing Myeloencephalitis: Herpes-Associated Neurologic Disease of Horses, Vet Pathol., 13, 161-171. 28. Liu, K. M. and Castleman, W. (1977) Equine Posterior Paresis Associated with Equine Herpes I Vaccine in California: A Pre- liminary Report, J. Eq. Med. & Surg. 1, 397-401. 29. McKercher, D. G., Saito, J. K. and Mathis, R. M. (1969) Com- parative Aspects of Immunity Against Bovine and Equine Her- pesviruses, JAVMA, 155, 2 (Part 2), 300. 30. Neely, D. P. and Hawkins, D. L. (1978) A Two Year Study of the Clinical and Serologic Responses of Horses to a Modified Live-Virus Equine Rhinopneumonitis Vaccine, J. Eq. Med. & Surg., 2, 532-540. 31. Plummer, G. and Waterson, A. P. (1963) Equine Herpes Virus, Virology 19, 3, 412. 32. Roberts, S. J. and DeLahunta, A. (1975) Personal Communi- cation. 33. Saxegaard, F. (1966) Isolation and Identification of Equine Rhinopneumonitis Virus from Cases of Abortion and Paralysis, Nord. Vet. Med. 18, 504. 34. Smith, I. M., Girard, A., Comer, A. H. and Mitchell, D. (1972) The Fluorescent Antibody Technique in the Diagnosis of Equine Rhinopneumonitis Virus Abortion, Can. J. Comp. Med. 36, 303- 308. 35. Sprinkle, T. (1975) Diagnosis-Equine Rhino., Norden News Spring 1975, 16-18. 36. Studdert, M. J. (1974) Comparative Aspects of Equine Herpes- viruses, Cor. Vet. 64, 94-122. 37. Studdert, M. J., Simpson, T. and Roizman, B. (1981) Differ- entiation of Respiratory and Abortigenic Isolates of Equine Her- pesvirus I by Restriction Endonucleases, Science, 214, 562-564. 38. Turtinen, L. W., Allen, G. P., Darlington, R. W. and Bryans, J. T. (1981) Serologic and Molecular Comparisons of Several Equine Herpesvirus Type I Strains, Amer. J. Vet. Res., 42, 12, 2099-2104. 39. University of Kentucky Veterinary Science Department (1982) Equine Herpes Vims Abortion—A Review, A.A.E.P. News- letter (Mar.), 1, 97. Arteritis Virus 1. Bryans, J. T., Doll, E. R., Crowe, M. E. W. and McCollum, W. H. (1957) The Blood Picture and Thermal Reaction in Ex- perimental Viral Arteritis of Horses, Cor. Vet. 47, 1, 42. 2. Burki, F. and Gerber, H. A. (1966) Virologically Certified Large Scale Outbreak of Equine Arteritis, Berl. and Munich. Tierartzl. Wochschr. 79, 20, 391. 3. Cheville, N. F. (1980) Pathogenesis of Abortion in Equine Viral Arteritis Abstr., Mod. Vet. Pract., 61, 413-414. 4. Doll, E. R., Bryans, J. T., McCollum, W. H. and Crowe, M. E. W. (1957) Isolation of a Filterable Agent Causing Arteritis of Horses and Abortion of Mares, Its Differentiation from the Equine Abortion (Influenza) Vims, Cor. Vet. 47, 1, 3. 5. Funkunaga, Y. and McCollum, W. H. (1977) Complement-Fix- ation Reactions in Equine Viral Arteritis, Amer. J. Vet. Res. 38, 12, 2043-2046. 6. Gabel, A. A., Heuschele, W. P. and Kohn, C. W. (1980) Proc. 1980 Intemat. Workshop on Equine Viral Respiratory Diseases and Complications, A.A.E.P. Newsletter 2: 49-99. 7. Harry, T. O. and McCollum, W. H. (1981) Stability of Viability and Immunizing Potency of Lyophilized, Modified Equine Ar- teritis Live-Vims Vaccine, Amer. J. Vet. Res. 42, 9, 1501-1505. 8. Jones, T. C., Doll, E. R. and Bryans, J. T. (1957) The Lesions of Equine Viral Arteritis, Cor. Vet. 47, 1, 52.178 VETERINARY OBSTETRICS 9. Jones, T. C. (1969) Clinical and Pathologic Features of Equine Viral Arteritis, JAVMA, 155, 2 (Part 2), 315. 10. Knappenberger, R. E. and Bryans, J. T. (1957) An Outbreak of Abortion Caused by the Equine Arteritis Virus, Cor. Vet. 47, 1, 69. 11. McCollum, W. H. (1969) Development of a Modified Virus Strain and Vaccine for Equine Virus Arteritis, Symp. on Immunity to Selected Equine Diseases, Lexington, Ky., JAVMA, 155, 2 (Part 2), 31S. 12. McCollum, W. H. and Bryans, J. T. (1972) Serological Identi- fication of Infection by Equine Arteritis Virus in Horses of Sev- eral Countries, Proc. 3rd Intemat. Conf. Equine Infectious Dis- eases, Paris, 256-263 (Karger, Basel, 1973). 13. McCollum, W. H. (1981) Pathologic Features of Horses Given Avirulent Equine Arteritis Virus Intramuscularly, Amer. J. Vet. Res. 42, 7, 1218-1220. 14. McCollum, W. H., Doll, E. R., Wilson, J. C. and Johnson, C. B. (1961) Propagation of Equine Arteritis Virus in Monolayer Cultures of Equine Kidney, Amer. J. Vet. Res. 22, 89, 731. 15. McCollum, W. H., Doll, E. R. and Wilson, J. C. (1962) The Recovery of Virus from Horses with Experimental Cases of Equine Arteritis Using Monolayer Cell Culture of Equine Kidney, Amer. J. Vet. Res. 94, 23, 465. 16. Wilson, J. C., Doll, E. R., McCollum, W. H. and Cheatham, J. (1962) Propagation of Equine Arteritis Virus Previously Adapted to Cell Cultures of Equine Kidney in Monolayer Cultures of Hamster Kidney, Cor. Vet. 52, 200-205. Other Viruses 1. Ishii, S. (1963) Equine Infectious Anemia or Swamp Fever, Adv. in Vet. Sci. 8, 263. 2. Kemen, M. J. and Coggins, L. (1972) Equine Infectious Anemia; Transmission from Infected Mares and Foals, JAVMA, 161, 496- 499. Mycotic or Fungal Infections 1. Arnold, F. J. (1979) Problems Related to Pregnancy in Mares, Proc. 25th Amer. Conv. A.A.E.P. Miami Beach, 451-457. 2. Hall, A. D. (1979) An Equine Abortion Due to Histoplasmosis, Vet. Med. SAC. 74, 200-201. 3. Hensel, L., Bisping, W. and Schimmel-Pennig, A. (1961) As- pergillusabort biem Pferde, Berl. Munch. Tierartzl. Wchnschr. 74, 290. 4. Mahaffey, L. and Adam, N. (1964) Abortions Associated with Mycotic Lesions of the Placenta of Mares, JAVMA, 144, 1, 24. 5. Mahaffey, L. and Rossdale, P. O. (1965) An Abortion Due to Allescheria boydii and General Observations Concerning My- cotic Abortions of Mares, Vet. Rec. 77, 19, 541. 6. Powers, R. D. and Benz, G. W. (1977) Abortion in a Mare Due to Coccidioidomycosis, JAVMA, 170, 2, 178-179. 7a. Rooney, J. (1964) Cleanliness is the Best Safeguard Against My- cotic Placentitis, The Blood-Horse 87, 15, 772. 7b. Ryan, M. J. and Wyand, D. S. (1981) Cryptococcus as a Cause of Neonatal Pneumonia and Abortion in Two Horses, Vet. Pa- thol., 18, 270. Protozoal Infections 1. Duplessis, J. L. and Basson, P. A. (1966) Babesiosis in Aborted Equine Fetuses, J. South Afric. V.M.A. 37, 267. 2. Gibbons, W. J. (1968) Reproduction in Farm Animals, Edit, by E. S. E. Hafez, 2nd Ed., Lea and Febiger, Philadelphia, 399. 3. Fayer, R. (1980) Sarcocystis in Horses, (Abstr.) Eq. Vet. Data, I, 22, 263. 4. Frerichs, W. M., Holbrook, A. A. and Johnson, A. J. (1969) Equine Piroplasmosis; Complement Fixation Titers of Horses In- fected with Babesia caballi, Amer. J. Vet. Res. 30, 5, 697. 5. Madden, P. A. and Holbrook, A. A. (1968) Equine Piroplas- mosis; Indirect Fluorescent Antibody Test for B. caballi, Amer. J. Vet. Res. 29, 1, 117. 6. Meynard, J. A. (1951) Congenital Piroplasmosis in the Horse, Rec. Med. Vet. 127, 340. 7. Platt, H. (1975) Infection of the Horse Fetus, J. Reprod. Fert. Suppl. 23, 605 -610. 8. Neitz, W. O. (1956) Babesiosis: Some Protozoan Diseases of Man and Animals, Art. 2, Ann. N.Y. Acad. Sci. 64, 56. 9. Ristic, M. (1975) Equine Babesiosis and Trypanosomiasis, 1st Intemat. Suppl. Eq. Hematol., East Lansing, Mich. 393-407. 10. Sippel, W. L, Cooperrider, D. E., Gainer, J. H., Allen, R. W., Mouw, J. E. B. and Tiegland, M. B. (1962) Equine Piroplas- mosis in the United States, JAVMA, 141, 6, 694. Noninfectious Causes of Equine Abortion 1. Allen, W. E. (1975) Pregnancy Failure Induced by Human Cho- rionic Gonadotropin in Pony Mares, Vet. Rec. 96, 88-90. 2. Aim, C. C., Sullivan, J. J. and First, N. L. (1974) Induction of Premature Parturition by Parenteral Administration of Dex- amethasone in the Mare, JAVMA, 165, 721. 3. Asdell, S. A. (1964) Patterns of Mammalian Reproduction, 2nd Ed., Comstock Publishing Co., Ithaca, N.Y. 4. Arthur, G. H. (1958) An Analysis of the Reproductive Function of Mares Based on Post-mortem Examination, Vet. Rec. 70, 682. 5. Arthur, G. H. (1964) Wright’s Veterinary Obstetrics, 3rd Ed., Williams and Wilkins Co., Baltimore. 6. Britton, J. W. (1947) Clinical Studies of Early Abortion, Cor. Vet. 37, 1, 14. 7. Bums, S. J. (1973) Clinical Safety of Dexamethasone in Mares During Pregnancy, Eq. Vet. Jour. 5, 91. 8. Dinger, J. E. and McCall, J. P. (1981) Plasma Progesterone Levels in Pregnant Mares Following Administration of Exoge- nous Progesterone, Theriog. 15, 405-413. 9. Douglas, R. H. and Ginther, O. J. (1975) Effects of Prostaglan- din F2a on the Oestrus Cycle and Pregnancy in Mares, J. Reprod. Fert. Suppl. 23, 257-261. 10. Drew, B., Barber, W. P. and Williams, D. G. (1975) The Ef- fect of Excess Dietary Iodine on Pregnant Mares and Foals, Vet. Rec. 97, 93-95. 11. Errington, B. J. (1942) Equine Twin Placentation, Cor. Vet. 32, 4, 367. 12. Ganjam, V. K. and Kenney, R. M. (1975) Peripheral Blood Plasma Levels and Some Unique Metabolic Aspects of Proges- terone in Pregnant and Non-Pregnant Mares, Proc. 21st Ann. Conv. A.A.E.P., Boston, Mass. 263-275. 13. Garbers, G. (1967) Personal Communication.DISEASES AND ACCIDENTS OF GESTATION 179 14a. Ginther, O. J. (1979) Reproductive Biology of the Mare—Basic and Applied Aspects, Cross Plaines, Wise. 14b. Ginther, O. J. (1982) Twinning in Mares: A Review of Recent Studies, Eq. Vet. Sci. 2, 4, 127-135. 15. Hawkins, D. L. (1979) Injectable Progesterone Therapy in the Mare, Proc. 25th Ann. Conv. A.A.E.P., Miami Beach, Fla., 123-129. 16. Hawkins, D. L., Neely, D. P. and Stabenfeldt, G. H. (1979) Plasma Progesterone Concentrations Derived from the Admin- istration of Exogenous Progesterone to Ovariectomized Mares, J. Reprod. Fert., 27, 211-216. 17. Hillman, R. B. and Lesser, S. A. (1980) Induction of Parturi- tion in the Mare, Vet. Clin, of N. Amer. 2, 2, 333-344. 18. Knudson, O. (1964) Endometrial Cytology as a Diagnostic Aid in Mares, Cor. Vet. 54, 3, 415. 19. Lanman, J. T. (1968) Delays During Reproduction and their Effects on the Embryo and Fetus, New Engl. J. of Med. 278, 993, 1047, 1092. 20. Lein, D. (1967) Personal Communication. 21. Loy, R. G. and Swan, S. M. (1966) Effects of Exogenous Pro- gestagens on Reproductive Phenomena in Mares, J. An. Sci. 25, 3, 821. 22a. Mcllwraith, C. W. and James, L. F. (1982) Limb Deformities Associated with Ingestion of Locoweed by Mares, JAVMA, 181, 3, 255. 22b. Merkt, H. (1966) Foal Heat and Fetal Resorption, Zuchthyg, 1, 102. 23. Mitchell, D. (1967) (1969) Personal Communication. 24. Mitchell, D. and Allen, W. R. (1975) Observation on Repro- ductive Performance in the Yearling Mare, J. Reprod. Fert. Suppl. 23, 531-536. 25. Mitchell, D. and Lein, D. (1971) Veterinary Obstetrics and Genital Diseases, 2nd Ed., by S. J. Roberts, Woodstock, Vt. 142. 26. Nishikawa, Y. (1959) Studies on Reproduction in Horses, Japan Racing Assoc. Tokyo, Japan, 152. 27. Osborne, V. E. (1960, 1965) Personal Communication. 28. Osborne, V. E. (1966) An Analysis of the Pattern of Ovulation As it Occurs in the Annual Reproductive Cycle of the Mare in Australia, Austral. Vet. Jour. 42, 149. 29. Osborne, V. E. (1975) Factors Influencing Foaling Percentages in Australian Mares, J. Reprod. Fert. Suppl. 23, 477-483. 30. Patterson, A. W. (1962) Personal Communication. 31. Richter, W. (1963) Investigations into the Interruption of Preg- nancy in Mares, Zuchthyg. Fortpfl. und Besam. der Haust. 7, 2, 81. 32. Roberts, S. J. (1971) Veterinary Obstetrics and Genital Diseases 2nd Ed., Woodstock, Vt., 142. 33a. Roberts, S. J. (1978) Twin Pregnancy in a Mare: A Live Foal and a Mummified Fetus, Cor. Vet. 68, 196-198. 33b. Roberts, S. T. and Myhre, G. (1983) A Review of Twinning in Horses and the Possible Value of Supplemental Progesterone to Prevent Abortion of Equine Twin Fetuses, Cor. Vet., In Press. 34. Romane, W. M., Adams, L. G., Bullard, T. L. and Dollahite, J. W. (1966) Cystitis Syndrome of the Equine, Southwestern Vet. 19, 2, 95. 35. Sager, F. (1962) Personal Communication. 36a. Squires, E. L., Hillman, R. B., Pickett, B. W. and Nett, T. M. (1980) Induction of Abortion in Mares with Equimate: Ef- fect on Secretion of Progesterone PMSG and Reproductive Per- formance, J. An. Sci. 50, 490-495. 36b. Squires, E. L., Eikenberry, D. J., Voss, J. L., Nett, T. M. and Shideler, R. K. (1981) The Effect of Progestin Therapy on Preg- nancy Maintenance in Mares, J. An. Sci., 53, Suppl. 1, 594, 368. (Abstr.) 37. VanKampen, K. R. (1970) Sudan Grass and Sorghum Poisoning of Horses: A Possible Lathyrogenic Disease, JAVMA, 156, 5, 629. 38. Van Niekerk, C. H. (1965) Early Embryonic Resorption in Mares, J. S. Afr. Vet. Med. Assoc. 36, 1, 61. 39. Wohanka, K. (1961) Untersuchungen Der Ursachen Der Ver- fohlens, Proc. 4th Intemat. Cong, on An. Reproduction, the Ha- gue, III, 622. Miscellaneous Causes of Equine Abortion: (Nutritional, Genetic, Teratogenic, Physical, Twinning, Early Embryonic, Managerial) 1. Arnold, J. F. Jr. (1979) Problems Related to Pregnancy in Mares, Proc. 25th Ann. Conv. A.A.E.P., Miami Beach, Florida. 2. Arthur, G. H. (1964) Wright’s Veterinary Obstetrics, 3rd Ed., Williams and Wilkins Comp., Baltimore, 6. 3. Blue, M. G. (1981) A Cytogenetical Study of Prenatal Loss in the Mare, Theriog., 15, 3, 295-309. 4. Britton, J. W. (1947) Clinical Studies of Early Equine Abortion, Cor. Vet. 37, 1, 14. 5. Dimock, W. W., Edwards, P. R. and Bruner, D. W. (1947) Infections Observed in Equine Fetuses and Foals, Cor. Vet. 37, 88. 6. Errington, B. J. (1942) Equine Twin Placentation, Cor. Vet., 32, 4, 367. 7. Garbers, G. (1967) Personal Communication. 8a. Ginther, O. J. (1979) Reproductive Biology of the Mare, Cross Plaines, Wise., 348-358. 8b. Ginther, O. J. (1982) Twinning in Mares: A Review of Recent Studies, Eq. Vet. Sci., 2, 4, 127-135. 9. Jeffcott, L. B. and Whitwell, K. E. (1973) Twinning as a Cause of Fetal and Neonatal Loss in the Thoroughbred Mare, J. Comp. Path. 83, 91-106. 10a. Klein, N. W., Plenefisch, J. D., Carey, S. W., Fredrickson, W. T., Sacked, G. P., Barbacher, T. M. and Parker, R. M. (1982) Serum From Monkeys with Histories of Fetal Wastage Causes Abnormalities in Cultured Rat Embryos, Science 215, 66-69. 10b. Knudson, O. (1964) Endometrial Cytology as a Diagnostic Aid in Mares, Cor. Vet. 54, 3, 415. 11a. Lansman, J. T. (1968) Delays During Reproduction and Their Effects on the Embryo and Fetus, New Eng. J. of Med. 278, 993, 1047, 1092. lib. Layton, G. E. (1982) Personal Communication. 12. Merkt, H. (1966) Foal Heat and Fetal Resorption, Zuchthyg. 1, 102. 13. Mitchell, D. and Allen, W. R. (1975) Observation on Repro- ductive Performance in the Yearling Mare, J. Reprod. Fert. Suppl. 23, 531-536. 14. Mitchell, D. and Lein, D. (1971) Veterinary Obstetrics and Genital Disease, 2nd Ed., by S. J. Roberts, Woodstock, Vt., 142. 15. Osborne, V. E. (1966) An Analysis of the Pattern of Ovulation as it Occurs in the Annual Reproductive Cycle of the Mare in Australia, Austral. Vet. J. 42, 149. 16. Platt, H. (1973) Aetiological Aspects of Abortion in the Thor- oughbred Mare, J. Comp. Path. 83, 199-205.180 VETERINARY OBSTETRICS 17a. Richter, W. (1963) Investigations into the Interruption of Preg- nancy in Mares, Zuchthyg. Fortpfl. und Besam. der Haust. 7, 2, 81. 17b. Roberts, S. J. and Myhre, G. (1983) A Review of Twinning in Horses and the Possible Therapeutic Value of Supplemental Pro- gesterone to Prevent Abortion of Equine Twin Fetuses., Cor. Vet., 73, In press. 17c. Squires, E. L. (1982) The Pregnant Mare (Abstract), Eq. Vet. Data, 3, 22. 18. Swerczek, T. W. (1976) Pathology and Pathogenesis of Equine Fetal Diseases, Proc. Ann. Mtg. Soc. for Theriog., Lexington, Ky. 19. Van Niekerk, C. H. (1965) Early Embryonic Resorption in Mares, J. So. Afr. Vet. Med. Assoc. 36, 1, 61. 20a. Whitwell, K. E. (1975) Morphology and Pathology of the Equine Umbilical Cord, J. Reprod. Fert. Suppl. 23, 599-603. 20b. Whitwell, K. E. (1980) Investigations into Fetal and Neonatal Losses in the Horse, The Vet. Clin, of N. Amer. 2, 2, 313— 330, W. B. Saunders Co., Philadelphia. 21. Wohanka, K. (1961) Untersuchungen Der Ursachen Der Ver- fohlens, Proc. 4th Intemat. Cong, on An. Reprod., the Hague III, 622. 22. Zent, W. W. (1982) Personal Communication. Abortion in Swine Abortions in swine, as in other species, are comprised of early embryonic deaths and abortions or absorptions, fetal deaths and either abortion of the entire litter or mummification and stillbirths at term of a variable por- tion of the litter. The latter two categories in contrast to uniparous animals are common in swine. In a herd rel- atively free of infectious bacterial and viral diseases an incidence of 3 to 8 percent stillbirths and 1 to 5 percent fetal mummification in 551 litters of over 5000 pigs in a ten year period was reported.- Abortions were uncom- mon. Over 58,000 pigs had an incidence of 5 to 14 per- cent stillbirths.- Stillbirths comprise those fetal deaths occurring within the last 20 to 30 days of gestation which terminate in abortion at term; mummification comprise those deaths occurring from 35 to approximately 85 days of gestation.- The incidence of swine abortion is vari- able, possibly about 5 percent, and abortions usually oc- cur from 75 to 95 days of gestation.-— Stillbirths and mummification will be discussed later in more detail but are an integral part of the porcine prenatal death loss. About 40 to 50 percent of the causes of abortions in swine are diagnosed when investigated by competent veterinary laboratories. This level of diagnosis is only slightly better than in cattle and lower than in sheep and horses. A 1978 study of infectious agents associated with 824 abortions in swine in the midwest indicated that 38.8 percent of the fetuses revealed an infectious agent; 22 percent were viral and 16.5 percent were bacterial. Of the bacterial infections leptospiral agents were most common, 9.8 percent.^ Infectious Causes of Swine Abortion Bacterial Causes Leptospirosis first recognized in 1950 is the most common bacterial cause of swine abortion in the U.S. now that brucellosis is on the decline due to regulatory activities. The causative agent is usually L. pomona al- Table 11. Summary of Causes of Abortion in Swine Infectious causes: Bacterial-Leptospirosis (L. pomona, L. grippotyphosa, L. icterohemorrhagiae and L. canicola), Brucellosis (Br. suis) Miscellaneous bacterial-streptococci, Staphylococcus aureus, E. coli, Salmonella spp., Mycobacterium avium, Listeria monocytogenes, C. pyogenes, Erysipelothrix rhusiopathiae, Pseudomonas spp. Nocardia asteriodes, Pasteurella spp, Mycoplasma, Actinobacillus equuli, Actinomyces, Hemophilus, Proteus, Chlamydia, Hemophilus parahemolyticus Mycobacterium tuberculosis, and Klebsiella pneumoniae. Viral-enteroviruses or picomaviruses, parvovirus, pseudorabies (Aujesky’s disease) Miscellaneous viral-hog cholera, reovirus, cytomegalovirus, vesicular exanthema virus and vesicular stomatitis virus, foot and mouth disease virus, Japanese B. encephalitis virus, hemagglutination virus, influenza vims and African swine fever vims. Mycotic or fungal-Aspergillus fumigatus and other molds Protozoa-Toxoplasma gondii, eperythrozoonosis, and sarcocystosis. Noninfectious Causes: Chemical, Dmg and Plant-dicoumaral, zearalenone and trichothenes (moldy com), pentochlorophenols (PCB’s), carbon mon- oxide and creosote Hormonal-estrogens, glucocorticoids, prostaglandins Nutritional-deficiencies of iodine, vitamin A, iron, and calcium Physical-stress and exhaustion coincident to transportation, fighting and injury Genetic, congenital or chromosomal-anomalies, early embryonic deaths Miscellaneous-poor management, increased stillbirths associated with large or small litters and in older anemic, fat sows.DISEASES AND ACCIDENTS OF GESTATION 181 though L. grippotyphosa, L. hardjo, L. canicola, L. hyos, L. sejroe (hebdomadis), L. icterohemorrhagiae, L. ballum and L. autumnalis have also been reported as causing abortion, stillbirths or weak pigs that die shortly after birth.--'----'1'2 Leptospirosis in swine due to var- ious serotypes is widespread in the U.S., Europe and other countries throughout the world. It is more preva- lent than commonly suspected because certain serotypes (serovars) produce an inapparent clinical disease.- The incidence of leptospirosis in swine in the U.S. varies from 8 to 25 percent36'5 with the higher incidence in Florida and Georgia. Leptospiral organisms usually enter the body of the susceptible pig through breaks in the skin or through the mucous membrane of the nasal, conjunctival, digestive or reproductive tracts. A leptospiremia and general in- fection develops in which organisms invade all the vis- ceral organs. This lasts for 5 to 10 days after which serum antibodies can be detected. The highest serum antibody titers are observed about 3 to 4 weeks after exposure and persist for a year or more. The organisms usually lo- calize in the kidney tubules and are discharged in the urine for 1-1/2 to 6 months. In a few pigs the renal carrier state or leptospiruria may persist for 2 years. The greatest number of organisms are shed 20 to 30 days after exposure.1,5 - Leptospiral organisms may be spread directly by the urine or indirectly by contaminated feed and water to susceptible pigs. As reported previously un- der abortions in cattle, leptospira can survive in a moist environment outside the body for a period of over a week.-9 Infected boars might infect susceptible sows at coitus and have been shown to introduce the infection into a susceptible sow herd. It is possible that leptospi- rosis might be spread from infected boars by artificial insemination. Infection, but not abortion, was produced by infecting sows intravaginally after coitus.1 Abortions occurred only in sows infected late in the second month, during the third month or early in the fourth month of gestation. Leptospira spp can also be spread from cattle to swine or swine to cattle by infected urine. As in lep- tospirosis in cattle, wild animals such as rodents, skunks, opossums and raccoons may be a source of infection for swine. Only occasionally do swine infected with Leptospira spp demonstrate acute or obvious clinical signs of illness such as hemoglobinuria. In experimental animals the in- cubation period is 1 to 2 weeks and inappetence, a mild fever and slight depression may be seen for several days during the leptospiremic stage of the disease but under farm conditions these signs are often not observed. Thus many leptospiral infections of swine are inapparent ex- cept for abortions that occur in pregnant females. Fol- lowing leptospirosis in swine small widespread greyish foci are found scattered throughout the kidneys and liver.5 9 Some degeneration and necrosis of kidney tubules may also be present. Abortions in susceptible sows infected with Lepto- spira spp occur 1 to 4 weeks prior to term. Of 800 abort- ing sows the earliest leptospiral abortions were from 72 to 78 days of gestation.4 Infections occurring between 55 and 88 days of gestation in sows most commonly pro- duce abortions. Abortions usually occur 3 to 4 weeks after the initial infection of the sow. Some or all of the fetuses may be infected and deaths are due to a leptospi- ral septicemia. Following fetal deaths mummification of the fetus may occur.- Stillbirths or deaths of fetuses late in gestation, and the birth of infected weak, “squealer” pigs that die within several days after birth are common in leptospiral epizootics in swine herds. The incidence of abortion in sows in a herd or of dead fetuses or dying newborn pigs may vary from 20 to 100 percent depend- ing on the number of susceptible sows in late gestation and the rate of spread and virulence of the organism.8 Aborted fetuses may be icteric and weak live pigs may die soon after birth.-- Leptospirosis may be diagnosed by leptospiral serum titers of 1:100 or higher in the aborting sows as deter- mined by the microscopic agglutination (MA) test using cultures or antigens of five serotypes.- Other serologic tests may be used. Low titers might indicate a prior in- fection or vaccination with L. pomona or other leptospi- ra and abortion due to another cause. A rising titer is highly diagnostic in blood samples taken at abortion and several weeks later. Leptospira spp can often be iso- lated on culture with special media or animal inoculation from the liver, kidneys, peritoneal or pericardial cavities of aborted fetuses, stillborn or weak, ill newborn piglets. Histopathological examination of silver-stained kidney sections or fluorescent antibody stained body fluids or tissues-'7 from fetuses may reveal the organism. Lepto- spira often cannot be isolated from the urine of acutely infected aborting sows but several weeks following abor- tion leptospira can frequently be cultured from the sow’s urine. Direct dark field examination of the fetal pericar- dial or peritoneal fluid or kidney scrapings may reveal the small, fine, fdamentous, motile “spinning” leptospi- ral organisms.-’-’1 Following abortion caused by lepto- spira the sows are immune and resistant to reinfection with that serotype for at least 11 to 14 months.6 Leptospirosis in swine may be controlled by sanita- tion, vaccination and antibiotic therapy, but is difficult to eradicate in a herd. Maintaining a herd free of lep- tospirosis is possible but may be difficult due to reser- voirs of infection in cattle, other domestic animals and182 VETERINARY OBSTETRICS in wild animals, such as skunks, mice and rats. A san- itary environment free of water holes and swampy areas may aid in preventing the spread of the disease. Covered feeding and watering troughs not easily contaminated by infective urine are also desirable. Cattle and swine should not be house together as leptospirosis may be transmitted between the species. By proper sanitation and manage- ment, frequent blood testing, segregation and isolation or measures used to produce a specific pathogen-free herd, a leptospirosis-free herd may be attained. If the swine herd is free of leptospirosis, purchased swine should be negative to the blood test, isolated away from the herd for a month and retested before placed in the herd. Since in chronically-infected swine herds the acute disease is inapparent, most commercial swine owners routinely vaccinate their sows and gilts before the breed- ing season, early in pregnancy or every six months with a multivalent leptospiral bacterin that provides a good but relatively short-lived immunity against abortions due to L. pomona, hardjo, grippotyphosa, canicola and icterohemorrhagiae. The bacterin may also be used early in an outbreak but abortions may continue for 3 to 4 weeks in infected sows. Vaccination of swine two weeks before going to fairs or shows is recommended. Lepto- spiruria may occasionally develop in exposed vaccinated sows but abortions do not occur, and the number of car- riers will be reduced.-1 Vaccination with the bacterin produces low serum titers. In recently infected susceptible herds, vaccination and antibiotics administered for a period of several weeks- have been effective in treating the carrier state as well as the acute infection and to reduce the incidence of abortion for a period of several weeks until immunity develops to vaccination. The following regimens have been recommended: for pregnant animals in an infected herd; 400 to 500 gm. of chlortetracycline (Aureomycin) or oxytetracycline (Terramycin) per ton of feed for 10 to 14 days should be provided. For treating the chronic carrier or shedder state in pigs of all ages, chlortetra- cycline or oxytetracycline at levels of 400 to 500 up to 1000 gm. per ton of feed should be fed for 7 to 10 days.--1 Individual treatment of swine may also be used with 5 daily intramuscular injections of tetracycline (Polyotic) at a dose level of 3 mg. per pound of body weight or a single injection of 25 mg, per kg. of body weight of dihydrostreptomycin.10 It is advisable to blood test boars or sows introduced into the breeding herd. If the breeding herd is infected, vaccination of these animals prior to entry is indicated. If the breeding herd is noninfected and the introduced animals are positive, isolation and administration of an- tibiotics to eliminate the carrier state is essential. Brucellosis in swine, due to Brucella suis, is a much more insidious disease than brucellosis in cattle. The dis- ease has been widespread especially in the hog-raising areas of the Midwest. In 1980 the incidence of animal infection in the U.S. was 0.08 percent and farm infection 0.87 percent.- An aggressive eradication program is con- tinuing in the U.S. under the direction of the U.S. Dept, of Agriculture and cooperating states to increase the numbers of validated (brucellosis-free) herds. Blood testing of adult sows and boars at slaughter to locate in- fected herds has proven highly effective in controlling and eradicating this disease. Swine brucellosis exists in all swine producing countries and occurs in wild pigs in Florida and Louisiana.7 In Florida infected feral swine have caused brucellosis in other swine and hunters.- Br. suis may also occur naturally in horses, cattle, dogs, fowl and the European hare. Br. abortus, Br. melitensis and Br. canis may cause brucellosis in swine but clinical signs are rare and the infections are selflimiting.- - - Bru- cellosis due to Br. suis until recently was the most com- mon type found in humans in the United States.- Br. suis is a facultative intracellular parasite that can survive in the host’s phagocytic cells.- Clinically the disease is endemic on certain farms. The level of resistance is high in young immature pigs nurs- ing infected dams. Clinical signs of the disease usually occur after sexual maturity.--'4 New infections in a herd are often traced to a recently introduced boar. The or- ganism, Br. suis, enters the body through the conjunc- tiva, nose or mouth, the latter by ingestion of feed and water contaminated by uterine discharges, urine, or feces of infected animals or by eating aborted fetuses and membranes. An important cause of infection in the sow is mating with an infected boar. Brucellosis is a venereal disease of swine. Most infected swine develop brucel- losis with clinical signs and a bacteremia starting 1 to 7 weeks post exposure and continuing for 5 weeks and then in a few swine an intermittent bacteremia may last for 8 months to 3 years.- A diagnostic level of serum anti- body develops 10 to 21 days after exposure. Antibody levels are higher and persist longer in adult than in im- mature swine. The principal clinical signs of brucellosis in swine are abortion, birth of stillborn or weak pigs, infertility due to early embryonic deaths, and less commonly orchitis in boars and posterior paralysis and lameness due to ver- tebral lesions. Abortions may occur at any stage of ges- tation.-- Nearly all brucella-infected boars had lesions in the epididymis and vesicular glands and produced nor- mal appearing but infected semen.6 Pus in the semen was uncommon and fertilization was normal. Following ser- vice to infected boars abortions may occur as early asDISEASES AND ACCIDENTS OF GESTATION 183 22 days of gestation and are usually not observed under field conditions as no vaginal discharge is present. Sows or gilts infected at coitus frequently return to estrum in 30 to 45 days. Infections acquired by the sow after 30 or 40 days of gestation result in abortions from 46 to 105 days, average 65 to 80 days.--4 Genital infection may persist from 1 to 30 months in females. The period of infertility in sows is related to the duration of the gen- ital infection and the degree of pathology present. Many sows overcome the genital infection within one to two months and then have good conception rates thereafter. Br. suis may persist in granulomatous lesions and in mu- cosal cysts of the endometrium and catarrhal endome- tritis may occur. About 75 percent of susceptible gilts bred to an infected boar become pregnant and 80 percent of these have a normal gestation period. But when an infected sow was bred to a clean boar only a 35 percent conception occurred due to chronic endometrial lesions causing early embryonic deaths and prolonged periods between estrums.6 Nodular or granulomatous lesions containing Br. suis may also be found in lymph glands, spleen, liver, kidneys, testes, ovaries, and accessory male reproductive glands. A good herd history is very helpful in a diagnosis of swine brucellosis. The disease may be definitely diag- nosed by recovering the organism by cultural methods from organs, especially lymph glands, of the infected sow or boar, from the stomach contents of aborted fe- tuses or from the chorion of the placenta. Fluorescent antibody tests on fetal or placental tissues may aid di- agnosis. The tube or plate agglutination tests may be per- formed on blood serum from suspected or infected swine. This test is not as reliable as the blood test in cattle. Certain swine harboring and spreading the organism may have low serum titers or be negative to the agglutination test. Most swine with localized infections and those with clinical signs of brucellosis will have an agglutination titer of 1:100 or higher on the standard tube test at some stage of the disease.-'4 Nonspecific antibodies to other organisms producing titers of up to 1:50 are common in swine. The blood titer in swine drops more rapidly than in cattle. Testing the herd and eliminating the reactors is not a practical method of eradicating the disease. The agglutination test is of value, however, as a herd test for indicating the presence of infection. In the adult swine herd the presence of any reactors with a titer of 1:100 or a higher indicates that the herd is infected.3 A herd with no animals with titers over 1:50 on repeated tests and no clinical signs of brucellosis is considered nega- tive. Supplemental tests such as the acidified plate an- tigen test, the heat inactivation test, the Rose-Bengal test, the rivanol test, the complement fixation test and espe- cially the Card test may be helpful in the diagnosis of carriers of Br. suis.--- In the future the ELISA (en- zyme-linked immunosorbent assay) test may prove to be a superior test.- A single negative blood test on one in- dividual is of no diagnostic value. The prognosis is guarded in this insidious disease, since sterility may fol- low abortion and the sow may spread the disease for several months or more. In respect to the herd situation, rather drastic steps need to be taken to eradicate the dis- ease, as there are no treatments that have proven effec- tive in curing an infected animal or herd. No safe or reliable vaccines have been developed and in this coun- try the present incidence of brucellosis does not justify a possible vaccination approach to control. The methods of eradicating the disease in commercial herds consist of-3 (1) selling all the stock for slaughter, cleaning and disinfecting the premises or moving to clean quarters and then restocking from known noninfected or validated herds. This has been the most successful and economical approach. (2) In valuable purebred herds in which it is desired that breeding lines be maintained, the pigs may be raised on infected sows until eight weeks of age, weaned, and moved from the infected herd, iso- lated, and raised on clean ground. These pigs are tested individually by the agglutination test at intervals of 1 to 2 months. Any reactors are sold for slaughter. Methods of blood collection from the anterior vena cava and the tail of swine have been described.21 When the isolated gilts are of breeding age they are bred to noninfected boars. After farrowing in isolation the gilts are retested and if they are negative their litters, when weaned at 8 weeks, are the basis of a new, clean herd. The original herd is disposed of as soon as practical. (3) Repeated blood testing at 30-day intervals together with the slaughter of reactors may occasionally be advisable and success- ful. In most herds this is not as satisfactory or successful as the two previous methods. If only one or two animals in a herd are serologically positive there is a question whether brucellosis actually is present in the herd.-'3 Chemotherapy is of no value in this disease. Br. abortus strain 19 vaccine does not immunize swine. Natural re- sistance or immunity to Br. suis is present in about 30 percent of swine.-4 Animals purchased from herds of unknown brucellosis status should not be placed in a bru- cellosis-free herd. Miscellaneous bacterial causes of abortion in swine have been described in sporadic cases or occasional out- breaks. The following organisms have been recovered in pure culture from freshly-aborted porcine fetuses: Staphylococcus aureus,4 Mycobacterium avium,6 Lis- teria monocytogenes,7 Salmonella sp., E. coli, Strep- tococci,96 Coryn. pyogenes,-- Erysipelothrix rhu-184 VETERINARY OBSTETRICS siopathiae; Pseudomonas spp., Pasteurella,2 la Campylobacter fetus, mycoplasma,— Nocardia aster- oides,4 Actinomyces spp.4 5 Actinobacillus equuli,11 Haemophilus parahemolyticus, Mycobacterium tu- berculosis, chlamydia and Proteus.-- An outbreak of abortions, stillbirths and moribund neonatal pigs apparently due to streptococci and E. coli has been described.Ia The former organism was resistant to 4 antibiotics that had been used in the herd in prior years as a feed additive. The use of effective oral anti- biotics, determined by sensitivity testing, for the last 30 days of gestation greatly increased the numbers of live pigs per litter at birth, 10 vs. 6, and the number of weaned pigs per litter over the untreated controls, 8.5 vs. 3.8, respectively. E. coli endotoxin caused abortion when in- jected into pregnant sows by apparently inducing pros- taglandin release and luteolysis.12 Nine of 30 sows given a live avirulent erysipelas vaccine 30 days before far- rowing aborted and the organism was isolated from the fetuses.3 Viral Causes for Porcine Prenatal Losses The major viral causes for prenatal loss in swine are parvovirus infection, pseudorabies or Aujesky’s disease and various entero-picoma (SMEDI) viruses. Hog chol- era, formerly an important viral cause of abortion, has been eradicated from the United States. SMEDI is an acronym coined by Dunne3 referring to stillbirth-mum- mification-embryonic death and infertility associated with the above and other viral diseases of swine. Other viral agents of swine that produce signs of the SMEDI syn- drome are hog cholera virus, reovirus and influenza vi- rus.123 Of 824 porcine abortions in the midwest U.S.A. 22 percent were due to a viral agent; 10.9 percent en- terovirus, 4.9 percent parvovirus, 4.4 percent reovirus and 1 percent pseudorabies virus.- Dual infections with two viruses or a virus and bacteria are fairly common in swine abortions. Since the etiologic agents causing the SMEDI syndrome are now well-known and diagnostic tests have been developed, the term SMEDI should be discarded. It should be noted that leptospirosis and bru- cellosis may also exhibit similar signs. It is important to recognize that in swine these and other viruses may af- fect the developing embryos or fetuses and result in: (1) infertility or sterility related to early embryonic deaths that are aborted unseen or absorbed, (2) fetal mummi- fication, (3) defective or anomalous fetuses (4) stillbirths (5) birth of live but poorly viable pigs and (6) birth of live normal pigs that may be carriers of the virus. Abor- tions of entire litters late in gestation are rare. Enteroviruses or Picornaviruses,3 have been shown to cause occasional abortions but mainly the aforemen- tioned effects on intrauterine embryos or fetuses in sows. (See Figure 74.) These enteroviruses are ubiquitous in all swine. The only known natural host for porcine enter- oviruses is the pig. These viruses are quite resistant to disinfectants and very resistant to environmental influ- ences.2 Transmission is directly by the fecal-oral route and indirectly by fomites. Several serogroups of porcine enteroviruses are endemic in all commercial swine herds. Pigs of any age are susceptible but most adults have high antibody titers and rarely excrete virus.2'4 In a tenative classification of over 40 porcine picomavirus strains iso- lated in North America, Japan, England and Czechoslo- vakia, 17 groups were determined serologically. The 5 strains of enteroviruses isolated in Pennsylvania fell into Groups 1, 6, 7 and 13.5 These 5 strains of enteroviruses when inoculated into cholera-immune or cholera-suscep- tible pregnant swine cause a similar syndrome to that caused by hog cholera, pseudorabies, parvovirus, or other viruses that will be mentioned. Susceptible pregnant gilts inoculated with enteroviruses at 25 days of gestation had embryonic deaths within 5 days of the inoculation; death of fetuses and mummification occurred 15 to 40 or more days after inoculation; and thereafter stillbirths and weak pigs dying within 6 hours after birth were observed. Fe- tuses in the same sow may become infected and die at different stages of gestation. If embryos die before 30 days of gestation when no skeletal development has oc- curred, absorption results; if fetuses die at later stages of gestation, 50 to 100 days, after skeletal development oc- curs mummification or stillbirths result. The position of the fetus in the uterus was not related to the time of fetal deaths. In some sows where early embryonic deaths oc- curred the sow returned to estrum at a varying interval following the initial service. In other cases where fetal deaths occurred at 30 to 60 days of gestation and mum- mification resulted, “parturition” did not take place at the end of gestation and the sow exhibited a prolonged “gestation” period. These signs are usually limited to one breeding season in a herd. Recovered immune sows have normal gestations during the next breeding season. The virus is apparently spread through the susceptible animals in the breeding herd after its introduction by an infected animal or from contact with infected pigs. The boar may also be a temporary spreader of the virus. The virus may be isolated in suspected outbreaks from cul- tures of the internal organs of stillborn fetuses or weak, poorly viable, newborn pigs. Usually there are no le- sions in aborted fetuses. Occasional lesions may be seen in the CNS, lungs (pneumonia) or heart (pericarditis or myocarditis). In mummified pigs the viral antigen mayDISEASES AND ACCIDENTS OF GESTATION 185 be detected by immunofluorescence. Serologic tests are of no value.2 Sows infected before breeding are appar- ently immune as are sows at the next breeding period following an episode or outbreak of stillbirths, mum- mified fetuses, abortions, embryonic deaths and infer- tility. Control measures depend on prevention rather than treatment.2 Because of the many serogroups no effective vaccine is available. So gilts and fresh stock introduced into the herd should be exposed to “resident” infection by contact with the older sows, weaned piglets, or fecal material a month or more before breeding. Comingling gilts with older sows also provides nose to nose contact as well as fecal exposure and the development of a nat- ural immunity before breeding.1,2 Pseudorabies (Aujezsky’s disease) due to a herpes- virus is widespread in swine in the U.S. with most out- breaks reported in the midwest. In the early and mid 1970’s there was a marked increase in the number and severity of outbreaks in the U.S. In 1981 the incidence in swine based on serological testing by the USDA was 8.3 percent. The disease incidence has also increased in Europe and is found world-wide.-,lb'5'3 The virus ap- parently persists in a latent form-3,5'7,11 in recovered swine and may be present in most domestic animals and many wild animals. In animals other than swine, which is the host of the virus, pseudorabies is usually a fatal disease. Humans are resistant. Up to 60 percent abortions have been reported in a susceptible breeding herd.5'8,12 The average live litter size was reduced from 7.7 pigs in con- trol gilts to 1.9 pigs in the exposed gilts.8 Forty-one per- cent of porcine fetuses from sows aborting or delivering stillbirths due to pseudorabies had pinpoint to poppy- seed-sized necrotic foci in the liver and intranuclear in- clusion bodies were observed.2'14 They also have isolated the virus from the vagina of sows and the prepuce of boars. If this herpesvirus is like others in domestic an- imals it is likely the boar may transmit the virus at coitus at rare intervals.9 The herpesvirus of pseudorabies in swine, as in virus infections in other species, such as IBR in cattle, may be transmitted in semen. Many states and the federal government have passed regulations in recent years controlling the shipping of infected swine or semen, the use of vaccines and the quarantining of known-infected herds. The greatest mortality in susceptible pigs infected with pseudorabies virus from nasal or oral exposure is in suckling pigs, up to 90 percent, and next greatest is in weanling and fattening pigs.4,5 Usually fever, difficult breathing and sneezing, salivation, vomition, anorexia, ataxia, convulsions, coma and death in 1 to 2 days in the former and 6 to 8 days in the latter is observed. The mortality rate in mature swine is less than 2 percent with mild signs of sneezing, coughing, anorexia. Blindness often is associated with central nervous signs. Most older pigs recover in 10 to 12 days.5 The main site of viral replication is the upper respiratory tract from which the virus invades the blood stream and the cranial nerves.5 7 Viremia allows passage of the virus to all organs of the body. In pregnant swine the virus readily crosses the pla- centa barrier and infects the embryo or fetus. If this oc- curs at 30 days of gestation the embryos die and are re- sorbed and pregnancy is terminated. If infection occurs after 40 days of gestation and before 60 to 80 days, fetal mummification and maceration of some or all of the fe- tuses may occur. If infection occurs after 60 or 80 days of gestation death and maceration, premature expulsion or the birth at term of stillborn or weak infected fetuses may occur. Delayed parturition of 2 to 3 weeks occa- sionally occurs if all the fetuses died in the later stages of gestation. Following fetal infections and expulsion, infertility may be present at the first breeding. Diagnosis of pseudorabies can be made by culturing tissues from infected fetuses or performing the immu- nofluorescent antibody (FA) test on fetal tissues.514 Se- rologic tests on live pigs or sows include the virus neu- tralization test, the enzyme-linked immunosorbent as- say. (ELISA) test, agar gel immunodiffusion test,7b the complement fixation test and the indirect hemaggluti- nation test. A skin test based on cell-mediated immunity has been developed. Biologic tests of animal inoculation of suspect material subcutaneously into rabbits or mice or into embryonating chicken eggs can also be per- formed.5 Treatment cannot greatly alter the course of the dis- ease once signs of the disease are present. Eradication or control are topics being seriously debated currently between those concerned with the control and prevention of pseudorabies.13a Because of the nature of herpesvi- ruses and their ability to remain latent in the ganglions of the cranial (trigeminal) nerve711 and recrudesce under stress,lb the wide-spread incidence of the virus in the swine population, the failure of diagnostic tests to indicate all carrier or infected animals, and the difficulties of ac- quiring a pseudorabies virus-free herd and maintaining it with the other livestock or wild animals that can carry the virus on to the farm, the author believes a pseudora- bies virus-free commercial or conventional swine herd would be difficult to develop and maintain. The cost of this effort would probably not be economically possible for most swine breeders and the country.133 Attenuated (MLV) and inactivated vaccines are available15,6'10 and when used properly before breeding in young pigs will produce a good immunity and largely186 VETERINARY OBSTETRICS prevent losses due to pseudorabies. Vaccines will not prevent infection with virulent virus and these infected animals shed the virulent virus for a period of time and often develop a latent infection that can recrudesce under stress.3,7,11 One bivalent commercial inactivated vaccine contains both pseudorabies and parvoviruses.10 Vaccines will produce positive serologic titers.6 These titers can interfere with serologic tests used to eliminate virus from a herd. Another inactivated P.R. vaccine has been com- bined with a multivalent leptospiral vaccine. It is rec- ommended that cattle, sheep and dogs be kept away from infected or pseudorabies-free herds. Additions to herds should be blood tested and retested after a 4-week iso- lation period or purchased from pseudorabies-free herds to prevent the possible introduction of virulent virus es- pecially when sows are pregnant or have recently far- rowed. Pseudorabies vaccines have proven helpful when given to pregnant sows early in an outbreak.1,10 Porcine Parvovirus (PPV), the most common cause of embryonic and early fetal loss or mummification, was first described in 1967 in England.1,5 Since then it has been found to be an ubiquitous virus throughout the world and is enzootic in most swine herds.5 It causes repro- ductive failure in sows with signs of embryonic and fetal death with resorption or mummification without produc- ing any clinical signs of illness. In 1977 a study at an abattoir in Iowa found 62 of 203 pregnant sow uteri con- taining dead or mummified embryos or fetuses.3 Forty six or 74.2 percent of these litters were positive for por- cine parvovirus (PPV) based on isolation of the virus or demonstration of the PPV antigen. Most of the fetuses (392 or 84 percent) died and became mummified before 71 days of gestation and antibody was found in nearly all of the serums of the 68 or 14.8 percent live fetuses at 81 to 105 days of gestational age. The incidence of PPV infection in pregnant uteri in abattoir material in Minnesota and Iowa was 9.4 to 23 percent.3,9 Porcine parvovirus is not related to other parvoviruses including canine parvoviruses, feline panleukopenia virus or mink enteritis virus.5 Because of the ubiquitous nature of porcine parvovirus nearly all sows in most herds have become naturally in- fected by the oral and nasal routes and are immune as determined by seroepidemiologic data. This immunity persists for a lifetime. The parvovirus is quite stable, and remains infectious in the secretions and excretions of acutely infected pigs for months.5 It is resistant to com- mon disinfectants. Parvovirus may be spread by acutely- infected boars by several routes including the semen. Acute infection of susceptible young pigs, pregnant gilts or sows and boars is usually subclinical even though the virus is found throughout the body and can pass trans- placentally to the fetuses. Thus the only clinical signs are referrable to reproductive failure with embryonic and fetal death. Transplacental infection apparently requires 10 to 14 days from maternal exposure. Infection of the conceptus between 10 and 30 days of gestation causes embryonic death and resorption and between 30 and 70 days causes fetal death and mummification. Intrauterine spread of the virus may also occur causing deaths at different times with mummified fetuses of different sizes.4,5 Immuno- tolerance to PPV may develop in fetuses infected prior to 55 days of gestation and they may be bom alive with no antibody but carrying the virus.5 After midgestation, 70 days, fetal infection also occurs in acutely infected susceptible gilts or sows but the fetus survives without clinical disease because it develops an immunologic re- sponse to the virus.5,6 Even though a direct causal role of porcine parvovirus in semen in reproduction failure has not been completely confirmed, the susceptible female infected by semen may spread the vims to other swine.5 Conceptuses are ap- parently infected transplacentally during or after mater- nal viremia. Infected embryos or fetuses contain the vi- ms in most of their cells at death especially in the endothelium as determined by immunofluorescent mi- croscopy. Macroscopic lesions seen in fetuses before they are immunocompetent include congestion, edema, hem- orrhage, and bloody fluids in the body cavities. Micro- scopic lesions include cellular necrosis and inflammation and possibly intranuclear inclusions.5 Meningoencepha- litis with perivascular cuffing has been described in fe- tuses or stillborn pigs after they have become immuno- competent. PPV may be suspected when gilts, not sows, show evidence of early embryonic deaths, return to estrus, have abortions, fetal mummification, resorptions, infertility and failure to farrow. Stillbirths or reduced numbers of pigs and neonatal deaths occur occasionally.5 Fetal mummification or death of all embryos and their resorp- tion has caused prolonged gestation. Diagnosis is con- firmed by fluorescent antibody test of tissues, especially the lungs, of mummified fetuses less than 16 cm in length.5 Remnants of autolyzed tissues of embryos may be similarly examined by immunofluorescent micros- copy. Viral isolation from infected autolyzed tissues of fetuses is difficult. Serologic tests are recommended only when small mummified fetuses are not present indicating a recent infection. Maternal blood samples taken from sows or gilts if negative for PPV antibody would exclude this virus as a cause of reproductive failure. Because PPV virus is so ubiquitous a positive hemagglutination inhi- bition (HI) test, serum neutralization (SN) test, immu- nodiffusion test, or modified direct complement fixation (CF) test is meaningless.5 Detection of PPV antibodiesDISEASES AND ACCIDENTS OF GESTATION 187 in the serum of fetuses or stillborn pigs or neonatal pigs before nursing or body fluids of fetuses would indicate fetal infection since maternal antibody cannot cross the fetal-maternal junction.2 There is no treatment for porcine parvoviral repro- ductive failures. Preventive measures include either the natural exposure and infection or vaccination of gilts be- fore they are bred. Natural exposure and infection is ef- fected by close contact or intermingling of seronegative gilts with seropositive sows, placing the former in a con- taminated area or exposing the susceptible gilts to mum- mified conceptuses, stillbirths and placentas of recently infected aborting sows. This method of exposing gilts to PPV may inadvertently expose them to pseudorabies vi- rus and other diseases and is not as reliable as vacci- nation. In herds where PPV is enzootic usually 50 per- cent or more of the gilts are infected and immune before breeding.5 In 2 swine herds with enzootic PPV, the pro- portion of seronegative, susceptible gilts at breeding was 40 percent and only 50 percent of these became infected during their first gestation. The incidence of mummified fetuses in pigs bom previously to seropositive gilts, sero- negative gilts and gilts that seroconverted during gesta- tion was 0.6%, 1.0% and 3.0% respectively.213 By vaccination one month or more prior to breeding the swine breeder can be certain gilts are immune before conception. Both inactivated and MLV vaccines5'7,8 have been developed. Since seropositive sows produce anti- bodies to PPV in the colostrum passive antibodies in pig- lets persist for 4 to 6 months and interfere with vacci- nation immunity. Gilts should be vaccinated 15 to 60 days before breeding. The duration of immunity from the inactivated vaccine lasts 4 to 6 months and usually within this time natural exposure and active immunity will develop. Vaccination with an inactivated product is recommended for all seronegative sows and boars intro- duced into an infected herd. A few disease-free or other swine herds may be PPV-free but maintaining this status is very difficult and risky. Porcine parvovirus when in- troduced into a PPV-free herd produces very severe re- productive losses.5 Swine influenza due to the swine influenza virus (SIV) is primarily a respiratory disease common during the fall and winter in swine raising areas with a serologic inci- dence of 12 to 45 percent.7,5 Reproductive losses, in- cluding mummification and weak pigs, have been re- ported in susceptible dams infected with SIV during gestation, especially the first 30 days. Breeding sows that are more likely to have been previously exposed to SIV, in the fall for winter farrowing instead of gilts may re- duce the reproductive losses.7,5,11 Diagnosis of swine in- fluenza is based on the history and respiratory signs, and possibly the recovery of the virus from aborted fetuses or careful interpretation of serologic evidence by the hemagglutination-inhibition (HI) or serum neutralizing or complement fixation test on sows or newborn piglets before suckling. Presently there are no licensed vaccines for swine influenza nor any specific treatment.1 A recent study showed that SIV did not produce abortions, did not cross the placenta into the fetuses and was not a di- rect cause of reproductive failure in swine.lb It should be noted that influenza viruses in cattle and horses sel- dom affect the fetus or reproduction. Further studies are needed to determine the role, if any, of swine influenza in reproductive losses. Reovirus infection has been reported in 4.4 percent of 320 porcine abortions based on untyped virologic cul- tures.-8 Sows experimentally infected between 40 and 80 days of gestation produced stillbirths, mummified fe- tuses and weak pigs.7 Clinical signs of reovirus infection in swine usually includes mild respiratory or digestive signs. No lesions have been described in fetuses or neo- nates. Antibody detected by the HI test is widespread but might be used for detecting antibodies in stillbirths or neonatal piglets before suckling. Reproductive losses due to reovirus requires further investigation. Porcine cytomegalovirus (PCMV) infection is not accompanied by clinical signs in pigs over 3 weeks old but can be fatal for the fetus and newborn piglet.6 This ubiquitous organism is spread in the nasal and ocular secretions, urine and cervical secretions of infected preg- nant sows. Active immunity usually develops between 8 to 11 weeks in piglets receiving passive colostral im- munity from the dam. Early postnatal or congenital in- fection of piglets occurs in association with mummified fetuses, stillbirths, neonatal deaths, and stunted pigs. In- tranuclear inclusions are observed in the reticuloendothe- lial tissues and kidney of infected fetuses or neonates. Gross fetal lesions include petechiae, pleural and peri- cardial effusions and edema especially in the kidney. Viral cultures and serologic tests aid the diagnosis of PCMV infections. Hog cholera due to hog cholera virus (HCV), al- though eradicated from the United States, is present in many countries. Hog cholera virus strains differ mark- edly in virulence.10 Field strains of low virulence or at- tenuated or modified strains used as vaccines if inocu- lated into pregnant susceptible sows the first 10 to 20 days of gestation resulted in death and absorption of the embryos and fetal malformations.2,3 If the virus gained entrance to the sow’s body from 30 to 90 or more days of gestation, mummification of fetuses, stillbirths and weak pigs were common. The hog cholera virus in infected fetuses, stillbirths or live newborn pigs may be cultured on tissue culture media or demonstrated by the fluorescent antibody188 VETERINARY OBSTETRICS technique1,2,4'10 Pigs infected in utero may survive and after birth become tolerant carriers of HCV. Under stress these carrier pigs may become ill and die of cholera weeks or months after birth. Other viral causes for porcine fetal deaths, mum- mification and abortion include: Japanese B encepha- litis virus, Japanese hemagglutinating virus, and Af- rican swine fever virus.1,4,9 The latter virus caused outbreaks in the Dominican Republic and Haiti in 1978 and Cuba in 1979. This has been the closest African swine fever outbreaks have occurred to the United States. This virus causes porcine abortions at any stage of gestation, latent carriers and possibly immunotolerant offspring. The Dominican isolate caused 7 abortions in thirteen 38 to 92 day pregnant sows 5 to 8 days postinoculation as- sociated with the acute viremia of the sow.9 African swine fever virus was recovered from the aborted fetuses. Abortions have also been described accompanying acute cases of vesicular exanthema,- foot and mouth disease and possibly vesicular stomatitis.-’4 Mycotic or fungal porcine abortions due to Asper- gillus fumigatus, Nocardia asteroides and others have been described on rare sporadic occasions.^,la,b,c The parasitic protozoan causes of abortion in swine possibly include the agents of Toxoplasma gondii and Eperythrozoon suis and Sarcocystis spp. From sero- logical evidence toxoplasmosis is common in swine but few clinical cases have been reported.1,3 Pregnant sows may abort or farrow weak or stillborn pigs.-- - Epery- throzoonosis, although very common in herds in the United States, is suspected, but not proven to be asso- ciated with reproductive problems including delayed es- trus, embryonic death, absorption of fetuses and abor- tion.-'5 Sarcocystis suicanis was carried by host dogs and raccoons and affected 16.6 percent of sows in Geor- gia. This parasitic protozoa caused abortions and deaths in pregnant sows in Europe,13,4 when experimentally in- oculated in large doses. (See sheep.) Noninfectious Causes of Porcine Abortion Chemical, drug or plant poisonings are rather sel- dom causes for abortion in swine. Dicoumarol poisoning has been cited.5 Wood preservatives such as the pen- tachlorophenols and creosote have been reported to be toxic for prenatal and postnatal pigs.14 Wood so treated should be thoroughly dryed before placing sows or pigs in contact with it. Polychlorinated biphenyl (PCB) when fed to sows caused a reduction in live pigs farrowed and an increase in fetal mummification probably related to the immunosuppressive effects of the compound.6 Moldy corn toxicosis probably due to aflatoxin B associated with penicillin, aspergillus and rhizopus molds, caused bloody diarrhea, anorexia, depression, ataxia and abor- tion.3 Another mold, Fusarium spp, produces the my- cotoxins, zearalenone and trichothenes.7a,b,9b11 The for- mer causes an estogenic syndrome of swollen external genitalia, mammary gland development, testicular hy- poplasia, infertility, constant estrus, pseudopregnancy, small litter size due to early embryonic deaths and re- sorbtion, increased mummification and possibly in- creased stillbirths and weak pigs. The latter mycotoxin may also cause infertility and abortion. Ergot was not shown to be a cause of abortion in swine even when ergotism produced necrosis of the extremities.1 Ergot- infected feed did cause agalactia in sows and in one re- port lowered reproductive rates.3,7,9b,u Early embryonic deaths and mummification followed the consumption by sows of a tropical shrub legume, Leucaena leucocepha- la.16 Hormonal causes for porcine abortions are uncom- mon. Glucocorticoids have not been reported to cause abortion in swine but severe stress conditions have been associated with premature births and abortions. Exoge- nous glucocorticoids in large doses such as dexametha- sone and prostaglandins or their analogues have been used to induce premature or “timed” parturition by injection between 110 and 113 days of gestation.- (See Chapter XI). Administration of 500 p.g cloprostenol to gilts be- tween 30 and 100 days of gestation resulted in abortion in 34 to 42 hours requiring a duration of 4 to 14 hours. Estrus occurred 9 to 10 days after abortions with 90 per- cent conceptions in this estrus.llb Nutritional causes of swine abortion, stillbirths and anomalous fetuses include deficiencies of iodine, vita- min A, iron and calcium.5,9,10,12 Iodine deficiency is characterized by hairlessness, goiter, edema of the fetus and a slightly prolonged gestation. This condition is rare at present because iodine is commonly added to salt in most rations. Vitamin A deficiency usually related to a lack of pasture, alfalfa hay and the feeding of 2 or more- year-old com may result in weak, moribund newborn pigs or stillbirths with edema, ascites, cleft palate, an- ophthalmia, microphthalmia, hydrocephalus and cardiac defects. Iron deficiency may cause stillbirths or weak newborn pigs suffering from a severe anemia. Chronic calcium deficiency due to exclusive grain feeding, a lack of roughage or pasture or no mineral or tankage supple- mentation results a progressive increase in the number of mummified fetuses and stillbirths with each litter pro- duced. Physical causes of porcine abortion include stress and exhaustion due to transportation and excessive fight-DISEASES AND ACCIDENTS OF GESTATION 189 ing between sows.5 Abortions were associated with se- vere outbreaks of pneumonia in many swine herds.93 Genetic or chromosomal causes for stillbirths or moribund pigs include the congenital or genetic lethal defects described previously (See Chap. III). About 10 to 12 percent of the blastocysts from normal sows had chromosomal defects, mainly polyploidy, which may account for about 30 percent of the total pregnancy wast- age in swine.8 These defective zygotes that die early in gestation may comprise a significant number of the ova released and fertilized that fail to result in pigs produced at parturition. This loss may be estimated by counting the corpora lutea in the ovaries at farrowing. Miscellaneous abortions or loss of neonatal pigs may be due to poor management at the time of farrowing resulting in smothering, crushing or chilling of newborn pigs. These are often called “stillbirths.” About 5 to 10 percent of all porcine fetuses expelled at parturition are stillbirths. These may be divided into prepartum deaths usually due to infectious causes late in gestation and in- trapartum deaths associated with delayed or abnormal expulsion of fetuses.- Attendance of a caretaker at far- rowing is highly desirable. At parturition sows should be neither too fat nor too thin. Farrowing crates or guarded stalls and heat lamps or heated floors are very helpful in preventing neonatal losses. The larger the litter or the smaller the litter, above 12 or below 4, the greater the percentage of stillbirths that occurred.- The number of stillbirths increased as the duration of parturition in- creased from one to 8 hours and as the age of the sow increased. Most of the dead pigs, 80 to 85 percent, were bom late in the act of parturition. In large litters deaths might have been due to delays in birth associated with exhaustiion of the sow or uterine inertia and anoxia of the fetus due to intrauterine rupture of the umbilical cord. In small litters the larger-sized fetuses presented may have resulted in slower expulsion. Administration of oxytocin to hasten farrowing did not reduce the mortality. If par- turition is more than 6 to 7 days early or late the inci- dence of stillbirths increase. Weak pigs at birth may be due to hypoxia and may be revived by artificial respi- ration and small amounts of supplemental oxygen.-15 Sows that are anemic, with hemoglobin levels below 9 gm/ 100 ml, have a higher incidence of stillborn pigs. Iron supplementation during pregnancy is indicated in these sows. Induction of parturition with prostaglandins so at- tendants may be present to supervise births has reduced the incidence of stillbirths. After about one-half or two- thirds of the litter has been bom administration of fre- quent small doses of oxytocin or the single injection of neostigmine (5 mg/sow)-15 increases the speed of far- rowing and reduces the number of stillbirths. Sows in late pregnancy were exposed for 48 to 96 hours to various atmospheric carbon monoxide concentrations such as might occur in poorly maintained gas-fired heat- ers in farrowing houses. There was a close correlation between the rates of stillbirths (8 to 80 percent) and the concentrations of carbon monoxide (200 to 350 ppm).417 Gross lesions in the stillborn pigs were cherry-red dis- coloration of subcutaneous tissues, muscles and viscera and a serosanguinous pleural effusion. Other distinctive microscopic lesions were also described. Abortion in Swine General References 1. Blood, D. C. and Henderson, J. A. (1979) Veterinary Medicine 5th Ed., Lea and Febiger, Philadelphia. 2. Dunne, H. W. (1968) Abortion and Stillbirth in Swine, from Abortion Diseases of Livestock, edit, by L. C. Faulkner, Charles C. Thomas, Springfield, 111., 139. 3. Gillespie, J. H. and Timoney, J. F. (1981) Hagan and Bruner’s Infectious Diseases of Domestic Animals, 7th Ed., Cornell Univ. Press, Ithaca, N.Y. 4. Kirkbride, C. A. and McAdaragh, J. P. (1978) Infectious Agents Associated with Fetal and Early Neonatal Death and Abortion in Swine, JAVMA, 172, 4, 480-483. 5. Lawson, J. R. (1963) Bacterial and Mycotic Agents Associated with Abortion and Stillbirth in the Domestic Animals, from In- fertility of Livestock, Animal Health Branch monograph No. 5, F.A.O., Rome. 6. Leman, A. D. (1981) Diseases of Swine, 5th Ed., Iowa State Univ. Press, Ames, Iowa. 7. Leman, A. D., Cropper, M. and Rodeffer, H. E. (1974) Infec- tious Swine Reproductive Diseases, Theriog. 2, 6, 149-156. 8. Lucas, L. E. and Wagner, W. C. (1970) Effect of Disease and Stress on Reproductive Efficiency in Swine, Symposium Proc. Iowa State Univ., Ames, Iowa. 9. Pond, W. G., Roberts, S. J., Dunn, J. A. and Willman, J. P. (1960) Late Embryonic Mortality and Stillbirths in Three Breeds of Swine, J. An. Sci. 19, 881. 10. Saunders, C. N. (1958) Abortion and Stillbirths in Pigs, An Analysis of 67 Outbreaks, Vet. Rec. 70: 48, 965. 1_1. Wrathall, A. E. (1975) Reproductive Disorders of Pigs, Review Series 11 of the Commonwealth Bureau of Animal Health, Farm- ham Royal, Slough, United Kingdom. Infectious Causes Bacterial Causes Leptospirosis 1. Bohl, E. H. (1961) Leptospirosis in Swine—Review and Com- ments, Proc. 65th Ann. Meeting, U.S.L.S.A., 133. 2. Fennestad, K. L. and Borg-Petersen, C. (1968) Experimental Leptospirosis in Pregnant Sows, J. of Infect. Dis. 116, 57. 3a. Ferguson, L. C. and Powers, T. E. (1956) Experimental Lep- tospirosis in Pregnant Swine, Amer. J. Vet. Res. 17, 471.190 VETERINARY OBSTETRICS 3b. Hanson, L. E. (1982) Leptospirosis in Domestic Animals: The Public Health Perspective, JAVMA, 181, 12, 1505. 4. Kemenes, F. and Szemeredi, G. (1961) Effect of Leptospirosis in Sows, Acta Veterinaria (Budapest), 11, 1 (Abstr. Vet. Med. 56, 9, 398.) 5. Morse, E. V., Bauer, D. C., Langham, R. F., Lang, R. W. and Ullrey, D. E. (1958) Experimental Leptospirosis, IV Pathogen- esis of Porcine Leptospira pomona Infections, Amer. J. Vet. Res. 19, 71, 388. 6. Morter, R. L., Morse, E. V. and Langham, R. F. (1960) Ex- perimental Leptospirosis VII Reexposure of Pregnant Sows with Leptospira pomona, Amer. J. Vet. Res. 21, 80, 95. 7. Nakamura, R. M. (1964) The Fluorescent Antibody Technique. Its Use in Diagnosis of Disease of Animals, Proc. 65th Ann. Meeting, U.S.L.S.A., 427. 8. Powers, T. E., Bohl, E. H. and Ferguson, L. C. (1956) Clinical Studies on Leptospirosis as a Cause of Abortion in Swine, JAVMA, 129, 12, 568. 9. Ryley, J. W. (1956) Leptospirosis in Swine, Austral. Vet. J. 32, 1, 4. 10. Stalheim, O. H. V. (1971) Chemotherapy of Renal Leptospirosis in Hamsters and Swine, Proc. 75th Ann Mtg. U.S.A.H.A. Brucellosis 1. Becker, H. N., Belden, R. C., Breault, T., Burridge, M. J., Fran- kenberger, W. B. and Nicoletti, P. (1978) Brucellosis in Feral Swine in Florida, JAVMA, 173, 9, 1181-1182. 2. Getty, R. and Ghoshal, N. G. (1957) Applied Anatomy of the Sacrococcygeal Region of the Pig as Related to Tail-Bleeding, Vet. Med. 62, 4, 361. 3. Hoerlein, A. B., Hubbard, E. D., Lieth, T. S. and Biester, H. E. (1954) Swine Brucellosis, Vet. Med. Res. Inst., Iowa State Coll., Ames, Iowa. 4. Manthei, C. A. (1968) Brucellosis as a Cause of Abortion Today, in Abortion Diseases of Livestock, edit, by L. C. Faulkner, Charles C. Thomas Co., Springfield, 111. 5. Nicoletti, P. (1967) Utilization of the Card Test in Brucellosis Eradication, JAVMA, 151, 12, 1778. 6. Vandeplassche, M. (1969) Brucella suis Infection and Infertility in Swine, Medel. der. Veeartsenijsch. van de Rijkuniv. Gent., 11, 37, (Abstr. JAVMA 154, 9, 1050). 7. Zygment, S. M., Nettles, V. F., Shotts, E. B. Jr., Carmen, W. A. and Blackburn, B. O. (1982) Brucellosis in Wild Swine in Southeastern United States, JAVMA, 181, 11, 1285. Miscellaneous Bacterial Causes la. Cornish, J. D. and Naylor, R. D. (1982) Abortion in Sows and the Isolation of Pasteurella ureae, Vet. Rec. 110, 25, 582. lb. Davis, J. W. and Thomas, H. R. (1966) The Use of Gallimycin Injectable, Erythromycin and Furacin Water Mix in a Problem Herd of S.P.F. Sows, Vet. Med. 61, 1, 62. lc. Ellsworth, S. R., Kirkbride, C. A., Johnson, D. D. and Vorhies, M. W. (1979) Mycobacterium avium Abortion in a Sow, Vet. Path. 16, 310-317. 2. Fennestad, K. L., Pedersen, P. S. and Moeller, T. (1955) Staph- ylococcus aureus as a Cause of Reproductive Failure and So- Called Actinomycosis in Swine, Nord. Vet. Med., 7, 929. 3. Henry, S. and Kelly, B. (1979) Swine Abortion Associated with Use of Live Erysipelas Vaccine, JAVMA, 175, 453-454. 4. Koehne, G. and Giles, R. C. (1979) Nocardia asteroides Abor- tion in Swine, JAVMA, 179, 5, 478, 479. 5. Palmer, N. C., Kierstead, M. and Wilson, R. W. (1979) Abor- tion in Swine Associated with Actinomyces spp., Can. Vet. J. 20, 199. 6. Plum, N. (1937) Tuberculous Abortion in Cattle, Acta Pathol, et Microbiol. Scand., Suppl. 37, 438. 7. Ray, J. D. (1952) Abortion in Swine, N.A. Vet. 33, 626. 8. Robl, M. G., McAdaragh, J. P., Phillips, C. S., Knudtson, W. U., Pierce, R. L., Wohlgemuth, K. and Kirkbride, C. A. (1972) Porcine Abortion Studies in South Dakota, Proc. 76th Ann. Mtg. U.S.A.H.A., Miami, Fla. 9a. Sanford, S. E. and Josephson, G. K. A. (1981) Porcine Hae- mophilus Pleuropneumonia Epizootic, Can. J. Comp. Med. 45, 2. 9b. Sanford, S. E. and Tilker, A. M. E. (1982) Streptococcus suis Type II-Associated Diseases in Swine, JAVMA, 181, 7, 673. 9c. Thome, H. and Nilsson, P. O. (1961) Staphylococcus aureus as a Cause of Abortion in Swine, Acta Vet. Scand. 2, 311. 10. Wilson, R. W. and Kierstead, M. (1976) Haemophilus para- hemolyticus Associated with Abortion in Swine, Can. Vet. J. 17, 222. 11. Werdin, R. E., Hurtgen, J. P., Bates, F. Y. and Borgwardt, F. C. (1976) Porcine Abortion Caused by Actinobacillus equuli., JAVMA, 169, 704-706. 12. Wrathall, A. E., Wray, C., Bailey, J. and Wells, D. E. (1978) Experimentally Inducted Bacterial Endotoxaemia and Abortion in Pigs, Brit. Vet. J., 134, 225-230. Picornaviruses (Enterovirus) 1. Biehl, L. G. (1977) Management Practices Can Control SMEDI, Abstr. An. Nutr. and Health, 32, 5, 11. 2. Derbyshire, J. B. (1981) Porcine Enterovirus Infection, in Dis- eases of Swine 5th Ed., edit, by A. D. Leman, Iowa State Univ. Press, Ames, Iowa. 265-270. 3. Dunne, H. W., Gobble, J. L., Hokanson, J. F., Kradel, D. C. and Bubash, G. R. (1965) Porcine Reproductive Failure Associ- ated with a Newly Identified “SMEDI” Group of Picoma Viruses, Amer. J. Vet. Res., 26, 115, 1284. 4. Huang, J., Gentry, R. F. and Zarkower, A. (1980) Experimental Infection of Pregnant Sows with Porcine Enteroviruses, Amer. J. Vet. Res. 41, 4, 469-473. 5. Wang, J. T. and Dunne, H. W. (1969) Comparison of Porcine Picornaviruses Isolated in North America and Their Identification with SMEDI Viruses, Amer. J. Vet. Res. 30, 9, 1677. Pseudorabies, Aujesky’s Disease la. Bass, E. P. (1978) Immunization of Swine with a Modified Live- Vims Pseudorabies Vaccine, Proc. 82th Ann. Mtg. U.S.A.H.A., 426-431. lb. Crandell, R. A. (1982) Pseudorabies (Aujeszky’s Disease), Vet. Clin, of N. Amer., L.A. Pract. 4, 2, 321-331. 2. Csontos, L., Hejj, L. and Szabo, I. (1962) A Contribution to the Etiology of Aujesky’s Disease in the Pig. Fetal Damage and Abortions Due to the Vims, Acta. Vet. Acad. Sci. (Hungary), 12, 17. 3. Davies, E. B. and Beran, G. W. (1980) Spontaneous SheddingDISEASES AND ACCIDENTS OF GESTATION 191 of Pseudorabies Virus from a Clinically Recovered Postpartu- rient Sow, JAVMA, 176, 1345-1347. 4. Gordon, W. A. M. and Luke, D. (1955) An Outbreak of Au- jesky’s Disease in Swine with Heavy Mortality in Piglets, Ill- ness in Sows and Deaths in Utero, Vet. Rec. 67, 591. 5. Gustafson, D. P. (1981) Pseudorabies, in Diseases of Swine, 5th Ed., A. D. Leman Edit., 209-223. 6. Gutekunst, D. E. and Pirtle, E. C. (1979) Humoral and Cellular Immune Responses in Swine After Vaccination with Inactivated Pseudorabies Virus, Amer. J. Vet. Res., 40, 1343-1346. 7a. Gutekunst, D. E., Pirtle, E. C., Miller, L. I. and Stewart, W. C. (1980) Isolation of Pseudorabies Virus from Trigeminal Gan- glia of a Latently Infected Sow. Amer. J. Vet. Res. 41, 8, 1315. 7b. Johnson, M. E., Thawley, D. G., Solorzano, R. F. and Wright, J. C. (1983) Evaluation of the Microimmunodiffusion Test for the Detection of Antibody to Pseudorabies Virus, Am. J. Vet. Res. 44, 1, 28. 8. Kluge, J. P. and Mare, C. J. (1974) Swine Pseudorabies: Abor- tion, Clinical Disease and Lesions in Pregnant Gilts Infected with Pseudorabies Virus (Aujesky’s Disease), Am. J. Vet. Res. 35, 7, 911-915. 9. Larsen, R. E., Shope, R. E., Leman, A. D. and Kurtz, H. J. (1980) Semen Changes in Boars after Experimental Infection with Pseudorabies Virus, Am. J. Vet. Res., 41, 733-739. 10. Mengeling, W. L., Gutekurst, D. E., Pirtle, E. C. and Paul, P. S. (1981) Immunogenicity of Bivalent Vaccine for Reproductive Failure of Swine Induced by Pseudorabies Virus and Porcine Parvovirus, Amer. J. Vet. Res. 42, 600-603. 11. Mock, R. E., Crandell, R. A. and Mesfin, G. M. (1981) In- duced Latency in Pseudorabies Vaccinated Pigs, Can. J. Comp. Med. 45, 56-59. 12. Saunders, J. R., Gustafson, D. P., Olander, H. J. and Jones, R. K. (1963) An Unusual Outbreak of Aujesky’s Disease in Swine, Proc. 67th Ann. Meeting, U.S.L.S.A., 331. 13a. Thawley, D. G., Gustafson, D. P. and Beran, G. W. (1982) Procedures for the Elimination of Pseudorabies Virus from Herds of Swine, JAVMA, 181, 12, 1513. 13b. Trainer, D. O. and Karstad, I. (1965) Pseudorabies, A Disease of Wild and Domestic Animals, Zoonoses Res. 2, 146 (Abstr. JAVMA, 146, 10, 1058.) 14. Wohlgemuth, K., Leslie, P. F., Reed, D. E. and Smidt, D. K. (1978) Pseudorabies Virus Associated with Abortion in Swine, JAVMA, 172, 478-479. Porcine Parvovirus Abortion 1. Cartwright, S. F. and Huck, R. A. (1967) Viruses Isolated in Association with Herd Infertility, Abortions and Stillbirths in Pigs, Vet. Rec. 81, 196-197. 2a. Cropper, M., Dunne, H. W., Leman, A. D., Starkey, A. L. and Hoefling, D. C. (1967) Prevalence of Antibodies to Porcine En- teroviruses and Porcine Parvovirus in Body Fluids of Fetal Pigs from Small vs. Large Litters, JAVMA, 168, 3, 233-235. 2b. Cutler, R. S., Molitor, T. W., Leman, A. D. and Sauber, T. E. (1982) Effect of Porcine Parvovirus Serostatus on the Reproduc- tive Performance of Mated Gilts in an Infected Herd., Am. J. Vet. Res. 43, 6, 935. 3. Mengeling, W. L. (1978) Prevalence of Porcine Parvovirus-In- duced Reproductive Failure: An Abattoir Study, JAVMA, 172, 11, 1291-1294. 4. Mengeling, W. L. (1979) Prenatal Infection Following Maternal Exposure to Porcine Parvovirus on Either the Seventh or Fourteen Day of Gestation, Can. J. Comp. herd. 43, 106-109. 5. Mengeling, W. L. (1981) Porcine Parvovirus Infection, in Dis- eases of Swine, 5th Ed., edit, by A. D. Leman, Iowa State Univ. Press, Ames, Iowa, 352-365. 6. Mengeling, W. L. and Paul, P. S. (1981) Reproductive Perfor- mance of Gilts Exposed to Porcine Parvovirus at 56 or 70 days of Gestation, Amer. J. Vet. Res. 42, 12, 2074-2076. 7. Mengeling, W. L., Brown, T. T., Paul, P. S. and Gutekunst, D. E. (1979) Efficacy of an Inactivated Virus Vaccine for Prevention of Porcine Parvovirus Induced Reproductive Failure, Am. J. Vet. Res. 40, 204-207. 8. Paul, P. S. and Mengeling, W. L. (1980) Evaluation of a Mod- ified Live-Virus Vaccine for the Prevention of Porcine Parvovi- rus-Induced Reproductive Disease in Swine, Amer. J. Vet. Res. 41, 12, 2007-2011. 9. Thacker, B. J., Leman, A. D., Hurtgen, J. P., Sauber, T. E. and Joo, H. S. (1981) Survey of Porcine Parvovirus Infection in Swine Fetuses and their Dams at a Minnesota Abattoir, Am. J. Vet. Res. 42, 865-867. Other Miscellaneous Viral Agents Causing Porcine Abortion la. Aiken, J. M., Hoopes, K. H. and Stair, E. L. (1964) Rapid Di- agnosis of Hog Cholera. A Direct Fluorescent Antibody Tech- nique, Proc. Book, JAVMA, 282. lb. Brown, T. T., Mengeling, W. L. and Pirtle, E. E. (1982) Failure of Swine Influenza Virus to Cause Transplacental Infection of Porcine Fetuses, Am. J. Vet. Res. 43, 5, 817. 2. Cowart, W. O. and Morehouse, L. G. (1967) Effects of Atten- uated Hog Cholera Virus in Pregnant Swine at Various Stages of Gestation, JAVMA, 151, 12, 1788. 3. Dunne, H. W. and Clark, C. D. (1968) Embryonic Death, Fetal Mummification, Stillbirth and Neonatal Death in Pigs of Gilts Vaccinated with Attenuated Live Virus Hog Cholera Vaccine, Amer. J. Vet. Res. 29, 4, 787. 4. Dunne, H. W., Gobble, J. L., Hokanson, J. F., Kradel, D. C. and Bubash, G. K. (1965) Porcine Reproductive Failure Asso- ciated with a Newly Identified “SMEDI” Group of Picoma Vi- ruses, Amer. J. Vet. Res. 26, 115, 1284. 5. Easterday, B. C. (1981) Swine Influenza, in Diseases of Swine, 5th Ed., Edit, by A. D. Leman, Iowa State Univ. Press., Ames, Iowa, 184-194. 6. Edington, N. (1981) Porcine Cytomegalovirus (PCMV) Infec- tion, in Diseases of Swine, 5th Ed., edited by A. D. Leman, 271-277. Iowa State Univ. Press., Ames, Iowa. 7. McAdaragh, J. P. and Robl, M. G. (1976) Experimental Reo- virus Infections of Pregnant Sows, Proc. 4th Intern. Congr. Pig. Vet. Soc., Iowa State Univ., Ames, Iowa, 001. 8. McFerran, J. B. (1981) Reovirus Infection, in Diseases of Swine, 5th Ed., edit, by A. D. Leman, 330-334, Iowa State Univ. Press, Ames, Iowa. 9. Schlafer, D. H. and Mebus, C. A. (1981) African Swine Fever in Pregnant Sows, 85th Ann. Mtg., U.S.A.H.A., St. Louis, Mo., 281-288. 10. Stewart, W. C. (1981) Hog Cholera, in Diseases of Swine, 5th Ed., edit, by A. D. Leman, 224-236, Iowa State Univ. Press, Ames, Iowa. 11. Woods, G. T. and Mansfield, M. E. (1974) Transplacental Mi-192 VETERINARY OBSTETRICS gration of Swine Influenza Virus in Gilts Exposed Experimen- tally, Res. Common. Chem. Path. Pharm. 7, 629-632. Fungal Infections la. Ainsworth, G. C. and Austwick, P. K. C. (1958) Fungal Dis- eases of Animals, Commonwealth Agric. Bureau, Farmham Royal, Bucks, England. lb. Eustis, S. L., Kirkbride, C. A., Gates, C. and Haley, L. D. (1981) Porcine Abortions Associated with Fungi, Actinomycetes and Rhodococcus sp., Vet. Path. 18, 608-613. lc. Robl, M. G., McAdaragh, J. P., Phillips, C. S., Knudtson, W. U., Pierce, R. L., Wohlgemuth, K. and Kirkbride, C. A. (1972) Proc. 76th Ann. Mtg., U.S.A.H.A., Miami, 711-718. Protozoan Infections la. Erber, M., Meyer, J. and Boch, J. (1978) Aborte beim Schwein- durch Sarcosporidien. (Sarcocystis suicanis), Berl. Muench. Tierartzl Wochenschr. 91, 393. lb. Garcia, Z., Ruppanner, R., and Behymer, D. (1979) Toxo- plasma gondii Antibodies in California Swine, JAVMA, 174, 6, 610-612. 2. Koestner, A. and Cole, C. R. (1960) Neuropathology of Porcine Toxoplasmosis, Cor. Vet. 50, 4, 362. 3. Moriwaki, M., Hayashi, S., Minami, T. and Ishitani, R. (1976) Detection of Congenital Toxoplasmosis in Piglets, Jap. J. Vet. Sci. 38, 377-381. 4. Prestwood, A. K., Cahoon, R. W. and McDaniel, H. Thomas (1980) Sarcocystis Infections in Georgia Swine, Amer. J. Vet. Res. 41, 11, 1879-1881. 5. Smith, A. R. (1981) Eperythozoonosis, in Diseases of Swine, 5th Ed., edit, by A. D. Leman. Iowa State Univ. Press, Ames, Iowa, 600. Noninfectious Causes of Abortion 1. Asdell, S. A. andWillman, J. P. (1941) The Causes of Stillbirth in Swine and an Attempt to Control It, J. Agr. Res. 63, 6, 345. 2. Blevins, D. I., Glenn, M. W., Hamdy, A. H., Brodasky, F. F. and Evans, R. A. (1969) Mycotoxicosis Associated with Hem- orrhagic Enterocolitis and Abortion in Swine, JAVMA, 154, 9, 1043. 3. Burfening, P. J. (1973) Ergotism, JAVMA, 163, 11, 1288-1290. 4. Dominick, M. A. and Carson, T. L. (1983) Effects of Carbon Monoxide Exposure on Pregnant Sows and Their Fetuses, Amer. J. Vet. Res. 44, 1, 35. 5. Dunne, H. W. and Hokanson, J. F. (1963) A Modem Approach to Abortion and Stillbirth Problems in Swine, Proc. AVMA Nat. Meeting, N.Y.C., 54. 6. Hansen, L. G., Byerly, C. S., Metcalf, R. L. and Bevill, B. F. (1975) Effect of a Polychlorinated Biphenyl Mixture on Swine Reproduction and Tissue Residues, Amer. J. Vet. Res. 36, 1, 23-26. 7a. Knight, A. P. (1981) Mycotoxicosis of Food Animals, Comp, on Cont. Educ. 3, 3, 5112-5118. 7b. Long, G. G., Diekman, M., Tuite, J. F., Shannon, G. M. and Vesonder, R. F. (1982) Effect of Fusarium roseum Com Cul- ture Containing Zearalenone on Early Pregnancy in Swine, Am. J. Vet. Res. 43, 1599. 8. McFeely, R. A. (1967) Chromosome Abnormalities in Early Embryos of the Pig, J. Reprod. and Fert. 13, 379. 9a. Moore, R. W., Redmond, H. E. and Livingston, C. W. (1965) Iron Deficiency Anemia as a Cause of Stillbirths in Swine, JAVMA, 147, 746. 9b. Morehouse, L. G. (1981) Mycotoxins—Their Toxicology and Principal Lesions, Proc. 85th Ann. Mtg. U.S.A.H.A., St. Louis, Mo., 232-267. 10. Palludan, B. (1961) The Teratogenic Effect of Vitamin A De- ficiency in Pigs, Austral. Vet. J. 26, 1, 4. 11a. Pier, A. C., Richard, J. L. and Cysewski, S. J. (1980) Impli- cations of Mycotoxins in Animal Disease, JAVMA, 176, 8, 719— 724. lib. Podany, J., Vanicek, J., Stejskal, J. and Jelenek, L. (1982) In- duction of Abortion with PGF2a in Gilts and Their Subsequent Fertility, Theriog. 17, 4, 393. 12. Pullar, E. M. (1950) Nutritional Abortion and Stillbirth in Vic- torian Pigs, Austral. Vet. J. 26, 1, 4. 13. Reid, J. T. (1949) Relationship of Nutrition to Fertility in An- imals, JAVMA, 114, 158 and 242. 14. Schipper, I. A. (1961) Toxicity of Wood Preservatives for Swine, Amer. J. Vet. Res. 22, 88, 401. 15. Sprecher, D. J., Leman, A. D. and Carlisle, S. (1975) Effects of Parasympathominetics on Porcine Stillbirth, Amer. J. Vet. Res. 36, 9, 1331-1333. 16. Wayman, O., Iwanga, I. and Hugh, W. I. (1970) Fetal Re- sorption in Swine Caused by Leucaena Leucocephala in the Diet, J. An. Sci. 30, 4, 583. 17. Wood, E. N. (1979) Increased Incidence of Stillbirths Associ- ated with High Levels of Atmospheric Carbon Monoxide, Vet. Rec. 104, 283-284. ABORTION IN SHEEP AND GOATS Abortions in sheep and goats, as in other larger do- mestic animals, are due to a wide variety of infectious and noninfectious agents. Because of the methods of breeding and management of sheep in flocks, many an- imals are at the same stage of pregnancy at the same time and exposure of pregnant ewes to introduced infectious diseases is favored. When an abortion outbreak does oc- cur in a flock it is usually possible to secure 2 to 5 or more fresh fetuses and their placentas for examination and laboratory diagnosis. For this reason, the percentage of confirmed or accurate diagnoses for abortions in ewes is higher than in cattle, about 40 to 60 percent. In most flocks an incidence of 1 to 5 percent abortion and still- birth is considered “average” or acceptable.- Higher rates of abortion or stillbirth should be carefully investigated. For this purpose fresh fetuses and placentas from abort- ing ewes should be collected in a clean container, chilled and promptly transported to a well-equipped diagnostic laboratory.DISEASES AND ACCIDENTS OF GESTATION 193 Infectious Causes of Ovine and Caprine Abortion Bacterial Causes Campylobacteriosis, Vibrionic abortion (vibriosis) due to Campylobacter fetus var intestinalis is the most common cause for epizootic ovine abortion in the United States.-'-—-— Campylobacter abortion is rare in goats.-- It is a cause of serious economic losses in bands of sheep in the Rocky Mountain states and elsewhere in the U.S. It is widespread, occurring in nearly all the sheep-raising areas of the world. The C. fetus intestinalis organism in sheep is similar to C. fetus venerealis in cattle in some bacteriologic and morphologic characteristics. The former organism in sheep seldom spreads to or infects cows under natural conditions. C. fetus intestinalis (C. jejuni) can cause abortions in humans so it is of public health significance.- C. fetus intestinalis is catalase positive and H2S pos- itive; while C. fetus venerealis is catalase positive and H2S negative. The former will grow in 1% glycine while the latter will not. These organisms may be confused with nonpathogenic vibrios, C. bubulus, which is cat- alase negative and C. fecalis which is catalase positive but resembles C. bubulus. There are 5 whole-cell sero- types (I—V) with two serotypes I and V (C) causing most outbreaks.--’3 In recent months an intestinal strain of Campylobacter called Campylobacter jejuni has been recovered from feces from a number of species including ducks, goats, sheep, cattle, dogs and humans. In these species it may cause an acute diarrhea and in sheep and goats it causes abortions in late pregnancy. C. jejuni and C. fetus intestinalis are possibly identical, based on se- rological and cultural characteristics.lb'4b llb In affected flocks the incidence of abortion due to vi- briosis varies from 5 to 70 percent, with an average of 20 to 25 percent with deaths in about 5 percent of the affected ewes.-’2 These authors reported that the disease was observed uncommonly in flocks kept on range the year around, but that it was more commonly seen in sheep kept in feed lots for a part of the winter especially if sanitation was poor. Ewes will frequently smell of and lick aborted conceptuses of other ewes. The disease has been transmitted orally by feeding infective material from aborting ewes as well as by intravenous injection of cul- tures of C. fetus intestinalis. Following oral exposure of susceptible ewes, a period of bacteremia of 7 to 14 days follows as in brucellosis.-11 Under natural condi- tions infection is probably introduced into clean flocks by carrier sheep that may carry the organisms in their intestines or gall bladder, whether they aborted or not, and shed them in their feces for weeks or months. Car- rion birds such as magpies and crows may also carry the organisms in their gut from one flock to another.13,16'17 C. fetus is rather easily destroyed by sunlight, heat or drying, but may remain viable for some time at low tem- peratures in moist surroundings. This may partly account Table 12. Summary of the Causes of Ovine and Caprine Abortion Infectious causes Bacterial causes—Campylobacter fetus var. intestinalis and jejuni; Listeria monocytogenes; Brucella melitensis, abor- tus, and ovis; Salmonella abortus ovis, dublin, typhimurium and others; Leptospira pomona and others; Coryne- bacterium pyogenes, pseudotuberculosis and others; and Pasteurella tularensis, pseudotuberculosis and others. Miscellaneous bacterial causes—E. coli and other coliforms, streptococci, staphylococci, Clostridium feseri, Bacteroides fragilis and Mycobacterium paratuberculosis. Viral and rickettsial causes—Enzootic abortion (EAE) due to Chalmydia psittaci Miscellaneous viral and rickettsial causes—Tick-borne fever, Wesselbron virus, Rift Valley fever, Nairobi sheep disease, rinderpest, foot and mouth disease, bluetongue, Coxiella (Rickettsia) burnetii, Akabane virus and Border Disease and/ or BVD-MD virus. Mycoplasmal causes—M. agalactiae, M. mycoides var capri and ureaplasma. Mycotic causes—Aspergillus fumigatus. Protozoan causes—Toxoplasma gondii and Sarcocystis spp. Noninfectious Causes Drugs, chemical and plant poisonings—phenothiazine, tetramisole, carbon tetrachloride, lead, nitrate, locoweeds, lupines, Veratrum, and onion grass. Hormonal—estrogens, progesterone deficiency, cortisol and ACTH excess, prostaglandins, and stress. Nutritional—Deficiency of TDN, copper, cobalt, iodine, selenium, vitamin A and manganese, debility and parasitisms. Miscellaneous—chromosomal or genetic lethals, severe physical stress, possibly twinning or greater multiples.194 VETERINARY OBSTETRICS for the higher incidence during the winter months. Vibriosis in sheep in contrast to vibriosis in cattle is not a venereal disease. The ram is not a factor in the transmission of the disease except as he may be an in- testinal carrier of the infection.4,7 Infertility due to em- bryonic deaths is not present in ewes mated to experi- mentally infected rams. The disease is transmitted from infected or aborting sheep to susceptible pregnant ewes the third through the fifth month of gestation. Pregnant ewes infected prior to the third month of gestation do not abort.2 There is an incubation period of 7 to 25 days. During the bacteremic period the vibrio enter the ma- ternal placenta where inflammatory changes occur with extension of the infection to the fetal placenta and cho- rion. The organisms are then carried to the fetus by the placental circulation causing fetal bacteremia.8 Abor- tions may continue in a flock for 6 to 12 weeks. In Cam- pylobacter abortion there are often no premonitory symptoms. Occasionally the vulva will swell and a slight reddish discharge may be present. The fetuses are usu- ally expelled the last trimester or 4 to 6 weeks of preg- nancy. Abortions occur 1 to 3 days after the death of the fetus. In some cases lambs may be expelled prematurely as stillbirths or at term but die soon after birth. At the time of abortion the fetuses are fairly fresh and only sel- dom are they decomposed or mummified. The aborted fetuses usually have subcutaneous edema and reddish serum in the body cavities due to autolytic changes. The fetal membranes, especially the cotyledons, show in- flammatory changes characterized by edema and necro- sis. About 5 percent of aborting ewes may die due to secondary uterine infections, macerating fetuses and peritonitis.-2 About 20 to 60 percent of the fetuses have characteristic necrotic areas or infarcts 1/2 to 3 cm. in diameter in the liver. These contain large numbers of organisms. The cotyledons may be necrotic and organ- isms may be recovered from these placental structures. C. fetus may be identified by stained smears or cultures from the fetal stomach, lungs, cotyledons or uterine ex- udate.8 The latter is usually necessary for a positive iden- tification. The agglutination test on the blood has been of very limited value in the diagnosis of the disease. Flu- orescent antibody technique may be of value in the rapid diagnosis of the disease.1,2 Most workers agree that sheep that abort one year are usually immune the second and possibly the third year and carry their lambs normally, but immunity is prob- ably not permanent.9,10 In some flocks the disease may appear two years in a row but usually the incidence is much lower the second year. Aborting ewes should im- mediately be removed from the rest of the flock and iso- lated for 2 to 4 weeks until genital discharges cease. The fetus and membranes should be buried or destroyed. Dis- infection with a cresylic compound of the infected pen or area after an abortion is desirable.1 Other precautionary sanitary measures to prevent the contamination of feed and water by infective material is indicated. Injection of 300,000 units of penicillin and 1 gm. of dihydrostreptomycin intramuscularly for 2 daily doses or the daily feeding of 80 mg of chloretetracycline in grain until lambing if done in the early stages of an outbreak of vibriosis will reduce the incidence of abor- tion about 10 percent.6,12 Feeding of antibiotics was not highly effective unless started prior to an outbreak.10 Al- though additional injections of antibiotics might be in- dicated, it is probably not practical. C. fetus intestinalis serotypes I and V (C) are the most common causes of ovine vibriosis. Cross immunity between these two serotypes does not occur.10 Two in- jections 15 to 30 days apart of a commercial bivalent, alum-adjuvanted, killed bacterin before breeding or dur- ing the first half of pregnancy provided an excellent im- munity if done at yearly intervals.14 Susceptible replace- ment ewes should also be vaccinated when entering the flock.15 Recent work has shown that an oil adjuvanted bacterin produced an immunity that lasted for 3 years.10 Vaccination has been recommended in outbreaks of ovine vibriosis. Since 10 to 14 days are required for immunity to develop, early and prompt diagnosis and administra- tion of the vaccine is indicated for even fair results to be obtained.5 The combination of bacterin and antibiotic injections may be used. This disease is rare in does.— Listeriosis caused by Listeria monocytogenes is a worldwide disease affecting a variety of species includ- ing man with the septicemic, the encephalitic or the re- productive or abortifacient forms of the disease.-12 It is uncommon to see more than one of these forms in a group of animals at one time. The septicemic form occurs most commonly in newborn or very young ruminants even though the dam may appear normal. The encephalitic form is most common in sheep and cattle. The reproductive form occurs naturally as an epizootic outbreak in occa- sional flocks of pregnant ewes and does. Listeria is a cause of habitual abortion in women. Humans can con- tract this disease from animals; thus it is of public health significance. Listeriosis in sheep due to Listeria monocytogenes is a much less common cause of abortion than C. fetus. In flocks experiencing listerial abortion outbreaks, sheep were recently purchased from flocks where listeriosis had previously been demonstrated.12 Apparently the disease can be carried latently by clinically normal sheep and excreted during periods of stress. The disease may spread from cattle to sheep on the same farm. Nearly all casesDISEASES AND ACCIDENTS OF GESTATION 195 of ovine and caprine abortions due to listeria will follow by 1 to 3 weeks some radical change in management that caused a lowering of the animal’s resistance such as withholding food and water, feeding poor silage in which Listeria organisms might have multiplied,2'3'10 or heavy feeding to condition ewes for show. The incidence of abortions due to listeriosis varied from 1 to 25 percent which is lower than in vibrionic abortion. Abortions usu- ally occur late in gestation and may take place over a period of several months. A few fetuses may be aborted at an earlier stage of gestation. Sheep showing the en- cephalitic form of listeriosis may rarely also be observed in the flock. The mode of spread is not known but ex- perimental abortions were produced by oral administra- tion of the organisms.2 3’10 Intravenous injections of L. monocytogenes regularly produced abortions in 7 to 12 days.9 The fetuses had usually been dead for several days before expulsion. Thus autolysis and decomposition of the fetus and membranes were often present. Retained placentas were common and associated with metritis.-'5 Placental lesions and fetal lesions were not distinctive.6 However, listeric abortions resulted mainly from a pla- centitis.5 Postmortem examination of the fetuses revealed evenly distributed small foci of necrosis in the liver and edema and congestion of the meninges. Some lambs near term may be born alive but die within several days with ker- atitis and liver necrosis. Listeria may be recovered by culture from the placenta, brain, abomasum, meconium and other fetal organs.- The genital tract of infected ewes sheds organisms in the uterine discharge for several days after the abortion. Isolation of the organism may be dif- ficult and require repeated cultures of large amounts of refrigerated material (See listerial abortion in cattle). The uterus is usually free of organisms 2 to 3 weeks after abortion. It is assumed that after one abortion the ewe is immune inasmuch as second abortions or consecutive yearly flock outbreaks due to L. monocytogenes have not been reported. The fluorescent antibody technique is a helpful aid in diagnosis. Serological tests have been tried with only limited success.—'7 Treatment would logically call for division of the flock into small units, isolation of aborting or convalescent ewes, and proper sanitation and disinfection of premises. Silage feeding should be discontinued. Environmental stresses should be eliminated. Purchase of ewes should be confined to flocks free of listeriosis. Preliminary stud- ies on various types of vaccines have been performed8 but none have been developed commercially. The value of antibiotics in an epizootic outbreak has not been de- termined but could be of value.— Brucellosis due to Brucella melitensis, Brucella abortus or Brucella ovis is presently rare in the United States as a cause for abortion in sheep and goats. There are no published reports of Br. ovis abortions in goats.11 In certain areas in and around the Mediterranean region of Europe and Africa, in Russia and possibly Central and South America brucellosis due to Br. melitensis is an enzootic and a common cause for abortion, especially in goats.---'9 Ovine abortion due to Brucella melitensis has not been reported in recent years in the United States. An outbreak of ovine abortion due to Br. abortus in Minnesota apparently contracted from infected cattle was reported. Infections and abortions persisted in this flock for more than 40 months.10'11 This was apparently a rare occurrence as sheep are quite resistant to Br. abortus.—— The third form of brucellosis, due to Brucella ovis (ram epididymitis organism) (REO) has been reported in Aus- tralia and New Zealand, Central Europe, S. Africa and the United States where its principal pathologic effect has been in rams causing infertility. In California the incidence of infected rams was 20 to 25 percent.— Abor- tion in ewes due to Br. ovis is of little importance and is seldom reported except in New Zealand where an in- cidence of 7 to 10 percent was noted in some flocks.514 In brucellosis in goats due to Br. melitensis the in- cidence of abortion may reach 40 to 60 percent. Abor- tions occur the last third of gestation and weak moribund kids or lambs may be bom at term or prematurely. Like brucellosis in cattle the disease is contracted by pregnant sheep or goats by ingestion of food and water contam- inated with organisms from aborted fetuses and their membranes or genital discharges. After intravenous in- oculation of Br. melitensis abortions may occur 10 to 21 days later. A placentitis involving the placentomes with necrosis of the chorioallantois occurs in advanced cases. The fetus is also infected with inflammatory and necrotic foci in the liver and other organs.215 Diagnosis of the disease is based on cultures of aborted fetuses or stillbirths and serologic tests, the most useful of which is the agglutination test. Following abortions or infection some ewes or does may carry the infection for months, years or a lifetime in various organs, especially the udder and uterus.—'12 Control of the infection is patterned after the control of brucellosis in cattle and swine. Sanitation, blood test- ing by the tube agglutination, CF and card tests,-'— iso- lation or quarentine and slaughter are necessary. Agglu- tination titers of 1:25 are positive. Milk tests such as the whey agglutination test have not proven as satisfactory for the diagnosis of brucellosis in goats as in cattle. As in swine serologic tests may be unreliable in individual goats but on a herd basis even one positive sample in- dicates a herd infection.-— Vaccines have been tried in196 VETERINARY OBSTETRICS the control of Br. melitensis. Br. abortus strain 19 vac- cine is of questionable value. Two other vaccines have been more effective; one is an oil and water adjuvanted killed vaccine of Br. melitensis that produces a severe local reaction and persistent titers and the other is an avirulent living Br. melitensis vaccine (Rev 1) recom- mended for use in sheep and goats at 3 to 8 months of age.--'6-7 Vaccination is not practiced in the United States since the incidence of Br. abortus and melitensis is ex- tremely low. In brucellosis due to Br. abortus in sheep and goats the signs, lesions and diagnosis are similar to those with Br. melitensis. The disease may rarely spread from in- fected cattle to pregnant sheep or goats and cause abor- tions the last third of gestation. The occurrence of this form is rare. It should be controlled promptly in a man- ner similar to brucellosis in cattle, except for vaccina- tion. Isolation, quarentine and slaughter procedures are recommended. Brucellosis due to Br. ovis in ewes is lower in patho- genicity than Br. melitensis or Br. abortus. Ewes abort only if infected during pregnancy especially the first or second month of pregnancy since it requires 1-1/3 to 3 months or more to produce severe enough lesions of edema and coalescing areas of necrosis in the placen- tome and intercoteledonary placenta to interfere with fe- tal nutrition and result in the death of the fetus and abor- tion or the birth of weak diseased lambs.913,16 Apparently ewes are difficult to infect with Br. ovis unless they are pregnant. Breeding ewes with infected rams seldom causes the disease in ewes. Ewe to ewe passage of infection is rare. Ram to ram infection occurs most commonly by a susceptible ram breeding a ewe recently bred by an in- fected ram and contaminating his prepuce with the Br. ovis organism. Oral infection from pasture, feed, or water contaminated with material from aborted fetuses, mem- branes or genital discharges can occur but is of little im- portance. The disease can be produced in pregnant ewes by the inoculation of the conjunctival, nasal or rectal mucous membranes or by parenteral injection.8 9 Since intravaginal deposition of infected semen, as in cattle, seldom produces the disease it has been suggested that intrarectal ejaculation of infected semen or sodomy may be a means of spread of this form of ovine brucellosis from ram to ewe or ram to ram.8 The incidence of abortion due to Br. ovis is low.2,4,8,9,13'14 New Zealand workers5 indicated a high in- cidence of 7 to 10 percent in 40 naturally-infected flocks. Abortions usually occur the last trimester of pregnancy. Chronic placental lesions of necrotic plaque-like thick- ening and edema of the intercotyledonary areas of the placenta is characteristic of Br. ovis infection.9,16 Smears of these areas stained with Stamp’s modification of Ziehl- Neilsen stain often reveal the organism.14 The organism may be cultured from the fetus, the membranes and the uterine discharges for a week after abortion or premature lambing. The complement fixation (CF) test is a highly satisfactory serological test for determining the presence of Br. ovis in a flock or individual.10 The fluorescent antibody technique may also be used to detect Br. ovis in contaminated material in the placenta or semen. In- fection in ewes persists from one breeding season to the next in only a few ewes.8 However, rams may be chron- ically infected for 3 or more years. There is no evidence that lambs bom from infected ewes retain infection. There is little evidence Br. ovis causes infertility in ewes. In- fertility in rams is the major cause for losses from this disease. Since the effects of Br. ovis infection in the ewe are limited and the infection is transient, most control efforts are aimed at the rams. Palpation of the testes for the presence of lesions, especially in the region of the cauda epididymis will clinically diagnose most individ- ual infected rams. The use of the CF test on all rams will detect clinically and nonclinically infected males. Repeated clinical and serological testing and the elimi- nation of infected rams will rapidly reduce the infection rate and eliminate the infection in a flock. Replacement rams should be raised or purchased from disease-free flocks and tested prior to and after a 2 to 3 months iso- lation period. An effective vaccination procedure for young rams combining the simultaneous use of Brucella abortus Strain 19 and a formalin-killed oil adjuvant Br. ovis vaccine has been used widely in Australia and New Zealand.1 A vaccination procedure consisting of inject- ing an alum-precipitated Br. ovis bacterin subcutane- ously in 2 doses 30 to 60 days apart and followed by a single injection each year has been used in California.3 Because of the nature of the disease it is probably un- necessary to vaccinate ewes.9 Antibiotic therapy, espe- cially in chronic cases, is of doubtful value.- Salmonella (paratyphoid) abortion in sheep is prin- cipally caused by Salmonella abortus ovis, S. typhi- murium and S. dublin and others.-— 14,6 Salmonella spp. infections have caused outbreaks of abortions in goat herds.— These are uncommon and detailed clinical re- ports are not available. This type of infection has been described in England and Europe, especially Germany, but not in the U.S. The incidence of abortion varied from 8 to 60 percent.—’6 The infection is contracted orally by contamination of feed and water with aborted material or organisms from other common animal sources. An outside carrier animal added to the flock may introduce the disease. Stress situations often precede an out- break.-’2 In a few cases diarrhea or other evidence ofDISEASES AND ACCIDENTS OF GESTATION 197 infection of the ewe such as high fever and depression has been noted but in most cases no signs other than abortions in the last third of gestation or stillbirths at term are observed. Occasionally deaths may occur in newborn lambs and 5 to 7 percent of affected ewes.-5 The organisms are readily isolated from the internal organs of the fetus, the placenta, and the uterine dis- charges for a few days after abortion. An agglutination test can demonstrate antibodies in the blood serum of infected ewes or rams. Aborting ewes should be isolated and aborted fetuses and placentas should be destroyed. Contamination of feed and water must be prevented. Ro- dent control is essential. Although autogenous bacterins have been used very early in an outbreak, or as a preven- tative in reducing the incidence of abortion, their use has not been scientifically evaluated. Individual ewes may benefit from antibiotics, 10 mg/kg tetracycline daily, and supportive fluid therapy.--—2 Leptospirosis due to L. pomona and L. icterohem- orrhagiae and others is seen much less frequently in sheep and goats than in cattle and swine as they appear more resistant to infection. The disease is more common in young lambs than in older ewes.-- — —'4 Leptospirosis as a clinical disease of goats has been reported infrequently. Outbreaks of leptospirosis in older pregnant ewes that caused abortion in up to 20 percent of the flock have been described.2 Other symptoms in- cluded icterus, hemoglobinuria and death of the ewes. An outbreak of abortion in goats due to L. grippoty- phosa was reported in Israel.1 Based on experimental infections, sheep may have a leptospiruria for 40 to 100 days.5 No fetal infections were observed before 21 days after intraarterial inoculation of L. pomona. Leptospira may be cultured from fresh fetal or placental material, and seen by histologic or fluorescent antibody (FA) tech- niques.8 In autolyzed fetal or placental tissues cultural methods may be unsuccessful. As in cattle and swine, serologic tests are of limited value in the diagnosis of the disease. Treatment of the disease with an inactivated vaccine, usually multivalent, and antibiotics should be conducted along lines similar to those employed in cat- tle.-^'3 Miscellaneous Bacteria Causing Ovine and Caprine Abortion Pasteurella tularensis and P. pseudotuberculosis are sporadic causes of abortion in ewes the latter part of the gestation period.- — —'4 The latter organism was reported13 to produce white necrotic foci in the liver of fetuses. Tularemia due to P. tularensis is common in western United States where it causes enzootic outbreaks of dis- ease in wild rodents and can be transmitted to sheep by the common wood tick, Dermacentor andersoni and other ticks. Man is also susceptible to infection. The dis- ease has been described in Europe and Japan. Affected sheep show depression, anorexia, elevated temperature, increased pulse and respiratory rates, coughing, pre- mature births, stillbirths and abortions. One attach con- fers a long-lasting immunity with a persisting antibody titer. The agglutination test on the serum is useful for diagnostic purposes but may cross react with Brucella organisms. Injections of streptomycin or oxytetracycline produced a prompt clinical response and reduced losses. Controlling tick infestation of sheep by dipping or by keeping sheep from infected ranges is indicated.4 Cornynebacterium pyogenes, C. pseudotubercu- losis and even C. renale and C. equi have been re- covered from aborted ovine fetuses. C. pyogenes is the most common strain.1'3 This organism may also cause deaths in newborn lambs. Other miscellaneous bacteria causing abortion in ewes include: E. coli and other coliform organisms, strepto- cocci and staphylococci.- — Blackleg of the fetus due to Clostridium feseri infection following shearing wounds resulted in death of the fetus and distension of its tissues and the uterus and abortion.--2 Bacteroides fragilis was described as a cause of abortion in ewes,—'5 as was an organism resembling Bacillus cereus.6 Johne’s disease or Mycobacterium paratuberculosis in goats is a chronic condition resulting in debility, failure of conception, abortions and births of weak kids. There is no effective treatment.— Viral and Rickettsial Causes of Abortion in Ewes and Does Enzootic abortion of ewes (EAE) chlamydiosis or ovine virus abortion is caused by a viral agent of the psittacosis-lymphogranuloma (PL) group (Chlamydia psittaci). There is good evidence that the agent causing epizootic bovine abortion, EBA, and EAE are the same.-'--'—'2'6’12 Enzootic abortion of ewes and goats has been described in Scotland and England, Europe and in Western United States. In these latter states EAE or chla- mydiosis is a common occurrence in sheep and goat flocks.-’-’—'16 Chlamydial viruses have also been de- scribed as causing pneumonia and polyarthritis in sheep and goats.--—’10’13 Latent persistent chlamydial infec- tions of the ovine and caprine intestinal tract are com- mon.-'1011 Further study is necessary to determine the relationship of these chlamydial agents to each other and198 VETERINARY OBSTETRICS to abortion in ewes and goats. Evidence indicated that all these agents caused abortion in experimental ewes. Ewes with latent intestinal Chlamydia spp infection showed no increased resistance to superinfection and often aborted when challenged.11 The causative agent is an ob- ligate intracellular parasite that forms elementary bod- ies.- Chlamydiosis is characterized by abortions from 100 days of gestation to term but most commonly the last month of pregnancy. Occasionally macerated or mum- mified fetuses are observed. The birth of dead fetuses or weak, moribund lambs and kids is not uncommon. One fetus of twin lambs may be affected. The incidence of abortions in a flock where the disease is enzootic, is usu- ally 1 to 5 percent but in susceptible flocks the incidence may reach 30 percent. Most abortions occur in two- and three-year-old ewes in the chronically-infected flocks. Retained placenta may occur and be associated with a brownish genital discharge. Occasionally ewes and does may die from metritis and other complications after abortion. Most ewes bred satisfactorily following abor- tion as an immunity was developed.- — —12 The disease may be difficult to differentiate from campylobacteriosis (vibriosis). In fact, occasionally both infections may oc- cur concurrently in a flock.3 This chlamydial agent caus- ing abortion in sheep and cattle also causes abortion in goats.--1'9 Enzootic abortion of ewes (EAE) or chlamydiosis due to Chlamydia psittaci can be produced by oral feeding of the agent to susceptible ewes and does. The incuba- tion period is about 50 to 90 days.- Infection is probably most commonly due to ingestion of feed or water con- taminated with infective material from aborting ewes and does. Although rams may become infected as deter- mined by the CF test on serum there is no indication they are implicated in the spread of this disease. Ewe lambs or does bom in infected flocks may later show evidence of disease during pregnancy. Susceptible ewes or does contracting the infection at one lambing period may abort during their next pregnancy. The disease is not tick-bom. The fetal membranes are grossly similar to the fetal membranes present in bovine abortions due to Br. abor- tus. The chorionic membranes and cotyledons are thick- ened, edematous, necrotic and leathery and often re- tained. The aborted fetuses usually show signs of autolytic changes that are not distinctive. Staining of placental smears and examination with the microscope usually demonstrate the elementary coccoid viral bodies in the epithelial cells. The fluorescent antibody test is reliable but staining is just as reliable and easier.-’-’— The vims from the fetal membranes may be cultured in chick em- bryos and mice. Vims is seldom found in the fetus. Va- ginal swabs taken soon after abortion are the best sam- ples for the isolation of chlamydia.- Most ewes and does show a complement fixation titer in the semm from two weeks to 4 months after abortion. The CF test is not highly accurate because some infected individual ewes and goats may show no titers. Other nonaborting ewes may carry a titer due to natural infection or due to the latent agent commonly found in the digestive tract.-'-’— — —’2 Workers in Scotland and the U.S. produced a for- malized killed adjuvanted vaccine that proved effective as an immunizing agent for EAE. The immunity lasted for 2 to 3 years after a single injection. This vaccine given prior to the first breeding and to susceptible ad- ditions to the flock has also proven of value in Idaho and California and federal licensing is expected.-'14 Experi- mentally chlortetracycline fed at a rate of 100 to 250 mg per head per day- — to exposed or inoculated ewes or does may prevent abortions. Injection of tylosin and tet- racyclines might also prove helpful. However treatment is not completely effective. Once the infection was es- tablished in the placenta abortions could still occur. Miscellaneous viral and rickettsial diseases of sheep causing abortion are as follows: Tickborne fever is due to Rickettsia phagocytophi- lia. It has been reported in the United Kingdom and Scandinavia in goats, sheep and cattle and is transmitted by ticks, Ixodes ricinus.-’-’—13 After inoculation of in- fected blood, fever developed in 4 to 8 days and lasted for 10 days. During this period abortions occurred. When susceptible pregnant animals are moved from tick-free to tick-infested pastures late in gestation abortions may occur in up to 50 percent of the ewes and does and deaths in aborting animals may occasionally reach 20 percent. The causative agent may be found by microscopic ex- amination of the blood in aborting ewes. The inclusion bodies of this organism are seen in the cytoplasm of neu- trophiles and large monocytes. A complement fixation test has proven to be an accurate diagnostic serologic procedure.- Ewes and does reared on tick-infected pas- tures are apparently immune.8 Wesselsbron virus is a cause of abortion in sheep and death in newborn lambs in South Africa.— —11 A few affected ewes may die. The virus is transmitted by mos- quitoes. Antibodies to the virus are present in the serum of sheep after recovery. The virus apparently affects and kills the fetus in utero and may be cultured from the aborted fetus. Presently a modified live virus (MLV) vaccine is given annually to all ewes before breeding.- Rift Valley Fever virus or enzootic hepatitis, was a major cause of abortion in Kenya and South Africa in sheep, goats and cattle- - until a vaccine was developed and used extensively. Signs of abortion and deaths inDISEASES AND ACCIDENTS OF GESTATION 199 newborn lambs resembled disease due to Wesselsbron virus. Occasional deaths occurred in older ewes and goats. This disease is also transmitted by insects. As with Wes- selsbron virus the disease may affect man causing an in- fluenza-like syndrome. Viral isolation and serologic tests can confirm a clinical diagnosis of the disease.1,8 Nairobi sheep disease virus in Africa- - or rinder- pest and foot and mouth disease2,11 although not present in the United States cause abortions in sheep in countries where these diseases are prevalent. Bluetongue virus vaccine, a live viral preparation, if used on pregnant ewes, or a natural infection occurs in ewes and goats between the fourth and eighth week of gestation cause up to 20 percent fetal losses character- ized by stillbirths, mummified fetuses or spastic neo- nates with a variety of developmental central nervous system defects.--3,7 Goats, like cattle, are occasionally affected by bluetongue virus but are more naturally re- sistant than sheep.- Bluetongue has been reported in most southern and western states6 and in many other coun- tries. It is spread between animals during warm weather by insect vectors, especially the culicoides fly.-— The viremic stage may last for four months in sheep even though neutralizing antibodies are in the blood. Cattle may also harbor the virus and be a factor in the spread of the disease to sheep.4 Bluetongue (MLV or inacti- vated) vaccines are now available but since there are a number of serotypes of bluetongue virus a heterologous vaccine would be more effective than the homologous vaccine presently used.--6 Coxiella or Rickettsia burnetii or Q fever virus has been recovered from the placenta of cattle, ewes and goats in North America, Australia and Europe. In several flocks abortions occurred and antibodies were found in the blood of ewes and Coxiella organisms were recovered from the placenta.--—1,12 This rickettsial agent was not highly pathogenic for sheep and goats and seldom was a cause for abortion.—’9 Positive serologic tests and cultures are common where Q fever virus is endemic, even in ewes, goats and cattle having a normal birth and offspring. However when outbreaks of abortions occur in sheep and goats and this rickettsial agent is found culturally and serologically and no other cause for the abortions can be ascertained, veterinarians will believe this is the proba- ble cause of the abortions. Possibly when infections are severe abortions can result.1 12 Akabane virus causing fetal arthrogryposis and hy- dranenaphaly described previously in cattle (Chapter III) also affects ovine and caprine fetuses. It has been re- ported in lapan, Australia and Israel. The virus is trans- mitted by Culicoides insect vectors. It may also cause abortion, premature birth or stillbirths.- Border disease, “Hairy Shaker’’ Disease, Hypo- myelinogenesis congenita in sheep and goats is caused by a virus closely related to or identical with BVD-MD and hog cholera viruses. It has been reported in the United Kingdom, New Zealand, Australia and Europe1-- and possibly in the United States.5 Affected pregnant ewes and does may abort or produce defective newborn. Hair coat defects common in sheep are not observed in new- born kids with signs of CNS disease.11 Pregnant sheep and goats should be separated from cattle8 as cattle shed- ding virulent BVD-MD virus in large amounts may in- fect pregnant ewes and does. Two studies5,1,b reported on “Border Disease” in California and northwest United States based on serologic tests for BVD-MD virus in ewes and lambs and the recovery of the virus from the nasal and vaginal cavities of ewes and experimental reproduc- tion of the disease. However Ward in 197113 and English workers in 198010 showed that the inoculation of BVD- MD virus into pregnant ewes from 22 to 105 days and 25 to 40 days of gestation, respectively, resulted in 40 to 70 percent “empty” ewes at the time of lambing, up to 40 percent abortions, a few mummified fetuses and a number of stillbirths and neonates exhibiting growth re- tardation with hypomyelinogenesis, cerebellar hypopla- sia and hydrococephalus. Border disease virus may be recovered from infected newborn fetuses and the dams’ genital tract in the early postpartum period.16 Border dis- ease was produced in lambs following the artificial in- semination of their dams with semen from persistently infected rams. Certain infected rams and ewes producing infected lambs may not have circulating antibodies to BD vims. There were marked differences between strains of BD and BVD viruses in their antigenicity.16 Further studies are indicated on the very close relationship of BD and BVD viruses and the similar disease conditions pro- duced in sheep and cattle.56 Inoculation of the ovine progressive pneumonia vi- rus (OPPV) into the fetal amniotic sac at 45 to 85 days of gestation caused resorbtion, maceration or abortion of the fetus. Inoculation after 100 days of gestation had no clinical effect but the healthy lambs could be carriers of OPPV.la Mycoplasmal and Fungal Abortions Mycoplasma agalactiae causing mastitis (contagious agalactia), arthritis and keratoconjunctivitis in sheep and goats may occasionally be associated with vulvovaginitis and abortion,11 Mycoplasma mycoides var capri and other mycoplasma have been isolated from goats and sheep in the United States.3 Although the former mycoplas- ma causes contagious caprine pleuropneumonia, myco-200 VETERINARY OBSTETRICS plasma have been recovered from esophageal-pharyn- geal fluids from dead fetuses from does. Ureaplasma spp has been associated with infertility and abortion in sheep in Texas.2 Aspergillus fumigatus, a fungus, has been described only occasionally as a cause for abortion in ewes and goats.1 Parasitic Protozoal Infections Causing Abortions Toxoplasma gondii, a protozoa, may infect all do- mestic animals but only in sheep and goats is it a com- mon and serious cause of abortion. Toxoplasmosis oc- curs widespread throughout the world and in the United States and Canada. The infective form of Toxoplasma gondii is found as a coccidial oocyst in cat feces resem- bling that of the coccidia.I'5-5’ii-1'2-4'5-6a-b-7-8-11 Experimen- tal infections have been produced by inoculating infec- tive material.11 Control of the cat population on the farm may help prevent toxoplasmosis in sheep and goat flocks. The presence of cats on small farms make this disease more frequent in small flocks than in large range flocks.- Natural outbreaks in goat flocks are uncommon.--4 Heavy rainfall favors the spread of the disease. Stress may cause latent toxoplasmosis to become active. Occasional cases of congenital or intrauterine infections of the newborn have been described in most species of domestic ani- mals. If antibodies are present in the dam no transmis- sion of the infection to the fetus occurs.113 The impor- tance of toxoplasmosis as a cause of early fetal resorption, maceration, mummification, abortion and neonatal deaths varies in different countries. In New Zealand 50 to 60 percent of abortions and neonatal deaths were due to this disease; in Yorkshire, England about 15 percent and in the U.S. only sporadic outbreaks have been reported. The incidence of abortion in a flock may vary from 3 to 30 percent. Ewes and does infected prior to breeding do not abort. Those infected from 30 to 90 days postbreed- ing usually have fetal resorption or mummification. Most observed abortions occur the last trimester of gestation, 2 to 3 weeks before term after infection during the latter half of gestation. The incubation period from the feeding of sporulated oocysts to abortion in sheep was 28 to 34 days.1 One normal twin and one dead twin may be born at term. Ewes aborting due to toxoplosmosis often have a retained placenta. Affected ewes bred back and pro- duced normal lambs the next season. Chronically in- fected ewes do not have abortions or diseased newborn as do acutely infected pregnant ewes.1,11,13 Stillbirths, living, defective, ataxic, weak and dull lambs and nor- mal lambs, as well as aborted fetuses may carry Toxo- plasma gondii. This organism produces a characteristic placentitis with multiple small, 1 to 3 mm., soft white nodules amongst the fetal villi in the dark red caruncle or cotyledon. (See Figure 70.) The organism is readily identified either free or in cysts. The intercotyledonary placenta is often edematous. Fetuses or stillbirths show no gross lesions but organisms may be recovered from the liver, lungs, or brain. The Sabin-Feldman dye test or the indirect hemagglu- tination method on ewe’s or doe’s blood detects antibody usually present at the time of abortion and the titer con- tinues to rise for several weeks. The CF test and skin sensitivity test have also been used but the latter is of less value in the diagnosis of toxoplasmosis.— — — The indirect fluorescent antibody test on imprints of fresh cut tissues has proven valuable.1 Occasionally campylobac- teriosis (vibriosis) or other causes of abortion are found associated with toxoplasmosis. There is no satisfactory treatment for this disease. Sulfonamides and pyrimeth- amine have been tried.- It should be noted that animal to man transmission of toxoplasmosis can occur and acute infections in pregnant women should be prevented as the organism has a great affinity for the human fetus.—14 Vaccination with a nonpathogenic coccidium may prove of value to protect susceptible ewes and does against tox- oplasmosis.5 A recent review of toxoplasmosis in hu- mans has been published.15 Sarcosporidiosis (Sarcocystosis) caused by Sarco- cystis spp is similar to the life cycle of toxoplasma ex- cept most carnivores can excrete the various protozoal oocysts. Sarcosporidial cysts can be found in striated muscle in sheep and goats. S. ovicanis is a parasite in the dog’s intestinal tract which when ingested in large numbers by susceptible sheep or goats results in anemia, anorexia, ataxia and abortions during the period when the vascular endothelium is parasitized by schiz- onts.5,2,3,9,1I,12,13b Large experimental infections induced in pregnant ewes caused premature births and deaths of the ewes. Their lambs did not have congenital sarco- cystosis.131’ (See swine.) Sarcosporidiosis is distributed world-wide. The S. tenella infection in cats can be passed to sheep but apparently it is nonpathogenic.2 Globidiosis caused by the coccidia Eimeria (Globidium) gilruthi and Besnoitia may be transmitted in a manner similar to the above parasitic protozoa. There is no good evidence however, that they cause prenatal or neonatal deaths in fetuses or newborn domestic animals. Noninfectious Causes for Ovine or Caprine Abortion Drugs, Chemical or Plant Poisonings: Although the following causes of abortion in ewes and does have been reported, some of these causes are prob-DISEASES AND ACCIDENTS OF GESTATION 201 ably questionable and require further documentation and experimentation to ascertain their significance. Some abortions may be due to a combination of causes of which only one was recorded. Phenothiazine administered to ewes in late pregnancy may cause abortions within 4 days postworming.26 The author has observed dead, emphysematous, macerating fetuses causing severe dystocia, metritis and death fol- lowing this practice. This may be due to the stress of handling rather than the drug. Tetramisole and pheno- thiazine, but not thiabendazole has been reported to cause abortion in goats.— Carbon tetrachloride, a chemical seldom used cur- rently in parasite control, may cause abortion if admin- istered to pregnant ewes, and goats.—12,13 Chronic lead poisoning may cause abortion in preg- nant ewes.3 Nitrate feeding in doses in excess to that occurring in forage and causing a severe methemoglobinemia may occasionally cause abortion in ewes.10 Locoweeds (Astragalus lentiginosis, A. pubentisi- mus and Oxytropis sericea) caused abortions in all stages of gestation, and deformed and small weak newborn if fed to pregnant ewes and goats as hay or if grazed upon in pasture.-14,16,17 Lupine ingestion resulting in chronic lupinosis has been associated with abortions and fetal deaths in ewes as has consumption of broomweed (Gutierrezia microceph- ala) by goats- 20 Indigofera spicata, (creeping indigo) caused abortions in sheep.16 Veratrum californicum (False Hellebore) if con- sumed by pregnant ewes will cause early embryonic deaths, aborted fetuses and deformed lambs.16,23 Ergot fed to ewes at levels of 0.1 to 0.7 percent of the ration reduced the percent of ewes that lambed by 20 percent.7 Onion grass (Romulea bulbocodium) when ingested by pregnant ewes may cause abortion.— — Hormonal Causes for Abortion in Sheep Estrogens—The ingestion of excessive estrogens in subterranean clover by sheep in Australia often resulted in uterine inertia, dystocia, and the birth of stillborn lambs.4 Dystocia and sterility remained at a rather high level even though the sheep were removed from the clo- ver pasture because of permanent uterine damage by the estrogens. An isoflavone derivative, genistein, was the active estrogen in the clover.8 It has estrogenic activity equal to one-fifth that of estrone. In certain fresh-cut subterranean clovers, such as the dwalganup variety, concentrations of 100 mg. of genistein per 100 gms of clover was found. Small amounts of hexoestrol in the grain ration the last few weeks of pregnancy caused abortion in 11 of 14 ewes.—— Progesterone deficiency, or cortisol or ACTH ex- cess has been reported as causes of abortion in goats and sheep. Many Angora goat farms in South Africa had over 30 percent abortions each year.22 The condition did not affect other herds of goats and so it was considered to be genetic in nature. Abortions occurred from 2 weeks of gestation to term with over 60 percent occurring from 100 to 120 days of gestation. Fetuses were partially au- tolyzed when expelled. A higher incidence was present in the older does. Does conceived promptly after abort- ing. Abortions were caused by regression of the corpus luteum, necessary in the goat to maintain pregnancy. There was evidence of a lack of luteotrophic hormone from the anterior pituitary gland. Stress, such as shearing, seemed to contribute to an increased incidence of abortion. As discussed in cattle abortion the pituitary-adrenal axis largely controls the onset of parturition in sheep and goats. In habitual abortions occurring in Angora goats22 hyper- plasia of the adrenals was observed in aborting does and their fetuses.24,25 It was considered that selection for fleece quality in Angora goats raised for mohair production fa- vored animals with adrenal hyperplasia. If ovine fetuses were given ACTH, corticotropin, or cortisol abortion would occur within 3 to 7 days.18,25 If the former hormone was given the fetal adrenals would become as large as those in fetuses at term. Conversely if the fetal pituitary was destoyed or the fetal adrenals removed, prolonged gestation resulted. Injections of cor- tisol (hydrocortisone) or dexamethasone (Azium) in rel- atively small doses into ewes in late gestation caused the premature induction of parturition.2 25 Larger doses of cortisol administered to ewes during early gestation had no effect but after 85 days of gestation they proved lethal to the fetus. Prostaglandin F2a at a dose of 15 mg caused abortions in goats at 30 and 65 days of gestation and premature births at 140 or 142 days of gestation.5 When the pros- taglandin analogue, cloprostenol (Estrumate, ICI) was injected at a dose level of 0.5 or 0.50 ml per goat IM or SC between 72 and 132 days of pregnancy abortions occurred 30 to 50 hours later.9 High ambient temperatures and high humidity causing adrenal hyperactivity and hydrocortisone injections shortly after breeding caused increased embryonic deaths.15 Stress factors and their effect on the pregnant ewe especially in late pregnancy may play a definite role in inducing abortions as in toxoplasmosis, phenothiazine poisoning, and reduction in energy intake or ketosis.202 VETERINARY OBSTETRICS Nutritional Causes of Ovine Abortion Lack of TDN or energy has been widely reported in England and elsewhere as a cause of abortion. A high incidence of up to 80 percent abortions and/or maternal deaths have been associated with pregnancy toxemia or ketosis in ewes, especially those having 2 or more fe- tuses, and on a restricted energy intake and lack of ex- ercise in late pregnancy. Ewes fed only roots during pregnancy had a high abortion rate due to the reduced energy intake.-— Severe parasitisin, malnutrition and exposure or a combination of these may induce abortion prior to death of the doe.— 20 Copper deficiency was reported to be associated with stillbirths in ewes.— — A manganese deficiency has been associated with abortion in does at 80 to 100 days of gestation.- Cobalt deficiency has been reported asso- ciated with a high death rate in neonatal lambs.19 Vitamin A deficiency of long standing caused a high incidence of stillbirths or poorly viable newborn lambs and kids.——— Iodine deficiency has also resulted in congenital goi- ter and abortion or stillbirths in sheep and goats.— — — Selenium deficiency in ewes in New Zealand has been reported to cause abortion or neonatal deaths of lambs with congenital white muscle disease affecting the heart. It has been associated with farms having a large number of barren ewes and reduced lambing percentage.12'13 Ex- perimental diets high in sulfur caused fetal deaths and abortion with evidence of white muscle disease despite the administration of selenium and vitamin E to the preg- nant ewes.6 The administration of sulfur probably inter- fered with the absorption or utilization of selenium. The administration of 5 mg of sodium selenate or selenite monthly for 3 doses before breeding and again one month before lambing was recommended.13 A muscular dystro- phy in sheep with early neonatal deaths not associated with selenium deficiency has been described.21 Chromosomal, physical and miscellaneous causes Lethal genetic defects causing fetal deaths, abortions and stillbirths have been described previously. (See Chapter III.) Severe physical stress, fright and exhaus- tion, such as caused by dogs chasing a flock of ewes in advanced pregnancy, has occasionally been reported as a cause of abortions or premature births. Young ewes have a higher incidence of stillbirths than older ewes.—— Ewes carrying twins or greater multiples especially if on a low protein ration were more apt to abort or have still- births than those carrying single fetuses. References on Ovine Abortion General References L Blood, D. C. and Henderson, J. A. (1979) Veterinary Medicine, 5th Ed., Lea and Febiger, Philadelphia, Pa. 2. Dennis, S. M. (1968) Comparative Aspects of Infectious Abor- tion Diseases Common to Animals and Man, Intemat. J. of Fert. 13, 3, 191. 3. Dillman, R. C. (1968) Sequential Sterile Autolysis in the Ovine Fetus, Proc. 72nd Ann. Meeting, U.S.L.S.A., 478. 4. Faulkner, L. C. (1968) Abortion Diseases of Livestock, Charles C. Thomas Company, Springfield, 111. 5. Gall, C. (1981) Goat Production, Academic Press, N.Y.C., London. 6. Gillespie, J. H. and Timoney, J. F. (1981) Hagan and Bruner’s Infectious Diseases of Domestic Animals, 7th Ed., Cornell Univ. Press, Ithaca, N.Y. 7. Hawkins, W. W., Jr. (1968) Diseases Affecting the Reproduc- tive Capacity of the Ewe, Symposium on Sheep Diseases and Health, Univ. of Calif., Davis, Calif. 8. Jensen, R. and Swift, B. L. (1982) Disease of Sheep, 2nd Ed., Lea and Febiger, Philadelphia, Pa. 9. Lawson, J. R. (1962) Bacterial and Mycotic Agents Associated with Abortion and Stillbirth in Domestic Animals, Livestock In- fertility, Animal Health Branch Monograph No. 5, FAO, Rome. 10. Marsh, Hadleigh (1965) Newsom’s Sheep Diseases, 3rd Ed., Williams Wilkins Co., Baltimore, Md. 11a. Smith, M. C. (1980) Caprine Reproduction, in Current Therapy in Theriogenology edit by D. A. Morrow, W. B. Saunders Co., Philadelphia, London. 1 lb. Smith, M. C. (1981) Management and Diseases of Goats (Re- vised) N.Y.S. Col. Vet. Med., Ithaca, N.Y. 12. Watson, W. A. (1962) Abortion and Stillbirth in Sheep, Vet. Bull. 32, 5, 259. 13. Watson, W. A. (1962) Ovine Abortion, Vet. Rec. 74, 49, 1403. Bacterial infections Campylobacteriosis (Vibriosis) la. Anderson, K. L., Urbance, J. W., Hammond, M. M., Bryner, J. H. and McEntee, K. (1982) Caprine Camylobacter Abortion. Isolation from an Abortion Outbreak and Experimental Repro- duction of the Disease, Proc. 3rd Intemat. Goat Mtg., Tuscon, Arizona. lb. Ardrey, W. B., Armstrong, P., Meinershagen, W. A. and Frank, F. W. (1972) Diagnoses of Ovine Vibrioses and Enzootic Abor- tion of Ewes by Immunofluorescence Technique, Am. J. Vet. Res. 33, 12, 2535-2538. 2. Dennis, S. M. (1961) Vibrio fetus Infection in Sheep, Vet. Re- views and Annot., 7, Part 2, 69. 3. Firehammer, B. D. (1965) The Isolation of Vibrios from Ovine Feces, Cor. Vet. 55, 482. 4a. Firehammer, B. D., Marsh, H. and Tunnicliff, E. A. (1956) The Role of the Ram in Vibriosis of Sheep, Amer. J. Vet. Res. 17, 65, 573. 4b. Firehammer, B. D. and Myers, L. L. (1981) Campylobacter fetus subsp. jejuni. Its Possible Significance in Enteric Disease in Calves and Lambs, Amer. J. Vet. Res. 42, 6, 918-922. 5. Frank, F. W., Waldhalm, D. C., Meinershagen, W. A. andDISEASES AND ACCIDENTS OF GESTATION 203 Schrivner, L. H. (1965) Newer Knowledge of Ovine Vibriosis, JAVMA, 147, 12, 1313. 6. Hulet, C. V., Ercanbrack, S. K., Price, D. A., Humphrey, R. D., Frank, F. W. and Meinershagen, W. A. (1960) Effects of Certain Antibiotics in the Treatment of Vibriosis in Sheep, Amer. J. Vet. Res. 21, 82, 441. 7. Jensen, R., Miller, V. A., Hammarlund, M. A. and Graham, W. R. (1957) Vibrionic Abortion in Sheep—Transmission and Immunity, Amer. J. Vet. Res., 18, 67, 326. 8. Jensen, R., Miller, V. A. and Molello, J. A. (1961) Placental Pathology of Sheep with Vibriosis, Amer. J. Vet. Res. 22, 87, 169. 9. Meinershagen, W. A., Frank, F. W., Hulet, C. V. and Price, D. A. (1969) Immunity in Ewes Resulting from Natural Ex- posure to Vibrio fetus, Amer. J. Vet. Res., 30, 2, 203. 10. Miller, V. A. (1968) Ovine Genital Vibriosis, in Abortion Dis- eases of Livestock Edit, by L. C. Faulkner, C. C. Thomas Co., Springfield, 111., 128. 11a. Miller, V. A., Jensen, R. and Gilroy, J. J. (1959) Bacteremia in Pregnant Sheep Following Oral Administration of Vibrio Fe- tus, Amer. J. Vet. Res. 20, 77, 677. lib. Prescott, J. F. and Bruin-Mosch, C. W. (1981) Carriage of Campylobacter jejuni in healthy and Diarrheic Animals, Amer. J. Vet. Res. 42, 1, 164-165. 12. Ryff, J. F. and Breen, H. (1961) Experimental Treatment of Ovine Vibriosis, JAVMA, 139, 6, 665. 13. Smibert, R. M. (1965) Vibrio fetus var intestinalis Isolated From Fecal and Intestinal Contents of Clinically Normal Sheep, Amer. J. Vet. Res. 26, 111, 315. 14. Store, J., Miner, M. L., Marriott, M. E. and Olson, A. E. (1966) Prevention of Ovine Vibriosis by Vaccination; Duration of Pro- tective Immunity, Amer. J. Vet. Res. 27, 116, 110. 15. Store, J., Miner, M. L., Olson, A. E., Marriott, M. E. and Eisner, Y. Y. (1966) Prevention of Ovine Vibriosis by Vacci- nation; Effect of Yearly Vaccination of Replacement Ewes, Amer. J. Vet. Res. 27, 116, 115. 16. Waldhalm, O. G., Mason, D. R., Meinershagen, W. A. and Schrivner, L. H. (1964) Magpies as Carriers of Ovine Vibrio fetus, JAVMA, 144, 5, 497. 17. Watson, W. A., Hunter, D. and Bellhouse, R. (1967) Studies on Vibrionic Infection of Sheep and Carrion Crows, Vet. Rec. 81, 10, 220. Listeriosis 1. Diplock, P. T. (1957) Ovine Listerial Abortion, Austral. Vet. Jour. 33, 68. 2. Gray, M. L. (1960) A Possible Link in the Relationship Between Silage Feeding and Listeriosis, JAVMA, 136, 205. 3. Gray, M. L. (1963) Listeric Infection in Animals in the U.S., 2nd Symp. on Listeric Infections, Montana College, Bozeman, Mont. 4. Gray, M. L., Singh, C. and Thorp, F., Jr. (1956) Abortion and Pre- or Postnatal Death of Young Due to Listeria monocyto- genes, Amer. J. Vet. Res. 17, 64, 510. 5. Ladds, P. W., Dennis, S. M. and Nojoku, C. O. (1974) Pa- thology of Listeric Infection in Domestic Animals, Vet. Bull. 44, 67-74. 6. Molello, J. A. and Jensen, R. (1964) Placental Pathology IV Pla- cental Lesions of Sheep Experimentally Infected with Listeria monocytogenes, Amer. J. Vet. Res. 26, 105, 441. 7. Njoku-obi, A. N. (1962) The Antigen-Fixation Test for the Sero- Diagnosis of Listeria monocytogenes Infection, Cor. Vet. 52, 3, 415. 8. Osebold, J. W., Njoku-obi, A. N. and Abare, J. M. (1959) Ac- quired Resistance of Sheep to Listeria monocytogenes and Pilot Studies on Vaccination, Amer. J. Vet. Res. 20, 79, 966. 9. Paterson, J. S. (1940) Studies on the Organisms of the Genus Listerella IV An Outbreak of Abortion Associated with the Re- covery of Listerella from Aborted Fetuses, Vet. Jour. 96, 8, 327. 10. Smith, R. E., Reynolds, I. M. and Clark, G. W. (1968) Ex- perimental Ovine Listeriosis I Inoculation of Pregnant Ewes, Cor. Vet. 58, 2, 169. 11. Smith, R. E., Reynolds, I. M. and Harris, J. C. (1968) Experi- mental Ovine Listeriosis. Immunofluorescent Methods Applied to Maternal and Fetal Tissues, Cor. Vet. 58, 3, 389. 12. Young, Stuart (1968) Listeriosis in Cattle and Sheep, in Abor- tion Diseases of Livestock, edit, by L. C. Faulkner, C. C. Thomas Co., Springfield, 111. Brucellosis 1. Buddie, M. D. (1958) Vaccination in the Control of Brucella Ovis Infection in Sheep, New Zealand Vet. J. 6, 41. 2. Collier, J. R. and Molello, J. A. (1964) Comparative Distribution of Brucella abortus, Brucella melitensis and Brucella ovis in Experimentally Infected Pregnant Sheep, Amer. J. Vet. Res. 25, 107, 930. 3. Crenshaw, G. L. and McGowan, B. (1966) Ram Epididymitis Vaccination, Proc. 70th Ann. Meeting U.S.L.S.A., 476. 4. FAO-WHO Joint Expert Committee (1964) Brucellosis, 4th Re- port FAO Agric. Studies 66, Tech, Report Series 289, Rome. 5. Hartley, W. J., Jebson, J. L. and McFarlane, D. (1954) New Zealand Type II Abortion in Ewes, Austral. Vet. J. 30, 216. 6. Jones, L. M. (1962) A Review of Experiments on Vaccination of Goats and Sheep Against Brucella melitensis Infection, Re- fuah. Vet. 19, 2, 101. 7. Jones, L. M., Garcia-Carrillo, C. and Alton, G. G. (1973) Bru- cella melitensis Rev. 1 and Brucella abortus 45/20 Vaccines in Goats: Serologic Tests. Amer. J. Vet. Res. 34, 2, 199-202. 8. Keogh, J., Doolette, J. B. and Clapp, K. N. (1958) The Epi- demiology of Ovine Brucellosis in South Australia, Austral. Vet. J. 34, 412. 9. Lawrence, W. E. (1961) Ovine Brucellosis: A Review of the Dis- ease in Sheep Manifested by Epididymitis and Abortion, Brit. Vet. Jour., 117, 435. 10. Lucksinger, D. W. and Anderson, R. K. (1967) Epizootiology of Brucellosis in a Flock of Sheep, JAVMA, 150, 9, 1017. 11. Lucksinger, D. W. and Anderson, R. K. (1979) Longitudinal Studies of Naturally Acquired Brucella abortus Infection in Sheep, Amer. J. Vet. Res. 40, 9, 1307-1312. 12. Mayer, H. (1958) Experimental Studies on Brucellosis in Sheep, Monatsch f. Tierheilk. 10, 21, 43. 13. McGowan, B., Biberstein, E. L., Harrold, D. R. and Robinson, E. A. (1961) Epididymitis in Rams: The Effect of the Ram Epi- didymitis Organism (R.E.O.) on the Pregnant Ewe, Proc. 65th Ann. Meeting U.S.L.S.A., 291. 14. Meinershagen, W. A., Frank, F. W. and Waldhalm, D. G. (1974) Brucella ovis as a Cause of Abortion in Ewes, Amer. J. Vet. Res. 35, 5, 723-724. 15. Molello, J. A., Flint, J. C., Collier, J. R. and Jensen, R. (1963) Placental Pathology II Placental Lesions of Sheep Experimentally204 VETERINARY OBSTETRICS Infected with Brucella melitensis, Amer. J. Vet. Res. 24, 102, 905. 16. Molello, J. A., Jensen, R., Flint, J. C. and Collier, J. R. (1963) Placental Pathology 1 Placental Lesions of Sheep Experimentally Infected with Brucella ovis, Amer. J. Vet. Res., 24, 102, 897. 17. Van Drimmelen, G. C., Botes, H. J., Claassen, N., Ross, F. W. and Viljoen, C. C. (1963) The Use of Fluorescent Antibody in the Diagnosis of Brucella ovigenitalium Infection in Sheep Se- men Smears, J. S. Afr. Vet. Med. Assoc. 34, 265. Salmonella Abortion 1. Long, J. R., Finley, G. G., Clark, M. H. and Rehmtulla, A. J. (1978) Ovine Fetal Infection Due to Salmonella arizonae, Can. Vet. J. 19, 260-263. 2. Fielden, E. D. (1980) Infectious Ovine Abortion, in Current Ther- apy in Theriogenology, edit, by D. A. Morrow, Wm. B. Saunders Co., Philadelphia, 910. 3. Rae, M. and Wall, M. (1952) A Case of Uterine Infection with Salmonella meleagridis in a Sheep, Austral. Vet. J. 28, 173. 4. Shearer, G. C. (1957) An Outbreak of Abortion in Ewes due to Salmonella dublin, Vet. Rec. 69, 693. 5. Vickers, C. L., Bierer, B. W., Atkinson, R. E., Mudge, C. and Baker, D. E. (1958) Paratyphoid Dysentery and Paratyphoid Abor- tion in a Flock of Bred Yearling Ewes. JAVMA, 132, 1, 22. 6. Watson, W. A. (1960) Salmonella dublin Infection in a Lambing Flock, Vet. Rec. 72, 62. Leptospirosis 1. Alston, J. M. and Brown, J. C. (1958) Leptospirosis in Man and Animals, E. and S. Livingstone Ltd., London. 2. Beamer, P. D., Hardenbrook, H., Jr. and Morrill, C. C. (1953) Studies in Leptospirosis in Domestic Animals I Leptospirosis in Sheep, Vet. Med. 48, 365. 3. Brightenback, G. E., Scheidy, S. F. and Jensen, J. H. (1960) L. pomona Vaccination Studies in Sheep, Vet. Med. 55, 4, 63. 4. Hartley, W. J. (1952) Ovine Leptospirosis, Austral. Vet. J. 28, 169. 5. Lindquist, K. J., Morse, E. V. and Lundberg, A. M. (1958) Ex- perimental Leptospira pomona Infection in Pregnant Ewes, Cor. Vet. 48, 3, 277. 6. Smith, R. E., Hench, E. C. and Reynolds, I. M. (1966) Experi- mental Leptospirosis in Pregnant Ewes, VI, Cor. Vet. 56, 4, 640. 7. Smith, R. E., Reynolds, I. M. and Clark, G. W. (1966) Experi- mental Leptospirosis in Pregnant Ewes, V, Cor. Vet. 56, 3, 418. 8. Smith, R. E., Reynolds, I. M. and Clark, G. W. (1970) Patho- genesis of Fetal Infection and Mechanism of Abortion in Experi- mental Leptospirosis in Ewes, Cor. Vet. 60, 1, 40. Corynebacterium, Pasteurella and Miscellaneous Bacteria 1. Addo, P. B. and Dennis, S. M. (1979) Experimental Production of Corynebacterium pyogenes Abortion in Sheep, Cor. Vet. 69, 20-32. 2. Butler, H. C. and Marsh, H. (1956) Blackleg of the Fetus in Ewes, JAVMA, 128, 8, 401. 3. Dennis, S. M. and Bamford, V. W. (1966) The Role of Cory- nebacteria in Perinatal Lamb Mortality, Vet. Rec. 79, 4, 105. 4. Jellison, W., Jacobson, H. and Flora, S. (1964) Tick-borne Tu- laremia and Tick Paralysis in Cattle and Sheep, Proc. 68th Ann. Meeting U.S.L.S.A., 60. 5. Lindquist, K. (1956) A Case of Bacteroides fragilis Abortion in a Ewe, Nord. Vet. Med. 5, 995. 6. Smith, I. D. and Frost, A. J. (1968) The Pathogenicity to Pregnant Ewes of an Organism of the Genus Bacillus, Austral. Vet. Jour. 44, 17. Viral and Rickettsial Infections Enzootic Abortion of Ewes (Chlamydiosis) 1. East, N. E. and Brooks, D. L. (1982) Causes of Abortion in a Large Goat Dairy over a Three-year Period, Proc. 3rd Intemat. Goat Mtg., Tucson, Ariz. (in press) 2. Foggie, A. (1977) Chlamydial Infections in Mammals, Vet. Rec. 100, 315-317. 3. Frank, F. W. (1963) A Comparison of Some Aspects of Viral Abortion and Vibriosis of Sheep, Proc. 67th Ann. Meeting U.S.L.S.A., 308. 4. Frank, F. W., Schrivner, L. H., Thomas, L. and Waldham, D. G. (1968) Artificially Induced Immunity to Enzootic Abortion in Ewes, Amer. J. Vet. Res. 29, 7, 1441. 5. McCauley, E. H. and Ticken, E. L. (1968) Psittacosis-Lympho- granuloma Venereum Agent Isolated During an Abortion Epi- zootic in Goats. JAVMA, 152, 12, 1758. 6. McKercher, D. G., McGowan, B., Wada, E. M., Harold, D. R. and Studdert, M. J. (1964) Isolation of the Virus of Enzootic Abortion of Ewes from California and Oregon Sheep, JAVMA, 145, 6, 564. 7. Page, L. A. (1966) Interspecies Transfer of Psittacosis—L.G.V.— Trachoma Agents, Pathogenicity of Two Avian and Two Mam- malian Strains for Eight Species of Birds and Mammals, Amer. J. Vet. Res. 27, 117, 397. 8. Parker, H. O., Hawkins, W. W., Jr. and Brenner, E. (1966) Epizootiologic Studies of Ovine Virus Abortion, Amer. J. Vet. Res. 27, 119, 869. 9. Shefki, M. D. (1963) Enzootic Abortion in Goats, Brit. Vet. Jour. 119, 430. 10. Shupe, J. L. and Storz, J. (1964) Pathologic Study of Psittacosis- Lymphogranuloma Polyarthritis of Lambs, Amer. J. Vet. Res. 25, 107, 943. 11. Storz, J. (1963) Superinfection of Pregnant Ewes Latently In- fected with a Psittacosis-Lymphogranuma Agent, Cor. Vet. 53, 4, 469. 12. Storz, J. (1968) Comparative Studies on EBA and EAE Abortion Diseases of Cattle and Sheep Resulting from Infection with Psit- tacosis Agents, in Abortion Diseases of Livestock, edit, by L. Faulkner, C. C. Thomas, Springfield, 111., 108. 13. Storz, J., Shupe, J. L., James, L. F. and Smart, R. A. (1963) Polyarthritis of Sheep in the Intermountain Region Caused by a Psittacosis-Lymphogranuloma Agent, Amer. J. Vet. Res. 24, 103, 1201. 14. Waldhalm, D. G., Delong, W. J. and Hall, R. F. (1981) Im- munization of Sheep with a Bacteria Prepared from Chlamydia psittaci Grown in Cell Culture, Proc. 85th Ann. Mtg. U.S.A.H.A., St. Louis, Mo., 440-444.DISEASES AND ACCIDENTS OF GESTATION 205 Miscellaneous Viral and Rickettsial Infections la. Cutlip, R. C., Lehmkuhl, H. D., Whipp, S. C. and McClurkin, A. W. (1982) Effects on Ovine Fetuses of Exposure to Ovine Progressive Pneumonia Virus, Am. J. Vet. Res. 43, 1, 82. lb. East, N. E. and Brooks, D. L. (1982) Causes of Abortion in a Large Goat Dairy Over a Three Year Period, Proc. 3rd Intemat. Goat Mtg., Tucson, Ariz., In press. lc. Evermann, J. F. and Roeder, P. L. (1982) Border Disease Virus Isolation from Postpartum Ewes. (Letters), Am. J. Vet. Res. 43, 7, 1322. 2. Hutyra, F., Marek, J. and Manninger, R. (1938) Pathology and Therapeutics of the Diseases of Domestic Animals Vol. I, 415. 3. Inverso, M., Lukas, G. N. and Weidenback, S. J. (1980) Caprine Bluetongue Virus Isolations, Amer. J. Vet. Res. 41, 2, 277-278. 4. Luedke, A. J., Jockim, M. M. and Jones, R. H. (1969) Blue- tongue in Cattle: Viremia, Amer. J. Vet. Res. 30, 4, 511. 5a. Niemi, S. M., Evermann, J. F., Huffman, E. M. and Kirk, J. H. (1982) Border Disease Virus Isolation from Postpartum Ewes, Amer. J. Vet. Res. 43, 1, 86-88. 5b. Potts, B. J., Osbum, B. I. and Johnson, K. P. (1982) Border Disease: Experimental Reproduction in Sheep, Using a Virus Replicated in Tissue Culture, Am. J. Vet. Res. 43, 8, 1464. 6. Reynolds, G. E. (Chm) (1980) Report Bluetongue-Bovine Leu- cosis Committee, Proc. 84th Ann. Mtg. U.S.A.H.A., Louisville, Ky., 215-217. 7. Schultz, G. and DeLay, P. (1955) Losses in Newborn Lambs Associated with Bluetongue Vaccination of Pregnant Ewes, JAVMA, 127, 224. 8. Stamp, J. T., Watt, J. A. and Jamieson, S. (1950) Tick-borne Fever as a Cause of Abortion in Sheep, Vet. Rec. 62, 32, 465. 9. Tamarin, R., Rosenfeld, S. and Landau, M. (1964) Experimental Infection of Pregnant Sheep with Coxiella burnetii, Refuah Vet. 21, 180. 10. Terlecki, S., Richardson, C., Done, J. T., Harkness, J. W., Sands, J. J., Shaw, I. G., Winkler, C. E., Duffell, S. J., Patterson, D. S. P. and Sweasey, D. (1980) Pathogenicity for the Sheep Fetus of Bovine Virus Diarrhoea—Mucosal Disease Virus of Bovine Origin., Brit. Vet. Jour. 136, 602-611. 11. U.S. Livestock Sanitary Assoc. (1964) Foreign Animal Diseases, Report of Comm., Seer. Treas., Trenton, N.J. 12. Waldhalm, D. G., Stoenner, H. G., Simmons, R. E. and Thomas, L. A. (1978) Abortion Associated with Coxiella burnetii Infec- tion in Dairy Goats, JAVMA, 173, 12, 1580-1581. 13. Ward, G. M. (1971) Experimental Infection of Pregnant Sheep with Bovine Viral Diarrhea-Mucosal Disease Virus, Cor. Vet. 61, 179-191. 14. Weiss, K. E., Haig, D. A. and Alexander, R. A. (1956) Wes- selbron Virus—A Virus not Previously Described Associated with Abortion in Animals, Onderst. J. of Vet. Res. 27, (2), 183. Mycoplasma and Fungal Causes of Abortion 1. Cysewski, S. J., Pier, A. C. and Richard, J. L. (1968) Mycotic Abortion in Ewes Produced by Aspergillus fumigatus, Amer. J. Vet. Res. 29, 6, 1135. 2. Livingston, C. W., Gauer, B. B. and Shelton, M. (1978) A Spe- cific Ureaplasmal Serotype Associated with Ovine Uterine Infec- tions, Am. J. Vet. Res., 39, 1699-1671. 3. Yedloutschnig, R. J., Taylor, W. D. and Dardiri, A. H. (1971) Isolation of Mycoplasma mycoides var. capri from goats in the United States, Proc. 75th Ann. Mtg. U.S.A.H.A., 166-175. Parasitic Protozoa Causing Abortion (Toxoplasma gondii, Sarcocystis spp. and Besnoitia spp.) 1. Beverly, J. K. A. (1976) Toxoplasmosis in Animals. Vet. Rec. 99, 123-127. 2. Dubey, J. P. (1976) A Review of Sarcocystis of Domestic An- imals and Other Coccidia of Cats and Dogs. JAVMA, 169, 10, 1061-1078. 3. Dubey, J. P. (1981) Abortion and Death in Goats Inoculated with Sarcocystis Sporocysts from Coyote Feces, JAVMA, 178, 7, 700-702. 4. Dubey, J. P. (1981) Epizootic Toxoplasmosis Associated with Abortion in Dairy Goats in Montana, JAVMA, 178, 7, 661- 670. 5. Dubey, J. P. (1981) Prevention of Abortion and Neonatal Death Due to Toxoplasmosis by Vaccination of Goats with the Non- pathogenic Coccidium, Hammondia hammondi, Amer. J. Vet. Res. 42, 12, 2155-2157. 6a. Dubey, J. P. (1981) Toxoplasma—Induced Abortion in Dairy Goats, JAVMA, 178, 7, 671-674. 6b. Dubey, J. P. (1982) Repeat Transplacental Transfer of Toxo- plasma gondii in Dairy Goats, JAVMA, 180, 10, 1220. 7. Dubey, J. P. and Schmitz, J. A. (1981) Abortion Associated with Toxoplasmosis in Sheep in Oregon, JAVMA, 178, 7, 675- 678. 8. Dubey, J. P., Sundberg, J. P. and Matiuck, S. W. (1981) Tox- oplasmosis Associated with Abortion in Goats and Sheep in Connecticut. Amer. J. Vet. Res. 42, 9, 1624-1626. 9. Dubey, J. P., Weisebrode, S. E., Speer, C. A. and Sharma, S. P. (1981) Sarcocystis in Goats: Clinical Signs and Pathologic and Hematologic Findings, JAVMA, 178, 7, 683-699. 10. Frenkel, J. K., Dubey, J. P. and Miller, N. L. (1970) Toxo- plasma gondii in Cats: Fecal Stages Identified as Coccidian Oocysts, Science, 167, 893. 11. Hartley, W. J. (1976) Sporozoa in Animals with Particular Ref- erence to Toxoplasma and Sarcocystis. N.Z. Vet. J. 24, 1-5. 12. Leek, R. G. and Fayer, R. (1978) Sheep Experimentally In- fected with Sarcocystis from Dogs, Cor. Vet. 68, 108-123. 13a. Munday, B. L. (1972) Transmission of Toxoplasma Infection from Chronically Infected Ewes to their Lambs, Brit. Vet. Jour. 128, lxxi. 13b. Munday, B. L. (1981) Premature Parturition in Ewes Inoculated with Sarcocystis ovicanis, Vet. Parasitol. 9, 17. 14. Sheffield, H. G. and Melton, M. L. (1970) Toxoplasma gon- dii: The Oocyst, Sporozoite, and Infection of Cultured Cells, Science, 167, 892. 15. Sikes, R. K. (1982) Toxoplasmosis, JAVMA, 180, 8, 857. Noninfectious Causes of Abortions in Ewes and Goats 1. Adams, W. M. (1970) Personal Communication. 2. Adams, W. M. and Wagner, W. C. (1969) The Elective Induc- tion of Parturition in Cattle, Sheep and Rabbits, JAVMA Pro- ceedings Research Section, 106th Nat. Meeting, Minneapolis,206 VETERINARY OBSTETRICS Minn, and (1970) Role of Corticoids in Parturition, Biol, of Re- prod., 3, 223. 3. Allcroft, R. and Blaxter, K. L. (1950) Lead as a Nutritional Haz- ard to Farm Livestock, J. Comp. Path. 60, 209. 4. Bennetts, H. W., Underwood, E. J. and Shier, F. L. (1946) A Specific Breeding Problem of Sheep on Subterranean Clover Pas- tures in Western Australia, Austral. Vet. J. 22, 1, 2. 5. Bosu, W. T. K., Serna Garibay, J. A. and Barker, C. A. V. (1979) Peripheral Plasma Levels of Progesterone in Pregnant Goats and in Pregnant Goats Treated with Prostaglandin F2a, Theriog. 11, 2, 131-148. 6. Boyazoglu, P. A., Jordan, R. M. and Meade, R. J. (1967) Sul- fur-Selenium—Vitamin E. Interrelations in Ovine Nutrition, J. An. Sci. 26, 1390. 7. Burfening, P. J. (1975) Feeding Ergot to Pregnant Ewes, Ther- iog. 3, 5, 193-198. 8. Cumow, D. H. and Bennetts, H. W. (1952) Estrogenic Hor- mones in Plants in Relation to Animal Physiology, Proc. 6th Grasslands Congress, Penn. State College. 9. Day, A. M. and Southwell, S. R. G. (1979) Termination of Preg- nancy in Goats Using Cloprostenol, N. Z. Vet. Jour. 27, 207- 208. 10. Davison, K. L., McEntee, K. and Wright, M. J. (1965) Re- sponses in Pregnant Ewes Fed Forages Containing Various Lev- els of Nitrate, J. Dairy Sci. 48, 7, 968. 11. Gamer, R. J. (1967) Veterinary Toxicology, Bailliere, Tindall and Cox, London. 12. Grant, A. B., Hartley, W. J. and Drake, C. (1960) Further Ob- servation on White Muscle Disease in Lambs, N. Z. Vet. Jour. 8, 1. 13. Hartley, W. J. (1961) Personal Communication. 14. Hartley, W. J. and James, L. F. (1975) Fetal and Maternal Le- sions in Pregnant Ewes Ingesting Locoweed (Astragalus lentigi- nosus), Amer. J. Vet. Res. 36, 6, 825-826. 15. Howarth, B., Jr. and Hawk, H. W. (1968) Effect of Hydrocor- tisone on Embryonic Survival in Sheep, J. An. Sci. 27, 1, 117. 16. James, L. F. (1974) Diet-Related Birth Defects, Nutrition Today, 9, 4, 4-11. 17. James, L. F., Shupe, J. F., Binns, W. and Keeler, R. F. (1967) Abortive and Teratogenic Effects of Locoweed on Sheep and Cat- tle, Amer. J. Vet. Res. 28, 126, 1379. 18. Liggins, G. C. (1968) Premature Parturition after Infection of Corticotrophin or Cortisol into Fetal Lambs, J. Endocrin. 42, 323. 19. Reid, J. T. (1949) Relationship of Nutrition to Fertility in Ani- mals, JAVMA, 114, 158 and 242, 864 and 865. 20. Smith, M. C. (1978) Some Clinical Aspects of Caprine Repro- duction, Cor. Vet. 68, (Suppl. 7) 200-211. 21. Stamp, J. T. (1960) Muscular Dystrophy in Sheep and Neonatal Mortality. J. Comp. Path. 70, 296. 22. Van Heerden, K. M. (1963) Investigations into the Cause of Abortions in Angora Goats in South Africa, Onderst. J. Vet. Res. 30 (1), 23. 23. Van Kampen, K. R., Binns, W., James, L. F. and Balls, L. D. (1969) Early Embryonic Deaths in Ewes Given Veratrum cali- fornicum, Amer. J. Vet. Res. 30, 4, 517. 24. Van Rensburg, S. J. (1965) Adrenal Function and Fertility, Jour. S. Afr. Vet. Med. Assoc. 36, 4, 491. 25. Van Rensburg, S. J. (1967) Gestation in Sheep after Fetal Adre- nalectomy and Cortisol Acetate Administration, J. Endocrin. 38 (1), 83. 26. Warwick, B. L., Turk, R. D. and Berry, R. O. (1946) Abortion in Sheep Following the Administration of Phenothiazine, JAVMA, 108, 826, 41. ABORTION IN THE BITCH Abortions in bitches are much less common than in the larger domestic animals. Most canine abortions are sporadic except for enzootic or epizootic outbreaks in kennels due to Br. canis. Limited experimental work has been done on other causes of abortions in small an- imals. Infectious Causes of Canine Abortions Bacterial Causes Brucella canis is the most common cause of third trimester abortion and infertility in bitches and epididy- mitis, testicular atrophy and infertility in males,8,9c’24 It can be a serious cause for losses in breeding kennels. This highly contagious disease is widespread in the United States and other countries. The incidence of canine bru- cellosis, based on serologic tests, varies from 1 to 10 percent of dogs in the United States.24 Since serologic tests are inaccurate the true incidence may be much lower. For example in the north midwest states 6.7 percent of 2,572 dogs were positive on the slide test, 1.5 per- cent 25,72 on the tube agglutination test and only 0.2 per- cent positive on blood culture.3 In northeastern U.S. about 0.5 to 1.5 percent of dogs are possibly infected.8,24 Al- though initially observed in Beagles in the late 1960’s, it now occurs in all breeds and in both kenneled and free- roaming dogs. The incidence is higher in states and countries where the climate is mild and free-roaming packs of dogs are common.7,24 The disease in dogs resembles brucellosis in swine due to Br. suis but is relatively mild. Br. canis is an intracellular pathogen morphologically similar to other Brucella. It cross reacts with Br. ovis and rough variants of other Brucella as well as Acti- nobacillus equuli and Pseudomonas aeruginosa.8 Ca- nine brucellosis is characterized by abortion occurring between gestation days 30 and 57 with about 85 percent of the observed abortions occurring between days 45 and 55. Some infected bitches may carry their fetuses to near term and deliver both live and dead pups. The living pups may survive and appear healthy but be bacteremic for at least two months. Up to 30 percent of infected bitches may abort two or three litters in succession. Ap- parent failure of conception was also commonly ob-DISEASES AND ACCIDENTS OF GESTATION 207 Table 13a. Summary of the Causes of Canine Abortion Infectious causes: Bacterial causes—Br. canis. Miscellaneous bacterial causes—Br. abortus and suis, staphylococci, streptococci, pseudomonas, coliform and salmonella organisms. Viral Causes—Distemper virus, adenovirus (infectious hepatitis) and canine herpesvirus (CHV). Other infections—Toxoplasma gondii Noninfectious Causes: Drugs, chemical, poisons—O-diazoacetyl-L-serine, N-desacetyl thiocolchicine, malucidin and others. Hormonal—progesterone deficiency, prostaglandins. Physical—severe trauma (?) Nutritional—manganese deficiency (?) Miscellaneous—genetic defects, parturient conditions and stillbirths. served and this was due to early unrecognized embryonic deaths between gestation days 10 to 25.8,22,24 Early abor- tions were largely unobserved because the affected bitches would ingest the expelled membranes and embryos. These early breeding failures may also be repeated three or four times after consecutive breeding periods.24 Occasionally a bitch would abort, have a normal pregnancy and then abort again. The incidence of abortion in a susceptible kennel of dogs may reach 80 percent. Retained placentas were not observed. However, prolonged vaginal dis- charges were commonly seen lasting from 4 to 6 weeks after an abortion. The living pups often died and some fetuses had degrees of autolytic changes. In adult male dogs epididymitis was a consistent sign and the scrotum was hyperemic, swollen and painful resulting in scrotal dermatitis secondary to excessive licking. The epididy- mides were enlarged and firm and testicular degenera- tion and atrophy were often observed. Primary orchitis is seldom noted but the prostate is commonly affected. Semen samples are abnormal with varying degrees of oligospermia to azoospermia and containing many neu- trophiles and monocytes. Other lesions due to Br. canis include lymph node and splenic enlargement, and oc- casionally discospondylitis and recurrent uveitis.7,24 Clinical signs of pyrexia, depression, anorexia are usu- ally absent and deaths due to Br. canis have not been reported.7,24 Transmission of the disease can occur by inoculation of fairly large numbers of infective organisms but prob- ably occurs naturally by oral, nasal, conjunctival or va- ginal exposure to infective material.7,24 Aborting bitches discharge large numbers of infective organisms. The in- fected male can transmit brucellosis to bitches at coitus for many months by infective semen.24 Organisms from the epididymis, testes and prostate are discharged inter- mittently in semen. The male dog might rarely spread infection in his urine.8,24 Spread of infection by fecal contamination does not readily occur. When like-sexed infected and uninfected dogs were housed together trans- mission did not occur.24 The practice of breeding popular stud dogs to large number of females from a wide geographic area or the use of artificial insemination or frozen semen could dis- seminate the disease widely if the stud should be in- fected. The aborting female can readily spread Br. canis throughout a kennel by contamination of food, runs, and water from aborted fetuses and membranes, genital dis- charges and even by her milk. Because of the prolonged bacteremia blood transfusions or even the use of con- taminated syringes and needles could spread the disease. Since dogs are the only known natural host for Br. canis, transmission to man probably comes from this ca- nine source. Humans appear relatively resistant to Br. canis infection unless massively exposed.7,90 Signs in humans vary but resemble those of undulant fever due to Br. abortus including intermittent fever, chills, mal- aise, muscle and joint pain and enlarged lymph nodes. In the U. S. seroprevalence rates in humans was 0.4 per- cent. Human infections have responded to treatments with tetracyclines. There have been only 18 cases of human brucellosis due to Br. canis reported and no known deaths.7,24 Following canine exposure to Br. canis a bacteremia develops within 1 to 3 weeks. A generalized lymphad- enitis and splenitis occurs and antibodies become de- tectable by the serum agglutination test. The brucella or- ganisms persist for many months or indefinitely in many organs of the body. After one year blood cultures may become negative in some dogs but a few dogs may have a bacteremia lasting for 26 to 33 months or more. Since clinical signs other than abortion and epididymitis are not specific, a definitive diagnosis is based on serologic and bacteriologic tests, especially the latter.7,24 The organisms can readily be cultured from organs of208 VETERINARY OBSTETRICS aborted fetuses, placental tissues and vaginal discharges. Blood cultures are often positive. Current available sero- logic screening tests for canine brucellosis must be per- formed carefully and interpreted cautiously. The slide agglutination test and tube agglutination tests are widely used. The agar gel immunodiffusion test shows promise and is presently being evaluated.24 The slide agglutina- tion test is commonly performed by mixing patient serum with a rose bengal-stained heat-killed Br. ovis suspen- sion. Clumping or agglutination is interpreted as suspi- cious of Br. canis infection. However 50 to 60 percent of positive test results are erroneous or false positives. While a negative test is highly reliable, false negatives are rare. Thus a positive test result must be confirmed by culture of the organism. The addition of mercapto- ethanol to the serum will eliminate about 90 percent of the false positive results.6 A recommendation to destroy, castrate or spay serotest positive dogs requires the re- covery of the organism by culture procedures. The false positive test results are due to cross reactions to a num- ber of ubiquitous canine organisms. The tube agglutina- tion test is the most widely used serologic procedure to detect Br. canis antibodies. The serotiters reported based on this test must be interpreted by the laboratory per- forming the test but usually a titer of 1:200 is considered positive. However some chronically infected male dogs may be negative by serologic testing. It is interesting to note that even though dogs have positive serologic tests indicating the presence of antibodies in the blood that these dogs may concurrently have a Brucella bacteremia. Antibiotic therapy for several weeks will result in a pe- riod of abacteremia and false negative serologic test re- sults. After therapy is discontinued the bacteremia will usually recur. A single negative blood culture does not completely indicate freedom from the disease so, espe- cially in treated male dogs, repeated blood cultures might be indicated. Since present serologic tests may not be reliable, a recommendation to destory, castrate or spay a serotest positive dog should not be made without blood culture.6,7'24 Efforts to develop an effective safe bacterin or MLV vaccine have been unsuccessful and probably is not in- dicated or desirable.6 7 Although Br. canis is susceptible in vitro to a combination of tetracyclines, dihydrostrep- tomycin, minocycline, rifamysin; sulfonamides or com- binations of antibiotics administered to infected dogs for a number of weeks,156,24,32 therapy has been unsatisfac- tory as only a one to three-month temporary cessation of the bacteremia resulted. A few antibiotic regimens es- pecially if given early in the disease have apparently re- sulted in a cure of the disease in certain bitches.32 Such treatment was long term, very expensive and required repeated confirmatory cultures over many months even after therapy was discontinued.6,7,24 Bitches naturally in- fected with Br. canis were treated sequentially for a pe- riod of 14 days each with tetracycline 20 mg/kg orally TID, dihydrostreptomycin 11 mg/kg IM, BID and tri- methoprim-sulfadiazine 15 mg/kg orally BID. These bitches became abacteremic after treatment and abor- tions did not occur while they were bacteremic.156 Prevention and control in kennels is based on eradi- cation by repeated monthly serologic and cultural tests of all dogs, young, old, male and female, segregation and destruction of infected animals, and concommitant sanitary measures. All dogs to be introduced into ken- nels should be isolated for 3 to 4 weeks and blood tested. Domestic livestock have been shown to be highly re- sistant to infection with Br. canis. There is no evidence that Br. canis on inoculation into cattle will cause sero- conversion on tests for either Br. canis or Br. abortus. Cats are resistant to natural infections with Brucella Miscellaneous bacterial causes of canine and feline abortion include: Brucella abortus,1 suis19 and melitensis4 7 can cause occasional sporadic abortions in pregnant bitches when they ingest infected material. These cases may be di- agnosed on culture of aborted, infected fetuses or mem- branes and by the serum agglutination test.17,226 As with Br. canis, dogs infected with these other species of Bru- cella may transmit infections to humans. Nonspecific or- ganisms such as coliforms, staphylococci, streptococci and Salmonella spp. are frequently associated with spo- radic abortions especially in older bitches and often ac- companied by chronic endometritis and low grade cystic endometrial hyperplasia.2,18,20,21,23 These abortions are usually associated with infertility, a persistent vulvar discharge, chronic metritis, and repeated abortions. Few bacteriological studies have been reported in dogs to in- dicate the incidence of the more common or even the occasional bacterial causes of abortion. By the administration of large doses of penicillin and streptomycin or other antibiotics for 7 to 14 days or longer, some veterinarians have reported apparent success in preventing abortion in dogs showing early symptoms of impending abortion. Bitches with a history of repeated abortions may carry the conceptus to term if infection was controlled or prevented by treating with broad range antibiotics for several weeks before and after service. Although a few reports have linked Leptospira pomona with abortion in dogs, evidence indicates that they do not abort from this cause. Dogs can become urinary shedders of leptospira.4 Salmonella spp. has been re-DISEASES AND ACCIDENTS OF GESTATION 209 ported as a cause of occasional canine abortion and still- births associated with the acute disease.23 Viral causes of abortion—In contrast to the large species of domestic animals, dogs relatively seldom abort due to viral infections of the fetuses. Abortions in dogs have been described following an acute attack of distem- per. Viral agents including distemper,10’1618 canine adenovirus18 (infectious hepatitis) and canine herpesvirus (CHV)14'18 have been isolated from aborted fetuses, pla- centas and neonates. Transplacental transmission of CHV to fetuses may occur late in gestation.I4b There is evi- dence that the latter two viruses may occasionally cause abortion. Canine distemper virus (CDV) can cause trans- placental infections and abortion and if late in gestation may cause congenital infections in the newborn pups.18a Vaccines are available for the prevention of disease caused by distemper and infectious hepatitis and should be given before breeding. Canine distemper virus (CDV) MLV or avirulent vaccines should not be administered to preg- nant bitches. Fungal causes of abortion have not been reported in dogs. Protozoal causes of abortion in dogs are uncommon. Toxoplasma gondii may cause abortions, birth of pre- mature, dead or moribund pups or living pups with con- genital toxoplasmosis.4 8’28 Toxoplasmosis may clinically resemble other infectious diseases of dogs. As with sheep the organism may be recovered from fetal organs and placenta, especially the brain or be observed in histo- logic sections. The Sabin-Feldman dye test and the com- plement-fixation test and others are useful serologic tests for toxoplasmosis.411 Noninfectious Causes for Canine Abortion A number of drugs have been described that when ad- ministered to pregnant bitches caused fetal death and abortion. These drugs include: N-deacetylthiocolchicine; O-diazoacetyl-L-serine (azoserine); malucidin; a yeast extract and other nonhormonal compounds.12 13 27,30 31 These drugs have been suggested for mismatings but have not been generally accepted for this purpose nor proven acceptable for causing abortion in bitches. Because the dog is highly susceptible to estrogen tox- icity by bone marrow depression, thrombocytopenia and leukopenia, large or repeated doses of estrogens to pro- duce abortion has not been attempted nor recommended. Small doses of 0.02 to 0.03 mg/kg of prostaglandin F2a given 2 or 3 times per day between 33 and 53 days of gestation resulted in abortion in 4 or 7 bitches at 56 to 80 hours after treatment was started.96 In some bitches not all the fetuses were expelled. Also undesirable side effects of salivation, vomition and diarrhea occurrred after the injections. A single effective dose of 1 mg/kg is too near the fatal dose of 5 mg/kg to administer. Presently 0.05 to 0.075 mg/kg is given twice a day up to 5 to 7 days to be certain all fetuses are expelled.93 In prelimi- nary studies 2 bitches pregnant 30 days and 2 pregnant 45 days were given 5 mg dexamethasone twice daily for 10 days. In the former the embryos died and were re- sorbed and in the latter dead fetuses were aborted one and 3 days after the end of the treatment.13 Further stud- ies are indicated. Thus in the bitch there is no satisfac- tory product or drug to induce abortion even in early pregnancy. The use of dexamethasone to induce abortion or cause premature births in bitches has not been ade- quately evaluated. Possibly the combination of dexa- methasone and prostaglandin might be satifactory but further trials are indicated. However surgical removal of the corpora lutea in the bitch will result in abortion at any stage of gestation and presently it is the only safe method for termination of pregnancy.5 Progesterone deficiency—Abortion in bitches with no evidence of infection may be due to hypoluteinization and occur the sixth to seventh week of gestation because of premature regression of the corpus luteum, or occur the second to fifth week of gestation due to faulty de- velopment of the corpus luteum. Five to 25 mg doses of progesterone in oil 2 to 3 times a week until the eighth week of pregnancy, or the “repositol” form could be used less often.2 More work needs to be done to assess the incidence of abortions due to endocrine deficiencies. Nutritional causes of abortion in dogs have rarely been reported. Manganese deficient bitches either failed to come into estrus or when bred, terminated gestation about three weeks later.26 It is rather significant that in our motor- ized society that only a few abortions in dogs following severe trauma have been described. Genetic defects of the developing embryo or fetus may result in embryonic or fetal death. In bitches, as in sows, the number of de- veloping embryos maturing to term is regulated by uter- ine factors and spacing of embryos. Most deaths due to these factors occur about 30 days of gestation and em- bryos dying at this time are usually autolysed and ab- sorbed. Dystocia due to achondroplasia in certain breeds of dogs and lack of proper growth in young animals may cause dystocia and stillbirths. References Abortion in the Bitch la. Austad, R., Lunde A. and Sjaastad, 0. V. (1976) Peripheral Plasma Levels of Oestradiol-17B and Progesterone in the Bitch During the Oestrus Cycle, in Normal Pregnancy and After Dex-210 VETERINARY OBSTETRICS amethasone Treatment, J. Reprod. Fert. 46, 129-136. lb. Bicknell, S. R., Bell, R. A. and Richards, P. A. (1976) Bru- cella abortus in the Bitch, Vet. Rec. 99, 85-86. 2. Bloom, F. (1968) Canine Medicine, Edit, by E. J. Catcott, Amer. Vet. Public. Inc., Wheaton, 111., 445. 3. Boebel, F. W., Ehrenford, F. A., Brown, G. M., Angus R. D. and Thoen, C. O. (1979) Agglutinins to Brucella canis in Stray Dogs from Certain Counties in Illinois and Wisconsin, JAVMA, 175, 3, 276-277. 4. Bruner, D. W. and Gillespie, J. H. (1973) Hagan’s Infectious Diseases of Domestic Animals, 6th Ed., Cornell Univ. Press, Ithaca, N.Y. 5. Burke, T. J. (1979) Birth Control for Dogs, DVM Magazine 10, 6, 9-12. 6. Carmichael, L. E. (1982) Personal Communication. 7. Carmichael, L. E., Flores-Castro, R. and Soha, S. (1980) Bru- cellosis caused by Brucella canis (Br. canis): An Update of Infection in Animals and in Humans, Paper submitted to W.H.O. #6, 2/12/80. 8. Cole, C. R., Sanger, V. L., Farrell, R. L. and Komder, J. D. (1954) The Present Status of Toxoplasmosis in Veterinary Med- icine, N. A. Vet. 35, 265. 9a. Concannon, P. W. (1982) Personal Communication. 9b. Concannon, P. W. and Hansel, W. (1977) Prostaglandin F2a Induced Luteolysis, Hypothermia and Abortions in Beagle Bitches, Prostaglandins 13, 533-542. 9c. Currier, R. W., Raithel, W. F., Martin, R. J. and Potter, M. E. (1982) Canine Brucellosis (Dog and Man), JAVMA, 180, 132. 10. Engstrom, D. S. (1964) Canine Distemper—Student-Faculty Seminar, Cornell Univ., Ithaca, N.Y. 11. Evans, J. M. (1968) Neonatal Diseases of the Dog II Neonatal Disease in Puppies Associated with Bacteria and Toxoplasma, J. Sm. An. Pract., 9, 453. 12. Friedman, M. H. (1957) The Effect of O-Diazoacetyl-L-Serine (Azoserine) on the Pregnancy of the Dog, JAVMA, 130, 4, 159. 13. Galliani, G. and Lemer, L. J. (1976) Pregnancy Termination in Dogs with Novel Nonhormonal Compounds, Am. J. Vet. Res. 37, 263-268. 14a. Hashimoto, A., Hirai, K., Okada, K. and Fugimoto, Y. (1979) Pathology of the Placenta and Newborn Pups with Suspected Intrauterine Infection of Canine Herpesvirus, Amer. J. Vet. Res. 40, 1236-1240. 14b. Hashimoto, A., Hirai, K., Yamaguchi, T. and Fugimoto, Y. (1982) Experimental Transplacental Infection of Pregnant Dogs with Canine Herpesvirus, Am. J. Vet. Res. 43, 5 , 844. 15a. Johnson, B. D. (1979) Use of Prostaglandins in Reproduction (Dog and Cat), DVM Magazine 10, 5, 18-21. 15b. Johnson, C. A., Bennett, M., Jensen, R. K. and Schirmer, R. (1982) Effect of Combined Antibiotic Therapy on Fertility in Brood Bitches Infected with Brucella canis JAVMA, 180, 11, 1330. 16. Kessler, S. M. (1949) Spontaneous Abortion in a Bitch, JAVMA, 114, 865, 210. 17. Kimberling, C. V., Lucksinger, D. W., and Anderson, R. K. (1966) Three Cases of Canine Brucellosis, JAVMA, 148, 8, 900. 18a. Krokowka, S. and Hoover, E. A (1977) Congenital Canine Dis- temper, Mod. Vet. Pract. 58, 440-442 and Amer. J. Vet. Res. 38, 919-922. 18b. Lein, D. H. (1977) Reproduction in Veterinary Medicine, Sem- inar Wash. D.C. Acad, of Vet. Med. 19. Leman, A. D. (1981) Diseases of Swine, 5th Ed., Iowa State University Press. Ames, Iowa. 20. Montovani, A., Restani, R., Sciarra, D. and Simonella, P. (1962) Streptococcus Infection in the Dog, J. Small Anim. Pract. 2, 185. 21. McEntee, K. (1970) Pathology of Domestic Animals, 2nd Ed., by Jubb, K. and Kennedy, P., Academic Press, Inc., N.Y.C. 22a. Moore, J. A. and Bennett, M. (1967) A Previously Undescribed Organism Associated with Canine Abortion, Vet. Rec. 80, 604. 22b. Morse, E. V. (1951) Canine Brucellosis—A Review of the Lit- erature, JAVMA, 119, 304. 23. Morse, E. V. and Duncan, M. A. (1975) Canine Salmonellosis: Prevalence, Epizooteology, Signs and Public Health Signifi- cance, JAVMA, 167, 817-820. 24. Pollock, Roy (1979) Canine Brucellosis: Current Status, Comp, of Cont. Educ. 1, 2, 255-267. 25. Schalm, O. W. (1978) Exogenous Estrogen Toxicity in the Dog, Canine Pract. 5, 5, 57-61. 26. Sheffy, B. E., Krinsky, M. M., Williams, A. J. and Banta, C. A. (1976) Re-evaluation of Trace Element Requirements of Dogs, Report of J. A. Baker Institute for An. Health. 27. Shille, V. M. and Stabenfeldt, G. H. (1980) Current Concepts in Reproduction of the Dog and Cat., Adv. in Vet. Sci. and Comp. Med. 24, 211-243. 28. Siim, J. C., Biering-Sorensen, U. and Moller, T. (1963) Tox- oplasmosis in Domestic Animals, in Advances in Veterinary Science, Vol. 8, Edit, by C. A. Brandley and E. L. Jungherr, Academic Press Inc. N.Y.C. 29. Sokolowski, H. H. and Geng, S. (1977) Biological Evaluation of Mibolerone in the Female Beagle, Am. J. Vet. Res. 38, 1371- 1376. 30. Thiersch, J. B. (1967) Abortion in the Bitch with N-Desacetyl- Thiocolchicine, JAVMA, 151, 11, 1470. 31. Whitney. L. F. (1960) Further Studies on the Effect of Malu- cidin on Pregnancy, Vet. Med. 55, 12, 57. 32. Zoha, S. J. and Walsh, R. (1982) Effect of a Two-Stage An- tibiotic Treatment Regimen on Dogs Naturally Infected with Brucella canis, JAVMA, 180, 12, 1474. Abortion in Queens Abortion in queens is probably more common than in bitches13 but much lower than in sows, ewes, cows and mares. The true incidence is not known because of early embryonic deaths and resorption of the conceptuses and the nature of carnivores to consume aborted material or fetuses. Most feline abortions are sporadic. An increas- ing number of studies have been performed on the causes of abortion in queens. Infectious Causes of Feline Abortions Bacterial Causes Nonspecific organisms including coliforms (E. coli), Pseudomonas spp. Staphylococci, Streptococci and Salmonella are associated with sporadic or repeated abortions, early embryonic deaths, mummified and still- born fetuses, in middle-aged or older queens that, as in bitches, may be associated with chronic endometritis and low-grade cystic endometrial hyperplasia. Most of theseDISEASES AND ACCIDENTS OF GESTATION 211 Table 13b. Summary of the Causes of Feline Abortions Infectious Causes Bacterial causes—none. Miscellaneous bacterial causes—coliforms, pseudomonas, staphylococci, streptococci and salmonella. Viral causes—feline panleucopenia virus, feline herpesvirus (feline viral rhinotrachditis), feline leukemia virus (?). Other infectious causes—mycoplasma, Toxoplasma gondii Noninfectious Causes Hormonal causes—progesterone deficiency (?), prostaglandins. Physical causes—severe trauma (?) Miscellaneous causes—genetic defects, parturient conditions and stillbirths. abortions are observed after 4 to 5 weeks of gestation with an apparent greater incidence in short-haired queens.313,14,19’20 These reproductive failures are often accompanied by a prolonged discharge from the genital tract and a history of infertility. Although of question- able value, prompt administration of broad-range anti- biotics may prevent abortion in queens exhibiting signs of impending abortion. Culture of the discharge and sen- sitivity testing might improve the results of treatment. Those with a history of repeated abortions might benefit from antibiotics given for several weeks before and after breeding. This above syndrome, not uncommon in queens, may be associated with immunosuppressive viruses such as the feline leukemia and possibly feline infectious peri- tonitis viruses14 as well as the abnormal uterine changes in older queens due to chronic hormonal stimulation as- sociated with estrous cycling and pseudo-pregnancy and the steroid hormones, progesterone and estrogen.15 Cats are resistant to natural infection with Brucella spp.15 Although when infected they can become urinary shedders of Leptospira spp., abortions do not occur. 1,6 Viral Causes Feline panleucopenia (FPL) virus, a parvovirus, causes embryo resorption, mummified fetuses, abor- tions, stillbirths and cerebellar hypoplasia or aplasia in neonates infected late in gestation.2’3’5’912’14 Signs of ataxia associated with cerebellar dysplasia is often not noted until the kitten is 2 to 3 weeks old. As in parvovirus infection in swine not all fetuses in a litter may become infected. Feline panleucopenia, feline infectious enteritis, or “distemper” is a highly contagious viral infection seen world-wide in all breeds of cats. It is characterized by a marked leucopenia, fever, depression, anorexia, vomit- ing and a profuse diarrhea especially seen in young sus- ceptible kittens after 2 or 3 months of age when they have lost their colostral immunity. Acutely infected an- imals shed virus in all body excretions and for up to one year in the urine. It is easily spread by indirect contact as the virus is very stable. The virus may be recovered by viral isolation from aborted fetuses or demonstrated by immunofluorescence of infected tissues. The serum-neutralization test is used to detect antibody which rises rapidly to reach a high level about 10 days after the onset of illness.2’5’9 The disease may be prevented by vaccination with an inactivated or MLV vaccine or combined FPL and FVR vaccines available commercially. The latter MLV vac- cines should not be used in pregnant queens. After the initial series of vaccinations as kittens, once a year re- vaccination is recommended for maximum protection. Treatment of exposed pregnant and possibly susceptible queens should be with antiserum or normal feline serum at a rate of 1 ml/lb. to provide immediate protection.914 Feline viral rhinotracheitis (FVR) or feline herpes- virus 1 is wide-spread and causes an upper respiratory disease that varies from a subclinical condition to marked respiratory signs and death. It is characterized by sudden onset, pyrexia, leucocytosis, sneezing, coughing, nasal and conjunctival exudate, and anorexia.2’3 51214 Occa- sionally secondary bacterial pneumonia, dendritic ker- atitis, and vulvo-vaginitis may occur. If pregnant sus- ceptible cats become infected about the sixth week of gestation, mummified fetuses, abortion, stillborn or con- genitally infected, weak newborn may result as this fe- line herpesvirus crosses the placental barrier. As with other herpesviruses a carrier or latent infection in the tri- gemimal ganglion often results with recrudescence spon- taneously or at periods of stress such as parturition.7 8 Carriers or acutely infected cats transmit this infection by the respiratory route. This feline herpesvirus 1 is dis- tinct from the herpesvirus virus described as the possible cause of feline urolithiasis.9 Other agents such as feline calici (picoma) virus, feline chlamydial infection (pneu- monitis), reovirus, and Bordetella and Pasteurella also cause respiratory disease in cats that may resemble feline viral rhinotracheitis. Diagnosis of FVR infection can be made by viral isolation from fetuses or placentae, by the fluorescent antibody test or by finding intranuclear in- clusion bodies typically seen in herpes virus infected tis- sues on histopathological examination. Inactivated and212 VETERINARY OBSTETRICS MLV vaccines for intramuscular use and an MLV vac- cine for intranasal and conjunctival administration are commercially available. The MLV vaccines should not be used in pregnant queens. Presently commercial vac- cines combining the feline viral rhinotracheitis and pan- leukopenia viruses are also available. Other feline viruses such as the calici (picoma), feline infectious peritonitis (FIP), reovirus and chlamydial or- ganisms have not been reported to cause abortion in cats.9 In the mid to late 1970’s a wide-spread syndrome oc- curred in a near epizootic manner in many catteries and breeding colonies in the U.S. This kitten mortality com- plex (KMC) was an apparently new disease character- ized by a high incidence of reproductive failures and kit- ten deaths including: repeat breedings and failure of conception, abortions the last trimester of pregnancy, stillbirths, congenital malformations, endometritis and pyometra with a bloody vulvar discharge, chronic upper respiratory disease and conjunctivitis, intermittent py- rexia, acute cardiovascular disease and kittens dying within a few days or weeks of birth.16b,18c Careful studies failed to reveal any bacterial or viral etiologic agent. However, nearly all affected cats were serologically positive for feline infectious peritonitis (FIP). In recent years the in- cidence of this KMC syndrome has greatly declined. Feline leukemia virus (FeLV) is probably world-wide in distribution and causes a number of clinicopatholog- ical syndromes including alimentary, thymic and multi- centric lymphomas, leukemia, anemia, panleucopenia- like syndrome, enlarged kidneys, thymic atrophy and other FeLV immunosuppressive diseases. The FeL virus may be transmitted horizontally, especially in young kittens, or vertically from viremic queens. More often, however, early embryonic deaths and resorptions or abortions have been reported.3 9'101114 Thus even if feline leukemia vi- rus doesn’t actually cause abortion or resorptions it may favor disease processes that produce them. Further stud- ies are needed to delineate the exact role of FeLV in reproductive losses. Unless obvious disease states such as tumors are pres- ent, a diagnosis of feline leukemia-sarcoma complex re- quires laboratory assistance.9 Blood examinations, his- topathological, serological and virological procedure may all be used. The most common simple rapid tests are the immunofluorescent antibody (IFA) test applied to blood smears11 and the commercially-produced ELISA test that can be performed in the veterinary hospital, which detect the FeLV or antigen in the blood. This latter test is more sensitive and may detect transiently infected cats so a second test about a month later is indicated to determine the chronically FeLV infected cat.18b The FOCMA (fe- line oncovirus-associated cell membrane antigen) test for the presence of antibody can help assess the resistance of a cat. On the basis of these and other tests the prog- nosis in a given case may be determined.9 Although work has been undertaken on the develop- ment of a FeLV vaccine, none is presently available. The greatest numbers or incidence of FeLV-infected cats have been found in large breeding catteries; while a much lower percentage of positive cats have been found in one or two cat households or in free-roaming cats. An IFA or ELISA test positive cat is carrying the FeL virus whether it appears healthy or diseased and is probably shedding the virus.911 By using the above tests FeLV- free colonies can be established and maintained by not allowing infected cats into the disease-free colony. This is essential for a breeding cattery. Mycoplasmosis due to M. gateae has been described as a cause of feline abortions at various stages of ges- tation.22 Fungal causes of abortion in cats has not been re- ported. Parasitic Protozoal Causes—Toxoplasmosis due to Toxoplasma gondii was formerly reported in queens as the occasional cause of embryonic resorptions, fetal mummification, abortion and death of neonates, possibly due to transplacemental infections.1,1417,21 A more recent well-controlled study indicated that T. gondii is not likely to be an important cause of abortion or perinatal mor- tality in cats and transplacental transmission could not be demonstrated.3,4a,b However cats can harbor and ex- crete oocysts from their intestinal tract of four coccidial parasites, Toxoplasma, Hammondia, Sarcocystis and Besnoitia.23 Toxoplasmosis in kittens or older cats can easily be clinically confused with other feline diseases.4b Noninfectious Causes for Feline Abortion Recurrent abortions in queens might be due to a pro- gesterone deficiency when other causes cannot be de- termined.13 These abortions usually occur from the sec- ond to seventh week of gestation. It was suggested that 5 to 25 mg doses of progesterone in oil be administered two to three times a week until the eighth week of ges- tation or the repositol form could be used once or twice a week. Further studies might be informative if a number of queens with habitual abortions could be examined throughout pregnancy by hormonal assays. Prostaglandin F2a at doses of 0.5 to 1.0 mg/kg once or, if necessary, twice at 24 hour intervals caused abor- tions in all pregnant cats over 40 days of gestation within 24 or 48 hours, respectively. Queens pregnant 55 daysDISEASES AND ACCIDENTS OF GESTATION 213 or longer gave birth to live kittens, lactated normally and suckled their newborn.16 This treatment in contrast to bitches given prostaglandin, was well tolerated. Another preliminary study24 indicated that PGF2ci alone did not cause abortion in queens in late pregnancy unless com- bined with ACTH. Prostaglandin did not induce abor- tions when administered prior to 40 days of gestation.183 Estradiol cypionate (ECP) in a single dose of 0.25 mg given intramuscularly will prevent conception if given within 1 to 5 days, preferredly about 40 hours after co- itus, if the time of coitus is known.14 This treatment ap- parently retards the passage or locks the fertilized ova in the uterine tubes where they degenerate. Signs of estrus may be prolonged. Repeated estrogenic therapy should be avoided in queens, although they are not as suscep- tible to estrogen toxicity with bone marrow depression and thrombocytopenia as the bitch.183 Nutritional causes of abortion in queens have not been reported. Some feline abortions have been associated with severe anemia or pregnancy toxemia.13 As in other spe- cies genetic or chromosomal defects can cause early em- bryonic deaths, abortions or defective weak neonates. References on Abortion in the Queen la. Bloom, F. (1968) Canine Medicine, Edit, by E. J. Catcott, Amer. Vet. Public Inc., Wheaton, 111., 445. lb. Bruner, D. W. and Gillespie, J. H. (1973) Hagan’s Infectious Diseases of Domestic Animals, 6th Ed., Cornell Univ. Press. Ithaca, N.Y. 2. Catcott, E. J. (1975) Feline Medicine and Surgery, 2nd Ed., Amer. Vet. Publicat. Inc., Drawer KK, Santa Barbara, Cal. 19-26. 3. Colby, E. D. and Stein, B. S. (1982) The Genital System, in Feline Medicine and Surgery, 3rd Ed., edited by E. J. Catcott, Amer. Vet. Publ., Santa Barbara, Cal., In press. 4a. Dubey, J. P. and Hoover, E. A. (1977) Attempted Transmission of Toxoplasma gondii Infection from Pregnant Cats to Their Kittens. JAVMA, 170, 5, 538-540. 4b. Dubey, J. P. and Johnstone I. (1982) Fatal Neonatal Toxoplas- mosis in Cats, J.A.A.H.A.. 18, 461. 5. Ettinger, S. (1975) Textbook of Veterinary Internal Medicine, Diseases of the Dog and Cat, Vol. I, W. B. Saunders Co., Phil- adelphia, London. 6. Fessler, J. F. and Morter, R. L. (1964) Experimental Feline , Leptospirosis, Cor. Vet. 54, 2, 176. 7. Gaskell, R. M. and Povey, R. C. (1977) Experimental Induction of Feline Viral Rhinotracheitis Virus Re-excretion in FVR-re- covered Cats, Vet. Rec. 100, 128-133. 8. Gaskell, R. M. and Povey, R. C. (1979) Feline Viral Rhino- tracheitis: Sites of Virus Replication and Persistence in Acutely and Persistently Infected Cats. Res. Vet. Sci. 27, 167-174. 9. Gillespie, J. H. and Timoney, J. F. (1981) Hagan and Bruner’s Infectious Diseases of Domestic Animals, 7th Ed., Cornell Univ. Press, Ithaca, N.Y. 10. Hardy, W. D. Jr. (1974) Immunology of Onconoviruses, Vet. Cline, of N. Amer. W. B. Saunders Co., Philadelphia, Pa. 11. Hardy, W. D. Jr. (1979) Current Status of FeLV Diseases. Part I, Friskies Research Digest 15, 2, 1-3. 12. Herron, M. A. (1977) Feline Reproduction, Vet. Clin, of N. Amer., 7, 4, 715-722, W. B. Saunders Co., Philadelphia. 13. Holzworth, J. (1964) Personal Communication. 14. Lein, D. H. (1977) Reproduction in Veterinary Medicine, Sem- inar—Wash. D.C. Acad, of Vet. Med. 15. McEntee, K. (1970) Pathology of Domestic Animals, 2nd Ed., by Jubb, K. and Kennedy, P., Academic Press, Inc., N.Y.C. 16a. Nachreiner, R. F. and Marple, D. W. (1974) Termination of Pregnancy in Cats with Prostaglandin F2a. Prostaglandins 7, 303- 308. 16b. Norsworthy, G. D. (1979) Kitten Mortality Complex, Feline Pract. 9, 2, 57-60. 17. Petrak, M. and Carpenter, J. (1965) Feline Toxoplasmosis, JAVMA, 146, 7, 728. 18a. Shille, V. M. and Stabenfeldt, G. H. (1980) Current Concepts in Reproduction in the Dog and Cat, Adv. in Vet. Sci. and Comp. Med. 24, 211-243. 18b. Scott, F. W. (1982) Personal Communication. 18c. Scott, F. W., Weiss, R. C., Post, J. E., Gilmartin, J. E. and Hoshino, Y. (1979) Kitten Mortality Complex (Neonatal FIP?), Feline Pract. 9, 2, 44-56. 19. Sheppard, M. (1951) Some Observations on Cat Practice, Vet. Rec. 63, 44, 685. 20. Spaulding, R. H. (1923) Reproductive Diseases of Cats. Cor. Vet. 13, 4, 312. 21. Siim, J. C., Biering-Sorensen, U. and Moller, T. (1963) Tox- oplasmosis in Domestic Animals, in Advances in Veterinary Science, Vol. 8, Edit, by C. A. Brandley and E. L. Junghess, Academic Press Inc., N.Y.C. 22. Tan, R. J. S. and Miles, J. A. R. (1974) Possible Role of Feline T-strain Mycoplasmas in Cat Abortion. Austral. Vet. J. 50, 142. 23. Wallace, G. D. and Frenkel, J. K. (1975) Besnoitia Species (Protozoa, Sporozoa, Toxoplasmatidae): Recognition of Cyclic Transmission in Cats. Science 188, 369-371. 24. Wyckoff, J. T. and Ganjam, V. K. (1979) Successful Termi- nation of Pregnancy in Cats by the Combination of ACTH and PGF2», Fed. Proc. 38, 1189 (Abstr.). Mummification of the Fetus Fetal death in domestic animals occurring the middle or last third of gestation that does not result in involution of the corpus luteum and abortion of the fetus within the next week or 10 days or decomposition or maceration of the fetus within the next several months, is followed by autolytic changes in the fetus, absorption of placental and fetal fluids, involution of the maternal placenta, and mummification of the fetus. Conditions necessary for the occurrance of fetal mummification include the mainte- nance of the dead fetus within the uterus by the presence of a normal viable fetus or fetuses or the persistence of the corpus luteum of pregnancy associated with a single, or rarely twin, bovine mummified fetuses. One or more mummified fetuses present in the uterus with one or more214 VETERINARY OBSTETRICS Figure 71. Mummification of twin, bovine, 3-month-old fetuses. These were spontaneously aborted at four months of gestation. normal viable fetuses is observed frequently in sows, oc- casionally in bitches and queens and uncommonly in ewes, does, cows and mares. Fetal mummification associated with a persistent corpus luteum is observed in the cow, doe, sow and bitch. The maintenance of pregnancy in these species is due to progesterone produced by the cor- pus luteum. In the other species progesterone is pro- duced by the fetal placenta or chorion after midgestation and the corpora lutea involute. Fetal mummification ap- parently does not occur the first trimester of gestation because embryonic or fetal death prior to the develop- ment of the fetal bones usually is followed by resorption of the fetal and placental tissues. Fetal death the last month or six weeks of gestation with beginning fetal mummi- Figure 72. Removal by cesarean section of a bovine mummified fe- tus that died at 7 months of age. fication may be undiagnosed at parturition and called a stillbirth, especially in multiparous animals. Williams19 described some of these fetuses in cows as “static fetal cadavers.” Fetal mummification may occur and subse- quently bacteria may invade or gain entrance to the uterus and cause secondary maceration of the uterine contents. Two types of fetal mummification have been de- scribed in animals, the hematic type in cattle and the papyraceous type in all the other species. The process by which these two types form are basically similar. In cows as the maternal placenta or caruncle undergoes in- volution a variable amount of hemorrhage occurs be- tween the endometrium and fetal membranes which after the plasma has been absorbed leaves a reddish-brown, gummy, tenacious mass of autolyzed red cells, clots and mucus. This imparts a reddish-brown color to the fetal membranes and fetus. A similar discharge of blood from the caruncles is noted in normal parturient cows 10 to 14 days after calving and is characterized by a bloody genital discharge. The similarity between the tenacious sticky reddish mucus around the membranes of the bo- vine mummified fetus and that found in the rectum fol- lowing intussusception of the intestine in cattle is strik- Figure 73. Death and mummification of a bovine fetus due to the displacement of the umbilical cord around the neck of the fetus.DISEASES AND ACCIDENTS OF GESTATION 215 Figure 74. Porcine fetal death and mummification at different times in gestation and a stillbirth, with abortion of the uterine contents near term. This might possibly have been due to a parvo-, entero-, or pseu- dorabies virus. ing. In the other species mummification is not char- acterized by placental hemorrhage and the fetus is usu- ally a brownish color and the fetal membranes are not covered with this reddish-brown tenacious material. In both types of mummification the longer the condition exists the greater the loss of fluids from the placenta, the membranes and the fetus. Mummification of the bovine fetus is observed most often in Guernsey cattle although other breeds are com- monly affected. The condition usually affects single fe- tuses but may occasionally involve one or both fetuses in twin pregnancies. Bovine fetal mummification occurs during the third to eighth month of gestation but most commonly the fourth, fifth and sixth months (See Fig- ures 71, 72, 73). If the condition is undiagnosed the mummified fetus may remain in the uterus for months beyond a normal gestation period. Spontaneous abor- tions before, near, or after the expected end of gestation are not uncommon. In one study of 32 mummified fe- tuses in one herd the range of the “gestation,” period from conception to spontaneous abortion, was 131 to 342 days with an average of 215 days.5 The sex of mum- mified fetuses are nearly equally divided between males and females.11 No premonitory signs are observed before the expulsion of a mummified fetus except occasionally those of estrus. The causes of fetal death and mummification in cattle are often the same as causes for fetal death and abortion. The cause of fetal mummification is often impossible to determine because the time of death is not known and autolysis and mummification of the fetus and mem- branes makes isolation and determination of the causa- tive agent difficult or impossible. Serologic tests of the dam weeks or months after fetal death are usually of little diagnostic significance. Fluorescent antibody stain- ing of tissues have been helpful in some cases. Genetic factors may be involved in bovine fetal mum- mification.11 There is a greater incidence in the Guernsey and Jersey breeds of cattle. Certain cow families will have mummified fetuses in two to four generations of cows bred to apparently unrelated males by artificial in- semination. In these and other studies the male did not seem to play a causative role in the genetic inheritance of this condition. However, one report16 suggested that abortions and fetal mummification experienced in a Hol- stein herd at 120 to 180 days of gestation when daugh- ters of two popular sires were mated artificially to the other sire were due to autosomal recessive genes. In an- other large Holstein herd5 the heritability of fetal mum- mification was only 16 percent when the service sire was excluded and the condition was not transmitted as a sim- ple recessive. When the owner used other bulls on these cows the losses stopped. Further evidence that this con- dition may be due to an inherited endocrine or other de- fect of certain cows is the fact that as many as 20 to 50 percent, average 30 percent, of subsequent conceptions in cows that have had mummified fetuses may result in fetal mummification whether the same or different sires were used.1' The author observed one Guernsey cow that had 5 normal calves and 5 mummified calves within a period of 9 years. In such cows abortions at midgestation not associated with fetal mummification are quite com- mon. The possibility of a latent virus or organism resid- ing in the uterine or other body tissue or cells and caus- ing the repeated occurrence of mummified fetuses in the same individual should possibly be considered although evidence for this has not been reported. Rare cases of mummified anomalous calves are recorded. Other causes for bovine fetal mummification include216 VETERINARY OBSTETRICS torsion of the umbilical cord or compression of the um- bilical cord by its passing around a fetal extremity (See Figures 66 and 73). This causes fetal death. Fetal mum- mification may then occur instead of prompt abortion. There is evidence that fetal mummification may follow infectious causes of fetal death such as C. fetus, molds, leptospirosis, IBR and BVD-MD virus.8'9*’11 Leptospi- rosis and BVD-MD virus may account for the occasional epizootic outbreaks of fetal mummification in a herd. Fetal death and a degree of mummification may occur in animals in which the duration of gestation has been prolonged by progesterone or progesterone-like com- pounds. Torsion of the uterus and trauma are not con- sidered to be causes of fetal mummification. Wound in- fection organisms causing an inflammatory response in the endometrium with possible release of prostaglandins are characterized by fetal death and prompt abortion and not by fetal mummification. Almost all mummified fe- tuses and uteri when examined and cultured are sterile and free of organisms and the endometrium is involuted and no inflammatory lesions are present. This is further substantiated by the observations that cows usually con- ceive the first or second estrum after the expulsion of the mummified fetus. The causes of fetal mummification in the other species should be noted as these might pro- vide leads for explaining the causes of the condition in cattle. As the fetus mummifies and fetal and placental fluids disappear, the uterine walls contract and tightly enclose the conceptus. The longer the condition exists, the dryer, firmer, and more leather-like the tissues of the fetus be- come. In the cow the uterine walls are fairly thick and no cotyledons are palpable. The uterine artery is small and has no fremitus. Fetal mummification in the cow is characterized by failure of estrum with a persistent cor- pus luteum. It is usually not suspected until late in ges- tation or until after the normal length of gestation, when normal development of the fetus, body and udder changes incident to parturition and calving fail to occur. Al- though the uterus may be drawn forward by the weight of the mummified fetus and a normal cervical seal may be present, a careful rectal examination will readily re- veal the nature of the disease. If the uterus is dropped downward out of reach it may be pulled up to the pelvic cavity manually by grasping the cervix or intercomual ligament, by placing Knowles cervical forcepts on the cervix and drawing the uterus back, or by having two men raise the caudal abdominal viscera by means of a pipe or bar held by each of them. Rarely a large mum- mified fetus may be ballotted through the flank. In cases where the uterus is examined very early after the death of the fetus and the occurrence of the interplacental hem- orrhage, the former feels distended by a doughy mass, which is the large, soft blood clot. The fetus is not easily palpated in this doughy mass within the contracting uterus. Within a few weeks the typical changes associated with fetal mummification in the cow become apparent. The bovine fetal mummy remains in this semi-moist state without odor or pus until spontaneous abortion re- sults in from 1 to 2 months to 1 to 2 years, or until the condition is diagnosed, treated, and corrected, or the an- imal is slaughtered. If spontaneous abortion occurs, the fetus may be expelled into the vaginal cavity and a por- tion of the dark brownish-red stained fetal membrane hangs from the vulva until noticed by the caretaker or owner. Estrum usually occurs about the time of the spon- taneous abortion and the cow will come into estrum again 16 to 24 days later. If the fetus should be large and pas- sage through the dilated cervix is not possible then fetal maceration may occasionally result. In large fetuses te- nesmus or straining, as noted in other abortions, may be observed. The incidence of fetal mummification in cattle is low and sporadic. In three large herds the incidence was 0.43 to 1.8 percent of the pregnancies.11 In some herds the incidence may be higher and in a few instances apparent epizootics of mummified fetuses may occur. To expel the mummified fetus in the cow the simplest treatment is to administer 50 to 80 mgs. of stilbestrol or 5 to 10 mg. of estradiol intramuscularly. The injected estrogen causes contraction of the uterine muscles, re- laxation of the cervix, involution of the corpus luteum and results in the expulsion of the fetus. In about 80 percent or more of the cases this single injection of an estrogen is all that is required and the fetus is expelled within 37 to 72 hours. If the fetus has not been expelled within this time, a similar dose of estrogen may be ad- ministered a second time. In unusual instances 3 or more doses at 48-hour intervals may be needed. Some veter- inarians use repositol diethylstilbestrol, 100 to 150 mg., intramuscularly. In one study of 50 cows with mum- mified fetuses, daily injections of estrogens were given and all expelled the fetuses in 3 to 11 days.17 Occasion- ally examination of a cow either after treatment or before will reveal the fetus entering into or wedged in the cervi- cal canal, with the cervix not yet dilated sufficiently to allow passage. Administration of a single large dose of estrogen at this time usually results in successful dilation of the cervix and the expulsion of the fetus within 24 to 36 hours. When the fetus is large, or mummification oc- curs at 6 to 8 months of gestation, or the cow is small or immature, the genital tract should always be exam- ined within 48 to 72 hours after the injection to make certain failure of expulsion or dystocia does not occurDISEASES AND ACCIDENTS OF GESTATION 217 with secondary infection of the uterus, closure of the cer- vix and maceration of the fetus. Occasionally a second dose of estrogen, much lubrication, gradual traction with a snare or Knowles cervical forceps by one hand and pushing on the fetus with the other hand in the rectum, may be needed to help remove the fetus. In recent years a number of reports have indicated that the injection of prostaglandin or its analogues in luteo- lytic or somewhat larger doses intramuscularly such as 25 to 50 mg of prostaglandin F2a or 500 ug cloprostenol (Estrumate), caused the involution of the corpus luteum and the expulsion of the mummified fetus 72 to 120 hours later.71718 Plasma progesterone levels dropped rapidly from about 10 ug/ml to 1 ug/ml and estradiol levels were low about 3 pg/ml during the postinjection sam- pling period. However in most reported cases it was nec- essary to withdraw the fetus from the cervix and cranial vagina by traction due to the incomplete relaxation and dilation of the vagina and vulva. Possibly the combi- nation of estrogens and prostaglandin would be more ef- fective in producing expulsion of the mummified fetus and relaxation of the genital tract. Further studies are indicated as in some cases after prostaglandin therapy and rare cases after estrogen therapy the corpus luteum would involute but the mummified fetus would not be expelled.1117 Glucocorticoid treatment of cows with mummified fetuses failed to induce luteolysis and ex- pulsion of the mummy. A live fetus is necessary for dexamethasone to effect abortion or premature deliv- ery.1,lb'17 Removal of the persistent bovine corpus luteum of pregnancy will usually result in estrum and evacuation of the uterus. There is the added danger of trauma and damage to the ovary by the forceful or surgical removal of the deeply imbedded corpus luteum of pregnancy. It has been found that massage of the uterus daily for sev- eral days frequently provides enough stimulus to cause evacuation of the uterus. Manual dilation of the cervix is not indicated. It has been reported that filling and dis- tending the vagina with cotton will cause the expulsion of a mummified fetus. The author has had no experience with this method of treatment. It is possible that manual uterine massage or distention of the vagina stimulate the release of oxytocin and prostaglandin to effect expul- sion. In exceptional cases in which the affected animal is a small heifer, or the fetal cadaver is very large or previous treatment has been unsuccessful, a cesarean op- eration through either the right or left flank is usually successful in correcting the condition. Following treatment and expulsion of the mummified fetus, most cattle recover promptly since no infection is present to delay recovery. Conception usually occurs within 1 to 3 months. Any cow with a history of having one mummified calf may abort at 3 to 8 months of ges- tation or have another one at any gestation period; hence the prognosis should always be guarded. Fetal mummification in horses occurs seldom and has only been reported in one of twin fetuses that has died during pregnancy probably due to a lack of placen- tal area. The equine mummified fetus remains in the uterus only as long as pregnancy is maintained by the viable twin.12 Since spontaneous abortion of twin fetuses is common in mares the discrepancy between the size and development of the partially mummified fetus and re- cently dead fetus often leads to the improper diagnosis of superfetation. Mummification of both fetuses in a twin pregnancy has not been reported in the mare. Fetal mummification in sheep is occasionally ob- served as affecting single ovine fetuses or one or both twin fetuses. It has been associated with and probably caused by infections in sheep causing fetal deaths and abortions. These include: toxoplasmosis, EAE (Enzootic abortion of ewes or Chlamydiosis), Listeria monocy- togenes, possibly L. pomona and unknown causes as- sociated with prolonged gestation." In does, as in ewes, fetal mummification is uncom- mon but it has occurred affecting one of twin fetuses in chlamydiosis, in toxoplasmosis, in Border Disease (BVD) and possibly in Coxiella infection.1314’15 Two rare cases were reported in does. One was a case of twin hybrid mummified fetuses resulting from a mating of a ram and a doe and the other in a doe that ingested a toxic dose of Japanese pieris.13,14 Fetal mummification in swine is an important cause of prenatal losses. Fetuses dying in utero from 40 to 90 days of gestation usually mummify and are expelled at parturition along with the normal fetuses. In a herd rel- atively free of disease, single mummified fetuses in a litter were more common than two or more.10 In three breeds of pigs in this herd, Berkshire, Chester White and Yorkshire, the percentages of mummified pigs were 4.97 and 1.95 and 1.08, respectively. The high incidence of mummified fetuses in Berkshires in this herd accounted in part for the smaller litter size in this breed. Single mummified fetuses were more common in large litters. The presence of occasional mummified fetuses were not related to the incidence of stillbirths. The cause of these occasional mummified fetuses in certain litters is not known. Epizootic herd outbreaks of abortions, early em- bryonic deaths, mummified fetuses and stillbirths have been described in swine (See Figure 74). A high inci- dence of mummified porcine fetuses has been reported due to the following viruses: Aujesky’s or pseudorabies, Japanese encephalitis B, Japanese hemagglutination, hog218 VETERINARY OBSTETRICS cholera, picorno or entero-viruses,3'4 parvovirus, reo- virus, cytomegalovirus and possibly swine influenza vi- rus. Fetal mummification also occurs due to leptospi- rosis in pregnant sows (see abortion in swine). In these viral diseases mummification, when it affected all or nearly all of the fetuses, occasionally resulted in a pro- longed gestation period.13 Following outbreaks of the above viral diseases, affected sows usually conceive promptly and produce normal litters. A natural immunity is apparently produced. Fetal mummification in dogs and cats is uncommon and sporadic in nature but apparently similar to that seen commonly in swine where one to three mummified fe- tuses are expelled with normal neonates at the time of parturition. Occasionally in the bitch and more often in the queen the uterus may rupture in late gestation due to torsion or trauma and some fetuses escape into the ab- dominal cavity and mummifyla'9b (see Extra-uterine Pregnancies and Fetuses). Fetal Maceration Maceration may occur at any stage of gestation and has been observed in all species. It is described most often in the cow. (See Figures 75 and 76.) When the fertilized ovum or embryo succumbs to bacterial or viral infection or other disease or abnormality early in ges- tation it is usually absorbed in the uterus or a slight and often insignificant purulent uterine or vaginal discharge may be evident. The embryo is seldom observed. The interval between estrual periods may be prolonged if the embryo did not succumb until 20 to 50 days after con- ception. Early embryonic death and maceration are prob- Figure 75. Maceration of a 4-month-old bovine fetus. Figure 76. Bones of a 6-months-old macerated bovine fetus in the uterus. Note the thickened uterine wall and degenerated fibrotic en- dometrium (Courtesy K. McEntee). ably caused by a variety of miscellaneous organisms that may be found in the uterus, and are of common occur- rence in cows affected with trichomoniasis or vibriosis. In occasional cases of pyometra seen in trichomoniasis, fetal shreds and placental remnants are often found float- ing in the purulent exudate. In cases of early fetal macer- ation the cervix may be tightly sealed or some discharge of pus may be evident in the vagina or from the vulva. These cases usually are diagnosed and treated as pyom- etra or endometritis. In the former, estrum is not present; in the latter estrum may occur. In multipara, maceration of early embryos and fetuses usually ends in their being absorbed. The other fetuses develop normally or occa- sionally some become macerated in turn by the extension of the infection. Rarely in cows, ewes, does and mares one fetus may die the first half of gestation and macerate and be expelled with the placenta and the normal twin at parturition. In the cow fetal maceration that occurs after the third month of gestation, by which time fetal bones are fairly well developed, may be caused by wound-infection type bacterial agents, especially C. pyogenes. Septic metritis of pregnancy, resulting in the death, emphysema, and maceration of the fetus in a closed uterus, is uncommon. It may be caused in the cow by the death or mummifi- cation of the fetus, followed by a dilation of the cervix and an incomplete abortion and/or dystocia usually oc- curring from the middle of gestation to near term. The symptoms of septic metritis of pregnancy are similar to septic metritis after parturition. The condition may be more serious or fatal due to the presence of the decom- posing fetus(es), failure of the cervix and genital canal to dilate normally, and a uterine inertia.DISEASES AND ACCIDENTS OF GESTATION 219 In rare instances fetal emphysema and maceration may be associated with uterine torsion during gestation. The two factors of an open cervix and a dead fetus at body temperature cause a rapid bacterial invasion of the fetus and membranes of organisms already present in the uterus or from the more caudal portions of the reproductive tract. Fetal emphysema and maceration follow. If the bovine fetus is beyond the third month of pregnancy and if the usual expulsive efforts are not observed or are unsuc- cessful, the fetus develops emphysema in 24 to 48 hours and in 3 to 4 days maceration begins. If fetal emphysema and maceration develop in a fetus late in gestation, the handling or treatment of the case is the same as similar cases occurring as a sequelae to an ordinary dystocia at or near term and will be described later under the han- dling of dystocia. Because of the relatively smaller size of the fetus, those cases of fetal emphysema and maceration accompanying an abortion during the middle period of gestation are treated differently. Usually these cases have a history of intermittent straining for several days accompanied by a foul, fetid, reddish-grey vulvar discharge. The temper- ature and pulse are often elevated. Anorexia and drop in milk production may be present. Occasionally diarrhea is present. Palpation per vagina or rectum of a distended, swollen fetus with gas crepitating in the tissues is di- agnostic of fetal emphysema. In bovine abortion from the fourth to seventh month with fetal emphysema, the fetus usually may be removed by careful and gradual traction if the cervix is sufficiently dilated and much lu- brication is used. In the mare the cervix may be carefully dilated manually prior to removal of the decomposing fetus. After removal the uterus should be reexamined to make certain another fetus is not present and to remove the placenta if possible. Aftercare is similar to that de- scribed for septic metritis and retained placenta. In those few cases in cattle in which the cervix is contracted and the fetus cannot be removed, heroic treatment is not in- dicated. Supportive treatment consisting of antibiotics and sulfanomides parenterally along with large doses of es- trogens, 50 to 100 mg. of stilbestrol or 5 to 10 mg. of estradiol daily or every other day for perhaps 4 to 7 days, is administered until the cervix is relaxed enough or the fetus is macerated sufficiently to effect its removal in its entirety or in pieces without injury to the cow. With this treatment the danger of excessive traction or fetotomy causing lacerations or rupture of the cervix and uterus is avoided. Because the uterus and its contents are rela- tively small the development of a septic metritis and a severe toxemia is prevented by the supportive therapy. Cesarean section should be considered as a last resort in the cow, ewe and doe but is seldom required. The ani- mal should not be rebred for at least three to four months and the outlook for her reproductive life is guarded. Af- tercare and treatment of the infected uterus is necessary. In long-standing cases of fetal maceration the acute emphysematous stage has passed, straining is seldom observed, and the cervix is usually contracted. Gener- alized symptoms of elevated temperature and pulse and anorexia are not present. There is often a history of a chronic, fetid, mucopurulent discharge from the vulva over a period of several weeks or months. Only rarely is the cervix sealed. There may be a history of a gradual drop in milk flow and a loss of weight. The presence of diarrhea is variable. Diagnosis in the bitch and queen is aided by abdominal palpation, for loss of fluids and crepitation, and radiographs besides observing the other symptoms. Radiographs in the bitch, queen, and possi- bly the ewe, doe and sow may reveal late fetal death and maceration by the presence of fetal gas and cranial bone overlap. In the bitch dead fetuses curl into a posture re- sembling the letter C.6 In the bitch and queen laparo- hysterotomy or hysterectomy may successfully correct fetal maceration and the former operation may be fol- lowed by conception.2 In most cases no external symp- toms of illness are noted except possibly a uterine dis- charge appearing occasionally at the vulva. On rectal examination in the cow or mare, fetal bones may be pal- pated in the uterus either floating in pus or crepitating against each other with some exudate around them. The uterine wall is thick and heavy and the cervix is usually large and hard. In these cases severe degenerative and sclerotic changes have occurred in the endometrium. The prognosis is poor. Treatment in the cow is dif- ficult. If much pus is present, treatment as for pyometra is indicated and possibly the bones may be passed through the cervix with the pus. More often the amount of pus is slight and the condition has existed long enough so that the bones are deeply imbedded in the endometrium and uterine wall. The cervix is hard and indurated and not dilatable even with estrogens and prostaglandins. La- parohysterotomy is difficult because of the small size of the uterus and its infected contents. It is seldom indi- cated and then only as a last resort in a valuable cow, since the future breeding life of these cattle is very ques- tionable. The longer the condition has existed the greater the damage to the endometrium and the poorer the prog- nosis. In most cases in cattle, slaughter is recommended. In multiparous animals hysterectomy or hysterotomy may be performed, depending upon the circumstances. In rare instances fetal emphysema and maceration may cause a local perimetritis or even rupture of the uterus, with the macerating fetus being walled off in the abdom- inal cavity where it may remain indefinitely; or the mass220 VETERINARY OBSTETRICS may slough through the abdominal floor, into the rumen or into the rectum. In rare cases, torsion of the uterus may cause a similar condition in the cow and multipara. References Fetal Mummification and Maceration la. Bark, H., Sekeles, E. and Marcus, R. (1980) Extra-uterine Mum- mified Fetus in the Cat, Feline Pract. 10, 3, 44-47. lb. Coggins, E. G. and First, N. L. (1977) Effect of Dexamethasone and Methallibure on Gestation, J. An. Sci. 44, 1041-1049. 2. Colby, E. and Stein, B. S. (1975) (1982) The Genital System, in Feline Medicine and Surgery, edited by C. J. Catcott, Amer. Vet. Publ. Inc., Santa Barbara, Cal. 3. Dunne, H. W., Gobble, J. L., Hokanson, J. F., Kradel, D. C. and Bubash, G. R. (1965) Porcine Reproductive Failures Asso- ciated with a Newly Identified “SMEDI” Group of Picoma Vi- ruses, Amer. J. Vet. Res. 26, 115, 1284. 4. Dunne, H. W. and Hokanson, J. F. (1963) A Modem Approach to Abortion and Stillbirth Problems in Swine, Proc. Book AVMA, 54. 5. Erb, R. E. and Morrison, R. A. (1957) Effect of Mummified Fetuses on the Prolificacy of Holsteins, J. Dairy Sci., 40, 1030. 6. Farrow, C. S., Morgan, J. P. and Story, E. C. (1976) Late Term Fetal Death in the Dog: Early Radiographic Diagnosis. Am. Vet. Radiol. Soc., Iowa, 17, 14. 7. Jenkins, A. L., Youngquist, R. S., Elmore, R. G., Kesler, D. J., Garverick, H. A. and Bierschwal, C. J. (1977) Response of Two Cows with Mummified Fetus to Treatment with Clopros- tenol. Theriog. 7, 4, 251-257. 8. Kahrs, R. (1970) Personal Communication. 9a. Miller, R. B., Smith, M. W. and Lawson, K. F. (1978) Some Lesions Observed in Calves Bom to Cows Exposed to the Vims of Infectious Bovine Rhinotracheitis in the Last Trimester of Ges- tation, Can. J. Comp. Med., 42, 438-445. 9b. Nicholl, T. K. (1979) Extrauterine Fetuses in a Bitch, Canine Pract. 6, 4, 16-22. 10. Pond, W. G., Roberts, S. J., Dunn, J. A. and Willman, J. P. (1960) Late Embryonic Mortality and Stillbirths in Three Breeds of Swine, J. An. Sci. 19, 3, 881. 11. Roberts, S. J. (1962) The Enigma of Fetal Mummification, JAVMA, 140, 7, 691. 12. Roberts, S. J. (1978) Twin Pregnancy in a Mare: A Live Foal and a Mummified Fetus, Cor. Vet. 68, 196-198. 13. Smith, M. C. (1979) Fetal Mummification in a Goat Due to Jap- anese Pieris (Pieris Japonica) Poisoning, Cor. Vet. 69, 85-87. 14. Smith, M. C. (1980) Caprine Reproduction, in Current Therapy in Theriogenology, edited by D. A. Morrow, W. B. Saunders Co., Philadelphia. 15. Smith, M. C. (1982) Personal Communication. 16. Stevens, R. W. C. and King, G. J. (1969) Genetic Evidence for a Lethal Mutation in Holstein Friesian Cattle, J. Hered. 59, 6, 366. 17. Vandeplassche, M., Bouters, R., Spincemaille, J. and Bonte, P. (1974) Induction of Parturition in Cases of Pathological Gestation in Cattle, Theriog. 1, 3, 115-121. 18. Wenkoff, M. S. and Manns, J. G. (1977) Prostaglandin Induced Expulsion of Bovine Fetal Mummies, Can. Vet. J. 18, 44-45. 19. Williams, W. L. (1943) Diseases of the Genital Organs of Do- mestic Animals, 34d Ed., Ithaca, N.Y. Prevention of Conception after Mismating and Induced or Artificial Abortion in Domestic Animals Induced or artificial abortion or preventing of concep- tion is occasionally desirable in veterinary medicine from an economic or therapeutic standpoint. For example if a purebred female is bred by accident to a scrub male or a male of another breed, or if a female is bred at too young an age, induced abortion is often indicated. The earlier this abortion is brought about, the less time is lost in the female’s reproductive life and the fewer compli- cations that may arise. Abortions are often desirable in meat-producing animals upon entering the feed lots. If the owner of an animal requests an abortion there are no legal complications to consider as in human medicine. Induced abortion by the administration of hormones has also been discussed under the causes for abortion in each species. Prevention of conception following accidental breeding will now be considered. The most conservative methods of preventing concep- tion or producing abortion should be used. Heroic mea- sures while often effective may adversely affect the an- imal’s health or its future potential as a breeding animal. Prevention of conception following an accidental or unwanted service is best accomplished in animals by the injection of an estrogen within 24 to 48 hours after the undesired service. In the cow or heifer 40 to 80 mg. of stilbestrol or 5 to 10 mg. of estradiol intramuscularly usually prevents conception. In the mare this dose should be repeated 48 hours later. In the bitch 0.1 mg/10 lb of body weight up to a maximum of 1.0 mg. of estradiol cypionate (ECP) may be given intramuscularly8,9 9 to 12 days after the onset of proestrus bleeding, 3 to 5 days after the onset of estrus or within 1 to 2 days after a mismating. Rarely toxic or fatal complications due to bone marrow depression may arise even with the modest but effective dose recommended. Estrogens are probably contraindicated in valuable bitches.8,9,12 Estrum is usu- ally prolonged 2 to 10 days. In the queen mismating may be treated with 0.25 mg. of estradiol cypionate (ECP) about 40 hours after coitus or from 1 to 5 days after the cessation of estrus. As in the dog this dose may be re- peated but excessive doses of estrogens are contraindi- cated.7,9 Conception fails to occur after estrogen therapy due either to the locking or slowing of the passage of the fertilized ovum through the uterine tube,7 its too rapid passage through the uterine tube and uterus, or else to the production of an uterine environment inimicable to the development of the early embryo. The practice of douching female animals with mild antiseptics immediately after service often fails to pre- vent conception because in the cow, sperm cells reach the pavilion of the oviducts in less than 4-1/2 minutesDISEASES AND ACCIDENTS OF GESTATION 221 and in other species it is apparently only a matter of min- utes for some of the spermatozoa to reach the oviducts and hence out of reach of the antiseptic douche fluid. There is no need or reason for a veterinarian to attempt to “separate” copulating dogs even when this is desired by the owners. This is difficult, dangerous and often highly embarrassing. By the time the dogs are separated sperm cells have advanced into the cranial portions of the uterus. In the bitch, a number of steroidal, usually progesta- tional, compounds have been used to prevent pregnancy in the past, but have proven unsatisfactory because they produced uterine disease.3,12 Presently megestrol acetate is satisfactory for use for short periods of time at a dose level of 0.25 mg/lb. daily for 30 days to prevent the development of estrus. It is also administered at a dose level of 1.0 mg/lb. for 8 days beginning during the first 3 days of proestrual bleeding and vulvar swelling to pre- vent ovulation and corpora lutea formation. This latter treatment usually shortens the interval between estrous periods to 3 to 5 months.3,12 Mibolerone, a potent or- ally-active synthetic androgen is now approved for long term estrus prevention in the bitch. Daily administration at a dose rate of 60 to 200 ug daily is required and treat- ment may be continued for up to two years.3,412 Side effects are minimal and consist of enlargement of the clitoris, vulvo-vaginitis and occasionally a worsening of seborrhea if this condition is present. These effective steroidal compounds suppress the release of gonadotro- pins and stop the estrous cycle by preventing follicle for- mation, ovulation and the formation of corpora lutea. Less research has been done with the use of steroids as contraceptive agents in queens. The administration of progestational compounds in cats causes less uterine dis- ease than in dogs. Mibolerone (19-norandrogen) is not approved for use in the queen, although daily oral doses of 50 ug prevent estrus.3,4 These and even smaller doses cause thyroid dysfunction, clitoral hypertrophy and he- patic dysfunction. Megestrol acetate (Ovaban) at a dose of 5 mg/day for 3 days and then 2.5 to 5 mg/week has suppressed estrus in young queens for over a year. Even queens in estrus will go out of estrus after 3 days on megestrol acetate. This product should not be used in cats with infections of the genital tract.9 Since the queen is an induced ovulator, one can apply coital stimulus with a vasectomized tom cat or a pseudocoital stimulus with a sterile rod or swab inserted into the vagina during es- trus. Also 25 units of HCG (human chorionic gonado- tropin) per lb. of body weight can be administered to induce ovulation which is followed by a diestrus or pseu- dopregnancy that lasts for 35 to 45 days.3,5 Progesterone- like agents used for prolonged periods in dogs have pro- duced cystic degeneration of the endometrium and sec- ondary endometritis and pyometra. They are of no value in preventing conception after coitus, in fact some of these agents actually promote conception and mainte- nance of pregnancy if given at this time. Experimentally in cattle the injection of oxytocin, 100 to 200 I.U. daily from day 2 to day 7 after estrus causes an inhibition of the growth and development of the cor- pus luteum and its secretion of progesterone necessary to maintain pregnancy. Usually cattle treated in such a manner return to estrus in 8 to 10 days. Thus this treat- ment should also prevent conception in bovine animals bred accidentally. In areas such as India where bulls and cows are not confined and the amount of feed available is limited, the value of a small stainless steel spring similar to a “bobby pin” inserted into the cervix of a heifer or cow and re- maining indefinitely has been demonstrated.11 Although under these conditions estrous cycles, coitus and con- ception may occur, abortion results due to the failure of the cervix to be able to seal itself properly. This tech- nique was an early application of the presently widely accepted intrauterine devices (I.U.D.) used in women to prevent conception. Depending upon the species of an- imals the I.U.D.’s prevent fertilization, prevent implan- tation or interfere with normal corpus luteum develop- ment. Intravaginal or preputial devices to prevent conception have not proven satisfactory for general use.3 Ovariec- tomy effectively suppresses the estrous cycle and to- gether with castration or vasectomy prevents conception in all domestic animals. The induction of abortion in domestic animals fol- lowing conception can be accomplished in a variety of ways depending on the species of animal, the duration of pregnancy, the desires of the owner and the ease of inducing abortions by physical, hormonal or surgical procedures. Generally the earlier in gestation an abortion is induced, the simpler and easier it is for the dam and the veterinarian and fewer complications will arise. In- ducing abortion after midgestation or early in the third trimester should generally be discouraged because of the difficulties in the induction and the problems of delivery and aftercare of the dam. (See Induction of Parturition.) Douching the uterus by means of a catheter or pipette with antiseptics such as 1 to 2 percent Lugol’s solution, 200 ppm. chlorine solution, dilute acetic acid or 2 to 3 percent potassium permanganate solution or even saline 7 to 20 days or longer after service in the cow or mare, is often successful, possibly by also introducing bacteria to cause an endometritis, and destroying or expelling the developing ovum or embryo. Injecting of irritating so- lutions such as dilute Lugol’s solution around the third to sixth day after service in the cow may result in similar changes as produced by the injection of oxytocin with a222 VETERINARY OBSTETRICS shortened time between estrous periods due to the re- lease of prostaglandins from the endometrium resulting in luteolysis. In mares abortion may be produced readily up to 8 months of gestation by manual dilation of the cervix in a sterile manner and injecting several hundred ml. of dilute Lugol’s solution or other suitable mild an- tiseptic. One author14 aborted over 100 army remount mares by injecting 500 ml of sterile iodized oil or phys- iological saline into the gravid uterus. Possibly manual dilation alone would be sufficient in the mare. Aborting mares with fetuses over 8 months of age may cause in- jury or result in infection or dystocia in the mare. Douching the uterus and dilating the cervix is not prac- tical or possible in the ewe, bitch, sow or cat. Injection of hormones to induce abortion has been reported in all species of domestic animals. The usual hormones used in early to midgestation are estrogens, prostaglandins and possibly cortisone (dexamethasone). The use of these hormones for inducing abortion has been described previously in this Chapter under abortion in the various species. Often a combination of several hor- mones is superior to a single product. Following these treatments the veterinarian should follow each case to be certain abortion occurred and no complications such as dystocia, fetal maceration or uterine infection devel- oped. Although seldom used at this time manual removal of the corpus luteum of pregnancy in the cow per rectum invariably results in abortion in about 3 to 5 days. Since there is some danger of hemorrhage and ovarian and uterine adhesions following manual removal or enuclea- tion of the corpus luteum in the cow, and early invo- lution and luteolysis is readily produced by estrogens and prostaglandins, the latter products have replaced the for- mer hazardous procedure. Removal of the corpus luteum during early pregnancy in the mare or other domestic animals is not possible except by laparotomy and ovari- otomy. Manual rupture of the amnionic vesicle in the cow and the chorionic vesicle in the mare with destruction of the embryo or fetus is possibly by digital manipulation through the rectal wall from 30 to 100 days of pregnancy in the cow and 17 to 40 days in the mare as described previously under physical causes of abortion in the cow and mare. It was interesting to note that in single bovine pregnancies when the embryo was destroyed that “preg- nancy” continued and the membranes grew for 2 to 3 weeks following the rupture of the amnionic vesicle.1'2 Estrus seldom occurred until 30 or more days after in- ducing embryonic death.1'2’13 Manual destruction of one of twin embryos was reported to be successful in the mare6 but in the cow when one embryo was manually destroyed, the other also succumbed.13 The re-establishment of a normal estrous cycle within 2 or 3 months in the mare after terminating pregnancy after 40 or more days of gestation is very unlikely. The endometrial cups and their secretion of PMSG have an adverse effect on the initiation of normal follicle devel- opment, ovulation and the normal expression of regular periodic estrous signs in the mare. The timed induction of parturition in the later stages of pregnancy by the use of glucocorticoids and prosta- glandins in cows, sows, ewes and does, and oxytocin in mares have been described briefly under abortion in the various species and will be discussed in greater detail under parturition. Prevention of Conception and Induced Abortion 1. Ball, L. and Carroll, E. J. (1963) Induction of Fetal Death in Cattle by Manual Rupture of the Amniotic Vesicle, JAVMA, 142, 373. 2. Ball, L. and Carroll, E. J. (1968) Rupture of the Amniotic Ves- icle, in Abortion Diseases of Livestock, edit, by L. Faulkner, C. C. Thomas Inc., Springfield, 111. 3. Burke, T. J. (1979) Birth Control for Dogs, D.V.M. Magazine, 10, 6, 9-12. 4. Burke, T. J., Reynolds, H. H. and Sokolowski, J. H. (1977) A 180-day Tolerance-Efficacy Study with Mibolerone for Suppres- sion of Estrus in the Cat, Amer. J. Vet. Res. 38, 469-477. 5. Colby, E. D. and Stein, B. S. (1982) The Genital System, Feline Medicine and Surgery, 3rd Ed. (In Press), E. J. Catcott, Editor, Amer. Vet. Publ. Inc., Santa Barbara, Cal. 6. Garbers, G. (1967) Personal Communications. 7. Herron, M. A. and Sis, R. F. (1974) Ovum Transport in the Cat and Effect of Estrogen Administration, Am. J. Vet. Res. 35, 1277. 8. Johnson, S. D. (1982) Infertility and Reproductive Disorders in Dogs. Proc. N.Y.S. Vet. College Conf. for Veterinarians, Ithaca, N.Y. 9. Lein, D. H. (1977) Reproduction in Veterinary Medicine: Canine and Feline Theriogenology, Wash. D.C. Acad, of Vet. Med., Inc. Seminar. 10. McEntee, K. (1968) Personal Communication. 11. Roy, A. and Rowson, L. E. A. (1955) A Method of Inducing Sterility in the Cow, Vet. Rec. 67, 10, 177. 12. Shille, V. M. and Stabenfeldt, G. H. (1980) Current Concepts in Reproduction of the Dog and Cat, Adv. in Vet. Sci. and Comp. Med., 24, 211-243. 13. Steere, J. H. (1959) Bovine Gynecology in Denmark, Mod. Vet. Prac. 40, 32. 14. Trum, B. (1950) Personal Communication. Extrauterine Pregnancies and Fetuses True Extrauterine Pregnancy is characterized by a fertilized ovum, embryo, or fetus that has established nutritive relations with organs or tissues other than the endometrium and has undergone in this location a degreeDISEASES AND ACCIDENTS OF GESTATION 223 of embryological development. In humans ovarian and tubal pregnancies may occur, the latter being fairly com- mon. True abdominal pregnancies, with the fetal pla- centa attaching to the mesentery and omentum, have been described as rarely occurring in humans. In ovarian, tubal, and abdominal pregnancies the embryonic development proceeds only a short time and then the fetus succumbs. In human tubal pregnancy the oviduct ruptures, usually accompanied by severe hemorrhage. No authentic cases of true extrauterine pregnancies have been described in domestic animals. This difference is apparently related to the manner in which the developing zygote establishes nutritive relationships with the dam. In humans and ro- dents the developing zygote erodes the mucosa and bur- ies itself in the maternal tissues while in domestic ani- mals the villi of the trophoblast attach themselves in the maternal crypts formed in the endometrium. False or Secondary Extrauterine Pregnancy is seen occasionally in all domestic animals and very rarely in the mare.2 In this condition the fertilized ovum, embryo, or fetus develops normal placental relationships with the endometrium and the fetus reaches recognizable size. It then escapes from the uterine cavity into the abdominal cavity. This condition usually occurs the last two-thirds of the gestation period. Almost all secondary extrauter- ine fetuses are dead by the time the condition is diag- nosed. The cause for uterine rupture, allowing the es- cape of the fetus into the abdominal cavity, is frequently unknown. The condition is seen in uterine torsion, fetal emphysema, chronic perimetritis with adhesions and fol- lowing dystocia and oxytocin administration especially in the bitch.34 It may occur spontaneously or possibly associated with violence or trauma in advanced preg- nancy. In multipara, uterine torsion may involve a part of one horn or the entire horn with the enclosed fetuses being separated from the rest of the uterus. The adhe- sions that take place may cause the condition to be di- agnosed as an extrauterine pregnancy or fetus. In many cases in domestic animals in which a sterile fetus is re- leased into the abdominal cavity little or no external symptoms may be evident. The fetus dies and with its membranes becomes walled off as a sterile foreign body in the ventral portion of the abdominal cavity and re- mains there as an inert mass for months.1'6'7 Often ex- tensive adhesions between it and other abdominal vis- cera develop. The site of the rupture may only be a small or invisible scar after the uterus involutes. Since most of these fetuses are well-walled off, no external symptoms are usually seen. Occasionally mild digestive distur- bances may be evident. In rare cases a large extrauterine fetus may be diagnosed on rectal examination in the cow if the fetus was near term when it escaped from the uterus. A differential diagnosis must be made, considering mummification of the fetus, tumors, and fat necrosis. Diagnosis of most cases in the larger domestic animals is made at the time of slaughter. In the dog and cat ab- dominal palpation, radiographs and exploratory laparot- omy may aid in revealing the extrauterine fetus(es) es- pecially in an ailing animal soon after parturition. Reports would indicate that secondary extrauterine pregnancy and extrauterine fetuses occur more commonly in queens than in bitches.1,6 These fetuses may be or become infected, macerate, cause peritonitis and the death of the dam or rarely be walled-off and be expelled into the alimentary tract or through the abdominal wall.3'8 If extrauterine fetuses are diagnosed in large animals the prognosis is guarded and the animal is usually slaughtered. A laparatomy operation to remove the ex- trauterine fetus would be difficult and many adhesions would remain. In the dog and cat an operation might be considered in cases of chronic, walled-off extrauterine fetuses. In animals with uterine rupture late in pregnancy or at the time of parturition, secondary to trauma, torsion, fe- tal emphysema or possibly spontaneous rupture, the fe- tus and uterine contents escape into the abdominal cav- ity. If the fetus is emphysematous or grossly infected, fatal peritonitis and shock frequently follow. In rare cases the fetus may still be found alive and the dam and pos- sibly the young can be saved by an immediate laparot- omy to remove the dead or live fetuses and repair the ruptured uterus. In the mare a rotated or compound bicomual preg- nancy may be confused with an extrauterine fetus. In this condition the birth passageway is very long and the fetus may be palpated beneath the stretched vagina and uterine body and simulate an extrauterine fetus. In humans some long-existing extrauterine fetuses become quite firm and encapsulated with calcium laid down in the capsule, causing them to be spoken of as lithopedions. These well- encapsulated extrauterine fetuses in animals may occa- sionally be referred to as extrauterine fetal mummies. Dropsy of the Fetal Membranes and Fetus These pathologic conditions in pregnant domestic an- imals may include hydramnios, hydrallantois, edema of the allantois chorion, fetal anasarca, or fetal edema with ascites and hydrothorax. These conditions are usually found singly but on rare occasions may be associated. In hydramnios and hydrallantois in uniparous animals the abdomen is usually distended as if twins or triplets are present. All cows in which twins are suspected should224 VETERINARY OBSTETRICS be examined promptly for these possible dropsical con- ditions. Of these conditions hydramnios and hydrallan- tois are most common with the latter occurring 10 to 15 times more frequently than the former. In 7 percent of cases both hydramnios and hydrallantois were present together.23 Hydramnios or hydrops of the amnion is charac- terized by a gradual enlargement or filling of the am- niotic cavity that is associated with a genetic or congen- itally defective fetus. The condition is seen most commonly in cattle, occasionally in sheep, rarely in pigs and carnivores, and it has not been reported in horses.3 It may affect one of twin fetuses. At midgestation the amniotic fluid is watery and slightly yellow and in nor- mal bovine conceptuses only increases in amount very slowly until the last month of pregnancy when it nearly doubles in amount.13,4 In normal sheep there is a sudden increase around the 100th day of pregnancy. From mid- gestation onward the amniotic fluid becomes more viscid and glairy because the early watery fluid is swallowed or possibly inhaled into the large bronchi and absorbed and a large volume of saliva is continually produced. In defective fetuses swallowing is impaired and the amounts of amniotic fluid increase gradually to 5 to 30 gallons. Hydramnios is not solely due to a failure of deglutition in the fetus as other mechanisms besides swallowing reg- ulate the volume and composition of amniotic fluid.25 During the last few months of gestation, when hydram- nios becomes apparent, the amount of amniotic fluid in normal cows is only 1 to 2 gallons. Genetic or hereditary conditions resulting in defective fetuses often associated with hydramnios are: 1) Dexter cattle pregnant with “bull dog” calves. In these animals the disease is apparent at 3 to 4 months of pregnancy.7 Figure 77. Jersey cow about 7 to 8 months pregnant affected with hydrops and a transverse rupture of the abdominal muscles 8 inches cranial to the pubis. The cow was unable to stand. Figure 78. Same Jersey cow with marked ventral hernia with signs of rupture of the prepubic tendon two weeks after a cesarean section. 2) Angus cattle pregnant with small brachygnathic, defective calves with osteopetrosis. These exhibit in- creased abdominal enlargement the last month of ges- tation. 3) A muscle contracture monster associated with hydrops of the amnion has been described in Red-Danish cattle.12 4) Prolonged gestation in Guernsey cattle char- acterized by an immature defective small fetus with pi- tuitary hypoplasia or aplasia may be associated with hy- dramnios. 5) A lethal muscle contracture monster in sheep accompanied by dropsy of the amnion has been de- scribed.18 Hydramnios was commonly observed with hy- drocephalic fetuses in Hereford cattle.50 All of the above defective fetuses have been caused by recessive auto- somal genes (See chapter on Anomalies of the Fetus). Hydramnios is also seen in cattle with congenitally anomalous fetuses such as conjoined twin monsters, Schistosomus reflexus, and fetuses with anomalies of the cranial portions of the body. Hybrids produced by mating of an American bison bull with a domestic cow resulted in hydrops of the amnion.24 Anencephaly is fre- quently the cause of hydramnios in women.6 Hydramnios develops slowly over several months dur- ing the latter half of pregnancy. If the condition causes obvious abdominal enlargement it is usually the last month or six weeks of the gestation period. Often the condition is not recognized until parturition when large quantities of syrupy, viscid amniotic fluid, occasionally containing meconium, is released. The differential diagnosis be- tween hydramnios and hydrallantois has been described. (See Table 14.) The prognosis for the future breeding life of the dam is fair to good in hydramnios but the fetus is invariably defective and dies. Retention of the pla- centa and metritis are not serious problems as with hy- drallantois. Abortions and premature parturitions are fre- quent in cases of hydramnios. Because of the enlargedDISEASES AND ACCIDENTS OF GESTATION 225 Table 14. The Differential Diagnosis Between Hydrallantois and Hydramnios in Cattle Hydrallantois Hydramnios Occurs in 85 to 90% of cases of uterine dropsy. Abdominal enlargement develops rapidly within 5 to 20 days. Abdominal wall is round, distended and tense. Distended horns of uterus easily palpated per rectum and fill the abdominal cavity. Fetus and placentomes are not able to be palpated or ballotted per rectum or through the abdominal wall. Sporadic in incidence. Allantoic fluid is watery, clear and amber, with characteristics of a transudate. Fetuses are normal but small twins are occasionally present. Placenta, especially the allantois chorion, is usually diseased and abnormal with a reduced number of greatly hypertrophied placentomes. After removing much fluid by caesarean section or by allantocentesis, the allantoic cavity rapidly fills again. Retained placenta and severe metritis usually occurs. Sequelae such as uterine rupture, abdominal hernias and dislocation of the hips are common in severe cases. Prognosis—guarded to poor for life and fertility. Occurs in 5 to 10% of cases of uterine dropsy. Abdominal enlargement develops slowly over weeks and months. Abdominal wall is pear-shaped and less tense. Uterine horns hard to palpate, not very tense and don’t fill the upper and caudal abdominal cavity area. Placentomes and often the fetus may be palpated per rectum and the latter may occasionally be ballotted through the abdominal wall. Usually sporadic but in an inbred herd may have a number of cases. Amniotic fluid usually syrupy and viscid, and often contains meconium. Associated with a defective, small, anomalous fetus. Placenta, allantois chorion and placentomes normal. After removing much fluid by caesarean section or by amniocentesis, the amnion does not refill in the former and only slowly in the latter. Retained placenta may occasionally occur and metritis is much less common or severe. Adverse sequelae are rare due to gradual onset and the nature of the disease. Prognosis—fair to good for life and fertility. uterus, uterine inertia, and defective fetuses, dystocia at parturition is not uncommon. It is usually easily handled because of the small size of the fetus. In hydramnios associated with prolonged gestation and fetuses with de- fective or missing pituitary glands injections of large re- peated doses of glucocorticoids, prostaglandins, and es- trogens might be indicated to produce abortion or parturition. If the fetus is dead, glucocorticoids are of questionable value.4'19'21 Combinations of these hor- mones may avoid repeated large doses of a single hor- mone. Further trials are indicated. Cesarean section, as described under hydrallantois, can also be used to ter- minate a pregnancy with hydramnios. The genetic im- plication in salvaging an affected dam should be consid- ered. If the defective fetus and hydramnios is due to a recessive gene then the dam and sire are carriers. Such animals should be eliminated from the herd and any in- breeding in the herd should be discouraged. Hydrallantois, dropsy or hydrops of the allantois, is the single factor present in 85 to 90 percent of the dropsical conditions affecting the bovine fetus and its membranes. This condition is seen sporadically in dairy and beef cattle. It is often associated with a diseased uterus in which most of the caruncles in one horn are not functional and the rest of the placentomes are greatly enlarged and possibly diseased. Adventitious placentae are commonly observed. Portions of the placenta may be necrotic and edematous. Hydrallantois is seen quite commonly in cattle carrying twin fetuses or greater mul- tiples. Hydrallantois apparently is caused by structural or functional changes in the allantois chorion including its vessels with transudation and collection of fluid, dif- fering form normal allantoic fluid but resembling plasma.20 One may remove many gallons of this transudate from the allantoic cavity with a trocar but within 2 to 4 days it has been restored. This would tend to indicate that the fetal kidneys probably seldom play a role in causing this disease. The presence of cystic kidneys, hydronephrosis, or dysfunction of the fetal renal tubules resulting in poly- uria might be concerned in the pathogenesis of hydral- lantois.16 The author has seldom observed such abnor- malities in the fetal kidneys of fetuses from affected cows and further suggests these changes are probably second- ary to the hydrallantois. Torsion of the uterus and torsion of the umbilical cord are not associated with this con- dition. The navel cord in the cow is short and seldom twisted. In the mare torsion of the umbilical cord may occur and be severe enough to cause the death of the226 VETERINARY OBSTETRICS fetus but dropsy of the fetal membranes and fetus rarely occur. The author and others have observed mares with hydrops allantois that spontaneously aborted a small de- fective fetus. In one case there was evidence of moderate umbilical torsion with an area of adhesion between the amnion and chorioallantois. This condition appeared to be more prevalent in cattle in seasons when forage has been damaged, with a possible loss of vitamin A re- sulting in a lowered resistance of the endometrium to disease.13 24 In cases of hydrallantois associated with a reduced number of placentomes and uterine disease the fetuses are usually growth-retarded and show some edema and ascites. Hydrallantois usually affects cows 3 or more years of age although rarely the condition may be seen in heifers in which possibly a congenital lack of uterine caruncles was present. In older cows this lack of carun- cles characteristic of hydrallantois may be due to prior uterine infection or even tuberculous metritis.3 The signs of dropsy of the allantois vary depending on the degree of the involvement and the stage of preg- nancy. In mild cases, where the amount of fluids is mod- erate, 10 to 20 gallons, the condition may not be diag- nosed until parturition. At this time an excessive amount of clear, watery, amber fluid with the characteristics of a transudate is expelled. The fetal membranes may be tough and rupture with difficulty. The uterus is greatly enlarged and atonic and the small, growth-retarded fe- tus may exhibit some edema and ascites. Dystocia may result at the time of abortion or parturition due to uterine inertia. The fetus is usually dead at birth or dies shortly thereafter. Retention of the fetal membranes and septic metritis are common sequelae to this dropsical condi- tion. In severe cases, symptoms of hydrops of allantois may occur as early as the fifth month of pregnancy but nearly all cases develop the last 3 months of gestation.4 Hydrallantois usually develops rapidly within 5 to 20 days and is characterized by a distended uterus and enlarged abdomen (See Figure 77). Spontaneous abortion at 6 to 9 months may frequently be observed.21,23 In the more severe cases the amounts of fluid may reach 30 to 60 gallons. The fetal membranes may be heavy and edema- tous and the cow frequently has ascitic fluid in her ab- dominal cavity. Thus the weights of the dropsical fluids, membranes, and uterus frequently total 350 to 550 lbs. This excessive volume of fluid distending the abdomen causes the owner to believe his records of breeding dates are wrong or else the cow is going to have triplets. Later, digestive symptoms with anorexia, lack of ruminations, and constipation are noted. The condition is frequently misdiagnosed as indigestion, bloat, or traumatic gastri- tis. The cow may drink excessive amounts of water. The temperature is normal. The pulse is elevated to 90 to 140 per minute and is weak and wiry. The cow may exhibit anxiety, restlessness, and an expiratory grunt. Because of the excessive volume of fluid, the fetus can seldom be ballotted or felt per rectum. On rectal examination the uterus is greatly distended and tense. Placentomes can seldom be felt, due to the tense uterine wall, but the uterine arteries are “whirring” indicative of a live fetus. The uterus appears to fill the abdominal cavity. As the condition progresses—and it may progress quite rapidly at any time during the last trimester of pregnancy—the abdomen becomes more distended. The gait is stiff, slow, and cautious. The cow loses body condition, and even- tually is unable to rise. Dislocation of the hips or back- ward extension of the rear limbs may occur and the cow lies on her sternum looking like a “bloated bull frog” (See Figure 77). Rarely in the cow and mare rupture of the prepubic tendon or ventral hernia may occur due to the excessive weight of the uterus. Rupture of the uterine wall has also been described.9,17,23 For a differential di- agnosis between bovine hydrallantois and hydramnios see Table 14. In mares hydrops allantois is rare.22 It may occur in mares of any age. The condition becomes evident the last trimester of gestation with signs similar to those ob- served in cows. Dystocia and retained placenta second- ary to the uterine inertia caused by the greatly distended uterus is common. The fetus in affected mares is often defective, growth retarded and some may exhibit hydro- cephalus but while most all are alive at delivery, they invariably die within a short time. Other dropsical con- ditions affecting the fetus are much less common. Edema of the allantois chorion characterized by ex- tensive and severe edema distending these tissues to a thickness of 4 to 6 inches has been associated with Bru- cella abortus infection causing placental disease in cat- tle and therefore is rarely seen at present in the United States. Hydrallantois is rarely associated with Brucella abortus infection. Fetal ascites severe enough to cause dystocia may also rarely be due to Br. abortus infection. Slight fetal as- cites and edema as well as mild placental edema is fre- quently associated with intrauterine fetal death and ster- ile autolytic changes. Fetal anasarca or excessive edema of fetus is seen most commonly in cattle but may affect sheep. It may develop in a single fetus or one of twins. It is also rarely observed in one or two of a litter in swine or carnivores. Rarely mild hydrops of the amnion and/or allantois and edema of the placenta may accompany fetal anasarca. Abortions of affected fetuses are fairly common from 4 to 8 months of gestation in uniparous animals. The con- dition has been described affecting Ayrshire cattle.8 ThisDISEASES AND ACCIDENTS OF GESTATION 227 is caused by a recessive autosomal character. Most an- asarcous fetuses were expelled dead. In all of these latter conditions with the possible exception of edema of the allantois chorion, enlargement of the abdomen is not noted. The prognosis for hydramnios is fair to good for the dam unless she is a carrier of a recessive gene respon- sible for the defective fetus producing the condition. Sal- vage of the defective fetus is usually impossible. In many of these cases following induced abortions or caesarean section the placenta is often expelled or if it is retained, metritis associated with uterine inertia is not as severe as that following hydrallantois. The prognosis in cases of hydrallantois is poor. In advanced cases in which the cow is unable to rise, the prognosis is often hopeless. Even if the fetus can be removed, the mortality in cows is high, because the uterus is very atonic, the membranes diseased, and shock or severe septic metritis usually fol- lows the expulsion or removal of the fetus. If the cow should survive, its future reproductive life is question- able. In almost all cows with hydrops except the occa- sional slight or moderate one that goes to term and spon- taneously delivers, the fetus dies in utero or soon after birth. Milk production in dairy cows for the next lacta- tion after either hydramnios or hydrallantois is usually poor. Dropsy of the allantois at term is often associated with dystocia due to a dead edematous fetus in an ab- normal position or posture, uterine inertia, and a cervix that may fail to dilate completely. If the dystocia is not handled promptly emphysema of the fetus soon devel- ops. In the rare cases of hydrops allantois seen in mares the prognosis is guarded but better than in cattle unless rupture of the prepubic tendon occurs. The prognosis in rare cases of edema of the allantois chorion is similar to hydrops allantois. In both severe fetal ascites and fetal anasarca, dystocia usually results at the time the overly large fetus enters the birth canal, whether the fetus is aborted or expelled at term. The treatment or handling of cases of hydramnios and hydrallantois varies with the duration and severity of the condition. In mild cases undiagnosed until the time of abortion, premature birth or at normal parturition, ex- cessive volumes of fluids are observed accompanied by the presence of a poorly viable, small, growth-retarded or defective fetus, dystocia related to the diseased or dead fetus, and uterine inertia secondary to the uterine dis- tention. Mutation and forced extraction of these fetuses is usually easily effected. In mares about one-half of the cases terminate by spontaneous abortion or birth at or near term.22 In cases of fetal anasarca or ascites greater amounts of traction and lubrication may be needed. In a few cases fetotomy might have to be resorted to in order to mutilate the fetus to allow the excess fluid to escape. Retained placenta and a secondary severe me- tritis frequently follows hydrallantois and edema of the allantois chorion but is less frequently observed and is less severe in hydramnios. Early treatment for these con- ditions with parenteral and local antibiotics and ecbolics such as oxytocin, stilbestrol and ergonovine are indi- cated. In severe cases of hydramnios and hydrallantois oc- curring during the gestation period with a closed cervix, the prompt termination of the abnormal pregnancy is usually desired. In some slowly developing cases late in gestation it may be expedient to observe the cow or mare and wait for or induce parturition. In other severe cases an early decision to slaughter the cow while she is still in good physical condition is often the best method of handling these cases when all factors are considered. Daily administration of large doses of stilbestrol, 50 to 120 mg., or estradiol, 8 to 10 mg. for 4 to 7 days alone or together with large doses of prostaglandins, and gluco- corticoids and antibiotics may frequently result in cervi- cal dilation and abortion.414,15'19'21'23 Precipitating abor- tion is more successful with hydramnios than hydral- lantois. Because the uterus is atonic and distended and the cervix usually dilates poorly, the cow should be watched carefully. The abortion should be aided when necessary. Pituitrin or oxytocin may be given but its ef- fect may be negligible because of the atonic, stretched, and diseased uterine wall. . In the mare abortion or premature birth may be in- duced by manual dilation of the cervix, rupture of the usually thick, tough allantois-chorion and very slow drainage of the allantoic fluid to prevent shock. Oxy- tocin, 50 units, in a liter of saline given slowly intra- venously, and repeated if necessary, to aid uterine con- traction and delivery as well as promote expulsion of the placenta has been recommended.22 Injection of estradiol, 20 mg., 24 hours before induction of abortion might be indicated to promote relaxation of the cervix and genital tract. Manual removal of the fetus is usually necessary. Cesarean section has been attempted in many cases with success but in some the cow succumbs. Various authors5b-10'16 have recommended the use of a sterile tro- car or plastic tube inserted by a surgical procedure through the abdominal and uterine walls to draw the fluid off gradually at a rate of one liter per minute before the Ce- sarean is performed. This helped to avoid possible shock from removing too much fluid too rapidly. The draining of 25 to 50 liters of allantoic fluid often induces abortion within one to three days. In a few cases it may be in- dicated to repeat this treatment.5b Since most severely affected cows are very dehydrated with marked electro-228 VETERINARY OBSTETRICS lyte imbalances, appropriate fluid therapy in large vol- umes is indicated before, during and after the operation. Once the cow is down and unable to rise due to the weight of the fluid, any treatment is usually unsuccessful be- cause of complications such as abdominal hernia, severe myositis and nerve damage or dislocated hips. Following the relief of these severe dropsical conditions metritis usually associated with retained placenta almost invari- ably follows. The severity of this metritis varies with the severity of the condition and is a common cause for the high mortality. In all hydrops cases the treatment for septic metritis should begin before or at the time the condition is relieved with supportive fluid therapy, antibiotics, both parenteral and locally in the uterus and frequent injec- tions of ecbolics. Since treatment of this condition is not very successful, most of the more severe cases are sent to slaughter as soon as they are diagnosed. This is es- pecially true if the cow is of only moderate value. Three cases of hydrops allantois were successfully corrected by Cesarean section after slowly draining off 20 to 30 gal- lons of allantoic fluid in the one-half hour before the Cesarean operation.4b The pulse and respirations were monitored and Ringer’s solution with dextrose was ad- ministered intravenously during the operation. Subse- quent treatment with estrogens, antibiotics and further supportive therapy was necessary to control metritis as the placenta was retained for up to three weeks. It was recommended that the cows not be rebred. If more than 1 or 2 cases of hydramnios occur in a herd the hereditary nature of this disease should be suspected and investi- gated, and further inbreeding prevented. An interesting observation is that after terminating hy- drops of the allantois by cesarean section the uterus may continue to fill with transudative fluid for about 48 hours and require further draining.15 Abdominal Hernias Resulting in Hysterocele The pregnant uterus may drop into, or be present in, umbilical, inguinal, perineal, diaphragmatic, or ventral hernias. In cases of rupture of the prepubic tendon, the pregnant uterus will drop into the sac formed by the skin and cutaneous muscles. This may cause dystocia or death of the fetuses or dam or both. Umbilical and inguinal hernias may, if large enough, contain a portion of the uterine horn and developing fe- tus. Umbilical hernias have been described as heredi- tary in all species of animals. In cows most of them are small. Such animals should not be used as breeding an- imals. Umbilical hernia in cattle, especially Holsteins, is probably an autosomal dominant with low pene- trance.413 Most female animals with large umbilical her- nias are not bred. In males an umbilical hernia may pre- vent copulation. Inguinal hernias are hereditary or acquired and are described as common in the bitch, and rare in the queen, sow and mare. They have not been described in the cow or ewe. Bitches over 5 years of age are most commonly affected.10 Spayed bitches given large amounts of estrogen developed inguinal hernias within 90 days.8 One bitch with an inguinal hernia was spayed through a midline incision and the hernia was left intact. One year later the hernia had spontaneously disappeared. These observations indicate a close relationship between estrogen production by the ovary and the development of inguinal hernia in bitches. Inguinal hernias may be bilateral or unilateral, usually the latter, and are char- acterized by a swelling in the inguinal region. This be- comes larger as pregnancy progresses if a portion of the pregnant uterine horn is present in the hernial sac. In the bitch one to three fetuses may develop in the hernial sac. If pregnancy is allowed to progress it results in the death of the fetuses or in dystocia at the time of parturition. In the bitch this condition should be differentiated from a mammary neoplasm and a local abscess. Diaphrag- matic hernia is usually secondary to trauma in the bitch and other multiparous female animals and in rare cases a pregnant uterine horn may be present in the thoracic cavity.6,9 A perineal hernia containing a portion of the fetus has been described in the goat.1 Ventral hernias are usually traumatic in origin and may occur in all spe- cies. In the mare they may occur at the time of partu- rition in the caudal, ventral abdominal area just lateral to the midline. If possible, surgical repair should be de- layed several months or more until the edges of the her- nial rupture have healed and organized.7 If they are large a portion of the uterine horn and fetus may develop therein. If ventral hernias in large animals are extensive they are difficult if not impossible to repair. Fortunately, in large animals the uterus in early pregnancy does not drop far enough downward or forward to drop into most hernial sacs and in later pregnancy the uterus is too large to enter them. In the bitch, an inguinal hernia containing a portion of a pregnant horn can be handled surgically early in pregnancy by reducing and repairing the hernia, if nec- essary by enlarging the ring and/or using a synthetic mesh for a lasting support. From midpregnancy to near term, hysterotomy can be performed and the fetus or fetuses removed, the uterus replaced in the abdominal cavity, and the hernial ring sutured. Occasionally the portion of the herniated uterine horn containing fetuses may be re- moved by a partial hysterectomy. In other cases ovar- iohysterectomy may be indicated. The rare cases of um-DISEASES AND ACCIDENTS OF GESTATION 229 bilical or ventral, diaphragmatic or perineal hernias encountered containing a portion of the pregnant uterus could be handled in a manner similar to the repair of inguinal hernias. Extensive unilateral ventral hernias in large animals occur occasionally in advanced pregnancy in cows, ewes, and does, but rarely in mares. These hernias are usually due to trauma. The greatly increased weight of the gravid uterus and fetus, and possibly other changes, weaken the abdominal floor. These extensive hernias are seen most commonly in ruminants on the right side of the abdom- inal floor. They are observed most often on the left side in the mare.2 In rare instances they may be associated with twins or greater multiples or with hydrops of the amnion and allantois. Large unilateral ventral hernias are characterized by a unilateral ventral sagging of the ab- dominal floor, 6 to 8 inches or more below that of the normal side. Calving or foaling may be difficult because of the inability of the abdominal muscles to contract equally and strongly and force the fetus toward and through the birth canal. Following calving, the abdom- inal floor of the affected side may retract in some cattle and the abdominal contour become nearly normal. This may occasionally remain normal during subsequent pregnancies. However, it usually recurs during the latter stage of each gestation period. The involvement is so great that treatment or operations other than those out- lined under rupture of the prepubic tendon are not in- dicated. Rupture of the prepubic tendon or prepubic des- morrhexis of pregnancy is seen most commonly in the mare, and rarely in the cow and ewe. This condition is seen most frequently in the draft mare that is idle and well-fed, and infrequently in light mares. It is rare in Figure 80. Acute rupture of the prepubic tendon in a mare. cattle because the subpubic tendon, a structure that does not exist in horses, gives added support to the prepubic tendon.4 (See Figures 78, 79, 80.) Rupture of the pre- pubic tendon occurs during the last 2 months of gesta- tion. In the mare and occasionally the cow it is often preceded by a marked tense, painful edema, 6 to 14 cm. thick, on the abdominal floor, starting at the udder and extending to the xiphoid region. Severe edema of the abdominal floor in the mare in advanced pregnancy should always be viewed seriously. Physiological edema of the abdominal floor in the cow is common and does not in- dicate a possible weakness or rupture of the abdominal floor as in the mare. Rarely massive hematomas in the region of the bovine udder may be mistaken for rupture of the prepubic tendon.5 (See Figure 81.) The rupture is predisposed by the increased weight of the gravid uterus on the abdominal floor and possible degenerative changes due to the edema and the weight. Occasionally, due to violence or trauma, the condition Figure 79. Impending rupture of the prepubic tendon in an old mare. A proper support has been applied. Figure 81. A massive hematoma cranial and dorsal to the mammary gland of a pregnant cow resembling a rupture of the prepubic tendon.230 VETERINARY OBSTETRICS occurs suddenly without the development of edema. Twins or greater multiples,3 hydrops of the fetal membranes, fetal giants in prolonged gestation, as in Veratrum poi- soning in ewes, favor rupture. In this condition there is a transverse rupture of the prepubic tendon, the ventral abdominal muscles, abdominal tunic, and peritoneum letting the viscera and gravid uterus drop downward into a sac formed by the skin and cutaneous muscles. Only very rarely does complete eventration occur. In rupture that occurs suddenly due to violence, besides the sudden enlargement in the ventral abdominal region and the sinking of the flanks, there usually occurs intense pain and colic together with a cold sweat, fast respirations, rapid weak pulse, and a tendency toward collapse due to shock, and possible hemorrhage (see Figure 80). Oc- casionally a mare and her intrauterine fetus will perish at this time despite supportive treatment of blood, saline, stimulants, and support for the abdominal wall. In most cases the onset is more gradual, with a preceding painful edema of the abdominal floor, a stiff, careful, cautious gait, and refusal to lie down. After rupture has occurred the udder and teats are stretched forward and downward on the abdominal floor. The attitude is a typical “saw- horse” one, with an elevation of the tail head and the ischial tuberosities and a lordosis. The pelvis is tilted backward because the prepubic tendon is not intact to maintain the pelvis in its proper relationship to the spinal column. The prognosis in rupture of the prepubic tendon is al- ways poor, as most mares and foals succumb before foaling occurs. If foaling should terminate successfully the mare’s condition will improve, and she might do light work; but usually the mare is so unsightly that she is destroyed. Rebreeding these mares is definitely not in- dicated. Affected cows are usually sold after calving and lactation because of difficulty in milking and because rebreeding is contraindicated. Treatment is usually unsatisfactory, once rupture of the tendon has occurred. Preventive treatment of mares showing marked edema of the ventral abdominal floor and a stiff cautious gait should consist of confining the mare in a large comfortable box stall and restricting ex- ercise. Large bulky feeds should be withheld and a light concentrate ration should be fed. In some mares mild laxatives might be indicated. A suitable heavy, wide canvas webbing should be tightened securely with straps around the abdomen, to transfer the weight of the ab- dominal viscera to the spine. Padding over the back usu- ally is necessary to prevent pressure necrosis. (See Fig- ure 79.) The mare should be watched closely for the beginning of parturition so that aid may be given at once and the fetus withdrawn by traction. This aid is neces- sary since abdominal contractions are very weak and parturition cannot take place without aid and direction. In most cases uterine contractions and cervical dilation may take place but since the fetus does not engage or enter into the pelvic cavity, abdominal contractions, or labor do not begin. Periodic vaginal examinations may be necessary. In some cases the wide band in a horse sling to support the abdominal viscera may be useful and the mare can be kept standing. Possibly parturition should be induced in the mare in late pregnancy by the injection of estradiol and 30 to 40 units of oxytocin. Another pos- sibility in these mares is cesarean section which, though often successful permits the fetus to be saved, while the affected mare is usually destroyed. This latter procedure is indicated in sudden rupture, with impending collapse and death of the mare. In the cow abdominal support or slings are not tolerated. Induction of premature birth by the administration of large, repeated doses of glucocor- ticoids, prostaglandins and estrogens in the cow is usu- ally successfully accomplished with fewer complications than a cesarean operation. By confinement and careful observation, the fetus may be promptly withdrawn by traction. In the cow cesarean section is more successful than in the mare and may occasionally be indicated in this condition. In relieving dystocia due to rupture of the prepubic tendon, rolling the cow or mare on its side or back will aid in bringing the fetus to the pelvic inlet for removal. If the mare is in a standing position, horse slings may be applied and tightened to bring the fetus near the pelvic inlet. Torsion of the Uterus Torsion of the uterus may occur in all species of an- imals. Uterine torsion is usually defined as the revolu- tion or twisting of the uterus on its long axis. This might be true in the mare, where torsion of the uterus is un- common due to the dorsally attached broad ligaments that tend to prevent torsion. In other species of animals such as the cow, ewe, and doe, the gravid horn is in the shape of an arc or a U-shaped loop with the vagina and ovary at the respective ends of the arc. Torsion involves the rotation of this arc on its transverse axis, similar to an intestinal volvulus. This same type of torsion occurs in multipara when one horn rotates at its base. A mod- ification of this same volvulus type of torsion occurs in multipara when only a portion of one horn, containing usually only one fetus, may be twisted or rotated. In un- ipara, because of the strong intercomual ligament and the distention of the uterine horns and body with pla- centa and fluid, both gravid and nongravid horns are in-DISEASES AND ACCIDENTS OF GESTATION 231 volved in the torsion. Torsion involving both horns of the uterus cannot occur in the bitch and queen.2 Torsion of the uterus is most commonly observed in dairy cows and is occasionally seen in beef cows, bitches, queens, ewes, does and mares and rarely seen in the sow.415 Two rare cases of torsion of both uterine horns in sows were reported.15 Uterine torsion was reported to be more common in draft mares than in light mares.1 The incidence of uterine torsion in dairy cattle was 7.3 percent in 1555 dystocia cases treated over a 10-year pe- riod in the Ambulatory Clinic of the New York State Veterinary College. The incidence of uterine torsion may vary from 1 to 3 percent in Australia to 18 to 25 percent of referred cases in England, Germany and Switzer- land.5b,1° Uterine torsion is rare in the Bos indicus type of cattle. The possible causes for torsion of the uterus in the cow are many. The lesser curvature of the uterus in ad- vanced pregnancy is supported dorsal laterally by the mesometrium. The greater curvature lies free in the ab- dominal cavity resting on the abdominal floor and sup- ported by the rumen, the viscera, and the abdominal walls. The ovarian end of the gravid horn of the bovine uterus is a relatively small or narrow base upon which the uterus rests. If the nongravid hom is small or nonfunctional the instability of the uterus is increased. This anatomical ar- rangement, together with the manner in which the cow lies down, with the fore quarters going down first, and rises, by elevating the rear quarters first, so that each time the cow lies down or rises the gravid uterus is sus- pended in the abdominal cavity, means that a sudden slip or fall in either lying down or rising could cause torsion. Other factors aiding torsion of the uterus in advanced pregnancy are lack of fetal fluids, and violence such as sudden falls or rolling. In bitches and queens this latter factor is probably important. Confinement in stables for long periods favors torsion in the cow. The incidence of torsion as a cause of dystocia in pastured cattle was 2.7 percent and in stabled cattle 8.6 percent.16 In the expe- rience of many veterinarians in New York State most of the cases of uterine torsion occur during the early spring months after cows have been stabled for 4 to 6 months. Torsion is observed more commonly in pluriparous than in primiparous animals. A lack of tone of the pregnant uterus—a condition composed of a lack of fluids, flaccid uterine walls, a small nongravid hom, a long flaccid me- sometrium—favors uterine torsion. A deep capacious abdomen predisposes to uterine torsion. Twins in rum- inants tend to prevent torsion by making a broader base for the uterus to rest upon and by filling the abdominal cavity. However, 5 of 10 cases of uterine torsion in ewes were in bicomual twin pregnancies56 even though the ovine mesometrial attachment is sub lumbar as in mares.1 In some cases strong movements of the fetus in the early stages of parturition probably can cause uterine torsion. Uterine torsion is observed most commonly in ad- vanced pregnancy. However, cases of uterine torsion in the cow have been observed from 70 days of gestation to term. Torsions occurring before the seventh month of pregnancy in the cow are unusual. Several cases in cows16 and queens12 have been recorded in which uterine torsion occurred in nonpregnant uteri containing purulent exu- date. Most bovine torsions occurred during the early part of the second stage of labor or the latter part of the first stage.1 This conclusion was based on observations that the cervix is found to be dilated immediately after the torsion is relieved in most of the bovine dystocia cases due to torsion of the uterus. In only occasional cases is there a severe edema due to venous congestion or other circulatory disturbance in the uterus or its contents. In cases diagnosed early the fetus may still be alive. Uter- ine torsion at this time may be favored by unequal con- tractions of the uterus or by active movements of the large bovine fetuses.1 These movements are greatest dur- ing the first stage and early second stage of parturition. One mare developed uterine torsion immediately after a period of intense fetal activity.8 Probably other factors may be involved in the torsion, as it appears difficult for either uterine contractions or fetal activity alone to pro- duce torsion. Uterine torsions of cattle of 180° may occasionally be present for days or weeks without clinical symptoms un- til labor begins and dystocia results. In these cases16 and the occasional similar cases observed by the author, no evidence of circulatory interference was present. If cir- culatory interference of the blood supply to the uterus was present, acute clinical symptoms and death of the fetus would probably occur. During pregnancy 45° to 90° torsions or rotations of the uterus are rather fre- quently found on rectal examination. These often appear to correct themselves before or at parturition. For the above reasons this writer believes that some cases of bovine uterine torsion of 90 to 180° occur during the last few months of gestation, persist for days, weeks or months and only become evident at the time of par- turition. In unusual instances torsion of the uterus may involve a 360° or more rotation of the uterus. One author cited a case involving two complete turns.16 In torsions of greater than 180° to 240° the birth canal at parturition is usually tightly closed, so that the cervix and the fetus are not palpable per vagina. These severe torsions may cause obstruction of the blood supply to the uterus, with resulting congestion, edema, shock, death of the fetus, and even gangrene of the uterus. In neglected cases232 VETERINARY OBSTETRICS transverse rupture of the uterus or vagina, emphysema and maceration of the fetus, shock, collapse, and death may occur. In rare cases one of the large uterine vessels may rupture, followed by severe hemorrhage into the ab- dominal cavity. In the bitch transverse rupture of the twisted segment of the uterus often occurs at parturition when the uterus contracts and the fetuses are released into the abdominal cavity. Rarely uterine torsion may be associated with mummification of the fetus late in ges- tation, instead of emphysema and maceration. In torsion in cows, ewes and does the cephalic portion of the vagina is usually twisted. Occasionally in a uterus lacking fluid or tone the torsion may occur cephalad to the cervix and in severe torsions at the time of parturition the twist may actually involve the cervix. In multiparous animals, since there is no intercomual ligament, usually one entire horn rotates at the point of its junction with the body and the other horn. Occasionally only a portion of the horn is involved, the twisted portion may occur anywhere throughout the horn. In rare cases in multipara in which both uterine horns are involved in the torsion, the cranial portion of the vagina is twisted. There are a number of reports in the literature on multipara in which the twisted portion of the horn or the entire horn with its fetuses separated completely from the body of the uterus during pregnancy. The fetuses may rupture from this blind sac into the abdominal cavity at the time of parturition, or this separated portion of the horn may be walled off as a passive body in which the fetus or fetuses may mac- erate or mummify. Torsions in uniparous animals are either torsions to the right (clockwise) or to the left (counter-clockwise). Most authors agree that left torsion occurs more often than right.1 Sb 10 if the right horn is gravid the torsion is apt to be to the right.10 The signs, prognosis, and handling of torsions causing dystocia at the time of parturition will be discussed later. The following paragraphs will deal with the symptoms and prognosis of severe torsions during the gestation pe- riod that may be recognized prior to parturition. Al- though treatment of these antenatal torsions will be men- tioned at this time they are similar for torsions resulting in dystocia and so will be discussed in detail in Chapter 10. The symptoms of torsions of the uterus in the cow prior to parturition may be completely lacking if the tor- sion is of a mild degree, 45° to 90° or even 180°. When the torsion is 180 degrees or more, definite signs of ab- dominal pain usually may be noted, such as anorexia, constipation, lack of ruminations, weak and slow rumen contractions, rapid pulse rate, restlessness or colicy symptoms, treading, and tail switching. These symp- toms may be confused with traumatic gastritis, indiges- tion, pyelonephritis, or intestinal intussusception. Uter- ine torsion during pregnancy in the ewe is characterized by a stiff, stilted gait and a stretched, “sawhorse” atti- tude resembling signs of peritonitis and intussusception or volvulus.6 Whenever any cow over six months preg- nant shows these suggestive symptoms, a rectal exami- nation should always be made to determine if torsion of the uterus is present. In right torsion the right broad lig- ament is pulled strongly downward and under the twisted uterine body or vagina, and the left broad ligament is pulled tightly across over the top of the cervix, the body of the uterus, and the vagina, toward the right side. In counter-clockwise, or left torsion the location and direc- tion of the two broad ligaments is reversed, with the right broad ligament crossing over the top of the twisted por- tion of the birth canal (See Chapter X). The uterine ar- teries on both sides are tightly stretched. The amount of tension on the broad ligaments and arteries will help de- termine the severity of the torsion. The fetus is often difficult to palpate but the position of the fetus in the uterus in advanced pregnancy may further indicate the degree of torsion. A dorso-pubic position of the fetus usually occurs when the torsion is 180°. A rectal ex- amination is preferred over a vaginal examination be- cause occasionally the twisted portion of the genital tract may lie cephalad to the cervix in the region of the body of the uterus and not extend back into the vagina. In most cases of torsion of the uterus in cows the cephalic portion of the vagina is involved, the vaginal walls are spirally twisted and a stenosis of the vagina is present. Starting from the dorsum of the vagina, if the folds spiral forward and downward to the left, or counterclockwise left torsion is present; and if the folds spiral downward and forward to the right or clockwise it is a right torsion of the uterus. Rarely torsion may be suspected on ex- ternal examination of the vulva by the dorsal commis- sure being pulled forward to the left or right. This is more noticeable in advanced pregnancy when the vulva is relaxed and edematous. In severe cases of torsion oc- curring in late pregnancy the blood supply to and from the uterus is severely restricted or cut off. In these cases marked symptoms of complete anorexia and constipa- tion, fetid diarrhea, complete lack of ruminations and mmen activity, very rapid and weak pulse, rapid respi- rations, expiratory grunt, normal to subnormal body temperature, cold extremities, shock, collapse, and death may occur within 24 to 72 hours. In other cases the fetus may die, become emphysematous and macerate or rarely become mummified and the cow develop only slight or mild symptoms. A rectal examination may reveal chronic adhesions, perimetritis, or even an extrauterine fetus ifDISEASES AND ACCIDENTS OF GESTATION 233 the uterus has ruptured. This latter condition usually oc- curs at the time of parturition. In ewes symptoms are similar to those in cows. In multipara, symptoms of ab- dominal involvement in advanced pregnancy should al- ways cause suspicion of torsion of the uterus. An ex- ploratory laparotomy in ewes and multipara is often indicated. In a review53 of uterine torsions in mares, most cases occurred from 8 months of gestation to term, average 9 months, with torsions of 180 to 360 degrees. Unlike tor- sion in the cow, uterine torsion in the mare rarely in- volves the cervix and vagina. Thus vaginal examination as an aid to the diagnosis of equine uterine torsion is seldom of value. In the cow over 90 percent of uterine torsions are recognized at term while in the mare nearly all uterine torsions are recognized late in gestation with very few mares being in labor when the torsion is di- agnosed. All pregnant mares exhibiting signs of colic in the last trimester of gestation should be examined rec- tally for evidence of uterine torsion as revealed by the location and tension on the twisted broad ligaments and a narrowing of the lumen of the small colon. In the mare torsions to the left or right are reported with near equal frequency.58 If possible the fetus should be palpated to determine if it is alive or dead. Also if mares show se- vere colic, uterine rupture or incarceration of a portion of the intestine in the torsion may have occurred. The method preferred by some veterinarians of correcting uterine torsion in the mare is the standing laparotomy operation in the flank region on the same side as the direction of the torsion. The alternate lifting and pushing or rocking of the uterus by grasping the fetal limbs through the uterine wall greatly facilitates the correct replace- ment of the uterus. By this procedure over 50 percent of the fetuses and 70 percent of the mares survived.58 This is possibly a higher recovery rate than the simpler Schaeffer technique of rolling the mare under sedation or anesthesia preferred by the author. If complications are present, alternate surgical approaches should be con- sidered. The prognosis in torsion of the uterus prior to partu- rition depends upon the degree of torsion, the severity of symptoms, and the length of time it has existed. In mild cases without symptoms—found by accident on rectal examination—in which the torsion is occasionally 180° but usually 90° or less, the prognosis is good, since the torsion seldom worsens, and treatment is often not necessary. In 180° to 270° torsions causing definite symptoms that are diagnosed and treated early, the im- mediate prognosis is usually good for the dam and fetus, but the torsion may occasionally recur prior to parturi- tion. In advanced, severe, and neglected cases the prog- nosis is poor for the life and reproductive life of the dam and usually the fetus is dead. Depending upon the circumstances the two treatments most apt to be successful in antenatal cases of 180° to 270° torsions in which the condition is diagnosed promptly are: rolling of the cow or mare by Schaeffer’s method described by Arthur2'7 or correcting the torsion manually by means of a laparotomy. This latter technique was highly satisfactory by a flank approach in either the recumbent or standing mare.58'9,13'14 These authors reported that 5 of 10 mares in which torsion of the uterus was corrected by rolling died;3,14 this technique was apparently more dangerous than a laparotomy. The author and others have successfully corrected uterine torsion in mares by roll- ing.31’ Attempts at correcting torsion by manipulation through the rectum or vagina or both in cows in which the cervix is sealed are usually not successful. Hoisting the rear parts of the cow to effect reduction of the torsion is crude and unnecessary, but may be effective in the ewe.1 In rare cases cesarean section may be indicated when pregnancy is near term. Extrauterine fetuses, fetal maceration, or mummification associated with torsion are handled as described previously. In advanced severe cases in which gangrene of the uterus is present, laparohysterectomy is indicated in the bitch and queen but is usually unsuccessful in the cow. Further detailed description of the handling of uterine torsions is discussed in Chapter 10 under handling of torsions causing dystocia. Vagino-cervical Prolapse Prolapse of the vagina usually involves a prolapse of the floor, the lateral walls and a portion of the roof of the vagina through the vulva with the cervix and uterus moving caudad. Not infrequently the entire vagina and cervix are prolapsed through the vulva. Vagino-cervical prolapse is seen in all species of domestic animals but most commonly in the cow, especially Herefords and Santa Gertrudis and the ewe. The incidence of ovine va- ginal prolapse was reported to be about 0.5 percent but in some flocks this may reach 20 percent.16 In dairy cat- tle it is observed most often in the larger dairy breeds such as Holstein and Brown Swiss. In young, brachy- cephalic dogs prolapse of the vagina at the time of es- trum is fairly common. It is practically unknown in cats.4 The causes of prolapse of the vagina and cervix are probably multiple. It is observed in the cow most com- monly the last 2 to 3 months of gestation when a large amount of estrogenic hormone is being secreted by the placenta. This causes a relaxation of the pelvic ligaments234 VETERINARY OBSTETRICS and adjacent structures and an edema and relaxation of the vulva and vulvar sphincter muscles. When the cow lies down the intra-abdominal pressure especially in late pregnancy is transmitted to the flaccid pelvic structures tending to force the relaxed and loosely attached vaginal floor and walls through the vulva. The vesico-genital pouch is the least restraining part of the pelvic structures and when subjected to increased abdominal pressure the bladder and other viscera are forced against the most yielding part—the floor of the vagina." Why this con- dition affects certain cows and not others is not known but it can be theorized that certain cows produce more estrogens and develop a greater relaxation of the pelvic structures earlier in pregnancy. Conformation may favor prolapse. Prolapse of the vagina may be influenced or due to hereditary or genetic factors in Hereford cattle and sheep and Boxers and Bulldogs.4'16 29'38 Since prolapse of the vagina is observed more commonly in pluripara than primipara, injuries or trauma of the caudal vagina and vulva at the first or subsequent parturitions may pre- dispose to prolapse during later gestation periods. This is probably a very common predisposing cause in older cattle especially if they were immature or poorly grown heifers and required great traction to relieve dystocia oc- curring at the first parturition. The condition is favored by close confinement especially in stanchions in which the cow’s rear parts project over the gutter and in sheep, especially those confined on lush pastures and carrying twins.12 It is seen less commonly in pastured cattle. Over- distention of the abdomen or excessive amounts of loose pelvic fat favor the condition by increasing the intrapel- vic pressure. These factors are not important unless the pelvic and vulva structures are relaxed enough to allow the vaginal wall to prolapse. An hereditary cause is sus- pected occasionally in cattle if a dam and her daughter both develop vaginal prolapse. The high incidence of this condition in Hereford cattle may indicate a possible he- reditary factor in this breed. This condition is occasionally observed in dairy cattle following parturition. At this time it is often associated with cystic ovaries, another condition characterized by excessive estrogen production. In dogs, especially noted in Boxers and the larger breeds, most cases of vaginal prolapse occur during proestrus and estrus and regress during metestrus, only to recur again at the next estrus. Protrusion of the hy- pertrophied vaginal mucosa or prolapse may occur. The latter is usually due to heredity, excessive estrogens and their relaxing effect on pelvic and perineal structures, tenesmus, forcible separation of the male before the end of coitus and disproportion in size between the two sexes. In a few instances the ration may play a role in the cause of this condition. In swine and occasionally cattle the feeding of moldy com or barley containing an estrogenic mycotoxin, may cause edema of the vulva, relaxation of pelvic ligaments, tenesmus, and prolapse of the vagina and even the rectum. Young swine and cattle are more often affected.17 20 This condition has been called vulvo- vaginitis and is generally considered to be due to a high estrogen content in the moldy feed.21 Certain types of legumes such as subterranean clover in Australia may contain a high level of estrogens and produce permanent sterility iti ewes due to cystic degeneration of the en- dometrium, marked mammary growth and development, great enlargement of the bulbo-urethral glands in weth- ers, uterine inertia and dystocia, as well as a high in- cidence, 10 to 12 percent, of prolapse of the vagina in nonpregnant ewes.3 The development of vaginal pro- lapse ceased after removing the ewes from the subter- ranean clover pastures.28 Proper fertilization and rotation of pastures to maintain a certain percentage of grasses largely prevented this condition in sheep pastured on this type of clover.7 The former use of stilbestrol or estrogens in fattening lambs in the United States produced vaginal prolapse.8 Once prolapse of the vagina or cervix has occurred the exposed mucous membranes as well as the vulvar and vestibular mucosa become very edematous, inflamed, ir- ritated, infected, and occasionally necrotic. The bladder may prolapse through the vulva within the vaginal floor and continue to fill with urine. These factors tend to pre- vent the return of the prolapsed structures when the cow rises, and favor tenesmus, or straining, that may lead to prolapse of the cervix and the rectum and to exhaustion. In most cases occurring during the late gestation period, the symptoms usually cease after parturition. There is no relationship between prolapse of the vagina and cervix prior to parturition and prolapse of the uterus after par- turition. Prolapse of the uterus is no more likely to occur when prolapse of the vagina has preceded parturition than in cows not affected. Prolapse of the vagina and cervix will invariably recur and become more severe during subsequent pregnancies. The symptoms of vagino-cervical prolapse are ob- vious and the condition is often spoken of by the farmer as “casting of the wethers.” In the cow this condition is usually observed the last 2 to 3 months of gestation with an increasing incidence as parturition is approached. Oc- casionally it is seen as early as 4 to 5 months of gesta- tion. In a few cases it is observed after parturition in the cow. In the ewe and other species of domestic animals it seldom occurs other than a few weeks prior to par- turition except in the dog. Prolapse of the vagina in the bitch is seen most commonly at the time of estrum. TheDISEASES AND ACCIDENTS OF GESTATION 235 Figure 82. Prolapse of the vagina in a first-calf heifer. symptoms may vary from a mild protrusion of the va- ginal mucous membrane through the vulvar lips when the cow lies down, to a severe necrotic vagino-cervical prolapse containing a greatly distended bladder and com- plicated by a prolapse of the rectum due to the constant tenesmus (see Figures 82, 83, 84). In mild cases the pro- lapsed vaginal wall returns to its proper position when the cow rises. The degree of vulvitis, vaginitis, and cer- vicitis will vary depending upon the length of time the condition has existed and the type of mechanical, ther- mal, or infectious agents acting upon the prolapsed mu- cous membranes. The symptom of straining or tenesmus may be absent, intermittent and mild, or severe and nearly constant, depending upon the degree of the prolapse, the degree of inflammation, edema and irritation involving the genital canal, and the degree of distention of the bladder. Edema of the prolapsed vagina and cervix oc- curs because of the irritation and trauma to the exposed mucous membrane, and because this portion drops over the ischial arch thereby causing a passive venous conges- tion. This edema tends to accumulate in the submucosa and cause a separation of the mucosa from the under- Figure 83. Prolapse of the vagina, including the bladder, in a cow. lying thin muscular vaginal wall. The cervical seal usu- ally remains intact; although if the cervix is prolapsed and inflamed, the external portion of the seal may be absent. Occasionally the cervix relaxes, the cervical seal is lost and abortion or premature parturition occurs within 24 to 72 hours. If breeding records are not available, a rectal or vaginal examination should be made to see if the fetus is still alive and to determine the approximate stage of gestation. These factors are important in the prognosis and treatment. If the fetus is alive, the uterine artery has its characteristic “whirr,” or fremitus, and the fetus moves when its foot or eyeballs are pinched or its leg or jaw is pulled. In some recently purchased cows vulvar scars may be found indicating previous treatments for vaginal prolapse during other pregnancies. In ne- Figure 84. Prolapse of the vagina and cervix with a secondary pro- lapse of the rectum in a cow.236 VETERINARY OBSTETRICS glected, severe cases the exposed mucous membrane may be necrotic resulting in a toxemia and septicemia. This together with exhaustion caused by the constant straining may cause a fast, weak pulse, anorexia, rapid loss of weight, general body weakness, death of the fetus, pos- sible uterine infection and death. Necrosis or gangrene may even involve the cervix and the caudal portion of the uterus secondary vascular insult and thrombosis. If prolapse of the vagina occurs postpartum, the ovaries should always be examined for the presence of cysts and if no cysts are present the vulva should be examined for injuries. In the ewe suffering from prolapse of the vagina or cervix, death and maceration of the fetus fol- lowed by the death of the dam is not uncommon. Severe infections of the birth canal associated with prolapse of the vagina may result in uterine infections or retained afterbirth following parturition or abortion. Differential diagnosis should rather easily distinguish between pro- lapse of the vagina and cervix, and cystic Bartholin’s glands, hematomas of the vulva, tumors of the vagina or vulva, prolapse or eversion of the bladder, rupture of the vagina and prolapse of perivaginal fat, and thick heavy fetal membranes. Cows will usually calve without as- sistance in nearly all uncomplicated cases. After partu- rition the prolapse is usually immediately relieved. The prognosis in prolapse of the vagina and cervix depends upon the severity of the condition and the length of time it has existed. Except in extreme or severe cases, the prognosis is generally fair to good for the life of the animal and the fetus if treatment is prompt and aftercare is good. The condition will recur at subsequent gestation periods unless suitable procedures are followed to pre- vent it. In the more extreme conditions complicated by prolapse of the rectum, death of the fetus, impending abortion, septic metritis, severe necrosis of the prolapsed organs, exhaustion, septicemia and toxemia, marked de- bility of the patient, or constant and violent straining, the prognosis is guarded to poor. Slaughter should be considered after parturition or weaning of the newborn because of the tendency for this condition to recur and the possible hereditary nature of the condition. In sheep the prognosis is more guarded, since 10 to 20 percent of pregnant ewes may die or expel dead fetuses. The method of treatment selected for handling pro- lapse of the vagina and cervix will vary with the species and breed of animal, the severity of the condition, the stage of pregnancy and the ability of the owner to care for and observe the animal until after parturition. Early prompt treatment often permits the use of simple con- servative methods and obviates the necessity of using more heroic techniques. Many methods of handling pro- lapse of the vagina are available. These will be discussed in order from the conservative to the more heroic meth- ods used in cattle and then the handling of prolapse in the other species will be mentioned. The operator should select the most conservative method possible under the circumstances and caution the owner that as pregnancy progresses other methods may need to be used to control the condition. Combinations of methods may be used. Of the 16 procedures or techniques described in the second edition (1971) to correct prolapse of the vagina and control straining or tenesmus, 4 have been elimi- nated in this third edition because they have not been generally accepted by practicing veterinarians even though some beneficial effects were originally ascribed to them. They are: (1) the use of progesterone injections to con- trol vaginal prolapse in mild or early cases,37 (2) the technique for removal of large deposits of perivaginal fat;1213 (3) the use of artificial pneumoperitoneum to control tenesmus,10 31 and (4) the technique of unilateral pudendal neurectomy.9,33 Although the vaginal reefing operation for chronic vaginal prolapse11 may only oc- casionally be used, the author has briefly described it because it may be of value in chronic vaginal hypertro- phy and prolapse in bitches. (1) In mild cases in cattle in which only a slight pro- lapse occurs when the cows lie down, the cow should be removed from the stanchion and placed in a box stall. In slightly more advanced cases (2) one may elevate the rear parts of the cow in a stanchion by means of an in- clined platform that raises the rear quarters 2 to 6 inches higher than the front quarters. In a stall this may be done by building up the bedding under the rear quarters or digging out the soil under the front quarters. This prac- tice has been frequently followed in many of the mild cases of prolapse without any untoward effects with the exception that the rear quarters of the dairy cow have been difficult to keep clean. This simple procedure has prevented many mild cases from becoming more severe and has circumvented the use of trusses or vulvar su- tures. It is most practical in dairy cattle. In replacing the prolapsed bovine vagina and cervix epidural anesthesia using 5 to 8 ml. of 2 percent pro- caine or xylocaine solution is very helpful and usually necessary particularly in the more severe cases where tenesmus is present. Blocking the internal pudendal nerves in cows, in the manner described for bulls,19 anesthetizes the vulva and vestibular structures without affecting any motor nerves which is often observed in epidural anes- thesia. It is advisable to have the animal standing, pre- ferredly with the rear parts elevated to facilitate replace- ment of the prolapsed organs. In smaller animals the lifting or even suspending of the rear parts off the ground is easily accomplished and greatly aids replacement. TheDISEASES AND ACCIDENTS OF GESTATION 237 prolapsed portions should be washed free of dirt and de- bris with a mild, nonirritating antiseptic solution or physiological saline. If irritation, infection, or straining is present a bland antiseptic oil, or sulfonamides or an- tibiotics in oil or ointment, might be of value when ap- plied to the prolapsed vagina before replacing, and in- jected into the vagina once to twice daily for several days or more after replacement. If difficulty is encountered in replacement of the prolapsed vagina with the distended bladder inside it, the prolapsed portion may be raised dorsally to reduce the sharp kink in the urethra, thus per- mitting the urine to escape. In exceptional cases it may be necessary to trocarize the bladder through the pro- lapsed vagina wall with a large-gauge needle. Once the vaginal floor and walls are replaced the normal circu- lation is restored and the edema in the vaginal walls and mucous membrane is rapidly reduced. If the vagina is badly infected the animal may have an elevated body temperature. In these cases or those in which the cervix is relaxed and dilated and abortion appears likely, a course of antibiotic or sulfonamide therapy is indicated to con- trol infection and septicemia, and if abortion does occur to prevent septic metritis. (3) The vulvar truss is of practical value in controlling prolapse of the vagina in dairy cattle confined in stan- chions or box stalls where the owner is able to check and adjust the truss as needed. These trusses may be made of rope, leather, or metal. An aluminum rod truss26 held in place with ropes is easily molded to fit the in- dividual cow. These trusses are held in place by ropes or leather straps securely fastened to a surcingle around the cow’s chest and neck. The truss, as it fits over the vulva, may be padded with toweling or burlap to prevent abrasions or necrosis where it lies against the ischial arch. When the cow arches her back to urinate or calve the truss will loosen. Cows have been reported to have calved with the truss in place. Many dairy farmers prefer these simpler, less drastic methods, 1 through 3, for handling vaginal prolapse. Most cases are mild and when treated early the results are satisfactory. The above techniques are not usually satisfactory when tenesmus is severe or vagino-cervical prolapse is marked. (4) Pessaries which are popular in Europe consist of a long narrow wine bottle or similar blunt round object inserted into the vagina after replacement. Pessaries are held in place by a narrow piece of wood or metal placed into the bottle with a ring or loop on the end projecting out of the vulva. A rope is fastened through this ring similar to ropes that hold a metal, plastic or leather truss in place. A light metal rod or plastic pessary shaped like a hairpin with long lateral arms containing eyes so it could be fastened to the wool of ewes has been described and is available commercially in the United States.16 Pessa- ries have not been popular in the United States because an object placed in the vagina tends to cause straining and expulsion of the pessary. (5) Vulvar sutures that do not pass through the vulvar lips are often a satisfactory method of treating vaginal prolapse for a limited period especially the last 2 to 3 weeks of gestation. The sutures should be located at least 2 to 3 inches lateral to the vulvar lips in the hair line. This affords a much tougher and thicker skin for the su- ture, which does not tear out as readily nor cause as much irritation as one in the vulvar lips. It is desirable to use a type of suture that can be untied or released, so that if a cow appears to be near or in the first stage of par- turition the vulvar sutures can be unfastened, so that calving can occur. If the calving time has been mis- judged and prolapse again results, the prolapsed vagina may be washed and replaced. If prolapse does not occur, the sutures can be retied. This is not possible with the simple horizontal figure-eight or horizontal mattress su- tures that do not pass through the vulvar lips or deep horizontal mattress sutures, usually of double thickness one-eighth to one-quarter-inch thick umbilical tape, that have been passed through each lateral wall of the vulvar vestibule and including the vulvar lips. Another advan- tage of the type of suture that can be untied is that if there is some possibility of postpartum prolapse of the vagina, or even the uterus, the sutures can be retied after parturition and left for several more days. Although some suppuration occurs around these stiches they may be left in place for as long as 6 to 8 weeks. The vulva-suturing technique preferred by the author is one employing 4 to 5 small separate loops of doubled 1/4-3/8 inch umbil- ical tape or heavy nylon on either side of the vulva in the hair line from the level of the anus to about opposite the lower commissure of the vulva.12 About 2 feet of 1- 1/2-inch to 3-inch gauze bandage, doubled, is used to lace up the loops in a manner similar to lacing a shoe. This gauze may be removed or replaced as desired. A similar but crude technique is the use of hog rings in- stead of umbilical tape loops. These tend to tear out or work out of the skin. A metal skewer type of needle with large wooden buttons to hold the vulvar lips together and other metallic clamp-like devices have been advocated by European veterinarians and are available commer- cially. Some veterinarians prefer quill, button, or deep horizontal mattress sutures of umbilical tape, through the vulvar skin, muscle, and mucous membrane.18,32 (6) A buried or “hidden” purse-string type of suture, Buhner's method, for the vulva following replacement of a prolapsed vagina has been described.16 27 This tech- nique may be used in chronic postpartum prolapse as238 VETERINARY OBSTETRICS well as prepartum prolapse. Under epidural anesthesia and with a near-sterile procedure, two one-half inch in- cisions are made one to two inches above the upper com- missure and below the lower commissure of the vulva, respectively. With a long eye-point needle similar to a seton needle, an 18-inch piece of one-eighth inch thick nylon cord, heavy “Vetafil” or nylon sashcord is passed within the tissues from one incision to the other near the hairline lateral to one vulvar lip. The needle is with- drawn and reinserted in the opposite direction lateral to the opposite vulvar lip to the lower incision site and again withdrawn. The purse-string suture around the vulva is tightened sufficiently to allow 4 fingers in the vulva, and a bow knot is tied with long ends. Thus, the farmer may loosen this suture if parturition is imminent and if nec- essary tighten and retie the suture after calving. (7) A vulva-closing technique modified from the Cas- lick operation in mares has been of great assistance in the treatment of chronic prolapse of the vagina 2 months or more before parturition or in postpartum prolapse in cows. It has also proved very valuable in controlling te- nesmus associated with “windsucking” and a highly in- flamed vaginal and vulvar mucous membrane. The drawing of air into and forcing it out of a highly in- flamed vagina appears to stimulate and produce violent straining. This operation is performed under epidural anesthesia. After replacement of the prolapsed struc- tures, the caudal 3/4 inch of mucous membrane of both vulvar lips from and including the superior commissure to about 1-1/2 inches above the ventral commissure is removed with scissors. These raw areas of both vulvar lips are sewn together with interrupted vertical mattress sutures of fine catgut, nylon or silk suture closely spaced. One or two deep horizontal mattress vulvar sutures of umbilical tape are placed through the skin 2 or 3 inches lateral to the vulva and through the vulvar muscles and mucous membrane to prevent the vaginal wall being forced against the fine sutures in the vulvar lips and thus tearing them out if tenesmus occurs (see Figure 85). After 10 days all sutures may be removed. The vulvar opening is then so small that the vaginal wall cannot prolapse and air cannot gain admittance to the vaginal lumen. Just be- fore or at the time of calving it is necessary to slit this adhesion between the vulvar lips to prevent its tearing out. Because of the tendency to repeated prolapse at each gestation period, resuturing is advised immediately after calving if artificial insemination is employed or after breeding if natural service is used. (8) Minchev’s method14'23 for controlling prolapse of the vagina by surgically fastening the cranial portion of the vaginal wall through the dorsolateral wall of the sac- roscatic ligament, muscles and skin of the croup was slightly modified5 to place the stay sutures dorso-cranial to the lesser sciatic foramen.14'15 25 After replacement of the prolapsed vagina under epidural anesthesia the an- terior portion of the vagina is fastened to either side of the pelvic cavity preventing a prolapse by means of an- choring devices including gauze rolls, heavy plastic but- tons, large overcoat buttons or 3/16th inch thick pads of industrial belting. In securing the vaginal walls to the pelvic walls with these anchors inside the vagina and outside on the skin of the croup, heavy suture material such as 1/4 or 3/8 inch umbilical tape doubled or heavy Vetafil or nylon cord so that if straining does occur the vaginal wall will not be lacerated freeing it from its at- tachment to the pelvic wall. The sutures fastening the vaginal and skin buttons together may be inserted under local anesthesia by making small incisions in the skin of the croup over the sacrosciatic ligament and inserting a small rumen trocar or a crochet-type hook into the va- ginal cavity to guide or carry the suture material fastened to the vaginal button to the outside button on the skin. One may also do this by carrying a 4 to 6 inch needle threaded on the suture material attached to the vaginal button into the vagina and forcing the needle dorsolat- erally through the skin. In inserting the needle or trocar care should be taken to avoid the rectum, the pudendal nerve and vessels and the sciatic nerve that can be pal- pated medial to the sacrosciatic ligament. The authors originally describing this technique recommended that the sutures be removed in 10 to 14 days at which time the vaginal wall was firmly adhered to the pelvic wall. Firm attachment frequently does not occur by this time and prolapse of the vagina may again recur. For this rea- son many veterinarians leave the buttons and sutures in place until after calving. (9) Another recently introduced technique (Winkler) for handling prolapse of the vagina is fixation of the cer- vix to the prepubic tendon, cervipexy.24,36 This proce- dure minimized tenesmus, required no aftercase during gestation or at parturition, prevented recurrent prolapse at subsequent pregnancies and could be used in all types of cases. Under epidural anesthesia the prolapsed vagina is carefully cleaned and replaced. A 3 or 4-inch half cir- cle cutting edge suture needle is bent into a U-shape and threaded with 36 to 48 inches of heavy 3 or 4 nylon or “Vetafil,” noncapillary suture material. Material such as umbilical tape should not be used. The needle and suture material are carried into the vagina. The bladder is pushed laterally away from the midline. The needle is passed through the floor of the vagina beneath the external os of the cervix in a lateral to medial direction just cranial to the pubic symphysis and just to the right or left of the prepubic tendon and through a small lateral portion ofDISEASES AND ACCIDENTS OF GESTATION 239 Figure 85. A technique for the control of chronic prolapse of the vagina. (Left) Under epidural or local anesthesia a three-quarter inch strip of mucosa is removed from just inside the vulvar lips. (Center) An interrupted vertical mattress suture is used to draw the wound edges gently together. (Right) If the animal is straining a deep mattress suture is placed through both vulvar lips cranial to the suture line. the thick prepubic tendon, and then back up through the vaginal floor. This suture should include 1-1/2 to 2 inches of vaginal floor and 1/4 to 3/8 inch of prepubic tendon. The needle is then passed through the ventral half of the cervix at least one-half inch cranial to the external os. The suture is tied outside vulva and the knot carried for- ward so the cervix is fastened closely to, but not nec- essarily tightly against, the floor of the pelvis. It may be desirable to pass a catheter into the bladder to make cer- tain it was not included in the suture. These latter two operations (10 and 11) avoid placing sutures in the re- gion of the vulva which is richly supplied with sensory nerves and thus tenesmus is minimized. The suture is left in place indefinitely as it does not interfere with breeding or calving. This operation is performed most easily several months after calving when the uterus has involuted. Cervopexy through a laparotomy in the left paralumbar area may facilitate placing the fixation su- ture.24 (10) Another surgical “reefing” technique for correc- tion of chronic vagino-cervical prolapse, particularly adapted to selected cases in beef cattle has been de- scribed." This consists of a submucous resection of the edematous, devitalized mucous membrane from the pro- lapsed portion of the vagina. If the prolapsed portion of the vagina is large due to the presence of a distended bladder this should not be reduced before the operation as it will make surgery more difficult. Surgery can be performed under epidural anesthesia. Adrenaline in- jected or applied locally may aid in reducing hemorrhage during the peeling-off of the diseased, often necrotic, edematous mucous membrane. The sleeve of vaginal mucous membrane that is peeled off is narrow at the dorsum and wide ventrally, as more of the floor of the vagina is usually involved in the prolapse. Incisions on the prolapsed vagina are made in the normal mucous membrane near the cervix caudally and near the urethral orifice or hymen cranially. As the diseased mucous membrane is peeled off, mostly by blunt dissection, No. 3 or 4 chromic catgut suture is used to approximate the two cut edges of normal mucous membrane, as the op- eration progresses. This is done to control hemorrhage, which is usually quite severe but of a capillary oozing type, and to get most of the incision sewed before the prolapsed vagina begins to drop back into its proper in- trapelvic position. In most operations traction applied to the cervix is necessary to keep the vagina retracted and outside the vulva until the suturing is completed. The vagina is greatly shortened by this reefing operation so that the cervix is nearer the vulva. Since the excess va- ginal wall is thereby eliminated, the prolapse will not recur during that particular gestation though in rare cases it may during subsequent ones. Tenesmus ceases after the operation. The muscular coat of the vaginal wall is drawn up in folds under the suture line that joins the cephalic and caudal edges of normal vaginal mucous240 VETERINARY OBSTETRICS membrane. In operating on cows in which most of the vagina is prolapsed, care should be exercised in remov- ing the mucous membrane on the dorsal surface of the vagina not to cut too deeply and enter the recto-genital pouch of peritoneum, that extends about 5 inches caudad on the dorsal surface of the vagina. Care should also be used to prevent incising the urethral opening or urethra. Obviously this operation should not be performed if the cow is due to calve within 3 to 4 weeks or if abortion appears likely. This is not an operation to select as a last resort in a neglected case, with the patient exhibiting symptoms of toxemia and exhaustion. The type of case indicated for this operative should be selected carefully. The prolapse should have occurred relatively early in the gestation period or be a chronic postpartum prolapse. The cow should be in good condition for the operation. It is particularly indicated in that type of cow, usually beef, in which regular observation and care of the cow is not possible. In the bitch, no treatment of mild cases of vaginal hy- perplasia and prolapse is indicated, as the condition cor- rects itself after estrum. In breeding dogs the removal of the prolapsed mucous membranes by a reefing technique similar to the one described in the cow gives good re- sults."'22'32 Episiotomy in the dorsal position may be necessary as an aid in resection of the mucous membrane in the dog.14 In nonbreeding dogs ovariectomy results in a permanent cure. (11) In chronic prolapse in postpartum cows treatment with a gonadotrophic hormone or GnRH is indicated if cystic ovaries are present.12 In unusual cases other meth- ods of handling might be indicated such as a cesarean section late in gestation. If prolapse of the rectum occurs along with prolapse of the vagina the prognosis is more grave and either a purse-string suture to retain the rectum, a reefing oper- ation, or amputation of the rectum might be indicated, along with feeding or administering mild laxatives or large amounts of fluids to prevent constipation. Prompt slaughter of many animals affected with severe prolapse of both vagina and rectum is advisable as persistent tenesmus is common in these animals. If constant tenesmus after replacement is a problem, repeated use of local epidural anesthesia at one to two hour intervals may be helpful if accompanied by intra- vaginal infusions of bland, protective antiseptics in oil. In certain beef cattle some veterinarians have injected 3 to 8 ml. of benzyl, ethyl or isopropyl alcohol epidurally that destroys the nerve tissue resulting in anesthesia to the perineum and paralysis of the tail lasting from 2 to 6 months. This technique is not desirable for dairy cattle for sanitary reasons. The old technique of a tracheotomy operation to prevent straining is rarely, if ever, necessary or recommended. Recently some of the local anesthetics such as benzocaine, nupercaine, and cyclaine have been incorporated into ointment bases. The application of these ointments to the vaginal and vulvar mucous membranes have been recommended to control local surface irrita- tion and the resulting tenesmus. However, the author has not found these local anesthetic ointments very effective. Paraplegia of Pregnancy There are numerous causes for paraplegia, or paresis, during pregnancy. Most of these conditions occur in, or are aggravated by, advanced pregnancy, during which period there is very rapid growth of the fetus and an increase in weight of the gravid uterus as well as a pro- gressive relaxation of the pelvic ligaments and an in- crease in the size and development of the udder. The factors, and several may operate together, that may cause a cow to exhibit paresis in advanced pregnancy are: Nutritional deficiencies and starvation—A lack of minerals such as phosphorus and calcium may result in debility, pica, bone and joint lesions, and even an in- crease in incidence of fractures. A lack of trace min- erals, principally copper, cobalt, and iron, has been re- ported as resulting in anemia and debility, which if extreme may cause weakness and inability to rise. In certain areas such as Florida with high molybdenum lev- els in the soil and forage, chronic diarrhea coupled with a lack of copper, iron, and cobalt favor debility. Lack of vitamin A in the ration may lower resistance and favor uterine infections. Most nutritional deficiencies are mul- tiple, including a lack of minerals, proteins, carbohy- drates, and fats. The classic symptoms of severe under- feeding or starvation are debility, cachexia, weakness, and finally inability to rise; and in advanced cases, death of the fetus, and abortion. In certain areas of the country specific deficiency diseases occur commonly and are known by the local veterinarians. In the high-producing dairy cow it is usually desirable to supply additional minerals to the ration as well as offering them free-choice to compensate for the loss of minerals in the milk and the developing large fetus. Ketosis—Pregnancy disease in ewes due to a lack of carbohydrates is a common cause for debility and par- aplegia in ewes and does in advanced pregnancy. Twin or triplet pregnancy is a predisposing factor. Usually the fetuses die and the ewe often succumbs. If the fetuses are aborted promptly the ewe may recover; or treatment administered early in the disease may bring about re- covery. Therapy for ketosis consists of glucose intra-DISEASES AND ACCIDENTS OF GESTATION 241 venously, propylene glycol or glycerol orally and glu- cocorticoids in small doses parenterally. Large doses of glucocorticoids may induce premature parturition or abortion in late pregnancy. In a valuable ewe near term, cesarean section may be indicated. The carbohydrate in- take of the rest of the pregnant ewes in the flock should be increased by feeding grain or molasses. Provision for increased exercise may be helpful. This condition may be observed in the cow and bitch prior to parturition.2,4'5 Grass tetany is seen in pregnant cattle on lush pas- ture, such as wheat pastures, particularly in the fall or early spring. In areas with soil deficient in calcium and magnesium, it may occur at any time of year even in stabled animals. It is apparently due to a lack of calcium causing hypoclacemia and/or magnesium causing hy- pomagnesmia. Some believe it is associated with the high potassium or high vitamin A levels of the lush, green immature forage. Mineral feed or feeding of good-qual- ity alfalfa or clover hay rich in calcium, magnesium and phosphorus tends to prevent the condition. It is probably best to remove the stock from the lush pasture for a time. The paretic cases usually respond to calcium therapy, or if paresis and nervous symptoms are present both cal- cium and magnesium therapy are indicated. Milk fever or parturient paresis may occur just prior to parturition in the high-producing dairy cow, at which time it is called preparturient milk fever or paresis. Most preparturient cases occur during the first stage of par- turition, when milk letdown is favored by the action of the oxytocin released at that time. Following treatment, active labor and calving will often follow within 4 to 6 hours. In a few cases preparturient milk fever, or hy- pomagnesemia due to a sudden drop in blood calcium and/or magnesium may be observed 24 to 72 hours be- fore parturition. Transport stress in cows late in preg- nancy may precipitate this condition.6 Puerperal tetany, or eclampsia in dogs and rarely cats associated with a hypocalcemia characterized by nervousness, restlessness, whining, and then staggering, stiffness of the legs, and finally collapse with clonic spasms, labored respirations, salivation, and elevation of temperature, may be seen occasionally prior to parturi- tion although it is far more commonly observed the first 2 weeks after parturition. Dropsy of the fetal membranes and fetus—This may occur from 5 months to term as has been discussed pre- viously and is associated with a great increase in abdom- inal weight and size and the inability to rise. The in- creased abdominal weight may lead to injury such as dislocation of the hips. Joint and tendon injuries, especially to the rear limbs, may render the animal unable to rise. Dislocation of the hip is common in the cow in advanced pregnancy, es- pecially after slipping on concrete floors or ice in the barnyard. Dislocation or subluxation of the stifle are oc- casionally observed. Separation of the ligaments of the ilio-sacral articulation is infrequently observed. Some- times painful lesions of the joints, due to chronic arthritis of the stifle or hip or suppurative lesions of the hock or coffin joint, may cause reluctance to rise; in time, stiff- ness, myositis, neuritis and weakness and paresis may result with inability to rise.3 Sudden rupture of the pre- pubic tendon in the mare or rupture of the gastrocnemius tendon, usually secondary to Zenker’s muscle degener- ation in the cow, may occasionally be causes in these animals of their being unable to rise or rising with dif- ficulty. Fractures of the rear limbs or spine—Fractures of the femur and pelvis are the most common of those oc- curring in advanced pregnancy. They may occur when a cow in advanced pregnancy is mounted by another cow. Osteomalacia due to a prolonged mineral deficiency fa- vors fracture. Excessive relaxation of joints and liga- ments due to estrogens present in advanced pregnancy may also lead to fractures. Spinal injuries or fractures in the lumbar region with severe posterior paresis, may oc- casionally occur. If a cow or bull mounts the pregnant animal, the impact of the sternum on the coccygeal and sacral vertebrae may cause a subluxation, dislocation, or fracture of these vertebrae and subsequent posterior weakness and paralysis of the tail. Septic or infectious processes associated with ad- vanced pregnancy may cause paresis. They may be any of the following: septic metritis of pregnancy with death and maceration of the fetus; rupture of the uterus with severe peritonitis secondary to an emphysematous fetus; traumatic gastritis with diffuse peritonitis; severe torsion of the uterus with gangrene and shock, or death of the fetus and rupture of the uterus; severe pyelonephritis ag- gravated by advanced pregnancy; or septic mastitis. Other conditions that may cause paresis or paraplegia in animals at any time may affect the pregnant animal. These are as follows: rupture of a large uterine vessel with hemorrhage, toxic indigestion, diseases of the cen- tral nervous system, such as rabies and listeriosis; severe prolonged illness resulting in debility such as: Johnes disease, severe mange or pediculosis, advanced actino- mycosis of the jaw, and senility; tumors especially of the brain and spinal cord, such as lymphocytoma; severe septicemic diseases such as: anthrax, blackleg, pasteu- rellosis, leptospirosis and anaplasmosis; and severe foot lesions.6 If an animal is down, struggles to rise, but remains down for a period of time particularly on a hard concrete242 VETERINARY OBSTETRICS floor, decubital injuries, contusions, abrasions, joint muscle, nerve and tendon injuries, and exhaustion are common. These cause progressive soreness, stiffness, awkwardness, and even greater difficulty in rising. Many so-called malingerers or “downer” cows2,3'6 have arthri- tis, myositis, neuritis or tendonitis painful and debilitat- ing enough so that they refuse or are unable to rise. These animals might benefit from good nursing, a dirt floor or heavily bedded box stall, and slings to get them up pe- riodically so as to restore movement and circulation to the legs. Occasionally butazolidin or similar drugs to control inflammation and pain are of value. The further handling of these animals in advanced pregnancy de- pends upon their value for food, their sentimental value, the value of the offspring, the nature and severity of their diseases or injuries, and the owner’s ability, means, and interest in nursing these paraplegic, paretic or “downer” animals. Miscellaneous Accidents of Pregnancy Hemorrhages of pregnancy—The most common hemorrhage of pregnancy is that associated with hematic mummification of the bovine fetus. This occurs in the utero-chorionic space of a sealed uterus. Slight hemor- rhages occur between the maternal and fetal placenta that may be noted on examination of the placenta after par- turition. In the cow “uterine sand,” occasionally found in the utero-chorionic space, is dried or inspissated gran- ules of serum about 1/64 to 1/16 inch in diameter. Oc- casionally due to trauma or violence causing rupture of the larger vessels, hemorrhage or large blood clots suf- ficient to cause death may be found around the vagina or in the broad ligament in the cow or mare in late preg- nancy. Mares should not be transported or subject to vi- olent exercise in late pregnancy for this reason. Hem- orrhage or bleeding from the genital tract appearing at the vulva during pregnancy is rare in domestic animals. It may be noted in pyelonephritis, in a traumatic injury to the vagina, vulva or bladder or in tumors of the vulva or vagina that bleed readily. In mares recurrent slight bleeding from a ruptured varicose or surface vein in the vagina or hymenal region is common but not serious; it may heal spontaneously or be corrected by cautery or by surgically ligating the lesion. Bleeding usually ceases after parturition. A reddish-brown vulvar exudate containing free blood may be associated with beginning abortion and a dead fetus or a septic metritis of pregnancy with an open cervix. Hemoglobinuria due to leptospirosis and other acute hemolytic diseases may be confused in the pregnant animal with bleeding from the genital tract. Rupture of the gravid uterus—This may occur either spontaneously due to unknown causes, or secondary to abortion, dystocia, emphysematous fetuses, chronic per- itonitis with uterine adhesions, torsion of the uterus, dropsy of the fetal membranes and fetus, and extreme violence and trauma in advanced pregnancy. Strangulation of the large colon by the gravid uterus—A mare with unexplainable symptoms of diges- tive distress proved to have, on postmortem examina- tion, a displacement of the large colon beneath the gravid uterus.7 Obstruction of the bowel may also occur asso- ciated with uterine torsion. Strangulation of the pregnant uterus by a pedun- culated lipoma—A case of a 4-month pregnancy in a cow was cited in which a pedunculated lipoma wrapped around the uterus.1 References Extrauterine Fetuses 1. Bark, H., Sekeles, E. and Marcus, R. (1980) Extrauterine Mum- mified Fetus in the Cat. Feline Pract. 10, 3, 44-47. 2. Freytag, K. (1972) A Clinical Report of a Secondary Extrauterine Pregnancy in a Mare. Deutsche Tierarztl. Wochsch. 79, 21, 522. 3. Keyser, D. D. (1964) Displacement of an Ovine Fetus. Vet. Med. 59, 465. 4. Krichel, J. H., Jr. (1969) A Report of Six Cases of Uterine Ul- ceration in the Dog. Vet. Med. 64, 10, 872. 5. Lederer, H. A. and Fisher, L. E. (1960) Ectopic Pregnancy in a Dog. JAVMA, 137, 1, 61. 6. Nicholl, T. K. (1979) Extrauterine Fetuses in a Bitch. Canine Pract. 6, 4, 16-22. 7. Spanabel, J. J. (1957) Extrauterine Mummified Fetus in a Bitch. N. A. Vet. 38, 8, 239. 8. Williams, W. L. (1943) Veterinary Obstetrics, 4th Ed., Ithaca, N.Y. 151. Dropsy of the Fetal Membranes and Fetus 1. Arthur, G. H. (1957) Some Notes on the Quantities of Fetal Fluids in Ruminants with Special Reference to Hydrops Amnii. Brit. Vet. Jour. 113, 17. 2. Arthur, G. H. (1965) Further Observations on the Fetal Fluids of Cattle. Vet. Rec. 77, 623. 3. Arthur, G. H. (1969) The Fetal Fluids of Domestic Animals. J. Reprod. and Fertil., Suppl. 9, 45. 4a. Arthur, G. H. (1975) Veterinary Reproduction and Obstetrics, 4th Ed., Bailliere and Tindall, London. 4b. Baker, J. F. (1983) Personal Communication. 5a. Baker, M. L., Payne, L. C. and Baker, G. N. (1961) The In- heritance of Hydrocephalus in Cattle. Jour. Hered. 52, 135. 5b. Ball, L. and Brand, A. (1980) Elective Termination of Unwanted and Pathological Gestation, in Current Therapy in Theriogenol- ogy, edit by D. A. Morrow, W. B. Saunders, Co., Philadelphia, 243-245.DISEASES AND ACCIDENTS OF GESTATION 243 6. Cassidy, G. and Cailliteau, J. (1967) Amniotic Fluid in Anen- cephaly. Amer. J. of Obst. and Gynec. 97, 3, 395. 7. Crew, F. A. E. (1924) The Bulldog Calf; a Contribution to the Study of Achondroplasia. Vet. Rec. 4, 785. 8. Donald, H. P., Deas, D. W. and Wilson, L. A. (1952) Genetical Analysis of the Incidence of Dropsical Calves in Herds of Ayr- shire Cattle. Brit. Vet. Jour. 108, 227. 9. Fox, F. H. (1980) Personal Communication. 10. Gibbons, W. J. (1957) Dropsy of the Fetal Membranes. N. A. Vet. 38, 8, 233. 11. Jakobsen, K. J. and Simesen, M. G. (1959) Hydrops Amnii in Cows. Nord. Vet. Med. 11, 81. 12. Loje, K. (1930) Letalegenuer hos Husdyrene Specielt hos Kvaeg of Rod Dansk Malkrease. Tidskr. f. Landokonomi, 10, 517. 13. Lynd, F. I. (1956) Amnioallantoic Dropsy in Cows. Southwest Vet. 9, 2, 137. 14. Memon, M. A., Lock, T. F. and Nelson, D. R. (1981) Induction of Parturition with Prostaglandin F,„ in Cows with Hydrallantois; A Case Report. Theriog. 16, 6, 681-683. 15. Milne, F. J. (1953) Treatment of Hydrops Amnii with E.C.P. JAVMA, 123, 520. 16. Neal, P. A. (1956) Bovine Hydramnios and Hydrallantois. Vet. Rec. 68, 5, 89. 17. Oehme, F. W. (1964) Hydrops Allantois Associated with Twin Pregnancy and Uterine Rupture in a Cow. JAVMA, 145, 7, 688. 18. Roberts, J. A. F. (1929) The Inheritance of Lethal Muscle Con- tracture in the Sheep. Jour. Genet. 21, 57. 19. Sharp, A. J., Bierschwal, C. J., Elmore, R. G., Youngquist, R. S., Jenkins, A. L., Kesler, D. J. and Garverick, H. A. (1978) Response of Two Cows with Hydramnios and Hydrallantois to Treatment with Cloprostenol. Theriog. 10, 1, 27-33. 20. Skydsgaard, J. M. (1965) The Pathogenesis of Hydrallantois Bovis. Acta Vet. Scand. 6, 193. 21. Vandeplassche, M., Bouters, R., Spincemaille, J. and Bonte, P. (1974) Induction of Parturition in Cases of Pathological Gestation in Cattle. Theriog. 1, 3, 115-121. 22. Vandeplassche, M., Bouters, R., Spincemaille, J. and Conte, P. (1976) Dropsy of the Fetal Sacs in Mares; Induced and Sponta- neous Abortion. Vet. Rec. 99, 67-69. 23. Vandeplassche, M., Oyaert, W., Bouters, R., Vandenhende, C., Spincemaille, J. and Herman, J. (1965) Uber die Eihautwasser- sucht beim Rind. Wiener Tierarztl. Monatsschr. 5, 52, 461. 24. Williams, W. L. (1943) Veterinary Obstetrics, 4th Ed., Ithaca, N.Y., 179. 25. Wintour, E. M., Barnes, A., Brown, E. J., Hardy, K. J., Hor- acek, I., McDougall, J. M. and Scoggins, B. A. (1977) The Role of Deglutition in the Production of Hydramnios. Theriog. 8, 4, 160. Abdominal Hernias Associated with Hysterocele 1. Benesch, F. (1952) Lehrbuch der Tierarztlichen Geburtshilfe und Gynakologie, Urban and Schwarzenberg, Wien-Innsbruck, Aus- tria. 2. Benesch. F. and Wright, J. G. (1951) Veterinary Obstetrics, Wil- liams and Wilkins Co.. Baltimore, Md. 3. Drost. M., Dunn, H. O. and Stormont, C. (1974) Bovine Quad- ruplets—a Clinical and Cytogenetic Report of Two Cases. Ther- iog. 1, 1, 35-37. 4a. Emmerson, M. A. (1944) Rupture of the Prepubian and Sub- pubian Tendons in the Cow. Univ. of Penn. Vet. Ext. Quart. 94, 3. 4b. Gilmore, L. O. and Fechheimer, N. S. (1969) Congenital Ab- normalities in Cattle and Their General Etiologic Factors, J. Dairy Sci., 52, 11, 1831. 5. Hughes, D., Moore, R. A. and Fincher, M. G. (1958) Massive Hematomas, Mod. Vet. Pract. 39, 7, 56. 6. Ladds, P. and Vestweber, J. (1972) Diagphragmatic Metrocele in a Pregnant Gilt. Cor. Vet. 62, 3, 403-405. 7. Meek, O. G., DeGrofft, D. L. and Schneider, E. E. (1977) Sur- gical Repair of Similar Parturition-induced Midline Ventral Her- nias in Two Mares, Vet. Med/Sm. An. Clin. 72, 6, 106-1074. 8. Riser, W. H. (1963) Inguinal Hernia Containing a Portion of the Uterine Horn and a Fetus. JAVMA, 143, 1, 64. 9. Snow, R. (1956) Inguinal Metrocele (Gravid) in a Bitch. JAVMA, 129, 8, 359. 10. Wright. J. C. (1964) Inguinal Hernia in the Bitch. Abstr. JAVMA, 144, 5, 500. Torsion of the Uterus During Pregnancy 1. Arthur, G. H. (1975) Wright's Veterinary Obstetrics, 4th Ed., Williams Wilkins Co., Baltimore, Md. 2. Arthur, G. H. (1966) Recent Advances in Bovine Obstetrics, Vet. Rec. 79, 22, 630. 3a. Bloom, F. (1954) Pathology of the Dog and Cat. Amer. Vet. Public, Inc., Evanston, 111. 3b. Guthrie, R. G. (1982) Rolling for Correction of Uterine Torsion in the Mare, JAVMA, 181, 1, 66. 4. Nijhof, W. J. (1959) Torsion of the Uterus in a Sow. Tijdschr. v. Diergeneesk 84, 774. 5a. Pascoe, J. R., Meagher, D. M. and Wheat, J. D. (1981) Surgical Management of Uterine Torsion in the Mare: A Review of 26 Cases. JAVMA, 179, 4, 351-354 (and Proc. Ann. Mtg. Soc. for Theriog, Spokane, Wa. 271-275) (Review). 5b. Pierson, H. (1971) Uterine Torsion in Cattle: a Review of 168 Cases Vet. Rec. 89, 597. 6. Pugh, D. M. (1963) Uterine and Abomasal Torsion in the Ewe. Vet. Rec. 75, 40. 1028. 7. Roberts, S. J. and Hillman, R. B. (1973) An Improved Tech- nique for the Relief of Bovine Uterine Torsion. Cor. Vet. 63, 111-116. 8. Settergren, I. (1969) Personal communication. 9. Skjerven, O. (1965) Correction of Uterine Torsion in the Mare by Laparotomy. Nord. Vet. Med., 17, 377. 10. Sloss, V. and Dufty, J. H. (1980) Handbook of Bovine Obstet- rics. Williams and Wilkins, Baltimore. 11. Stein, B. S. (1980) Obstetrics, Surgical Procedures and Anes- thesia, in Current Therapy in Theriogenology, edit by D. A. Mor- row, W. B. Saunders Co.. Philadelphia, 867-868. 12. Stein. B. S. (1980) Obstetrics, Surgical Procedures and Anes- thesia, in Current Therapy in Theriogenology, edit by D. A. Mor- row, W. B. Saunders Co., Philadelphia, 867-868. 13. Vandeplassche, M., Pardis, F. and Bouters. R. (1961) Surgical Correction of the Uterine Torsion in the Mare. Vlaams Dierge- neesk Tijdschr. 30, 10. 14. Van der Kaay, F. C. and de Bois, C. H. W. (1958) Torsion of the Uterus in the Mare. Berl. und Munch. Tierartzl. Wchnschr. 71, 112. 15. Wensvoort, P. (1956) Two Cases of Torsion of the Uterus in the Sow. Tijdschr. v. Diergeneesk 15, 71.244 VETERINARY OBSTETRICS 16. Williams, W. L. (1943) Veterinary Obstetrics 4th Ed., Ithaca, N.Y. Prolapse of the Vagina 1. Arthur, G. H. (1966) Recent Advances in Bovine Obstetrics, Vet. Rec. 79, 22, 630. 2. Arthur, G. H. (1975) Wright’s Veterinary Obstetrics, 4th Ed., Williams, Wilkins Co., Baltimore, Maryland. 3. Bennetts, H. W., Underwood, E. J. and Shier, F. L. (1946) A Specific Breeding Problem of Sheep on Subterranean Clover Pas- tures in Western Australia, Austral. Vet. J. 22, 1, 2. 4. Bloom, F. (1968) Canine Medicine, 1st Catcott Ed., Amer. Vet. Public, Inc., Wheaton, 111. 5. Bouckaert, J. H., Oyaert, W., Wijverkens, H. and Meirhaeghe, E. (1956) Prolapse of the Vagina in the Cow, Vlaams Dierge- neesk. Tijdschr. 25, 119. 6. Buhner, F. (1958) Eine Einfache Chirurgische Verschluss Meth- ode fur Alle Scheiden und Uterusvorfalle, Tierarztl. Umsch. 13, 183. 7. Came, H. (1955) Personal communication. 8. Clegg, M. T., Albaugh, R., Lucas, J. and Weir, W. C. (1955) A Comparison of the Effect of Stilbestrol on the Growth Re- sponse of Lambs of Different Age and Sex, J. An. Sci. 14, 1, 178. 9. Ebert, E. F. and Bierschwal, C. J. (1956) Pudendal Neurectomy, Veterinary Scope, Upjohn Comp., Winter. 10. Espersen, G. (1962) Artificial Pneumoperitoneum for Tenesmus in Cattle, Wien Tierartzl. Mschr. 49, 825. 11. Farquharson, J. (1949) Vaginal Prolapse in the Bovine, Rept. of the 14th Intemat. Vet. Congr., London, England, 3, 264. 12. Frank, E. R. (1953) Veterinary Surgery Notes, Burgess Publ. Co., Minneapolis, Minn. 13. Guard, W. F. (1953) Surgical Principles and Technics, 2274 Yorkshire Rd., Columbus, 12, Ohio. 14. Habel, R. E. (1957) Prevention of Vaginal Prolapse in the Cow, Transl. JAVMA, 130, 8, 344. 15. Hentschl, A. F. (1961) The Button Technique for Correction of Prolapse of the Vagina in Cattle, JAVMA, 139, 12, 1319. 16. Jones, B. V. (1958) Control of Vaginal Prolapse in Ewes, Vet. Rec. 70, 17, 362. 17. Koen, J. S. and Smith, H. C. (1945) An Unusual Case of Genital Involvement in Swine Associated with Eating Moldy Com, Vet. Med. 40, 4, 131. 18. Lamp, J. H. and Lamp, T. M. (1981) A Method for Correcting Vaginal Prolapse in a Cow, Vet. Med/Sm. An. Clin. 76, 3, 395- 396. 19. Larson, L. L. (1953) The Internal Pudendal (Pudic) Nerve Block for Anesthesia of the Penis and Relaxation of the Retractor Penis Muscle, JAVMA, 123, 916, 18. 20. Libke, K. G. (1960) Personal communication. 21. McErlean, B. A. (1952) Vulvovaginitis of Swine, Vet. Rec. 64, 37, 539. 22. Merrillat, L. A. (1943) Whipple’s Operation for Prolapse of the Vagina in Bitches, JAVMA, 103, 800, 286. 23. Minchev, P. (1956) The Use of a New Surgical Method in Ev- ersion and Prolapse of the Vagina in Animals, Veterinariya, 33, (see Habel). 24. Noordsy, J. L. (1981) Cervopexy as a Treatment for Chronic Vaginal Prolapse in the Cow, Vet. Med/Sm An. Clin 76, 383- 385. 25. Norton, E. S. (1969) External Fixation of the Bovine Vagina after Reduction of a Prolapse, JAVMA, 154, 10, 1179. 26. Payton, J. (1951) The Payton Uterus and Vaginal Prolapse Pre- venter, JAVMA, 119, 897, 434. 27. Pierson, R. E. (1961) A Review of Surgical Procedures for Cor- rection of Vaginal Prolapses in Cattle, JAVMA, 139, 3, 352. 28. Schinkel, P. G. (1948) Infertility in Ewes Grazing Subterranean Clover Pastures, Austral. Vet. J., 24, 289. 29. Schulte, A. P. (1967) Vaginal Prolapse in the Bitch, Jour. S. Afr. Vet. Med. Assoc. 38, 2, 197. 30. Sloss, V. and Dufty, J. H. (1980) Handbook of Bovine Obstet- rics, Williams and Wilkins Co., Baltimore, Md. 31. Svendsen, P. (1967) Artificial Pneumoperitoneum, Nord. Vet. Med. 19, 163 (also 18, 226). 32. Weiss, C. (1977) Surgical Correction of Vaginal Mucosal Hy- perplasia and Prolapse, Canine Pract. 4, 3, 39-42. 33. Watts, R. E. (1954) Preparturient Prolapse of the Vaginal Wall, Proc. AVMA, 91st Ann. Meeting, 382. 34. Williams, W. L. (1943) Diseases of the Genital Organs of Do- mestic Animals, 3rd Ed., Ithaca, N.Y. 35. Williams, W. L. (1943) Veterinary Obstetrics, 4th Ed., Ithaca, N.Y. 36. Winkler, J. K. (1966) Repair of Bovine Vaginal Prolapse by Cervical Fixation, JAVMA, 149, 6, 768. 37. Woelffer, E. A. (1953) Use of Progesterone to Control Habitual Abortion in Cattle, JAVMA, 123, 921, 505. 38. Woodward, R. R. and Quesenberry, J. R. (1956) A Study of (Postpartum) Vaginal and Uterine Prolapse in Hereford Cattle, J. An. Sci. 15, 1, 119. Paraplegia of Pregnancy and Miscellaneous Accidents 1. Benesch, F. (1952) Lebrbuch der Tierartzlichen Geburtshilfe and Gynakologie, Urban and Schwarzenberg, Wien-Innsbruck, Aus- tria. 2. Caple, I. W., Pemberton, D. H., Harrison, M. A. and Halpin, C. G. (1977) Starvation Ketosis in Pregnant Beef Cows, Austral. Vet. J. 53, 289-291. 3. Cox, V. S., McGrath, C. J. and Jorgensen, S. E. (1982) The Role of Pressure Damage in Pathogenesis of the Downer Cow Syn- drome, Am. J. Vet. Res. 43, 1, 26-31. 4. Jackson, R. F., Bruss, M. L., Growney, P. J. and Seymour, W. G. (1980) Hypoglycemia-Ketonemia in a Pregnant Bitch, JAVMA, 177, 11, 1123-1127. 5. Kingrey, G. W., Ludwig, V. D., Monlux, W. S. and Ramsey, F. K. (1957) Pregnancy Disease in Cows, N. A. Vet. 38, 11, 321. 6. Roberts, S. J. (1954) Ketosis-Parturient Paresis Complex, JAVMA, 124, 926, 368-372. 7. Williams, W. L. (see above)Chapter VI PARTURITION Parturition encompasses the various physiological pro- cesses involved in the birth of young including the de- livery of the fetus and placenta (fetal membranes) and the involution of the uterus. Prior to parturition the dam should have been fed a properly balanced ration in amounts sufficient to provide the necessary carbohy- drates, protein, fat, vitamins, minerals, and water so that at the time of parturition she is neither fat nor thin. Most livestock men prefer to feed their animals approaching parturition a light, slightly laxative feed. Under most systems of management the pregnant animal is provided adequate opportunity for exercise. For the last 2 to 3 weeks prior to parturition violence and excessive exer- cise or work should be avoided. The animals should be segregated from the rest of the herd in clean, sanitary, comfortable, quiet surroundings. One of the best locations possible for parturition of farm animals is a small pasture free of woods, steep slopes, wet or brush areas. This location is clean and the newborn are not exposed to the common bam or barn- yard diseases. The principal disadvantage of such a lo- cation is that frequently close observation or supervision of parturition cannot be followed. During periods of ad- verse cold and wet weather, a dry, relatively warm building or shed supplied with heat is desirable for par- turition for all domestic animals. A satisfactory place often used for parturition of the large domestic animals is a clean, well-bedded, roomy, disinfected box stall. Clean, fresh, dry straw, shavings or sawdust are usually avail- able as bedding but are not ideal because they readily contaminate the fetus, membranes and genital tract. A strong, sterilized, rubberized or plastic covering securely anchored over the above bedding material would be highly desirable. Facilities for sanitation and isolation at the time of parturition or abortion are of prime importance in most herds. A reliable birth detection system for animals, other than the time-consuming repeated checking of those near parturition, has not been developed although preliminary studies have been conducted.52b In swine in which heavy death losses of 20 to 30 per- cent of the newborn are frequently experienced during parturition and the following 48 to 72 hours, many life- saving innovations have been introduced. The farrowing pen should have guard rails. The bedding should not be too deep. Farrowing crates are highly desirable. Con- stant watch should be kept on farrowing sows to prevent them from lying on the newborn pigs. In many cases the newborn pig is removed immediately after birth. After farrowing is completed, the pigs are returned to the sow. To prevent the newborn pigs from becoming chilled, far- rowing houses are built singly and small, or larger far- rowing houses are artificially heated. The use of heat- lamp-type brooders placed in the comer of the pens not only prevents chilling but provides a safe place for pigs when they are not nursing. In some farrowing houses heating cable is placed in the concrete floor to provide heat for the pigs. The optimum environmental temper- ature for newborn pigs is 85° to 95° F. This temperature must be maintained for 3 to 6 weeks as piglets are unable to maintain a normal body temperature when the ambient temperature is low. For dogs, the owner should set aside a whelping place or box about two to three feet square with six to eight inch sides for medium-sized dogs. If possible the bitch should be kept in this familiar envi- ronment for at least a month before whelping. It is important that veterinarians be familiar with nor- mal parturition as it occurs in the various domestic an- imals so that there may be immediate recognition of any pathological symptoms. Assistance or interference with the birth process, occasionally necessary to save the fe- tus or dam, must be performed at the proper time. The time of parturition is one of the most critical stages in the life of any animal. It is one of the periods of highest death rate in animals. It can be a period in which not only the fetus, but also the dam, may be severely dam- aged or injured and thus affect its future reproductive and productive efficiency. This period, therefore, is of vital concern to the farmer who has a large economic investment in his animals. Symptoms of Approaching Parturition The signs of approaching parturition in domestic an- imals are somewhat similar but vary in certain important respects. The symptoms are inconstant between individ- 245246 VETERINARY OBSTETRICS ual animals and between consecutive parturitions. These symptoms therefore do not permit an accurate prediction as to the exact time of parturition in a certain animal but they are useful indications as to the approximate time parturition may be expected. The practicing veterinarian is frequently asked to examine and predict the time of parturition of an animal in advanced pregnancy. Al- though the following discussion will be helpful in this respect, he should refrain from making too positive or definite a statement concerning the exact time of par- turition, as subsequent events will more often than not prove him wrong. The breeding date, if known, is helpful in predicting the approximate time of parturition. Breeding records are necessary on the well-managed farm. Just prior to par- turition most animals tend to segregate themselves from the others. The sow, bitch, and queen attempt to make a suitable bed. Changes in the pelvis, genital organs, and mammary glands take place. In the cow the pelvic ligaments, especially the sacro- sciatic, become progressively more relaxed, causing a sinking of the croup ligaments and muscles. The caudal border of the sacro- sciatic ligament between the coccy- geal vertebrae and ischial tuberosity becomes less cord- like and tight, and more relaxed and flaccid. Relaxation of the pelvic ligaments, cervix and possibly the struc- tures around the perineum is due to edema and changes in the collagen fibers in connective tissue probably caused by an increase in estrogen from the placenta. Relaxin may also play a role. In most cows the presence of very relaxed ligaments indicates that parturition will probably occur in 24 to 48 hours. This relaxation of the ligaments is also noted by the elevation of the tail head. The vulva becomes progressively edematous and more flaccid until it is 2 to 6 times its normal size. The udder becomes enlarged and edematous. In heifers this udder enlarge- ment begins about the fourth month of gestation. In older, pluriparous cows it may not be noticeable until 2 to 4 weeks before parturition. In high-producing, younger cows, the amount of edema in the udder may be exten- sive and cause difficulty in walking. Edema may extend forward on the abdominal floor to the xiphoid region and be 2 to 6 inches deep. In the region of the navel it may resemble an umbilical hernia. It may extend caudally above the udder and involve the region of the escutcheon and even the vulva. This edema may occasionally be se- vere enough to interfere with circulation in the skin be- tween the udder and legs or in the region between the fore quarters of the udder, resulting in areas of necrosis at these sites. Just prior to parturition the udder secretion changes from a honey-like dry secretion to a yellow, tur- bid, opaque cellular secretion called colostrum. At this period the udder and teats are so distended with colos- trum that in “easy milkers” it may leak out. The cow usually exhibits a tenacious, whitish, stringy type of mu- cus coming from the cranial part of the vagina, starting about 7 months of pregnancy. This mucus becomes more profuse as parturition approaches. Just prior to parturi- tion the amount of mucus increases markedly and the cervical seal liquefies. During the last few hours before calving the cow may exhibit anorexia and restlessness. Heifers may show signs of abdominal discomfort with kicking at the abdomen, treading, raising and switching their tails and lying down and rising. A majority of cows, 67 percent, calve during the night hours.92 Other studies indicate that calvings occurred equally between day and night. However, feeding beef cows at night for 1 to 3 weeks before calving altered the calving pattern so 85 percent of 1331 cows calved during the daylight, 6 am to 6 pm, hours when they could more easily be ob- served.60,621’ Further studies are indicated. In the mare somewhat similar symptoms of ap- proaching parturition are present. The sinking of the sa- crosciatic ligaments is not so pronounced, due to the heavy croup muscles. The vulva does not become as edematous as in the cow but edema and flaccidity are noted the last few weeks of gestation. No discharge of vaginal mucus prior to foaling is noted in the mare. The udder starts to develop noticeably about 3 to 6 weeks before foaling. In most mares the udder and teats become filled and dis- tended with colostrum about 2 days before foaling, and oozing of this colostrum from the teats, called “wax- ing,” is usually observed in 95 percent of mares 6 to 48 hours before foaling. In a few cases no waxing is ob- served before foaling and in rare cases milk may leak from the teats up to a week or so before parturition. Within 4 hours of parturition slight sweating in flank region and behind the elbows is frequently noticed. Anorexia occurs only within 1 to 2 hours of foaling. As the first stage of labor advances the mare becomes restless, shows slight colicy symptoms, raises and switches her tail and lies down and gets up frequently. These symptoms become progressively more marked until the allantois chorion ruptures and the second stage with actual labor begins. The mare greatly prefers solitude and quiet at partu- rition and seems more able than other animals to control or suppress parturition until the night hours, when stable activities are at a minimum. Of 367 foals, 59.8 percent were bom from 6:00 p.m. to midnight, 23.4 percent from midnight to 6:00 a.m. and only 16.8 percent from 6:00 a.m. to 6:00 p.m. Thus about 83 percent of the foals were bom during the night. Other studies confirmed this percentage of nighttime foalings.6,85,99 In the ewe and goat the conditions are similar to thePARTURITION 247 cow with the exception that udder development is not so great. In the sow and queen the symptoms are some- what similar to those in the bitch. As pregnancy pro- gresses, the bitch becomes quieter and as parturition ap- proaches the vulva becomes flaccid, enlarged, and edematous. The mammary glands also become enlarged and edematous and milk may be present in the udder several days before parturition. The bitch becomes rest- less and shows anorexia for a few days before parturi- tion. This becomes more noticeable 12 to 24 hours be- fore whelping. During the first stage of labor, the bitch may pant or exhibit an increased respiratory rate. During the latter stages of pregnancy in the ewe, sow, and bitch a mucoid vulvar discharge is usually evident. Environ- mental disturbances, especially those caused by other dogs, will delay or interrupt the birth process in bitches.11 Seventy-three percent of farrowings occurred between 2:00 pm and 4:00 am.5 The Initiation of Parturition In recent years the exact mechanism concerned with the onset of parturition after a rather regular and definite length of gestation for each species of animals is becom- ing much better understood. Hormonal factors are of prime importance, as parturition can take place without inner- vation of the uterus.21,33,47,49,60,85 As described in Chapter IV progesterone from the cor- pus luteum is necessary throughout gestation in the cow, doe, sow and bitch. Ovariectomy at any stage of ges- tation in these species results in abortion or premature birth. While in the ewe, queen and mare progesterone from the corpus luteum is necessary to maintain preg- nancy only during the early stages of gestation. Ovar- iectomy may be performed without affecting pregnancy after 55 days of gestation in the ewe, 50 days of ges- tation in the queen and 70 to 150 days of gestation in the mare. In these latter species, progestogens or pro- gesterone are produced by the feto-placental unit to maintain pregnancy after luteal function ceases.21,33 Estrogen levels, arising from the embryo or fetus and the placenta, are much lower than progesterone levels during pregnancy. In the cow, ewe, sow, doe and queen the estrogen levels rise very slowly during early and midgestation and then rise more rapidly the third trimes- ter and an especially sharp rise in estrogen levels occur the last few days of gestation, except in the queen. In the sow there is a temporary rise in estrogen levels around 12 to 30 days of gestation and in the mare from 150 to 250 days of gestation. In the mare this rise corresponds to the increase in size of the fetal gonads. In the mare and bitch estrogen levels in the dam’s plasma declined slightly the latter stages of gestation. Initiation of parturition in the ewe, doe, sow, cow, bitch and probably the queen starts in the hypothalamus of the fetal brain, possibly from stimuli such as placental aging, nutritional and uterine restrictions to growth and the accumulation of waste products, followed by release of ACTH from the pituitary gland and the elevation of adrenal cortisol in the fetal and then maternal plasma.21,33 49,97,98 The manner in which the different spe- cies respond to this elevated cortisol level differs. In ewes the placental enzymes cause the placental progesterone to be made into estrogen. Blood levels of progesterone fall rapidly and placental estrogen causes the synthesis of PGF2a and uterine contractions occur. In cows, does and sows, cortisol stimulates placental estrogen produc- tion causing uterine release of PGF2a and the rapid in- volution or luteolysis of the corpora lutea, with a rapid decline in progesterone levels and subsequent uterine contractions. Cortisol production by the fetus late in ges- tation is essential for rapid lung maturation and pulmo- nary surfactant production necessary for the survival of premature or mature fetuses.19 In the mare a somewhat similar pattern may exist but a pronounced rise in fetal plasma cortisol levels just prior to parturition has not been shown to occur.21,47,54,64,76,85 Further studies are needed. At the time of parturition in the mare the blood proges- tagen level is quite high, as in the woman, but drops rapidly within 24 hours after birth. In the bitch proges- terone levels fall sharply just prior to parturition and cor- tisol levels reach a peak during the day prior to the onset of parturition. There was sharp fall of 0.8° C in body temperature of the bitch during the 24 hours prior to par- turition.22 21 In the bitch and queen there is need for fur- ther studies to determine the exact sequence of events that initiate parturition. Prostaglandin E2 as well as pros- taglandin F2a is found in the fetal fluids and plasma dur- ing the latter stages of gestation in the mare and other animals. The former prostaglandin probably plays an im- portant role in maintaining the fetal vascular system in- cluding the patency of the ductus arteriosus60,85 and di- lation of the cervix.636 It is likely that a synergistic action between the rise in estrogens and relaxin, the rapid decline in progesto- gens and the rise in prostaglandins (PGF2a) precipitate peristaltic uterine contractions, cervical dilation and par- turition. In sows a large amount of relaxin from the lu- tein cells of the ovaries is released the last few days of gestation. Prostaglandin stimulates release of relaxin that dilates the cervix, increases the pelvic area and facili- tates the expulsion of the fetuses.36 Relaxin levels in plasma rise rapidly late in gestation and just before par- turition from 4.2 to 7 to 8 ng/ml. in the mare,94c from 2.7 ng. to 42 to 257 ng/ml. in the sow906 and in the cow.77b248 VETERINARY OBSTETRICS These levels decline very rapidly after parturition. Dur- ing the second stage of labor in all domestic animals high levels of PGF2a are present and as the fetus engages in the birth canal oxytocin is released. The latter hormone from the posterior pituitary gland does not initiate par- turition as previously believed but augments it by stim- ulating the release of large amounts of PGF2a.49'5177a'98 However it is important, together with PGF2a, in causing peristaltic uterine contractions to assist in delivery of the fetus(es) and the placentas. Two to 3 IU oxytocin i.v. intensified normal myometrial activity in sows within 20 seconds but 10 IU caused uterine spasms for 10 to 15 minutes.!:b Recent studies established that estrogens are important for myometrial sensitivity to oxytocin. This is accomplished by the regulation of the concentration of oxytocin receptors in the myometrium by estrogens.41b’93 Within 24 hours after birth, progesterone and estrogen levels in maternal plasma drop to very low levels in all domestic animals. Postponement of parturition can be achieved by pro- gestins in cows, ewes and sows for a few days to a week but dystocia and poor viability of the neonate often oc- curs. For short term postponement of parturition for a few to 18 hours, long-acting sympathomimetic, betam- imetic or tocolytic agents such as clenbuterol or isoxsu- prine may be used to produce myometrial quiescence.6b,c These agents are not currently available to veterinarians in the U.S. (See Dystocia.) Induction of Parturition (and Abortion) The great increase in knowledge in recent years of the endocrine control of parturition has enabled veterinarians not only to produce abortions at nearly any stage of ges- tation in most domestic animals (See Chapter V) but to induce essentially normaly parturitions by the timely in- jection of certain hormones. The stage of pregnancy at which parturition is induced, although not critical for the dam, is very critical for the welfare of the neonate.33'35 When parturition is induced prematurely more than 3 days in the sow, 5 days in the ewe and doe and 7 to 14 days in the cow satisfactory lactation and neonate sur- vival and growth is severely affected. In the mare the mammary glands should be enlarged and developed and secreting a milk-like colostrum, the mare should be at least 330 or more days into gestation and the cervix and pelvic ligaments should be relaxed before parturition is induced.54 55'78 84 Because there are very few reasons for induction of parturition in the bitch and queen, few stud- ies have been performed. The principal reasons for inducing birth is to terminate the pregnancy and to allow delivery of the fetus(es) dur- ing the daytime when trained skilled assistance is avail- able. Other indications might include: a history of prior poorly viable neonates, prolonged gestation, abdominal hernias or severe edema, severe arthritis, possible injury or obstructions of the birth canal, fetal death or mum- mification and dropsy of the fetal sacs. There is no evi- dence to suggest that induced parturition can be more normal than natural birth. Therefore veterinarians should be both cautions and selective in their cases before rec- ommending it and then carefully monitor the process. As animal owners are understandably prone to be highly critical should any adverse incidents occur to the dam or offspring during or for a long period after the induced birth (See Chart 2). In mares the site for induced foaling should be in a clean, disinfected, quiet, isolated location. The most common technique or method is the injection of 20 to 100 IU of oxytocin into the mare with the criteria noted above.55,78 Forty to 60 I.U. given intramuscularly will usually result in a foaling within one hour. Recent stud- ies have shown that much lower doses are probably safer even if a second or third dose at 30 minute intervals are needed to initiate the second stage of labor.778 In mares ready to foal oxytocin in a dose as low as 0.5 to 10 IU caused the rapid release of endogenous PGF2a and the initiation of labor within 90 minutes. Thus large doses greater than 10 IU may be unnecessary and even dan- gerous.773 Large doses might cause uterine and muscle spasms,12b premature placental separation or malposition of the fetus. The fetal membranes are usually noted at the vulva within 30 minutes. The fetus may be checked at this time or earlier to note and correct, if necessary, the position and posture of the fetus. The hormonal pat- terns produced by induction with oxytocin are similar to those occurring during a normal parturition.54 Retained fetal membranes or subsequent infertility has not been experienced after inducing foaling in mares when the proper procedures were followed at full term. As described in Chapter IV, the hormonal pattern at the termination of pregnancy in mares is very similar to that in women and different from the other domestic an- imals. A recent report on parturition in humans, causes one to speculate on a similar pattern in mares.41b Namely, under the influence of estrogens during pregnancy there occurs a dramatic increase in myometrial oxytocin re- ceptors. This lowers the threshold so rather small doses of oxytocin probably from the fetus activates myometrial activity and contractions as well as producing prostag- landin from the placenta where oxytocin receptors have also greatly increased. Prostaglandin release is essential for the dilation of the cervix and both hormones further promote uterine contractions and birth through the re- laxed cervix.PARTURITION 249 Chart 2a. Hormones Used Effectively for the Induction of Parturition** Corticoids single multiple PGF2o and Species administration Estrogens analogues Oxytocin Cow + + + * + + + '* + + + + * 0 Ewe + + + * n.n. + + + * + + + 0 Doe + + n.n. + + +* + + + 0 Sow ± +++ n.t. + + + * 0 Mare ± +++ n.t. + + + + * 'May be necessary to assure the delivery of fetus; can be replaced by a single dose of a long-acting corticoid. n.n. = not necessary; single injection fully effective, n.t. = not tested. * Presently most preferred technique. Dose levels: Corticoids: Two to three times the optimal therapeutic dose. Estrogens: Large therapeutic doses, repeated if not long-acting. PGs: Equivalent or larger than the luteolytic dose in cycling animals. Oxytocin: 20-100 I.U., repeated small doses, 5 to 10 I.U. preferable. Legend: + + + = 90-100% effective; + + = 70-90% effective; + = 60-80% effective; ± = ca 50% effective; 0 = not effective. **Modified from W. Jochle.61 Chart 2b. Condition of the Fetus and the Maternal Endometrium and Response to Hormonal Induction of Parturition (close to term, in delayed, or in pathological gestations) in the Cow.* Condition of the conceptus2 Condition of the material endometrium Corticoids Estrogens Prostaglandin F2a and analogues Fetus alive, normal developed, normal + + + + + + + approaching term. Fetus alive, normal developed, normal + + + + + + + delivery delayed Fetus dead (shortly before term). unknown 0 + + + + + + Dropsy of the fetal sacs: hy- unknown + + + ' + + + + + + drallantois and/or hydram- nios. Fetus died and is mummified. normal 0 + + + + + + Legend: + + + = 90-100% effective; + = 60-80% effective; 0 = ineffective. 'Depends on stage of gestation and viability of fetus. "When fetal viability is unknown or fetus is dead, combined therapy of 2 or more hormones is probably indicated. *Modified from W. Jochle.61 Ordinary to large daily doses, 10 to 40 mg., of the glucocorticoid, dexamethasone, for 4 to 5 days did not induce foaling in mares late in the gestation period. However, when massive doses of 100 mg. of dexa- methasone were given daily for 5 days from 321 to 324 days of gestation parturition occurred 3 to 7 days after the first injection.34 Estrogens to induce foaling in mares has not been adequately investigated. Estrogen and dex- amethasone given 24 hours before giving PGF2a to mares between 325 and 354 days of gestation with none show- ing impending signs of foaling resulted in induced nor- mal parturition 3 hours after the third dose of PGF2a given at 12 hour intervals.102 The prostaglandin analogue, flu- prostenol, when given intramuscularly to mares (1000 ug) or to pony mares (250 ug) not showing imminent signs of foaling, produced the first stage of labor within 30 minutes and normal foaling occurred within 90 min- utes in mares that were apparently hormonally ready for induction.84 Further study on the use of prostaglandins to induce foaling in mares is indicated but presently ox- ytocin is the drug of choice.773 In sows induction of parturition may be produced by exogenous dexamethasone or PGF2a or prostaglandin an- alogues.35 Injection of dexamethosone results in a con-250 VETERINARY OBSTETRICS siderable variation and a longer time period to produce delivery. While the prostaglandins, 10 to 12 mg PGF2a, 175 ug Cloprostenol or 5 mg Prostalene, if given on days 111, 112 or 113 of gestation, preferably the latter two days, results in delivery of pigs in an average time of 33 hours.35,42,50,56 About 80 percent of the sows treated with PGF2a farrowed within the predicted 12 hour period and 95 percent within 48 hours. When parturition was induced before day 111 of gestation in sows, unaccept- able neonate losses resulted due to prematurity and poor viability.33 35 Thus if accurate breeding records with identified sows are available, treatment early one morn- ing results in nearly all sows farrowing during daylight hours the next day when attendants are available. Far- rowing could be planned for groups of sows 3 days a week, avoiding weekends and holidays. Cross-fostering of pigs would be more efficient. Induced farrowing might aid in reducing the incidence of M.M. A.166,26 The pros- taglandin analogues in sows, as in mares, produced less side effects of restlessness, rubbing and gnawing, sali- vation and increased respiration rates, defecation and ur- ination than PGF2a.27 Following the administration of prostaglandins, progesterone levels decline rapidly due to luteolysis of the copora lutea. During the day after the injection of prostaglandin about two hours after a stream of milk could be expressed from the teats or 28 hours after the injection of Cloprostenol, 50 IU of oxytocin will markedly shorten the time to birth.105 In cows 16 to 30 mg of dexamethasone or 5 to 10 mg of flumethasone induced parturition after day 265 of ges- tation in over 80 percent of the cattle. The time from treatment to parturition ranged from 30 to 60 hours. Fifty to 90 percent of the cows had a retained placenta.33'60'104 Evidence would indicate that the glucocorticoid stimu- lated the release of estrogen from the placenta followed by the release of PGF2a by the uterus which caused lu- teolysis. Treatment with estrogen, 25 mg of estradiol, before or at the same time as the injection of a gluco- corticoid increased the percent of cows delivering, tended to shorten the time to delivery of the fetus and somewhat reduced the incidence of retained placentas.12’88 How- ever the problem of estrogen residues in milk limits the use of this hormone in dairy cattle. The local treatment and manipulation of the retained placenta accompanying most cases of induced parturition in cattle should be avoided but parenteral injections(s) of antibiotics were indicated. The fetal membranes dropped from the uterus within 10 days and subsequent delayed conception and infertility was not a problem.33,60 104 The injection of 20 to 40 mg of prostaglandin F2a into cows after 265 days of gestation induced parturition in 90 to 100 percent within 57 to 100 hours. The time from treatment to delivery was longer with prostaglandin F2a than with the glucocorticoids.33,60,63 The incidence of dystocia was somewhat higher, the percent of live calves slightly lower and the incidence of retained placenta about the same as with the glucocorticoids. Estrogens will also induce parturition in dairy cattle but high doses of 100 to 150 mg of diethylstilbesterol or its equivalent must be used and residue problems would occur.60 Combinations of a glucocorticoid, 25 mg dexamethasone, and PGF2a or prostaglandin analogues, 500 ug Cloprostenol, have been used to produce abortions within 4 to 6 days in 93 to 100 percent of heifers from 1 to 8 months of gesta- tion.6c In New Zealand over 1 million late-calving dairy cows were induced to calve up to 3 to 5 weeks before term for economic and managerial reasons by the injec- tion of a slowly absorbed corticosteroid formulation of betamethasone. Treated cows were observed carefully for parturition and periparturient disease problems. Re- tention of the placenta was commonly observed. It was determined there was no economic benefit to such a practice unless the cows were normal, young and healthy and advantages were indicated beyond the first lacta- tion.716 Cloprostenol (Estrumate) at a dose of 500 ug IM in cows and heifers from 250 to 300 days of gestation induced parturition in 95 percent of 64 animals within 0 to 60 hours, average 47 hours. It was desirable to induce parturition within one week of the expected calving date. Retained placenta occurred in 62 percent of the cows and 91 percent of the calves were viable.616 Thus both the glucocorticoids and prostaglandins re- liably induce parturition in cattle after 265 days of ges- tation. Until further extensive comparative trials are con- ducted the glucocorticoids appear to be more desirable and safe in producing shorter gestation periods, none or very slight, increase in calving difficulty, slight reduc- tions in birth weights, healthy viable calves and a re- duced udder edema in dairy heifers and cows.88 Heifers tended to have a shorter time interval from treatment to delivery than cows.63 In ewes given 20 mg of estradiol benzoate at 142 to 148 days of gestation 65 percent lambed within 48 hours and 84 percent lambed within 96 hours.16 This treatment could not be recommended because of the high incidence of lamb mortality in the 16 percent of the ewes that did not respond to the treatment. In another trial ewes were given either 2 mg flumethasone or 15 mg prostaglandin Fja on day 141 of gestation.52 Eighty nine percent of ewes treated with flumethasone and 33 percent treated with PGF2a lambed within 72 hours after treatment. The av- erage or mean hours from the flumethasone treatment to lambing was 50.9 hours for those ewes lambing within 72 hours. Another study in which 2 mg of flumethasone was given to ewes on days 138 through 144 of gestation, 67 to 89 percent of ewes injected on days 140 to 144 ofPARTURITION 251 gestation lambed within 72 hours after treatment. Of those ewes injected on days 138 and 139 of gestation only 31 to 41 percent lambed within 72 hours.81 These studies further emphasized the need for more trials with pros- taglandins and the importance of accurate breeding dates and records. Although further evaluation is needed, the use of 10 to 20 mg of dexamethasone in ewes 140 days pregnant induced parturition, and pregnancy toxemia losses were reduced.2'57 In does the administration of 15 mg PGF2a at 140 to 142 days of gestation resulted in induced parturition within 36 to 70 hours. Retention of the placenta for up to 24 hours with secondary metritis occurred in a number of does.13 Induction of parturition in goats has also been produced with estrogens and glucocorticoids but because of a lack of economic interest extensive studies in the doe have not been made.33,60 The doe responds to the above hormones in a manner similar to that of the cow to produce luteolysis and a rapid drop in progesterone levels with subsequent delivery. Live birth only occurs when estrogen and PGF2a treatments are given after day 139 of gestation.33 The Stages of Parturition Although the act of parturition is continuous, for pur- poses of definition it is usually divided into three stages or phases. First Stage—This stage is characterized by the relax- ation of the cervix and active contractions of both the longitudinal and circular muscle fibers of the uterine wall. In ewes, does, and possibly the other domestic animals, the collagenous structural nature of the cervix probably requires a mechanism involving an enzymic degradation of collagen to cause cervical relaxation and softening. This is apparently brought about by a declining proges- terone level, an elevated estrogen level and an elevation of prostaglandins. The latter are probably within the cer- vix.36 In the sow and possibly the other species relaxin also plays an important role in cervical relaxation.21,33,49 The elevated levels of estrogen and prostaglandin and reduced progesterone induced in most species by an elevated level of glucocorticoids in the fetus result in uterine contractions. Oxytocin is seldom released from the hypohysis prior to the second stage of labor so is not essential for the induction of parturition or la- bor.21'38,49’69101 Uterine peristalsis starting in the apices of the uterine horns is initiated by circular muscle con- tractions synchronized by propagation of the action im- pulse through the longitudinal muscles. Uterine contrac- tions perform 90 percent of the work of parturition and these contractions are directly proportional to fetal re- sistance. There is a greatly increased activity of the uter- ine musculature the last 1 to 2 hours before birth. The average prepartum amplitude of uterine muscle contrac- tion was 80 cm. of H20. Uterine contractions force the fetal membranes and their fluids against and into the re- laxed cervix. The external os of the bovine cervix re- laxes sufficiently a week or so before calving to accom- odate 2 to 4 fingers.4 The cervix of heifers remained tightly closed until the day before parturition. In the first stage of parturition the cervix was not dilated by the allantois chorion but was pulled open by the contraction of the longitudinal uterine muscles. For most of the first stage the cervix easily contained the allantois chorion that pro- jected into it. True dilation of the internal os started 2 to 4 hours after the external os had reached a diameter of 8 to 12 cm and by 6 to 12 hours the whole cervix was 12 to 15 cm wide and the cervix and vagina were a con- tinous canal filled with the distended allantois-chorion. Once cervical dilation is complete, the bovine fetus is expelled within 2 to 4 hours unless fetal or maternal causes for dystocia are present.92 During the first stage in the cow, uterine contractions occur about every 10 to 15 minutes and last 15 to 30 seconds. As the stage advances they increase in fre- quency, strength, and duration until contractions occur about every 3 to 5 minutes.8,46 In uniparous animals the contractions start at the apex of the cornua while the cau- dal part does not contract but rather dilates from the pressure of the fetus and fluids forced caudally. In this stage in the mare4,85 and probably the bitch the fetus is rotating from its dorso-pubic or dorso-lateral position into the dorso-sacral position. As it passes through the cervix into the birth canal the legs and head are extended. In the bovine and ovine fetus no rotation is necessary, as it is already in a dorso-sacral position. By the end of this stage the cervix is completely dilated. The multiparous animals have a more complex mech- anism of uterine contractions.4,8 The contractions of the uterus occur just cephalad to the most caudad fetus forc- ing it through the cervix into the birth canal, while the rest of the uterus remains quiescent. Then the same pro- cess is repeated for the most caudad fetus in the other horn, or the fetus immediately cranial to the one just expelled. This may help explain why in the second stage two fetuses may be bom nearly simultaneously. The lon- gitudinal fibers of the parts of the horn just emptied con- tract, but the circular fibers remain relaxed, so that the next fetus may pass through. This shortens the uterus as parturition progresses, so that each fetus in turn is brought back nearly to the cervix. This is important in multipara so that the fetuses at the apex of the uterine horn do not have to traverse a long uterine hom after the placenta252 VETERINARY OBSTETRICS has been detached or the navel cord ruptured. The nor- mal and abnormal behavioral patterns, or ethology, of the various species of animals before, during and after parturition has been described.39,40 During this first stage of parturition which lasts about 1 to 4 hours, straining or labor is not exhibited in the mare. The symptoms of restlessness, anorexia, colicy pains, slight sweating behind the elbows and around the flanks, lying down and getting up, tail switching, ele- vating of the tail, repeated periodic sudden complete ar- rest in motion even chewing, repeated stretching as if to urinate, frequent small bowel evacuations, and looking at the flank are characteristic of abdominal discomfort in the mare during the latter part of this period. Usually the pulse and respiratory rates are accelerated. During the latter part of the first stage just prior to labor the mare may roll back and forth in an apparent effort to rotate the fetus into a dorso-sacral position. Both fetal and ma- ternal activity and movements result in the turning or rotation of the fetus.85 The mare may crouch, go down on her knees, rise again and be highly restless. The body temperature may become slightly lower than normal dur- ing this period.4 In the cow and ewe the symptoms of abdominal pain or discomfort may not be evident especially in pluripar- ous animals. In heifers, colicy symptoms and restless- ness usually are observed and may last for 1 to 24 hours. The cow and ewe will show anorexia, stand with an arched back and raised tail, strain occasionally, and ruminate irregularly. The cow may lie down and get up fre- quently. Pulse and respiratory rates increase but lower- ing of the body temperature is inconstant. In the bitch, sow, and cat nervousness, anorexia, and an increase in pulse and respiratory rates usually occur. In dogs this may result in panting. The signs of various stages of parturition in the bitch have been described.41 Occasionally vomiting is observed. This stage usually lasts for about 2 to 12 hours. In the dog there is usually a sudden drop of 1 to 2° F in body temperature to below 100° F just before or during this phase of parturition. A drop in body temperature of 1 to 1.5° F just before parturition in cows, ewes, sows and bitches has been reported.22,23'30,31,32 107 This decline in temperature is re- lated to the decline in progesterone levels. However be- cause of its variability under field conditions, this fall in body temperature is of little practical value in predicting the onset of parturition in the cow, sow or ewe. In all animals in which a drop in body temperature occurs dur- ing this first stage, the temperature afterwards rises and reaches a peak during and shortly after parturition due to exertion. This first stage is apparent for longer periods in pri- miparous than pluriparous animals. During this stage in some animals of all species, milk or colostrum may drip or run from the udder. Usually toward the end of this first stage the allantois chorion ruptures as it is forced through the dilated cervix into the vagina. After the al- lantois chorion ruptures, the amnion pushes into and through the cervix, and the fetus—because of the short- ening and contracting of the uterus and dilation of the cervix—passes into the cervix and vagina. Once a por- tion of the fetus enters the pelvis, reflex stimuli result in straining or labor. This is produced by contractions of the abdominal muscles and diaphragm together with a closing of the glottis; and the second stage of parturition begins. Presentation, Position and Posture of the Fetus— It is essential for the sake of accuracy to describe the various presentations, positions, and postures a fetus may assume at the time of its entrance into the birth canal or pelvis. These definitions were established by Williams106 and are commonly used in the description of both normal and abnormal births. The presentation includes: (1) The relation of the spinal axis of the fetus to that of the dam. Presentations are either longitudinal or transverse. (2) The portion of the fetus that is approaching or entering the pelvic cavity or birth canal. This portion of the fetus is anterior or pos- terior in the longitudinal presentation, or dorsal or ven- tral in the transverse presentation. The position includes: (1) The relation of the dorsum of the fetus in longitudinal presentation, or the head in transverse presentation, to the quadrants of the maternal pelvis. These are the sacrum, the right ilium, the left ilium, and the pubis. The posture signifies the relation of the extremities, or the head, neck, and limbs, to the body of the fetus. The extremities may be flexed or extended or retained beneath, on the right or left side, or above the fetus. In outline form the presentation and position include all possible variations of the manner in which the fetus may enter the birth canal at parturition. Presentations Positions Anterior, longitudinal Dorso-sacral Right dorso-ilial Posterior, longitudinal Left dorso-ilial Dorso-pubic Transverse ventral Right cephalo-ilial Transverse dorsal Left cephalo-ilialPARTURITION 253 The normal presentation in uniparous animals is the anterior longitudinal presentation, dorso-sacral position with the head resting on the metacarpal bones and knees of the extended fore legs. Birth can take place without assistance if the fetus is in the posterior longitudinal presentation, dorso-sacral position. Unless the fetus is small, other positions result in dystocia. The transverse presentation is seen only rarely in ruminants and mul- tipara. It can occur in the mare, in which the fetus de- velops in both horns, rather than in the body and one hom. Dystocia invariably results. The posterior longi- tudinal presentation, dorso sacral position, with the hind limbs retained or extended beneath the body, is com- monly spoken of as breech presentation. Two old terms, only rarely used, are “stemo-abdominal” presentation, which is a transverse ventral presentation in the mare, and “poll” presentation which is an anterior longitudinal presentation, dorso-sacral position, with the head flexed beneath the neck. The position of the fetus in the uterus was discussed in Chapter 4. Thirty to 40 percent of the fetuses of multipara are presented posteriorly and this is considered normal or physiological. Because of the short neck of swine fetuses, the head and neck are seldom deviated. Since the limbs in multipara are small, short and flexible, their posture is of no importance. They may be extended beneath or in front of the body or flexed without resulting in dystocia. In ewes 69.5 percent of fetuses were in normal anterior presentation with the ex- tremities extended and 17.8 percent of the fetuses were normal except for one retained or flexed leg.4 In sheep, fetuses may be expelled without assistance in anterior presentation with one fore limb extended beneath or alongside the body. When both forelimbs are retained beneath the body dystocia usually results. The Second Stage—This stage is characterized by uterine contractions, the entrance of the fetus or fetuses into the dilated birth canal; rupture of the allantoic sac; abdominal contractions, or labor; and the expulsion of the fetus through the vulva. In the cow abdominal con- tractions occurred only after the feet of the fetus were in the cervix or vagina.46 Breaking of the allantoic sac caused a sudden increase in abdominal contractions that were superimposed on the crest of each uterine wave with amplitudes of 80 to 320 cm. H20, average 180 cm. HzO. In the cow and mare following the rupture of the allan- toic sac, the amnion is pushed through the cervix and may appear at the vulva as a translucent distended mem- brane.85 During this second stage of labor, uterine con- tractions occurred in the cow about 4 to 8 times every 10 minutes and lasted 80 to 100 seconds.8 46 Intermittent tenesmus or straining continues and the feet of the fetus appear at the vulva. As the feet pass through the vulva the amniotic sac usually ruptures. Point pressure rather than diffuse pressure such as that exerted by the allantoic sac is the stimulus to abdominal contractions. Passage of the head, shoulders and hips of the fetus through the pelvis caused an increase in abdominal contractions. The fetal head starts through the vulva and at this point the greatest and strongest abdominal straining in the birth process usually occurs. In the larger uniparous animals as the head is being forced into the vulva, the chest is entering the pelvic canal. Often after the head passes the vulva the dam will rest for a few minutes before begin- ning straining again with strong abdominal efforts as the chest passes through the birth canal and vulva. The hips usually follow through the birth canal fairly rapidly but occasionally the hind limbs may remain in the vagina until the fetus or dam moves.85 In goats and cows during the passage of the fetus through the birth canal and when the vagina was dilated there was a great increase in the levels of oxytocin in the jugular blood over that present during the first and early second stages of labor when in general it was similar to the very low blood levels pres- ent during pregnancy.38'101 The release of oxytocin dur- ing most of the second stage of labor was continual in contrast to spurts in the release of oxytocin during the milking act. Oxytocin causes the release of prostaglan- dins which further increases uterine contractions and cervical dilation.47'51'85 The levels of oxytocin in the blood plasma of goats, sheep and cows during the second stage of labor was 77 to 381, 5 to 3000, and 400 to 1000 microunits per ml., respectively. The half life of oxy- tocin in the blood is one to one and one-half minutes. In the goat the posterior pituitary gland contains about 9 to 13 units of oxytocin and about one-tenth that amount is released during parturition.38'101 Passage of the fetus through the birth canal not only causes the release of oxytocin but also the release of prostaglandins in the mare85 and probably the other domestic animals. Almost all animals lie down as soon as straining com- mences. The foal or calf may be bom with the dam standing in only about 1.5 percent of mares and cows.85 92 The mare and sow usually lie out flat with the legs ex- tended, whereas the cow, bitch, and ewe are more likely to lie on their sternum. In the mare straining is usually characterized by several, 2 to 5, strong expulsive efforts followed by 2 to 3 minutes of rest. This procedure is repeated at fairly regular intervals. In the mare one fore- leg of the fetus precedes the other by 6 inches as the fetus passes through the birth canal.4 This indicates that one elbow and shoulder enters the birth canal before the other. The foal’s cheek is usually lying on the limbs with its muzzle midway between the knee and fetlock joints. Although parturition is quite rapid in the mare it is ac-254 VETERINARY OBSTETRICS companied by such great expulsive efforts that the mare is usually exhausted and will lie on her side for 15 to 30 minutes before rising.83 85 Since the umbilical cord in the mare is long it often does not rupture as the fetus passes through the birth canal. It will remain attached to the fetus for an average of 8 to occasionally 30 minutes until the mare or foal moves, when it breaks at a point about 3 to 5 cm from the foal’s body. Pulsations can usually be felt in the umbilical artery for one to 9 minutes. If the umbilical cord is separated immediately 400 to 1,500 ml of blood is lost to the fetus.83 In the cow the straining is not as forceful or as fre- quent as in the mare. During the early part of labor the cow may remain standing. Its body temperature may in- crease to a high normal level and the pulse and respi- ration rate will rise due to the exertion, as is observed in other animals. In the ewe the second stage of birth is similar to that in the cow. Once the second stage begins the abdominal contractions develop with gradually in- creasing frequency and intensity until birth has occurred. The periods or bouts of abdominal straining occur every 2 to 3 minutes and consist of 5 to 8 abdominal contrac- tions in the cow. These abdominal contractions will in- crease and resting time decrease as the fetus enters and passes through the birth canal.92 If these contractions be- come reduced in number or intensity usually assistance will be necessary to deliver a live fetus, as this condition does not occur in normal deliveries. Once the feet have passed through the vulva they should stay there and not appear and disappear at each abdominal contraction. This same pattern is followed in other domestic animals. In the bitch the amnion as it appears at the vulva be- fore the first pup is usually broken by the bitch as she licks the vulva. In the bitch the delivery of the head through the vulva requires the greatest expulsive efforts. The umbilical cord, which is still intact at birth, is usu- ally broken by the bitch. After the birth of each pup the bitch rests, licks the pup and her vulva. When the fetal membranes are expelled—in about 10 minutes after the birth of the pup—they are eaten by the bitch. It is prob- ably best to let the bitch eat only 2 or 3 placentas and then remove the rest, as consumption of too many pla- centas may cause vomiting and diarrhea. The greenish- black fluid that is discharged following the fetal mem- branes is normal and is due to the breakdown of blood resulting in the presence of bile-like pigments, uterover- din, around the edges of the placental zone of attach- ment. Straining begins again after 0.5 to 1 hour or more and another pup is expelled. Although it may take about 1 hour of labor for the first pup to be born, the periods of straining for the second and third pups are usually progressively shorter. The rate of expulsion of the fe- tuses is very irregular. Some bitches may not expel the second fetus for several hours after the first. Then the next 2 or 3 may be expelled rapidly within 10 to 30 min- utes of each other followed by another delay. Rarely are the pups expelled rapidly in a short time. They may also be expelled at somewhat regular intervals. The sow and queen have a second stage of birth similar to that in the bitch. The period of time between the expulsion of pigs varied from 3 to 45 minutes or rarely longer. The longest intervals were observed between the first and second pig and before the last pig.4'6169 About three-quarters of the pigs were bom with the umbilical cords intact and it took 2 to 6 minutes average time before rupture. After far- rowing the sow usually urinates copiously. In multipara the fetuses are expelled in an irregular and random manner from each hom, that is, one fetus may be expelled from one hom and then 2 or 3 from the other and then 2 from the first and one from the second, and so forth. In the bitch, but not the sow, the horn con- taining the most fetuses expelled the first fetus.95 About half of the pigs born came from the same hom as its predecessor and the other half from the opposite hom.25b In some sows most of one hom would empty and then all of the other and the remainder of the first horn and etc. In general porcine and canine fetuses came ran- domly. Porcine fetuses occasionally passed each other within the hom or uterine body and as many as 20 per- cent of the fetuses changed their presentations in late gestation or during parturition.95 In 73 canine fetuses marked by transuterine injections at laparotomy between 45 and 54 days of gestation, 56.2% were in anterior and 43.8% were in posterior presentation. Between marking and birth 6.9% changed from posterior to anterior pres- entation. At no time did a canine fetus located more tub- ally pass another fetus located closer to the cervix. After the birth of one pup, the next pup came from the con- tralateral hom in 78.2% of the births. Therefore the two horns did not alternate in presenting a fetus into the birth canal. In the 14 bitches in their first to third parities the average duration of gestation was 62.3 days and the du- ration of parturition from the first to last pup ranged from 100 to 875 minutes (1.6 to 14.5 hours). Eight of the 14 bitches were given 1 IU oxytocin during parturition with 33.3%, 66.6%, 71.4% and 88.1%, of the pups bom within 30, 60, 90 and 120 minutes, respectively of its prede- cessor.10"’ The presence of a dead fetus may delay the emptying of that hom. Occasionally in the mare, bitch, and only rarely in the other domestic animals, the fetus may be bom with the amnion or a portion of it wrapped around its head. In the mare this may cause suffocation of the foal if not promptly removed. In carnivora, death is notPARTURITION 255 likely from this cause since the bitch and queen promptly licks and eats the amnion. During this stage the contracting and shortening uter- ine walls force and direct the fetus into the birth canal and pelvis and abdominal contractions, or labor, drives the fetus through the birth canal. The intra-uterine pres- sure in the cow was 66 mm. of Hg between uterine con- tractions during the second stage of labor. The pressure reached about 170 mm. of Hg at the time of abdominal contraction. Thus the total pressure at the opening of the pelvic inlet is about 150 to 170 lbs., or about what one man could apply by traction on the fetus.7 The intra-abdominal pressure, caused by contraction of the abdominal muscles and diaphragm and closure of the glottis, is equal in all directions. The uterus is nec- essary to direct the fetus into the path of least resis- tance—the pelvic canal. If a large hernia is present ab- dominal contractions could force the uterus into the hernia. Not uncommonly traumatic gastritis or displacement of the abomasum may occur as a sequelae to parturition, due to the abdominal pressure. A healthy fetus, intact abdominal walls and a healthy uterus are necessary for normal birth. In uniparous animals the large fetuses pass through an arc from the abdominal cavity upward into and through the pelvis and then downward again as they pass through the vulva. In the cow the fetus must pass over the high ischial tuberosities. This arc-like direction of the fetus as it passes through the pelvis causes stretching of its dorsal and pelvic muscles and a relaxation of the linea alba and abdominal muscles. The latter is important be- cause it allows the pelvis to be extended backward on the fetal sacrum, thus reducing the sacro-pubic diameter of the fetal pelvis. The downward direction of the cranial portion of the fetus as it passes the vulva tends to push the fetal pelvis high in the maternal pelvis, where the bisiliac diameter is greater. This helps prevent a hiplock condition frequently encountered when traction is incor- rectly applied. In hiplock the greater trochanters fail to pass between the shafts of the ilia. The time for this second stage of birth in the cow is from 0.5 to 3 to 4 hours. In pluriparous cows this second stage usually requires 0.5 to 1 hour. Primipara may take longer, up to 3 hours or more. In ewes and goats the second stage of labor is completed in about 1 hour, range 0.5 to 2 hours, or slightly longer if twins or triplets are present. In mares this second stage is normally com- pleted in 5 to 60 minutes with an average of 20 min- utes.4'83,85 In multiparous or polytocous animals the length of the second stage of birth is variable, often depending upon the number of fetuses in the uterus. In the bitch the expulsion of the first pup may take up to 1 hour and a variable time for each fetus thereafter. The average total time for the second stage of parturition in a bitch is 3 to 6 hours. Twelve hours would certainly be near maximum. In the sow the second stage is usually com- pleted within 1 to 5 hours but occasionally may last up to 8 hours. In the sow the interval between the birth of pigs averaged 15 minutes but ranged from 1 minute to 3 hours.86 A longer time interval between pigs often pre- cedes the expulsion of a stillborn fetus. In the queen the time required to complete the second stage of labor is usually 1 to 2 hours with several minutes to an hour in- terval between kittens. In some cases delivery of fetuses may occur several days apart.20 In the sow and bitch after the second stage of parturition is completed they actively nurse their young, cease straining, and are quiet and con- tent. When the umbilical cord ruptures, the two umbilical arteries together with the urachus retract into the abdom- inal cavity of the fetus. By the contraction of the arteries into the body tissues, provision is made for the preven- tion of bleeding from the navel. The umbilical vein col- lapses, the blood drains from it and the fluids in the um- bilical cord drain out, often aided by the licking of the cord by the dam. The umbilical cord becomes necrotic, dries up and drops away in 7 to 21 days. The Third Stage—The third and last stage of par- turition is the expulsion of the fetal membranes and the involution of the uterus. These two conditions are dis- cussed separately because the expulsion of the fetal membranes is normally completed within a few hours after the expulsion of the fetus, whereas involution of the uterus to its normal nonpregnant state may take more than a month in some species. Fetal maturity is synchronized with parturition by the decline in progesterone and the elevation of prostaglan- din and cortisol in the doe and ewe and the other ani- mals. This alteration in hormone levels late in gestation also results in placental “maturation” and the initial early changes which after fetal birth result in the rapid sepa- ration of the fetal and maternal tissues at the microvil- lous junction and the initiation of lactation.24,94'98 Expulsion of the Fetal Membranes—With the birth of the fetus, the vessels in the fetal placenta collapse and the villi become small and shrunken. After the expulsion of the fetus the uterus still contracts strongly for 48 hours and less vigorously, but more frequently, there- after.46,62,92 This is necessary to prevent hemorrhage and to aid in the expulsion of the fetal membranes. These peristaltic and contraction waves besides reducing the size of the uterus and aiding in forcing the placenta and mem- branes into the birth canal probably markedly reduce the amount of blood circulating in the endometrium. This256 VETERINARY OBSTETRICS causes a dilation or relaxation of the maternal crypts. The shrinking of the villi and the dilation of the maternal caruncular crypts probably play a major role in the sep- aration of the fetal trophoblast and cryptal epithelium of the maternal placenta. No maternal tissue is shed in the afterbirth of cows. However a few fetal villi may be caught and left in the maternal crypts.10 The middle uterine ar- tery immediately contracts following parturition. The ar- tery becomes thickwalled and the characteristic thrill of “whirring” is absent although it may be several weeks or more before it involutes to near its normal size. In exceptional cases an aneurism of this artery may occur and a thrill or “whirr” may be palpated over a portion of the artery for several weeks or longer following par- turition. The uterine contractions during this third stage produce movement of the uterine wall and caruncles that may aid in freeing or separating the fetal placenta. There is no muscular tissue in the caruncles. The weight of the amnion and the portion of the allantois chorion in the birth canal tends to help remove the afterbirth from the uterus. The incidence of retained afterbirth was much higher in buffalo in which the young were not allowed to suckle, 22.7 percent, than when the young were al- lowed to suckle, 4.9 percent.103 It is well-known that suckling stimulates the release of oxytocin from the pi- tuitary gland. A lack of progesterone during the last month or so of pregnancy resulted in the occurrence of partu- ritions 10 to 20 days earlier than normal together with a high incidence of retention of the placenta.69a,69b Early parturition, twin pregnancy or a shortened gestation pe- riod have frequently been observed associated with re- tained placenta. In these instances infection may play a pathogenic role. This will be discussed further under re- tention of the fetal membranes. Normal expulsion of the fetal membranes can be said to be a complex process involving both mechanical and hormonal factors, al- though the exact mechanism is still not completely understood. In bitches and queens the fetal membranes are usually expelled irregularly between the fetuses; or one fetus may be expelled with its own placenta and that of a fetus expelled earlier. In rare instances expulsion of a few pla- centae may be delayed for 12 hours or more. In the sow, since a number of the allantois chorions may be fused, the fetal membranes may be expelled at only 2 to 3 in- tervals during parturition. Most porcine afterbirths were expelled from 20 minutes to 12 hours, average 4 hours, after the birth of the last pig.61 Occasionally placentas were retained with no observed ill effects. The fetal membranes of the last fetuses in the bitch are usually expelled shortly after the birth of the last pup. This third period of labor is characterized by relatively short, in- frequent, and mild periods of straining usually at the time the larger mass of membranes are expelled or when much of the placenta is hanging from the vulva especially in uniparous animals. In most unipara the amnion and um- bilical cord start through the birth canal first and as the allantois chorion separates from the endometrium at the apex of the horn due to peristaltic waves starting there, the chorion or fetal placenta is inverted and the allantoic surface is outside as the membranes are expelled from the uterus.62 If placental expulsion is delayed for a longer period of time than normal the chorion of fetal placenta may be exposed when it falls from the vulva. Occasion- ally when fetal expulsion is delayed the fetal placenta may separate, and later both the dead fetus and the fetal membranes are expelled or withdrawn together. Unlike the mare, placental separation in the cow is slower than in most other species of animals, so that the second stage of labor can be prolonged without the danger to the fe- tus. The umbilical cord of the bovine fetus is ruptured as the fetus passes through the birth canal. In the cow the length of time required for the expulsion of the fetal membranes is normally 1/2 to 8 hours. The ewe is sim- ilar to the cow. The mare normally expels its fetal mem- branes within 0.5 to 3 hours after the birth of the foal. Generally, the healthier the animal the more prompt is the expulsion of the fetal membranes. Domestic animals, with the exception of the mare, will usually eat the ex- pelled fetal membranes. Instances of cow’s choking and suffocating while eating their placentas have been re- ported.100'*'106 Ruminants will not eat their fetal mem- branes if the membranes are decomposed. Multipara usually eat the fetal membranes as well as any fetal ca- davers. The act of eating the fetal membranes is not known to be beneficial in any way. In ruminants the placenta may lie in the rumen and slowly macerate or decompose over a period of several weeks or more and is occasion- ally suspected of causing indigestion. This is question- able, since nearly all cattle eat their fetal membranes and symptoms of indigestion or toxemia rarely occur. Oc- casionally the cow may begin eating her fetal mem- branes before they have dropped away from the uterus. After the expulsion of the fetal membranes in a normal birth, the cervix secretes a rather thick tenacious mucus that tends to seal the cervix and thus helps prevent in- fection gaining entrance to the uterus. Involution or regression of the uterus in domestic animals, with the exception of the cow and the ewe, has not been extensively studied. In multiparous animals and the ewe, rebreeding the female within the next 1 to 6 months is seldom practiced. In the bitch, sow, and queen estrum usually does not occur until after the young are weaned. In the sow signs of estrus may be exhibited about 3 days postpartum but if copulation is allowed the con- ception rate is extremely low. In the mare, commonlyPARTURITION 257 bred 9 to 30 days after foaling, relatively few studies have been made on the involution of the uterus. Regres- sion of the mare’s uterus proceeds at a rapid rate.3,94b The endometrium, however, had seldom completely in- voluted by the onset of the foal heat. In many mares the endometrium must be largely restored by the third to fifth day after foal heat or 12 to 17 days postpartum when the early embryo enters the uterus. Conception often occurs from service at this estrum. By 13 to 25 days after par- turition the endometrium was fully restored in all normal foaling mares. At the time of onset of foal heat the sub- epithelial areas of glandular epithelium were highly dis- organized and contained large number of leukocytes. This would indicate the uterus was not yet in a completely involuted and normal state. However, after placental separation the uterine epithelium is relatively undamaged and by 7 to 10 days after a normal foaling involution of the endometrium is largely completed.94b By the end of foal heat both the gross and microscopic involution was nearly complete.4811 The mare may discharge a slight amount of grey to brownish lochia for about one week postpartum. Involution appears more rapid in primapa- rous mares than in pluriparous mares. Exercise appears to hasten involution. The rapid involution of the endo- metrium in the mare and sow is probably related to the simple diffuse placental attachments. The genital tract of all mares became infected, usually with streptococci, at the time of foaling or within one to three days. In normal mares this infection was overcome soon after the onset of foal heat or about the sixth to tenth day after partu- rition.14 Pregnant sows from 30 to 100 days of gestation may be aborted within 34 to 42 hours by a single dose of 500 ug. cloprostenol, a prostaglandin analogue. Es- trus occurred in these sows within 9 to 10 days and breeding on this first heat resulted in 90% conception.7811 Therefore uterine and endometrial involution in the sow is rapid as in the mare. In cows the involution of the uterus has been carefully studied.7,15,17,66~68,73,74,79,92 Following the expulsion of the fetal membranes in the cow the uterine contractions and peristalsis continue as strong rhythmical waves that gradually diminish through the fourth day. In the cow the uterine muscle cells shortened from 750 microns after parturition to 400 microns one day later. From the fourth to eighth days there are only irregular undulations of the horn.7 The maternal placenta involuted by the necrosis of the caruncular stalk due to vasoconstriction, leucocytic in- filtration and by the dissolution of the uterine caruncle by fatty infiltration, solution, sloughing and detachment of the entire superficial layer of the caruncle that became part of the uterine lochia.43,68 79 The caruncle and its stalk were necrotic by the fifth day after parturition. The dis- solution and sloughing of the caruncle was generally completed by the twelfth day leaving a raw surface with protruding blood vessels where the stalk was attached. The caruncles had returned to nearly their original size by the second or third week. This delayed loss of ma- ternal placental tissue through necrosis would lead to the observation that cattle and sheep are not true nondecidu- ate animals. By about 25 to 30 days postpartum, epi- thelium covered the caruncles and repair was complete. Thus a 70 gm. caruncle by 48 hours after birth reduced its size and weight to 26 gms. and was quite small 5 days later. Even when the caruncles are nearly normal in size at 30 days postpartum a large vascular bed of vessels remains. These feel rather fibrous and are present for a long period even if the animal does not become pregnant. The intercaruncular epithelium may be eroded by bacterial lysis but is normally repaired by 20 days postpartum.65,67 The lochia in the bovine uterus the first 48 hours after parturition was greatest in amount of any period, about 1400 to 1600 ml. By the eighth day postpartum the amount had decreased to 500 ml. and by 14 to 18 days there were only a few ml. of lochia. The amount of lochia discharged from the vulva was variable. Most primipara discharged about 50 ml. Some primipara discharged al- most no lochia but absorbed it from the uterus. Some pluripara discharged from 800 to 2000 ml. of lochia. Usually this discharge of uterine lochia, consisting of mucus, tissue, detritus, and blood, commenced about 3 to 4 days postpartum and increased until the ninth day. The detritus was light yellow-brown to red in color. After the ninth to tenth day postpartum, there was an increased amount of blood mixed with the lochia. This apparently originated from the surface of the caruncles. This bloody lochia usually ceased about the twelfth day. Hyperleu- kocytosis was found only the first 2 to 3 days postpar- tum. The process of normal involution took the course of an aseptic process. However, in the examination of apparently normal cows. A spontaneous puerperal in- fection causing a massive bacterial growth in the uterine lochia was often observed.79 About 93 percent of bovine uteri were infected from parturition to 15 days postpar- tum, 78 percent between 16 and 30 days, 50 percent between 31 and 45 days and 9 percent between 45 and 60 days.29 Lymphocytes were extremely numerous in the endometrium of infected uteri and only moderate in most bacteriologically sterile uteri.44 In puerperal cows infec- tions due to C. pyogenes, E. coli, staphylococcus, Pseudomonas aeruginosa, streptococci, or mixed in- fections were most commonly cultured. These infections in cows resulted in the lochia assuming a white, yellow- white or grey mucopurulent character toward the latter part of the puerperal period. Vaginal exudates of 5 to258 VETERINARY OBSTETRICS 200 ml. volumes in 30 to 35 percent of all cows were reported 10 to 20 days postpartum but only 2 to 5 percent had this volume at 30 to 50 days.96 These latter cases were probably those with persisting infections. Plasma levels of prostaglandin metabolite were high for 7 to 23 days postpartum. Cows with postpartum uter- ine discharges had longer periods of prostaglandin re- lease, 16.7 days, and longer periods for the completion of uterine involution, 39.6 days, than the cows with a normal postpartum uterine involution 13.5 and 29.6 days, respectively. Progesterone levels remained at baseline levels in the postpartum period until the prostaglandin release had ceased.643 The interval from parturition to complete involution of the uterus averaged 29.6 days (range 16 to 50 days). Prostaglandin increased uterine tone and promoted involution.643 Presence of ovarian cysts had little or/no effect on uterine involution. The involution of the bovine uterus and cervix based on rectal palpation during the postpartum period was re- viewed and reported upon.73 74 The size of the bovine utems decreased slowly between the fourth and ninth days postpartum. By the tenth day the involuting uterus could be completely defined by rectal examination. A marked decrease in uterine size and an increase in uterine tone occurred from days 10 to 14 coinciding with the onset of the first estrus in normal cows and the voluminous discharge of the uterine lochia. Fluid or lochia could be detected in the uterus by palpation on days 7 to 12 post- partum in many cows. During this period of 10 to 14 days postpartum the size of the postgravid uterine horn declined from 12 cm to 7 cm in diameter. The rate of uterine regression was quite rapid from 14 to 25 days postpartum. There was a decreased rate of involution be- tween days 26 and 39. Between days 40 and 50 there was little change noted. Prior to day 20 postpartum the diameter of the cervix, 4 to 7 or more cm, was smaller than the horn and after days 22 to 25 the cervical di- ameter, 3 to 4 cm, was greater than the horn diame- ter.7374,96 The following postpartum regression in the weight of cows’ uteri was 10 Kg. at parturition, 5 Kg. at 6 days, 2 Kg. at 12 days, 1 Kg. at 25 days and 0.7 Kg. at 50 days.65,68 Within 24 to 36 hours after a normal parturition the hand could not be passed through the cer- vix and by the fourth day postpartum only two fingers could be introduced. If a retained placenta was present the rate of closure of the cervix was delayed and the hand could still be inserted at 48 hours and often at 72 hours postpartum. In general the major gross palpable or physical involution of the uterus occurred by 25 to 30 days postpartum. Changes after 30 days were much less marked and more gradual. A summary of reports on bo- vine uterine involution as determined by palpation showed the time for involution varied from 26 to 56 days post- partum with a majority of authors reporting complete regression between 42 and 47 days.73,74,92 Clinical and rectal examination of the genital tract and ovaries of nor- mal post partum dairy cows revealed the first estrus to occur about 15 days after calving with the second estrus occurring about 33 days postpartum after a somewhat shortened estrous cycle. Subsequent estrous cycles were a normal length. Great variations were observed in high- producing cows and those with abnormal parturitions. Silent estrus occurred in 77 percent of the first postpar- tum ovulations, 54 percent of the second and 36 percent of the third ovulations.74 Hormonal profiles of individual dairy cows during the postpartum period of 40 to 78 days varied greatly but correlated fairly closely with clinical findings. The first preovulatory LH peak occurred at an average of 17 days (±10 days) and the first estrus oc- curred on postpartum day 28 (±16 days).883 During the spring and summer months cows’ uteri in- voluted more rapidly than cows calving during the fall or winter months. Cows suffering from periparturient diseases such as retention of the afterbirth had a slightly slower rate of uterine involution. The normally regress- ing uterus did not become histologically normal until 50 to 60 days postpartum or about 20 days after the uterus had returned to a clinically normal or involuted state. Following a retained placenta leucocytic infiltrations oc- curred in large numbers and remained for 20 to 30 days beyond the normal histologic involution in normal par- turition or until about 70 to 90 days postpartum. Corpora albicantia replacing the corpora lutea of pregnancy usu- ally are larger, containing more connective tissue, than are corpora albicantia replacing corpora lutea that were active for only a short period of time. In some cows these may persist for a number of years. In nearly 20 percent of the cattle, resorption of the corpora albicantia occurred after the fourth pregnancy.253 Postpartum involution of the canine uterus is a pro- longed process extending over a 12 week (3 month) pe- riod. Although the interplacental area returns to normal within a few weeks, the placental sites require many weeks to involute and heal.2b But as late as 3 months after par- turition, when the uterus is the size and appearance of the normal diestrous uterus, slight pigmented ring-shaped stripes may be observed in the endometrium indicating the former placentation sites. The bitch discharges much dark, mucoid, green lochia after parturition. This green pigment is uteroverdin and comes from the “green bor- der” of the placenta.37 This color is produced by the breakdown of hemoglobin. This decomposition product is the same as bilirubin and biliverdin. In the cat the placental border is brown. The first week the lochia is amber to red in color and by the second week it should be normal, clear mucus. The walls of the gravid hornPARTURITION 259 remain slightly thickened. In primipara and other young animals the uterus never returns to its pregravid size. The rate of involution in the other animals is not as well known but in sows a lochial discharge may be ob- served for about a week and involution of the uterus was fairly rapid.7 The uterine mucosa of the ewe was com- pletely involuted by 30 days after parturition and the pro- cess was described in detail.loob The uterine weight of postpartum ovine uteri was 700 gms at 3 days, 200 to 250 gms at 7 days, 60 gms at 21 days, and 30 gms at 35 days.70 Artificial Interference in Normal Parturition If parturition is a normal one there is no need or ne- cessity for outside aid by attendants. Such aid is ill-ad- vised. In the artificial environment under which many domestic animals are kept certain sanitary and preven- tive precautions may be necessary. Valuable animals should be observed during the act of parturition so that injury to the newborn is not caused by the dam or the surroundings, such as a mare or cow trying to give birth with its rear quarters wedged into a comer of a box stall. The afterbirth of ruminants should be removed after its expulsion so that the dam will not eat it or choke on it. Following parturition it is highly essential that the dam and newborn not be disturbed for several hours so that close “bonding” between them can occur.56b If the dam becomes excited after parturition, or for some other rea- son attacks the newborn, they should be separated. This condition is seen occasionally in the sow, the “berserk” sow, and in rare cases in the dog, in which the dam kills and even eats her young. The young cow may rarely attack her newborn offspring. Upon arising and feeling the placenta against her hocks or heels the mare may become excited, kick, and possibly injure the foal. Some horsemen tie up the amnion to the umbilical cord so the membranes are not stepped on and torn.83 85 Occasion- ally in young mares, heifers, gilts, and ewes the udder may be so sensitive, edematous, and sore that they will not allow the newborn to nurse. After dystocia or for other unknown causes, females may reject, ignore, or fail to accept and nourish their young. In these cases the dam must be restrained or given a sedative or tranquil- izer to allow the newborn to suckle or colostrum must be given and the newborn placed on a foster mother or fed milk replacer. If the cow or mare gave birth in a box stall, the wet, contaminated straw should be removed and replaced with clean, dry straw. If parturition took place in an unsanitary environment the navel requires disinfection. It is desirable to have a comfortable, quiet, isolated, sanitary place in which the animal can give birth. The dam and the newborn should be left alone unless the course of parturition is definitely abnormal. Close observation and knowledge of the normal course of parturition is necessary. If the first stage of parturition in the cow, doe and ewe is over 6 to 12 hours, in the mare over 4 hours, in the bitch, queen and sow over 6 to 12 hours; or if the second stage of parturition in the cow, doe and ewe is over 2 to 3 hours, in the mare over 20 to 40 minutes, in the sow, bitch and queen is over 2 to 4 hours, outside help is indicated. If at anytime the normal progression of the fetus(es) into and through the birth canal fails, assistance is usually needed. This should be obtained at once if severe injury to the dam or death of the fetuses is to be prevented. This aid to the dam is indicated if the frequency or intensity of abdominal contractions de- clines before the birth of the young or if the feet of the fetus in unipara appear and disappear with each labor contraction without progress in the passage of the fetus. In posterior presentation in primiparous, uniparous dams, outside traction may be desirable to avoid asphyxiation of the newborn. The help or assistance provided at par- turition should be competent and experienced. During the act of parturition it is not desirable or nec- essary to rupture the fetal membranes, either the amnion or allantois. It is not desirable to apply traction in phys- iological birth when the fetus first appears at the vulva. Such traction is likely to result in laceration and trauma of the dorsal commissure of the vulva or the perineum. Traction if applied too early before the cervix, vagina, or vulva is fully dilated, pulls these structures caudally and makes the lumen or diameter of the birth canal smaller, requiring trauma or rupture of the structures if birth is to be accomplished with traction. Williams stated, “In an experience exceeding 60 years I do not recall vul- var or perineal laceration in physiological birth in a do- mestic animal when not tampered with by attendants.” There is no indication for or advantage to the adminis- tration of oxytocin before or after normal parturition. The umbilical cord should be allowed to break of its own accord in the mare. In the cat and bitch the dam usually bites it off or it breaks off naturally by traction. Ligation of the umbilical cord in animals is usually unnecessary and frequently predisposes to umbilical infection. References Parturition and Involution 1. Adams, W. M. (1969) The Elective Induction of Labor and Parturition in Cattle, JAVMA, 154, 3, 261. 2a. Adams, W. M. and Wagner, W. C. (1970) Role of Corticoids in Parturition, Biol, of Reprod. 3, 223-228. 2b. Al-Bassam. M. A., Thomson, R. G. and O’Donnell, L. (1981)260 VETERINARY OBSTETRICS Normal Postpartum Involution of the Uterus in the Dog, Canad. J. Comp. 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(1979) Ultrastruc- tural Studies of the Equine Uterus and Placenta Following Par- turition, J. Reprod. and Fert. Suppl. 27, 579-586. 94c. Stewart, D. R. and Stabenfeldt, G. (1981) Relaxin Activity in the Pregnant Mare, Biol. Reprod. 25, 281. 95. Taveme, M. A. M., van der Weyden, G. C., Fontijne, P., Ellendorff, F., Naaktgeboren, G. and Smidt, D. (1977) Uter- ine Position and Presentation of Mini-pig Fetuses and Their Order and Presentation at Birth, Amer. J. Vet. Res., 38, 11, 1761-1764. 96. Tennant, B., Kendrick, J. W. and Petticord, R. G. (1967) Uterine Involution and Ovarian Function in the Postpartum Cow: A Retrospective Analysis of 2338 Genital Organ Examina- tions, Cor. Vet. 57, 4, 543. 97. Thorbum, G. D., Challis, J. R. C. and Currie, W. B. (1977) Control of Parturition in Domestic Animals, Biol. Reprod. 16, 18-27. 98. Thorburn, G. D., Challis, J. R. G. and Robinson, J. S. (1977) Endocrine Control of Parturition, in Cellular Biology of the Uterus, edit, by R. M. Wynn, Plenum, New York, 653-715. 99. Tram, F. F. (1947) What Time Will a Mare Foal, Blood Horse, 27, 2, 106. 100a. Ulrich, Carl (1969) Personal Communication. 100b. Uren, A. W. (1935) Involution of the Uterine Mucosa in the Ewe, Mich. State Col. Agr. Exp. Stat., Tech. Bull. 144. 101a. VanDongen, C. G. and Hayes, R. L. (1966) Oxytoxic Activity in Unextracted Blood Plasma During Calving, J. Reprod. and Fert. 11, 317. 101b. VanderWeyden, G. C., Taveme, M. A. M., Okkens, A. C. and Fontijne, P. (1981) Intrauterine Position of Canine Fetuses and their Sequence of Expulsion at Birth, J. Sm. An. Pract. 22, 503. 102. Van Niekerk, C. H. and Morgenthal, J. C. (1976) Plasma Pro- gesterone and Oestrogen Concentrations During Induction of Parturition in Mares with Flumethsone and Prostaglandin, Proc. Intern. Congr. for An. Reprod. and Art. Insem. 3, 386. 103. Vinattieri, E., Hayward, A. H. S. and Artioli, D. (1945) Re- tention of Placenta in the Buffalo, with Associated Sequelae, Vet. Rec., 57, 46, 509. 104. Wagner, W. C., Willham, R. L. and Evans, L. E. (1974) Con- trolled Parturition in Cattle, J. An. Sci. 38, 3, 485-489. 105. Welk, F. A. and N. L. First (1981) The Effect of Oxytocin on the Synchrony of Parturition Induced by PGF2a, 9th Intern. Congr. on An. Reprod. and Art. Insem., Madrid, Spain. 106. Williams, W. L. (1943) Veterinary Obstetrics, 4th Ed., Ithaca, N.Y. 107. Wrenn, T. R., Bitman, J. and Sykes, J. F. (1958) Body Tem- perature Variations in Dairy Cattle During the Estrous Cycle and Pregnancy, J. Dairy Sci. 41, 8, 1071. Care of the Newborn and the Dam At the time of the birth of the young especially in the mare, an attendant should be present to remove the am- nion that may be wrapped around the muzzle and nose and cause asphyxiation. The onset of fetal respirationPARTURITION 263 may begin before the fetus is completely expelled in some parturitions, especially those that are delayed. In normal parturitions respiratory movements in the fetus are ini- tiated by several deep inspirations about 10 to 60 sec- onds after expulsion. In the foal this will often occur before the umbilical cord has ruptured. It is believed that either a rise in the C02 levels in the fetal blood,7 an increased hydrostatic pressure in the fetal vessels when the cord ruptures, or removal of the amnion from over the nostrils, or a combination of these factors initiates breathing in the newborn. If respiration in the newborn is delayed various procedures should be used to stimu- late this activity. The mucus should be removed from the nose and mouth. The newborn should be laid on its side on straw, not loose chaff or shavings that might be inhaled, with the head and fore quarters slightly lower than the hind quarters. Vigorous rubbing of the newborn with straw, hay, towels or shaking its head, or tickling its nostrils, will help bring about respiratory activity. The use of an oxygen tank and an attached short rubber tube has proven useful in saving some weak newborn. The tube is passed into the pharynx and the nostrils and mouth are closed tightly. Oxygen under moderate pressure dis- tends the lungs. Opening the nostrils and pressure on the chest collapses the lungs and the process is repeated as often as necessary. A positive pressure “Bird” respirator may also be used. A warm oxygen tent or chamber may help save some weak pups or kittens. In recent years several simple resuscitators with attachments for an ox- ygen tank are commercially available. These actively re- move excess mucus from the lungs and provide oxygen. Other practices, such as artificial respiration, have not proved very satisfactory or saved many weak newborn animals. Electrocardiographic studies showed a rapid rise in the heart rate occurred at birth, from 54 to 60 to 108 to 216 beats per minute in the equine newborn and from 72 to 108 to 96 to 120 per minute in the newborn calf.110 Some veterinarians advocate dipping the pup or kitten in cold then hot water to stimulate respiration. Other work- ers advise holding the young up by their hind legs to aid cleaning mucus from the larger bronchi, throat, and nose. If this is done in the newborn calf a copious flow of mucus is often passed from the nose and mouth. Most of this mucus obviously must come from the stomach. It has been observed by the author that in the handling of nearly all newborn which at expulsion are so weak that respirations do not begin normally within 1 to 2 minutes, any treatment of a drastic nature is often un- successful, although such efforts are usually indicated and are appreciated by the owner. Umbilical disinfection may not be necessary if births occur on clean pasture. The licking of the navel and the absence of barn or barnyard infections usually ensure the rapid and normal healing of the newborn’s umbilicus. If parturitions take place in a bam or barnyard, particularly if navel infections are prevalent on the farm, careful dis- infection of the navel may help prevent disease. It is doubtful if a hasty, careless application of a disinfectant or antiseptic to the navel will be of any value. To be effective an antiseptic should be carefully applied 1 to 3 times daily for the first two days following birth. Tinc- ture of iodine, 1:1000 solution of alcoholic sublimate, 5 percent tannic and 5 percent salicylic acid in 70 percent alcohol, 10,000 ppm. neutral iodophor solution, 40,000 to 50,000 ppm. sodium hypochlorite solution with a very low hydroxide content, or any similar antiseptic, may be applied by carefully soaking the navel stump and squeez- ing it with cotton soaked in the antiseptic. Some prefer to use a powdered astringent such as alum or tannic acid and an antiseptic. This is carefully dusted on the navel stump to hasten dessication. In foals it is often advisable to administer a prophylactic dose of tetanus antitoxin. Two foals developed tetanus even though the dam re- ceived a booster injection of tetanus toxoid during preg- nancy.83 A contributing factor may have been that both mares leaked milk for a week before parturition. In a valuable newborn, antibiotics such as penicillin, strep- tomycin, tetracycline, ampicillin or Chloromycetin may be administered for several days to prevent navel infec- tion or septicemia. Clean, sanitary, well-bedded stalls for the calf and parturient cow help greatly in preventing navel infections. On farms or ranches where large num- bers of females give birth in a confined area sanitation practices and facilities are highly important to prevent navel infections, infectious diseases of the newborn as well as retained placenta, metritis and mastitis in the dam. If young calves are placed together they may suck the umbilical stumps and cause navel infection. In countries with the screwworm, Cochliomyia americana, infes- tation during the warm seasons, it may be necessary to treat the navels of newborn animals with a fly repellant to prevent screwworm infestation of the navel stump. The newborn should nurse and thus get colostrum within 1 or 2 hours after birth. From birth to suckling averaged 111 minutes, range 35 to 420, in the foal93 and an av- erage of 10 to 35 minutes, range 3 to 153, in the pig.60 In the sow this may be slightly delayed if the pigs are removed as they are bom—to prevent their injury by the sow—and returned after parturition is completed. The great importance of globulins in the colostrum, which are only absorbed from the gut 12 to 36 hours after birth by the newborn animal, has been discussed under pla- cental transfer of immunity. This does not occur in do- mestic animals except to a slight degree in the dog and264 VETERINARY OBSTETRICS cat.50 Under highly unsanitary or infected environmental conditions, it is desirable to get colostrum into the new- born promptly, within 15 to 30 minutes after birth. If necessary this may be given by stomach tube. The amount of colostral antibodies absorbed and available to the newborn is in direct proportion to their levels in the co- lostrum and the amount of colostrum consumed within a few hours after parturition. Premilking in cows, some- times practiced to avoid severe edema of the udder, may reduce the immunoglobulins available to the newborn calf because of their dilution in large quantities of milk stim- ulated by this practice. The principal transfer of globu- lins from the blood to the milk occurs the last 3 days of the gestation period.93 Besides the important immune bodies absorbed from the colostrum by the intestines during the first 24 to 36 hours of life there are laxative properties in the colostrum. In the cow the colostrum is about five times as high in protein, two times as high in fat and minerals, ten times as high in iron as ordinary milk. In the newborn lamb this first feeding of colostrum is essential to getting it on its feet, and making it strong and active. Clipping of the udder in heavily fleeced ewes may aid the lambs to find the teats and nurse promptly. If for some reason, such as preparturient leaking of milk, colostrum from the dam is not available, another source may be indicated. Colostrum may be frozen and stored for such emergencies. In calves and foals 1500 to 2000 ml. should be given in divided doses the first 12 hours after birth.226 The amount of immunoglobulins absorbed from the colostrum is directly related to the susceptibility of the newborn to the neonatal diseases of scours, sep- ticemia and pneumonia. In 300 baby calves purchased at auctions, deaths occurred in 16 percent of calves with 1 to 6 percent of the serum protein comprised of gamma globulins while only 1 percent deaths occurred in calves with 19 to 46 percent gamma globulins in their total serum protein fraction.53 Eighty to 90 percent of neonatal foals with failure of colostral immunoglobulin transfer devel- oped infections and died or required therapy. This was largely due, as in cattle, to low colostral immunoglob- ulin content.77 If colostrum is not available a transfusion of plasma or of dam’s blood or blood from an animal of the same species is indicated to provide the necessary antibodies.3311 Dam’s blood should not be used in new- born where hemolytic diseases are suspected. In large animals 500 to 800 ml. of blood or serum is usually ad- ministered subcutaneously,226 as large amounts of fluids are difficult to inject intravenously and the process fre- quently causes violent struggling in the newborn. In the smaller animals 20 to 100 ml. of blood or serum may be given. Lyophilized immunoglobulins may be pre- pared and stored and given by stomach tube to the new- born animal.336 The use of the antibiotics have been of further help in bringing these animals lacking immune bodies through the first few critical weeks of postnatal life. The new- born of animals except dairy cows and goats suckle the dam until weaned. In the sow each pig selects its own teat, the stronger often getting the better mammary gland, so that in a week or two there are only as many func- tioning glands as there are pigs. This teat preference oc- curs in kittens but not in pups.45'46 The other glands, that are not being suckled, involute. In uniparous animals the young suck all teats. There are many methods of man- aging the newborn calf to prevent digestive upsets or diarrhea, after he has suckled the dam for the first 12 to 24 hours. The Problem of Handling and Feeding of Orphan Animals is occasionally presented to the veterinarian when the dam dies at parturition or fails to give sufficient milk. It is well known that the young of a species thrives best on milk of its own kind. Therefore having the orphan adopted by another postparturient female of the same species is indicated. This is fairly easy and can often be done in all domestic animals when such an animal is available. Occasionally it is necessary in the sow to make the young smell like the foster dam’s offspring by rub- bing her fetal membranes or genital discharges over the orphan, or sprinkling the entire litter of orphans and sow with a material having a similar strong odor such as a weak cresol solution or an aerosol deodorant. In sheep it is a common practice to cover the orphan with the hide of the dead offspring or the wool of the ewe that is to be its foster mother. In the large animals, as in cows, the foster mother usually adopts the orphan fairly promptly but occasionally she may have to be restrained for a number of times to permit feeding. In the dog most post- parturient bitches will readily adopt the newborn of an- other. The problem is more difficult when a foster mother is not available. All domestic animals can be raised with proper care and attention by artificial nursing and feed- ing. In calves the problem is simple, since cow’s milk is nearly universally available. In the other animals the problem can be solved to a great extent by referring to Table 8 on the composition of the milk from the various animals. From this table it is noted that milk of the ewe, doe, and cow are nearly similar in composition. The milk of the sow is richer in fat. Mare’s milk is similar in com- position to human milk and foals therefore thrive on for- mulas for human babies. After foals are several months of age, cow’s milk might be satisfactory; but younger foals may develop a stubborn diarrhea when fed cow’s milk.88 Pigs, pups and possibly kittens may be raised on rich cow’s milk, evaporated milk, or prepared formu- las.66 Presently there are fortified powdered milk prod-PARTURITION 265 ucts for foals, “Foal-lac,”* for pups, “Esbilac,”* for kit- tens, KMR, and for pigs, “SPF-lac.”* These are mixed with the proper amounts of warm water and fed as are the synthetic or formulated starters for calves. The milk should be warm and fresh. The newborn animal should be fed every 1 to 3 hours for the first week or so and then every 4 or 12 hours thereafter. The amount of milk fed daily to the young of cattle, horses, sheep, goats, and swine should be about 10 percent of the body weight, divided into the aforementioned number of feedings. In dogs and cats the feeding of orphan young is discussed in Chapter 9 following cesarean section in the bitch. All animals can be fed by nipple bottle with either calf, lamb, human, or doll nipples. At an early age most animals except lambs usually may be taught to drink milk from a shallow pan or bucket. If symptoms of diarrhea de- velop, the amount of milk should be reduced markedly for 24 to 48 hours and oral and parenteral antibiotic, electrolyte and supportive therapy should be instituted. In some cases one may increase the amount of milk gradually to more than 10 percent of the body weight after the first week or so of age. It is hard to starve a young animal, but easy to overfeed it. Orphan pigs may be reared on special commercial pig starters or formulas containing antibiotics. The orphan young should be encouraged to eat solid food as early as possible so that the amount and fre- quency of milk feeding can be reduced. In general for the first 1 to 2 months of life the orphan young will not appear as well nourished as animals that are not orphans, and will more often have digestive disturbances. Care and nursing are of utmost importance in the proper rear- ing of orphan young on artificial diets; otherwise arti- ficial feeding is not particularly difficult. In some cases the addition of vitamins, especially A and D, may be necessary or advisable. In pigs, iron may be provided by injections of an iron dextran product intramuscularly, painting the sow’s udder with a weak solution of iron, or supplying clean soil to prevent anemia. A Persistent, Patent or Pervious Urachus is invari- able seen with infection of the navel either as a cause or a result of an open urachus. This condition is seen most commonly in the newborn foal and rarely in cattle. Since it is often followed by pyemia, septicemia, and navel or joint ill, the condition should be viewed seriously. An- tibiotics administered over a period of 10 to 14 days is indicated together with local treatment of the navel with antibiotics or disinfectants. If, after several days, the urine continues to flow through the urachus keeping the navel and the surrounding skin moist, the lower 4 to 5 inches *Borden Chemical Co., Box 419, Norfolk, Va. 23501 and other sup- pliers. of the urachus should be cauterized with a small swab containing Lugols’ solution or the instillation of about 2 to 5 ml. of 5 to 10 percent formalin solution. This or similar treatments will usually swell and close the ura- chus. Retained Meconium—In the newborn foal the me- conium in the rectum may be found in hard pellets from 1/2 to 2-1/2 inches in diameter that within 24 or 36 hours after birth become impacted just cranial to the bony pelvis. The condition is seen more often in colts than in fillies. The diameter of the bony pelvis is very small in the newborn foal. The affected foal usually nurses nor- mally but within 24 to 48 hours after birth exhibits symptoms of colic and persistent to intermittent strain- ing, frequently getting up and lying down, elevating the tail and assuming a straddled attitude similar to that as- sumed during defecation. Colicy symptoms may become more severe, and anorexia occur. Impaction may be con- firmed by inserting a lubricated finger into the rectum and palpating the mass of hard pellets of meconium. This disease is not uncommon in foals, and for that reason many veterinarians recommend that all newborn foals be given an enema soon after birth. This enema may be of physiological saline, mineral oil, olive oil, caster oil, mild soap and water, or several ounces of glycerin in a pint of soapy water; the author has found the commercial ob- stetrical lubricants like “Lubrivet” very satisfactory and nonirritating. About 4 to 6 ounces are introduced at a time through a soft rubber horse catheter. This may be repeated as often as necessary. In cases of impaction of meconium with colicy symptoms this may have to be repeated frequently at intervals of 10 to 30 minutes until the condition is relieved. Oral administration of laxatives such as castor oil, or the injection of “Lentin,” is not usually indicated as the fecal material in the rectum and small colon behind the hard meconial pellets is soft. Gentle, persistent treatment usually results in recovery. Heroic or drastic treatment with a looped wire or forceps is dangerous and rarely necessary. Rupture of the Bladder or Urachus may occur in rare instances in the newborn foal. This probably occurs due to a full bladder especially in male foals at partu- rition or when the navel cord is ruptured. The foal ap- pears normal for 12 to 24 hours; but by the second to fourth day the foal is depressed, pulse and respirations are increased, and the abdomen is slightly to markedly distended.39,76 115 Tapping the abdominal cavity with a needle in a sterile manner will release the urine and con- firm the diagnosis. Blood tests show a rise in blood urea nitrogen. Laparotomy on the midline, and repair of the ruptured bladder is indicated. Supportive and antibiotic therapy with good nursing often results in a successful termination.266 VETERINARY OBSTETRICS Many Congenital or Hereditary Conditions such as atresia ani, cleft palate, edema, undershot jaw, con- tracted tendons, blindness, cerebellar hypoplasia, and combined immunodeficiency (CID) and others may af- fect newborn animals. (See Chapter III). Some of these defects such as umbilical and scrotal hernias and cryp- torchidism noted at birth may spontaneously recover within a few weeks to months. The observation and study of anomalies in the newborn is interesting. It may be of value to the owner, if the condition has occurred several times in a herd, to check carefully for inbreeding and for a hereditary recessive factor causing the condition. If the veterinarian is acquainted with the reported hered- itary defects or anomalies in the newborn he may be able to advise his client properly even though only one de- fective individual has been produced. If the defects or anomalies are recognized early, treatment is possible in some; but in others slaughter must be recommended. Many anomalies or defects are observable at birth or cause no- ticeable symptoms to develop within several days after birth. Others may not be diagnosed for months or years. Infections of the Newborn Contracted in Utero are rather uncommon compared to the infections contracted after parturition due to contact with virulent organisms in the outside environment. Many diseases of the new- born such as various septicemias, enteritis, pneumonia, and others may develop shortly after birth. A few of these diseases may be contracted in utero or in the birth canal at parturition. Probably most of them are contracted after birth from infected surroundings either through the raw umbilical or navel area, by ingestion or by inhalation. Many diseases of the newborn are favored by improper nutrition, management and housing facilities. The nu- merous infectious, managerial and nutritional problems affecting the newborn will not be discussed in this text inasmuch as they are not directly associated with par- turition or gestation. Most of the organisms known to cause placental and fetal disease with abortion may cause disease or infec- tion of the newborn. Many of the organisms mentioned under causes for abortion may be present in fetuses bom at term and cause their early or delayed death. In cattle these include Brucella abortus, Leptospira spp., Listeria monocytogenes, E. coli, Streptococci, Toxoplasma gondii, Aspergillus spp., and Salmonella spp. Antibody titers for brucella, leptospira and IBR- IPV, influenza, BVD-MD and other viruses in the serum of newborn calves that have never suckled have been reported. This indicates a prenatal exposure and re- sponse by the fetus to these organisms whether the or- ganisms can or cannot be recovered from the fetus after birth. There is evidence67’71110 that Mycobacterium paratuberculosis may be transferred in utero from an infected cow to its fetus and be carried into the postnatal period. Bovine leukemia vims, similar to feline leuke- mia vims may occasionally pass to the fetus in utero although most spread occurs horizontally.43112 In horses the fetal infections contracted in utero caus- ing abortion, as well as early neonatal deaths after pre- mature abortion, as well as early neonatal deaths after premature or term births, include: Streptococcus zoo- epidemicus, E. coli, Actinobacillus or Shigella equuli,33 Leptospira spp, Salmonella abortus equi, and rhino- pneumonitis or herpesvirus 1.17 It may be difficult to de- termine in some infections, such as the first two, whether the fetus was infected before birth, during birth or whether the foal became infected soon after birth. If the newborn animals are visibly ill at the time birth or within a few hours then the infection was probably prenatal especially if retained placenta or metritis develops in the mare. Only 7 of 3,346 aborted fetuses yielded Actinobacillus equuli on culture but if postnatal death occurred within 24 hours of birth the Actinobacillus infection probably occurred prenatally.5,91’92 Intrauterine infection of fetuses with equine infectious anemia vims has been occasionally re- ported. In swine prenatal infections that may cause neonatal infections or death include: Leptospira spp., E. coli, hog cholera vims,19 42 parvovirus, pseudorabies vims, Toxoplasma gondii95 and Eperythrozoon suis (?).u Newborn pigs may become chronic carriers of the last five organisms. Poxvims was recovered from pustular skin lesions in a newborn pig.81 In sheep and goats intrauterine infections that may be present in newborn lambs and kids include: Vibrio fetus var intestinalis, Brucella melitensis, Salmonella spp., E. coli, enzootic abortion or Chlamydia, Toxoplasma gondii and Mycobacterium johnei.108 The latter organ- ism is not a cause for abortion in sheep. Occasional in- trauterine transmission of ovine progressive pneumonia vims and caprine leukoencephalomyelitis vims has been reported.22’28 In dogs and cats neonatal infections that may be con- tracted in utero include: Streptococci spp., Staphylo- cocci spp., E. coli, Pseudomonas aeruginosa, Leptos- pira canicola,64-66,70 canine herpes vims infection or “fading pup syndrome,”20'23 distemper vims, infectious canine hepatitis vims,70 Haemobartonella canis,70 and Toxoplasma gondii. The latter protozoal infection of prenatal fetuses has been reviewed in dogs and cats as well as in swine, sheep and cattle.95 102 In cats panleu- kopenia vims and leukemia vims may occasionally be transmitted in utero. The horizontal spread of these vi- ruses in young and older cats is much more common.82'85PARTURITION 267 Parasites Transmitted in utero from the Dam to the Fetus include: In horses—Strongylus vulgaris larvae.13 This is very rare.91 A verminous aneurysm in a 2 day-old fetus was infected with Actinobacillus equuli. Babesia caballi.111 Strongyloides westeri larvae may be transmitted to the foal in the dam’s milk as early as 5 days after parturition. Anthelmintic treatment of mares with Cambendazole within a few days after foaling prevented infection of the foals for several weeks and reduced the incidence of “foal scours.”73 As noted below strongyloides in swine and hookworm and ascarid larvae in dogs may also be trans- mitted to the newborn in the colostrum. In cattle—Neoascaris vitulorum,87 Theileria annu- lata,111 Anaplasma marginali (?),'“ Cysticercus bovis,79 Trypanosoma theileri,97 and Fasciola hepatica.86 Many other bovine parasites may be transmitted to the fetus in utero.36 In swine—Strongyloides ransomi and Stephanurus dentatus or swine kidney worm.8104 Although a few reports indicated that Ascaris suis infection of fetuses may occur, several studies84 proved that this does not occur. In dogs—Toxocara canis,38 68 70 Ancylostoma can- inum,170 and Dirofilaria immitis.70 75 Demodex canis infection of pups probably occurs the first few hours of life as there was no evidence it was acquired in utero.48 Several therapeutic regimens used to obtain ascarid-free pups have been described.21'49 There is presently no treatment to prevent Toxocara larvae from migrating from the dam to the fetus during pregnancy. Thus many bacterial, viral, fungal, parasitic and other diseases may be transmitted in utero resulting in the birth of infected neonates. In fact even rabies virus may pass transplacentally to fetuses of infected skunks.55 Neonatal Isoerythrolysis, or Hemolytic Icterus of the Newborn, has been described in the horse, pig, dog and cattle. In 1948 this condition was described in foals. 12,1516'34“37 Many workers have done much to clar- ify the causative factors and describe methods of diag- nosis and treatment.24 An incidence of 1 percent affected mares was reported in the New Market area in England. Neonatal isoerythrolysis of foals occurs when mares be- come isoimmunized to certain types of erythrocytes either through (1) placental breakdown and absorption of the antigens from placental tissue or fetal blood at previous gestation periods or (2) by transfusions of blood or (3) injection of fetal tissue vaccines. When these mares are bred to stallions which transmit to the fetus the type of erythrocyte to which the mare was previously immu- nized the disease develops. The icteric condition occurs when the apparently normal foal suckles and receives in the dam’s colostrum large amounts of antibodies com- posed of hemagglutinins and hemolysins. Hemolytic ic- terus has very rarely been observed in foals from pri- miparous mares. It is usually not observed in foals until the mare’s third or fourth parturition. Although most mares apparently become sensitized from the placenta of their foals. An early equine-fetal-tissue vaccine used for vac- cination against virus abortion caused certain mares to be immunized to the erythrocytes in the vaccine.36 Since vaccines prepared from equine tissues are not now used the incidence of neonatal isoerythrolysis has declined. Neonatal isoerythrolysis in foals is not due to an Rh-like factor as in humans but is caused by an isoimmunization of pregnancy due to intraspecies blood group factors (red cell antigens). Recent studies46'1056 on equine neonatal isoerythrolysis have shown that blood factors A and Q account for nearly all cases, especially in Thoroughbred and Arabian horses.1056 Brood mares possessing both blood factors A and Q are at low risk in producing affected foals. While mares lacking one or both factors and with a titer of anti- A or anti-Q of about 1:8 or 1:16 within 14 to 28 days of foaling are at high risk of having their foal develop this disease. Prognostic tests for these blood factors and their corresponding antibodies are now commercially available.46 1056 The symptoms, which may resemble foal septicemia, usually develop rapidly after the foal begins nursing, with mild to severe clinical symptoms occurring from 12 to 96 hours after birth. These include: somnolence; anorex- ia due to weakness; usually no rise in body temperature; increased pulse and respiration rate; slight to marked jaundice and anemia; and in severe cases prostration and hemoglobinuria. Foals which die rapidly have little ic- terus but an acute anemia. Foals that die of this disease after several days of illness usually show icterus and have severe liver and kidney damage.24 Icterus is also seen in foals that do not show illness until several days after birth. Hemoglobinuria and hemoglobinemia are unusual symptoms. The red blood cell count drops from a normal of 10 to 12 million, down to as low as 2 to 3 million in the most severe cases. In severe cases the death of the foal may result in 24 hours or less. In slight or mild cases where the amount of antibody from the ingested colos- trum is minimal, recovery may occur without treatment. The condition should be carefully differentiated from septicemia of the newborn usually characterized by el- evation of temperature, injection and congestion of the conjunctiva with icterus being absent or slight. Cases of septicemia, if treated fairly early, usually respond to treatment with parenteral antibiotics while cases of neo- natal icterus do not respond to antibiotic therapy. The268 VETERINARY OBSTETRICS red blood cell count does not fall below 5 to 6 million in septicemia of the newborn. The laboratory diagnosis was described by Bruner.12 The technique of testing the blood of mares and their foals, and stallions to which the mare was to be bred is relatively simple with proper equipment such as a cen- trifuge and microscope. In agglutination tests, using the serum of mares and a 50 percent suspension of carefully washed red cells of the foal or his sire, if the serum titer of the mare is no higher than 1:2 and the colostrum titer no higher than 1:4, the foal may safely nurse its dam. If the serum titer of the mare is 1:4 or the colostrum titer 1:8 the foal is likely to develop icterus and may or may not recover without treatment. If the serum titer in the mare is higher than 1:4 or the colostrum titer is 1:16 or higher it would be dangerous for the foal to nurse its dam. The development of an hemolysin titer of 1:10 or more is apparently necessary to produce marked symp- toms of the disease. The serum of sensitized mares may be tested against the red blood cells of a stallion and if a titer of 1:2 or less occurs the mare may safely be mated with that stallion. The prognosis in hemolytic icterus de- pends upon how early the condition is diagnosed and the promptness with which treatment is instituted. Advanced severe cases often die. The treatment of clinical cases consists of promptly removing the foal from the mare or muzzling it. If symp- toms are mild and the condition was not noted until the third to fifth day following foaling, treatment is unnec- essary. In severe cases several blood donors should be obtained and the blood of the dam and foal tested against various donors’ blood. If they are compatible, a large blood transfusion of 1500 to 2000 ml. of blood or more should be given the affected foal by injecting the blood into one jugular vein and removing an equal amount from the other by means of a 14-gauge needle. Occasionally another 500 to 1500 ml. of blood may be given the next day. In less severe cases 500 ml of blood may be trans- fused once or twice daily to carry the foal through the critical period of the disease which usually lasts only one to three days.24 Transfusions are usually necessary when the symptoms of the disease are exhibited within 24 hours of birth; when the foal is weak and unable to stand; and when the red blood cell number drops below 4,000,000 per cmm. or 8 gm. of hemoglobin per 100 ml. of blood. Up to 7000 ml. of blood may be transfused in a large exchange transfusion in severe or critical cases. In prac- tice this is often not possible and usually only about 50 percent of the foal’s original blood is removed. The blood volume of horses and foals is 8.11 to 9.7 percent of the body weight or in the average foal about 4000 to 6000 ml. The administration of antibiotics and confinement to prevent excessive exercise is advisable. The foal’s dam should never be used as a blood donor. Because of the low incidence of blood factor A in Shetland ponies they should be considered as potential blood donors.105b The dam should be milked out frequently by hand or by allowing another older foal to nurse her.15 37'94 The newborn foal can absorb antibodies from its digestive tract for only about 36 hours after birth. It had been shown in earlier work that the first colostrum had the highest titer and that this titer dropped rapidly in 12 to 18 hours with frequent milking even though slight amounts were secreted for several weeks postpartum. Most authors re- ported that after 48 hours postpartum it is safe to allow the foal to nurse if the mare has been milked out fre- quently. This disease in foals can usually be prevented if the sensitized mare is recognized because of having previ- ously produced an icteric foal, or by testing the mare’s serum against the red cells of the stallion to which it is to be bred. A positive test indicates that the disease will probably occur. A negative test is not significant as the mare may have become sensitized during pregnancy to the stallion’s red cells. A better procedure is to test the mare’s serum against the stallion’s red cells the last month, or preferredly the last week, of pregnancy.24 Even if the stallion’s blood is compatible with the mare’s serum when tested before breeding, the foals of sensitized or isoim- munized mares should not be allowed to nurse until its red blood cells are tested with the mare’s colostrum or serum. This is the most practical test. This may be done by immediately muzzling the newborn foal until the test is completed. If the foal’s erthrocytes agglutinate in a 1:4 dilution or higher with the dam’s serum or 1:8 or higher with the dam’s colostrum, the foal should be fed either “Foal-lac,” a human baby milk formula, low-fat cow’s milk to which some sugar syrup and possibly lime water have been added at a rate of 1 ounce syrup and 1 ounce lime per pint. The foal may be placed on another mare for several days. On the larger farms banks of fro- zen colostrum permit the foal to be provided needed co- lostrum after first crossmatching the red blood cells of the foal and the milk. These foals should be given pro- phylactic treatment with antibiotics for 4 to 6 days. The dam should be milked out thoroughly at frequent inter- vals by hand or by an older foal. After 48 hours the dam’s foal may be unmuzzled and allowed to suckle. Some veterinarians prefer to give the foal 500 cc. of compatible donor’s serum to replace the antibodies lost to the foal by not nursing its dam the first 48 hours after birth. In the convalescent period injections of iron dex- tran intramuscularly may aid recovery. Once a mare pro- duces a foal affected with neonatal isoerythrolysis, sub-PARTURITION 269 sequent foals are apt to be affected especially if the mare is bred to the same stallion. Recent further reviews on hemolytic icterus in foals have been published.37,58,90'94 A similar condition has been described in dogs pre- viously immunized by blood transfusions.44'107'116117 Nat- ural isoimmunization of the bitch during pregnancy is apparently rare. Although there are 7 blood types, A through G in the dog, only A is of significance in regard to incompatibility. In blood transfusions especially in breeding females, only A-negative donors should be used to avoid producing hemolytic disease in the pups after nursing. Leakage of blood from affected pups during parturition and subsequent uterine absorption may be one way of sensitizing the bitch.44 The signs of hemolytic anemia in affected pups are similar to those in foals. Most severely affected pups die within 72 hours of birth. Not all pups in a litter are usually affected, only those with type A positive blood. Treatment involves with- drawing 10 to 15 ml of blood from the jugular vein of affected pups and replacing it with a similar amount of A negative blood. In affected bitches the pups should be fed formula and not be allowed to nurse the bitch for 36 hours after birth. After this period their gut will not ab- sorb the antibodies present in the colostrum and they may be returned to their dam for nursing.66,99 Neonatal isoerythrolysis also occurs in pigs from 1 to 7 days after farrowing.14 Similar signs to that in foals and pups of weakness, depression, paleness of mucous membranes, anemia, icterus, prostration and occasion- ally hemoglobinuria are noted in some pigs, but not all, in a litter. As in dogs this condition may only rarely occur naturally. Most porcine cases have been due to vaccination of sows with crystal violet or swine tissue vaccines against hog cholera. In a few cases mildly af- fected pigs recover without treatment. Probably several blood group antibodies can cause the condition in swine.4 Other excellent reports on this disease in swine have been published.18,79 Bovine neonatal isoerythrolysis has been reported in Australia and the United States associated with the use of a vaccine that contains red blood cells as a preventive for tick-fever and an anaplasmosis (“Anaplaz”) respec- tively.98'105 The proper use of the latter vaccine, that is, vaccinating only nonpregnant cows, reduces the inci- dence to a very low level while still providing a degree of immunity to the disease. Hemolytic disease of the newborn has not been described in sheep, goats and cats but is a possibility. Nutritional deficiencies causing disease in the new- born animals include: (1) copper deficiency causing en- zootic ataxia, swayback of demyelinating encephalop- athy in lambs in Colorado, Peru, Australia, New Zealand and Great Britain. This is characterized by a progressive locomotor incoordination and partial or complete paral- ysis. Feeding additional, minute amounts of copper sul- phate to the pregnant ewes prevents this condition.59 (2) Iodine deficiency or excess causing enlargement of the thyroid glands or goiter is most frequently ob- served in foals. This may be prevented by feeding io- dized salt and by avoiding the excessive feeding of io- dides especially in the form of seaweed.6 (3) Selenium deficiency causes congenital white mus- cle disease or myopathy in newborn lambs in New Zea- land and other countries.51 This condition has also been described in dogs,74 and calves.69 Myocardial degener- ation and degeneration of skeletal muscles, especially of the neck, jaw and tongue are causes for weakness, in- ability to nurse and early death. (4) Vitamin A deficiency causes increased suscepti- bility for infectious diseases. This may occur rarely in newborn animals whose dams have been on a vitamin A deficient diet for many months. The teratogenic effects of vitamin A deficiency on fetal development have been described previously. Neoplasms of newborn animals are rare and have been reviewed.80 Tumors of the skin included papillomas of equine fetuses, and subcutaneous melanomas; a subcu- taneous mixed tumor and subcutaneous mixed tumor and a subcutaneous lymphangioma in bovine fetuses. Ab- dominal tumors included mesotheliomas of the perito- neum, a sublumbar lipoma and a retroperitoneal chon- drosarcoma in bovine fetuses. As in adult animals, mesotheliomas of the abdominal cavity produced ascites and resulted in dystocia that was relieved by caesarian section. Neoplasms of the gonads included adenomas of the testicles and granulosa cell tumors of the ovary of bovine fetuses.61 Congenital lymphoid leucosis often with skin involvement has been reported most often in bovine fetuses and newborn calves, and occasionally in a new- born piglet and a feline fetus.109 Other tumors included reticulosarcomatosis, carcinomatosis originating in the liver, nephroblastomas, a fibrosarcoma,25 and teratomas. Congenital leucosis has been reported in fetuses in cattle and cats. Most cases of leukemia are caused by the hor- izontal spread of the virus between animals. Miscellaneous diseases or causes of death of newborn animals include: Persistent bleeding from the navel stump. This oc- curred more often when the cord was cut with a sharp instrument instead of being broken by traction. If liga- tion of the cord is necessary to prevent excessive bleed- ing then the newborn should be placed on parenteral an-270 VETERINARY OBSTETRICS tibiotics for 3 to 7 days and the ligature removed in 24 to 48 hours. Repeated disinfection is indicated. A hem- orrhagic disease of calves was reported47 in which the dams were normal but had been fed sweet clover hay during the gestation period. Four newborn male and fe- male calves from one dam bled severely from the navel after birth. Three of the calves died but one survived after repeated transfusions. These calves suffered from a multiple coagulation defect of their blood. A possible hereditary nonsex-linked character might have been present.10 Hemophilia in foals and pups have been pre- viously described as affecting the male newborn in these species. Fibroelastosis of the heart valves due to an unknown cause has been described in pups and kittens and rarely in calves causing enlarged hearts and deaths of the new- born within 2 to 3 months after birth.41 Respiratory distress syndrome and convulsions in Thoroughbred newborn foals have been described.93,94 These foals have been called “barkers,” “dummies,” “convulsives” and “wanderers” depending upon the signs exhibited. Several different etiological factors or dis- eases were present in these foals including asphyxia, trauma (cerebral hemorrhage) and fetal stress. The res- piratory distress syndrome was described93,94 indicating the affected foals were normal for 24 hours. Respiratory distress began on the second day and became more se- vere. The respiratory rate went from 25 to 85 per min- ute. Inability to stand developed and extensor spasms occurred by the third day with death of the foals by the end of the third day or early on the fourth day. The lungs were atelectic and edematous with an absence of the sur- face-active lung lining or hyaline membrane. Thus this disease in foals resembled the respiratory distress syn- drome in human infants and piglets. A lethal autosomal recessive condition in swine characterized by respiratory distress (“barkers”) and hypothermia soon after birth to- gether with hypothyroidism, hairlessness, myxedema, reduced adcenocortical activity and immaturity of lung tissue with a surfactant deficiency has been reported.115b This syndrome resembles the condition in foals and hu- mans but a genetic component has not been reported in these latter species. Management and environmental conditions may cause or predispose the newborn to death or disease. Based on extensive and careful records 6 percent of calves die at parturition or within 25 hours of birth, 3 percent in multipara and 14 percent in primipara.113 There was a higher mortality rate in male calves and more abnormal parturitions associated with male calves. Calf mortality was eight times higher in moderately to severe abnormal parturitions or dystocia than in normal parturitions. The incidence of abnormal parturitions was twice as high for male calves than for female calves. Certain sires pro- duced calves having a higher mortality rate at parturition in primipara, 18 to 19 percent, than other sires, 8 to 10 percent.113 These sires should not be used on heifers. Dennis has reviewed the incidence and causes of peri- natal mortality in cattle, sheep and horses.30,31 Martens75b and Rossdale and Ricketts94 have further reviewed the diseases and therapy of newborn foals. In a survey of 790 feline litters 10 percent of the fetuses were stillborn and 27.1 percent of the live kittens failed to survive to one year of age. Malformations occurred in 6.8 percent of the kittens.9715 In a study of inbred matings, calves from certain sires had a much higher postnatal mortality rate than calves from other inbred sires.26 A higher than normal mortality rate occurred within several days after birth in Brahman cows calving on range during cold wet weather.32 A greater number of male beef calves were lost at parturition; these losses were greatest in primi- parous cattle, 9.5%, and least in pluriparous cows, 2.4%.3 Pups, pigs and lambs, in fact all newborn animals, have a poikilothermic nature and are often unable to re- spond to cold by increasing their metabolic rate until 3 to 7 days of age. This is most noticeable in thin, un- derweight, malnourished, “runty” newborn animals where nutritional reserves are not present. Many of these neo- nates appear immature. As high as 30 percent of baby pig losses after birth were due to chilling.27 It was also an important cause of death in pups.45,46 Hypoxia was the principal cause of 75 to 85 percent of stillbirths in swine.47b High death losses in newborn lambs occurred when the weather was cold and especially when the lambs were small and undernourished.2 Lambs weighing 4 pounds or less at birth suffered 65 percent or greater death losses compared to 5 to 8 percent losses in lambs weigh- ing 10 to 14 pounds.54 100 High environmental tempera- tures during gestation and underfeeding caused the birth of smaller lambs. The mortality in twin lambs with lower birth weights is 30 to 40 percent higher than in single births. Other causes for mortality in the newborn is lack of vigor due to inbreeding, prematurity, lack of nutrition for the dam during the gestation period and a failure of the dam to own or accept her newborn.103 Rarely certain Hereford cows may have such large teats that a small weak calf is unable to obtain colostrum. Occasionally postpartum dams suffer from agalactia due to disease, such as mastitis or endocrine causes and the newborn must be raised as an orphan. Disease factors causing mortality in lambs was carefully reviewed.9 Subcuta- neous edema associated with low serum protein levels was commonly present in all pigs for the first two days after birth. This edema disappeared after the ingestion of colostrum raised the serum protein levels of the pigs.40 Supplying artificial heat to the newborn and seeing thatPARTURITION 271 colostrum is ingested early to supply both energy and antibodies will save many weak neonatal animals. Injuries to the fetus during normal parturition are rare, but in dystocia forced extraction may result in fractures of the fore or hind limbs, especially in cattle. Fractures most often occur in the metacarpal or metatarsal bone in the region of the “break joint” or epiphysis, due to ap- plying the chain or rope above the fetlock and placing a severe strain on the leg by twisting, jerking, or excessive traction. If the fetus is dead this is of no consequence but if the fetus is alive the fracture may be highly em- barrassing for the veterinarian. By bandaging the leg and padding it well after correction of the displaced ends of the bone, and applying a plaster cast, the calf or young animal can walk. In 5 to 6 weeks this may be removed, and complete healing usually results. If a compound fracture occurs the prognosis is more guarded and anti- biotics locally and parenterally are indicated. Fracture of the jaw may result from excessive trac- tion or twisting. Occasionally the snare or chain may slip forward and fracture the bony plate holding the incisor teeth, thereby causing them to point forward. In cattle these fractures are difficult to hold in place after correc- tion. Frequently slaughter may be advised if both halves of the mandible are broken through the body, although surgery and wiring or pinning may be successful in se- lected cases. If only the incisor teeth are involved in the fracture, the animal will usually nurse satisfactorily or will drink from a pail, and healing occurs promptly even though the teeth may be at a more acute angle than nor- mal. Fractures of the ribs occur in foals due to injury of the fetus in its expulsion through the birth canal or due to the dam accidently stepping on the foal. Dyspnea often develops within a day or two with a jerky painful res- piration and an audible grunt on expiration. The foals move slowly and stiffly. Death often results. Occasion- ally taping the chest snugly with wide adhesive tape may be helpful if the lungs are not damaged. Dennis29 reported 174 hepatic ruptures and 1 splenic rupture in 4,417 lambs necropsied. Similar ruptures might occur in other species but they are rarely reported. Dislocation of the hip joint is very rare in the new- born of the larger domestic animals. If excessive traction or twisting is applied to the rear legs in posterior pres- entation dislocation is possible in the pup. In anterior presentation of the fetus when the head protrudes through the vulva and the fetal body is wedged in the birth canal, twisting or excessive traction on the head may cause dis- location of the occipital joint and the death of the canine or feline fetus. Subconjunctival hemorrhage is occasionally ob- served in newborn calves due to trauma during birth. If the cornea is not injured, therapy is not necessary and recovery occurs in about 7 to 10 days.114 Edema of the tongue is common in calves in anterior presentation, in which the normal passage of the fetus is delayed and the head is retained for several hours in the birth canal or protruding through the vulva. This edema of the tongue and often of the entire head is due to pas- sive congestion caused by the intrapelvic pressure ex- erted on the calf’s neck interfering with or blocking ve- nous circulation from the head. Edema of the forelimbs is observed frequently in prolonged dystocia when the forelimbs are extended so the fetlocks are outside the vulva. If the young is still alive the edema disappears within 3 to 24 hours after birth and the fetus can then suckle in a normal manner. Intertwined or twisted umbilical cords and straw in the nest of kittens may result in their starvation and death due to inability to move about freely. Occasionally the umbilical cord looped around a kitten’s leg may cause a slough. This may be due to the queen not properly cleaning the kitten and eating the long umbilical cord. Injury or death of the newborn caused by the dam— Occasionally the dam, usually a primiparous female, may become excited, belligerent, or vicious, and injure or de- stroy the young soon after birth. This is a further reason for having a quiet environment to which the animal is accustomed, and an attendent present during parturition. It occurs rarely in the cow or mare but is seen occa- sionally in sow and bitch. When the cow attacks, butts or kicks its calf, the calf should be removed or the cow restrained or tranquilized until it becomes reconciled to and accepts the calf. In a few mares colic associated with uterine involution and expulsion of the fetal membranes may be quite severe. A sedative or tranquilizer is indi- cated and in some instances the foal should be removed from the stall for several hours to prevent accidental in- jury by the dam. Occasionally a mare will refuse to al- low a colt to nurse and kicks him away from her flank. The mare-foal bond is established at birth by appear- ance, sound and smell. The latter comes from the fetal fluids. If the dam is highly nervous or exhausted from a painful or difficult birth and this bond does not occur soon after birth, it may not develop.553 This calls for re- straint and tranquilization of the mare at regular intervals even to an attendant employing a twitch to allow the foal to nurse. Between nursings the foal should be confined in a partitioned part of the box stall. The dam may accept the foal after 1 to 2 days when the congestion and sore- ness has left her udder. In swine this viciousness may be marked and the pri- miparous or young sow will attack and kill her offspring. About one percent of the pigs farrowed in Iowa, Illinois, and Indiana are eaten by sows.63 The sow may kill her272 VETERINARY OBSTETRICS pigs as they are farrowed or farrowing may be normal and then the sow kills the entire litter at one time. Some pigs are eaten but most are merely killed thus this con- dition is not a true “cannabalism.” This condition rarely occurs after 24 hours after farrowing. The “berserk” sow may even attack the owner. Obviously it is necessary to have this type of sow farrow in a farrowing crate or for the attendant to remove the pigs immediately after birth. Nutrition as a cause of this condition is doubtful since usually only one sow in a drove fed the same ration is affected. It may be due to an inherited or congenital ex- citability, psychosis, or viciousness. Gilts from affected or related sows may also develop a similar aggressive attitude after farrowing. The hereditary or genetic nature of this condition has not been proven but seems more likely than the nutritional theory as the cause of this con- dition. Quiet sows and gilts should be selected for breed- ing. In order to attempt to induce this type of sow to accept her pigs the surroundings should be quiet. Some owners and veterinarians truss the sow up and allow the pigs to nurse at regular intervals. Spontaneous recovery may oc- cur at any time. Often the sow is given a sedative or narcotic dose of chloral hydrate, pentobarbital or other strong sedative before the pigs are placed on her.63 Along with this, some veterinarians advise the injection of 2 to 5 ml., or 20 to 50 units, of oxytocin, but its value is questionable. The sow and her pigs should be closely watched, since as soon as they regain consciousness some sows will again attack their pigs. If this viciousness is pronounced and the sow refuses to accept her pigs in 1 to 2 days they should be placed on other dams or hand fed. Treatment frequently fails. This undesirable inher- ent disposition was aggravated by parturition. This type of sow is usually sent to slaughter. The same condition is also observed in bitches, es- pecially Cocker Spaniels, and rarely in queens after par- turition. Occasionally the dam, especially in primipara, will totally reject her offspring and not clean or nurse them. Their surviving offspring usually have to be reared as orphans.46,52 Animals should not be reared from such unstable psychotic dams for fear of perpetuating such individuals. Care of the Postpartum Dam—Following parturi- tion the dam should be allowed to lick and nurse her young. All undue excitement, noise, or unusual happen- ings should be eliminated or prevented. Rest and quiet following parturition is imperative. The roughage fed to large animals should be of good quality. The grain ration should be rather laxative and light, such as bran, oats, and a little linseed meal. In most animals the amount of grain should be increased gradually during the first three weeks after parturition. In the dairy cow it may have to be increased more rapidly, to prevent ketosis. In the sow the light grain feed should be continued for a week and then gradually increased. If it is increased too rapidly the pigs may get too much milk, and diarrhea may de- velop. In the mare a bran mash or two following foaling may be of value if the mare is constipated. Some veter- inarians routinely administer one gallon of mineral oil to mares soon after foaling to help prevent constipation due to the pain occasioned by the act of defecation the first few days after foaling. Milk yield in mares, as in cows, was maximal, 11.8 kg., at 30 days postpartum and de- clined to 9.8 kg. in late lactation.476 The cow should be watched carefully for several days after calving for symptoms of milk fever. Excess edema of the udder should be controlled by massage, frequent milking, or preferredly diuretics such as the carbonic anhydrase in- hibitors with or without the glucocorticoids as described under lactation. Udder suspensories may be indicated in some cows to help support the edematous udder. Al- though urticaria due to the absorption of milk proteins into a sensitized animal occurs most commonly at the time of drying off, especially in Guernsey and Jerseys, it may occasionally develop after parturition if milking is limited in order to prevent the occurrence of milk fe- ver. In most animals it takes about 10 to 14 days to re- turn the dam to full feed. Moderate and light daily ex- ercise is advisable in animals after parturition. Mares should be turned out for about one hour a day for the first week and then for longer periods thereafter. Draft or saddle mares can begin light work in two weeks. In domestic animals retention of the fetal membranes occasionally occurs. The membranes are considered as being retained if they are not expelled within 8 to 12 hours in the cow, 3 to 6 hours in the mare, and 8 to 12 hours in the ewe. Retained placenta occurred twice as frequently in cattle when the calf died at birth than in normal parturitions and these cows had a lower concep- tion rate.113 In multipara, membranes usually cannot be observed hanging from the vulva and they fequently go unnoticed until they are expelled in 1 to 2 days or de- compose and a mucopurulent discharge is noted in 4 to 10 days. It is desirable, especially in the cow and mare— in which species retained placenta occurs most com- monly—to have this condition treated by a veterinarian. Veterinarians prefer to treat retained placenta in the cow within 1 to 3 days after parturition. Mares should be treated earlier, within 12 to 24 hours, to avoid septi- cemia, toxemia, and possible parturient laminitis (See Chapter XI). If genital discharges persist beyond 14 to 20 days postpartum or if they are abnormal in amount or purulent in nature, the genital tract of the animal should be ex- amined and treated as described under uterine infections.PARTURITION 273 It is desirable especially in valuable cows to examine the genital tract about 30 days postpartum even when the calving and the postpartum period were apparently nor- mal. In mares a vaginal examination and possible uterine culture should be made about 6 days postpartum if breeding is to be at the foal estrum, or early in the sec- ond estrum if the mare is to be bred at that estrum. Early treatment of uterine infections or pathology or repair of vulvar lacerations after parturition is essential if the an- imal is to conceive promptly. Occasionally animals develop an acute septicemia from uterine or mammary infections within 24 to 48 hours postpartum. The symptoms may be severe and death re- sult. The dam may be so severely affected that lactation is greatly suppressed and the young may perish or must be raised as orphans. Any illness occurring immediately after parturition should be treated promptly. Agalactia, or a lack of milk after parturition, may be due to the failure of milk let-down or failure of milk production. In the former condition adrenalin, due to stimuli such as pain and fright, is thought to be secreted. This hormone antagonizes or prevents the let-down of milk by the posterior pituitary hormone, oxytocin. This condition is noticed occasionally in heifers with a greatly congested, edematous, painful udder; injections of pi- tuitrin or oxytocin intravenously or intramuscularly cause rapid and complete milk let-down. Sometimes repeated injections at each milking are required. The failure of milk production, if not caused by diseases such as: acute metritis, acute or chronic mastitis, traumatic gastritis, in- digestion and others, is due to a hormonal deficiency or to defective development of the mammary gland with a lack of secretory tissue. Prolactin from the anterior pi- tuitary gland apparently is important in initiating lacta- tion, while the growth or somatotropic hormone is re- sponsible for the maintenance of proper and high secretory levels. Injections of crude anterior pituitary extract have been used by veterinarians with questionable success as a possible aid in stimulating lactation. With the com- mercial production of the separate hormones of the an- terior pituitary gland, such as prolactin and growth hor- mone, the therapy of these animals with low production of milk after parturition, may be improved in the future. Marked agalactia in sows and mares was associated with the feeding of ergot the last few weeks of pregnancy.101 Mortality in piglets due to starvation was high. At pres- ent the treatment or correction of severe agalactia is un- satisfactory and usually the newborn must be reared as orphans. In most cases with no obvious cause, rebreed- ing is questionable and affected food-producing animals should be slaughtered. Occasionally it may be desirable to hasten mammary involution in animals that have lost their newborn young, or in bitches in pseudopregnancy. Cessation of milking; application of mild liniments, such as camphorated oil, to the udder; withholding or drastically reducing water and TDN intake, and injections of estrogens, in larger animals at repeated intervals if necessary, are valuable in reducing udder size and suppressing milk secretion. Care and Diseases of the Newborn Animal, Aftercare of the Dam 1. Adler, S. and Clark, E. J. (1962) Intrauterine Infection with Ancylostoma caninum in Dogs, Ann. of Trop. Med. and Paarasit., 15, 354. 2. Alexander, G. (1961) Energy, Expenditure and Mortality in Newborn Lambs, Proc. 4th Intemat. Congr. on An. Reprod., the Hague. 3. Anderson, D. C. and Bellows, R. A. (1967) Some Causes of Neonatal Calf Losses, J. An. Sci. 26, 4, 241. 4a. Andresen, E., Preston, K. S., Ramsey, F. K., and Baker, L. N. (1965) Further Studies on Hemolytic Disease in Pigs Caused by Anti Ba, Amer. J. Vet. Res. 26, 111, 303. 4b. Bailey, E. (1982) Prevalence of Anti-Red Blood Cell Anti- bodies in the Serum and Colostrum of Mares and Its Relation- ship to Neonatal Isoerythrolysis, Amer. J. Vet. Res. 43, 11, 1917. 5a. Bain, A. (1963) Common Bacterial Infections of Foetuses and Foals and Association of the Infection with the Dam, Austral. Vet. J. 39, 11, 413. 5b. Baines, F. M. (1981) Milk Substitutes and the Hand Rearing of Orphan Puppies and Kittens, J. Sm. An. Pract. 22, 555. 6. Baker, H. J. and Lindsey, J. R. (1968) Equine Goiter Due to Excess Dietary Iodide, JAVMA, 153, 12, 1618. 7. Barcroft, J. (1952) Fetal Respiration and Circulation, in Mar- shall’s Physiology of Reproduction, Vol. II, Longmans Green and Co., London, 398. 8. Batte, E. G., Moncol, D. J. and Barber, C. W. (1966) Prenatal Infection with the Swine Kidney Worm (Stephanurus den- tatus) and Associated Lesions, JAVMA, 149, 6, 758. 9. Beck, C. C., Bronson, G. M. and Henneman, H. A. (1968) Factors in Disease and Mortality of Lambs, in Proc. of Sym- pos. on Sheep Disease and Health, Univ. of Calif., Davis, Cal. 10. Bentinck-Smith, J., Roberts, S. J. and Katz, E. M. (1960) A Bleeding Disease of Newborn Calves, Cor. Vet. 50, 1, 15. 11. Berrier, H. H. and Gouge, R. E. (1954) Eperythrozoonosis Transmitted in utero from Carrier Sows to their Pigs, JAVMA, 124, 923, 98. 12. Bruner, D. W. (1950) Laboratory Diagnosis of Hemolytic Ic- terus in Foals, Cor. Vet., 40, 1, 11. 13. Bruner, D. W. (1954) and (1962) Personal Communication. 14. Bruner, D. W., Brown, R. G., Hull, F. E. and Kincaid, A. S. (1949) Blood Factors and Baby Pig Anemia, JAVMA, 115, 868, 94. 15. Bruner, D. W., Doll, E. R., Hull, F. E. and Kincaid, A. S. (1950) Further Studies on Hemolytic Icterus in Foals, Amer. J. Vet. Res. 11, 38, 22. 16. Bruner, D. W., Hull, F. E. and Doll, E. R. (1948) The Re- lation of Blood Factors to Icterus in Foals, Amer. J. Vet. Res., 9, 32, 237. 17. Bryans, J. T., Swerczek, T. W. and Crowe, M. W. (1977) Neonatal Foal Disease Associated with Perinatal Infection by Equine Herpesvirus I, J. Eq. Med. and Surg. 1, 1, 20-26. 18. Buxton, J. C., Brooksbank, H. H. and Combs, R. R. A. (1955)274 VETERINARY OBSTETRICS Hemolytic Disease of Newborn Pigs Caused by Maternal Isoimmunization, Brit. Vet. J. Ill, 463. 19. Carbrey, E. A., Stewart, W. C., Young, S. H. and Richard- son, G. C. (1966) Transmission of Hog Cholera by Pregnant Sows, JAVMA, 149, 1, 23. 20. Carmichael, W. E., Squire, R. A. and Krook, L. (1965) Clin- ical and Pathologic Features of a Fatal Viral Disease of New- born Pups, Amer. J. Vet. Res. 26, 113, 803. 21. Congdon, L. L. and Ames, E. R. (1973) Thiabendazole for Control of Toxocara canis in the Dog. Amer. J. Vet. Res. 34, 417. 22a. Cork, L. C. (1976) Differential Diagnosis of Viral Leukoen- cephalomyelitis of Goats, JAVMA, 169, 1303-1306. 22b. Crawford, T. B., McGuire, T. C., Hallowell, A. L. and McComber, L. E. (1977) Failure of Colostral Antibody Trans- fer in Foals: Its Effect Diagnosis and Treatment, Proc. 23rd Ann. Conv. A.A.E.P., Vancouver., 265. 23. Cornwell, H. J. C. and Wright, N. G. (1969) Neonatal Canine Herpes Virus Infection, Vet. Rec. 84, 2. 24. Cronin, M. T. I. (1955) Haemolytic Disease of Newborn Foals, Vet. Rec., 67, 26, 479. 25. Cowie, R. S. (1964) Cancer in the Newborn Calf, Vet. Rec. 76, 20, 566. 26. Cupps, P. T. and Laben, R. C. (1965) Physiological Changes Accompanying Decreased Vigor in a Group of Inbred Calves, J. Dairy Sci. 98, 6, 792. 27. Curtis, S. E., Heidenreich, C. J. and Harrington, R. B. (1967) Age Dependent Changes of Thermostability in Neonatal Pigs, Amer. J. Vet. Res. 28, 127, 1887. 28. Cutlip, R. C., Lehmkuhl, H. D. and Jackson, T. A. (1981) Intrauterine Transmission of Ovine Progressive Pneumonia Vi- rus, Am. J. Vet. Res. 42, 10, 1795-1797. 29. Dennis, S. M. (1970) Splenic Rupture in a Newborn Lamb, Amer. J. Vet. Res. 31, 1, 205. 30. Dennis, S. M. (1979) Perinatal Mortality of Ruminants, Comped. Cont. Educ. 1, 17-27. 31. Dennis, S. M. (1981) Perintal Foal Mortality, Comped. Cont. Educ. 3, 5, 206-217. 32. DeRouen, T. M., Reynolds, W. L. and Meyerhoeffer, D. C. (1967) Mortality in Beef Calves in the Gulf Coast Area, J. An. Sci. 26, 1, 202. 33a. Dimock, W. W., Edwards, P. R. and Bruner, D. W. (1947) Infections Observed in Equine Fetuses and Foals, Cor. Vet., 37, 2, 89. 33b. Divers, T. J., Byars, T. D. and George, L. W. (1981) Ly- ophilized Immunoglobulins as a Means of Passive Transfer of Antibodies in Foals., Proc. 27th Ann. Conv. A.A.E.P., New Orleans, 473. 34. Doll, E. R. and Brown, R. G. (1954) Isohemolytic Disease of Newborn Pigs, Cor. Vet., 44, 1, 96. 35. Doll, E. R. and Hull, F. E. (1951) Observations on Hemolytic Icterus of Newborn Foals, Cor. Vet., 41, 1, 14. 36. Doll, E. R., Richards, M. G., Wallace, M. E. and Bryans, J. T. (1952) The Influence of an Equine Fetal Tissue Vaccine upon Hemagglutination Activity of Mare Serums: Its Relation to Hemolytic Icterus of Newborn Foals, Cor. Vet., 42, 4, 495. 37. Doll, E. R. (1963) Neonatal Isoerythrolysis, in Equine Med- icine and Surgery, 1st Ed., Amer. Vet. Public Inc. Wheaten, 111., 517. 38. Douglas, J. R. and Baker, N. F. (1959) The Chronology of Experimental Intrauterine Infections with Toxocara canis in the Dog, J. of Parasitol., 45, 4, Sect. 2, 43. 39. DuPlessis, J. L. (1958) Repair of Ruptured Bladder in Foals, J. South Afr. Vet. Med. Assoc. 29, 261. 40. Edwards, B. L. (1961) Oedema in Newborn Pigs, Vet. Rec. 73, 22, 540. 41. Eliot, T. S., Jr., Eliot, F. P., Lushbaugh, C. C. and Slager, U. T. (1958) First Report of the Occurrence of Neonatal En- docardial Fibroelastosis in Cats and Dogs, JAVMA, 133, 5, 271. 42. Emerson, J. L. and Delez, A. L. (1965) Prenatal Hog Cholera Infection; A Potential Source of Hog Cholera, Proc. 102nd Meeting AVMA, 1346. 43. Ferrer, J. F. (1980) Bovine Lymphosarcoma, Comped, on Cont. Educ. 2, 11, 235-242, (Adv. Vet. Sci. Comp. Med. 24, 1). 44. Fluharty, D. M. (1965) Some Incompatible Reactions of Ca- nine Blood Group A, JAVMA, 147, 12, 1656. 45. Fox, M. W. (1963) Neonatal Mortality in the Dog, JAVMA, 143, 11, 1219. 46. Fox, M. W. (1966) Canine Pediatrics, C. C. Thomas, Co., Springfield, 111. 47a. Fraser, C. M. and Nelson, J. (1959) Sweet Clover Poisoning in Newborn Calves, JAVMA, 135, 5, 283. 47b. Gibbs, P. G., Potter, G. D., Blake, R. W. and McMullen, W. C. (1982) Milk Production of Quarterhorse Mares During 150 Days of Lactation., J. An. Sci. 54, 496. 47c. Glastonbury, J. R. W. (1977) Preweaning Mortality in the Pig. Pathobiological Findings in Piglets Dying Before and During Parturition, Austral. Vet. J. 53, 282-286. 48. Greve, J. H. and Gaafar, S. M. (1966) Natural Transmission of Demodex canis in Dogs, 148, 9, 1043. 49. Griesemer, R. A. and Gibson, J. P. (1963) The Establishment of an Ascarid-Free Beagle Colony, JAVMA, 143, 9, 965. 50. Harding, S. K., Bruner, D. W. and Bryant, I. W. (1961) The Transfer of Antibodies from the Mother Cat to her Newborn Kittens, Cor. Vet. 51, 4, 535. 51. Hartley, W. J. and Dodd, D. C. (1957) Muscular Dystrophy in New Zealand Livestock, New Zeal. Vet. J. 5, 61. 52. Hayes, F. A. and Perryman, B. S. (1958) Temporary Alle- viation of Cannibalism in a Staffordshire Terrier Bitch, N. A. Vet. 39, 1, 54. 53. House, J. (1968) Personal Communication (N.Y.S. Veterinary College). 54. Hoversland, A. S., Safford, J. and Van Horn, J. L. (1963) Some Charateristics of Newborn Lambs Associated with Mor- tality, J. An. Sci. 22, 3, 856. 55a. Houpt, K. A. and Wolski, T. R. (1979) Equine Maternal Be- havior and Its Aberrations, Eq. Pract. 1,1, 7-20. 55b. Houpt, K. A. (1982) Foal Rejection its Causes and Cures., Vet. Topics, N.Y.S. Coll, of Vet. Med. April, 1. 55c. Howard, D. R. (1981) Transplacental Transmission of Rabies Virus from a Naturally Infected Skunk, Am. J. Vet. Res. 42, 691. 56. Hubbert, W. T., Bryner, J. H., Foley, J. W. and Estes, P. C. (1975) Parasitic Infection of the Bovine Perinate: A Review, Theriog. 3, 2, 43-63 (141 References). 57. Ikede, B. D. and Losos, G. J. (1972) Hereditary Transmission of Trypanosoma vivax in Sheep, Brit. Vet. Jour. 128, 1. 58. Jeffcott, L. B. (1969) Haemolytic Disease of the Newborn Foal, Eq. Vet. J. 1, 4, 165. 59. Jensen, R., Maag, D. D. and Flint, J. C. (1958) Enzootic Ataxia from Copper Deficiency in Sheep in Colorado, JAVMA, 133, 6, 336. 60. Jones, J. E. T. (see preceding section).PARTURITION 275 61. Kanagawa, H., Kawata, K., Nakao, N. and Sung, W. K. (1964) A Case of Granulosa Cell Tumor of the Ovary in Newborn Calf, Jap. J. Vet. Res., 12, 1, 7. 62. Kilham, L., Margoulis, G., and Colby, E. D. (1967) Congen- ital Infections of Cats and Ferrets by Feline Leucopenia Virus Manifested by Cerebellar Hypoplasia, Laborat. Invest. 17, 465. 63. Kingrey, B. W. (1955) Hysteria in the Parturient Sow, Iowa State Col. Vet. 17, 2, 83. 64. Kirk, R. W. (1958) Canine Pediatrics, Mod. Vet. Pract. 39, 5, 45. 65. Kirk, R. W. (1965) Canine Pediatrics, JAVMA, 147, 12, 1475. 66. Kirk, R. W. (1968) Pediatrics, in Canine Medicine, 1st Cat- cott Ed., Amer. Vet. Public Inc., Wheaton, 111. 805. 67. Kopecky, K. E., Larsen, A. B. and Merkal, R. S. (1967) Uter- ine Infection in Bovine Paratuberculosis, Amer. J. Vet. Res. 28, 125, 1043. 68. Koutz, F. R., Groves, H. F. and Scothom, M. W. (1966) The Prenatal Migration of Toxocara canis Larvae and their Rela- tionship to Infection in Pregnant Bitches and in Pups, Amer. J. Vet. Res. 27, 118, 789. 69. Kradel, D. C. (1963) Developing Concepts of Nutritional Mus- cular Degenerations in Livestock, Proc. AVMA N.Y. City, 63. 70. Krakowka, S. (1977) Transplacentally Acquired Microbial and Parasitic Diseases of Dogs, JAVMA, 171, 8, 750-753. 71. Larsen, A. B. (1976) Johne’s Disease (Paratuberculosis) in 1976, 9th Ann. Conv. A.A.B.P., San Francisco, Cal., 20-23. 72. Leonard, E. P. (1954) Personal Communication. 73. Lyons, E. T., Drudge, J. H. and Tolliver, S. C. (1977) Ob- servations on Development of Strongyloides westeri in Foals Nursing Dams Treated with Cambendazole or Thiabendazole, Am. J. Vet. Res. 38, 6, 889-892. 74. Manktelow, B. W. (1963) Myopathy of Dogs Resembling White Muscle Disease of Sheep, New Zeal. Vet. J. 11, 52. 75a. Mantovani, A. and Jackson, R. F. (1966) Transplacental Transmission of Microfilaria of Dirofilaria immitis in the Dog, J. of Parasitol. 52, 116. 75b. Martens, R. J. (1981) Equine Pediatrics, Equine Vet. Data, 2, Nos. 6, 7, 8, 63-69, 74-82, 85-95. 76. McGee, W. R. (1954) Disease Problems in Foals, Vet. Med., 49, 8, 311. 77. McGuire, T. C., Crawford, T. B., Hallowell, A. L. and Ma- comber, L. E. (1977) Failure of Colostral Immunoglobulin Transfer as an Explanation for Most Infections and Deaths in Neonatal Foals, JAVMA, 170, 11, 1302-1304. 78. McManus, D. (1960) Prenatal Infection of Calves with Cys- ticercus bovis, Vet. Rec. 72, 41, 847. 79. Meyer, R. C., Rasmussen, B. A. and Simon, J. (1969) A He- molytic Neonatal Disease in Swine Associated with Blood Group Incompatibility, JAVMA, 154, 5, 531. 80a. Misdorp, W. (1965) Tumors of Newborn Animals, Path. Vet. 2, 328. 80b. Morrow, D. A. (1980) Parturition, Current Therapy in Ther- iogenology, W. D. Saunders Co., Philadelphia. 81. Neufeld, J. L. (1981) Pustular Dermatitis (Poxvirus) in a New- born Pig, Can. Vet. J. 22, 156. 82. Norsworthy, G. D. (1977) The Feline Leukemia Virus, Feline Pract. 7, 2, 52-58. 83. O’Dea, J. (1961, 1966) Personal Communication. 84. Olson, L. D. and Gaafar, S. M. (1963) Absence of Prenatal Infection with Ascaris lumbricoides in Swine, JAVMA, 143, 11, 1217. 85. Post, J. E. (1976) Feline Leukemia and Related Viruses, Feline Information Bulletin, Cornell Feline Res. Lab. No. 1, Apr. 86. Rees, J. B., Sykes, W. E., and Rickard, M. D. (1975) Prenatal Infection with Fasciola hepatica in Calves, Austral. Vet. J. 51, 497-499. 87. Refuerzo, P. G. and Albis-Jimenez, F. S. (1954) Studies on Neoascaris vitulorum, Amer. J. Vet. Res., 15, 57, 532. 88. Rice, V. A. and Andrews, F. N. (1951) Breeding and Im- provement of Farm Animals, 4th Ed., McGraw Hill Book Co., Inc., N.Y.C. 89. Rickard, C. (1970) Seminar, N.Y. State Veterinary College, Personal Communication. 90. Roberts, E. J. and Archer, R. K. (1966) Current Methods for the Diagnosis and Treatment of Haemolytic Disease in the Foal, Vet. Rec. 79, 61. 91. Rooney, J. R. (1962) Personal Communication. 92. Rooney, J. R. (1962) Joint 111, JAVMA, 141, Part II, 10, 1259. 93. Rossdale, P. D., Pattle, R. E. and Mahaffey, L. W. 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Res., 8, 47, 207.Chapter VII DYSTOCIA—ITS CAUSES When the first, or especially the second, stages of par- turition is markedly prolonged, becomes difficult or im- possible for the dam without artificial aid, the condition is termed dystocia. The term dystocia comes from the Greek and means difficult birth. Eutocia is safe, easy, natural or physiological parturition. There is no clear line between normal parturition and dystocia. Dystocia is one of the most important obstetrical conditions with which the veterinarian must cope. Because of the many vari- able managerial and genetic components the incidence of dystocia in the various species is not satisfactorily re- corded. Of the domestic species dystocia is most com- mon in cattle, especially in primipara and in the larger breeds.1,11’28'29,37 The overall incidence of bovine dysto- cia ranges from 3 to 25 percent. Dystocia in beef cattle corrected by means other than cesarean section reduced their future reproductive performance 5 to 16 percent while in cases corrected by the latter operation it reduced per- formance 30 to 40 percent.811 The incidence of dystocia in mares and sows is about 1 to possibly 2 percent and slightly higher in ewes due to twinning. In dogs it is highest in the Boston, Scotch Terrier, Pekinese, Sealy- ham, and other small brachycephalic breeds. It is lowest in the more natural breeds such as the hounds and mon- grels. In queens the incidence of dystocia is probably slightly lower than in bitches. It is obvious that the in- cidence of dystocia is highest in the more specialized breeds and those kept under greatest confinement in the most artificial manner. Dystocia is much more common in primipara than in pluripara. The incidence of dystocia is greater in pregnancies that terminate early due to uter- ine disease, fetal death, and twinning, or that terminate after a prolonged gestation period due to excessive size of the fetus. The causes of dystocia may be divided into the basic and the immediate causes. The basic causes should be studied for the purpose of obtaining knowledge that will help prevent the occurrence of dystocia. If basic causes are known and recognized, dystocia may largely be avoided; or if unavoidable the veterinarian and owner will know in advance that dystocia is highly probable. The latter circumstance requires certain preparations and precautions so that if dystocia should occur, prompt ob- servance and handling may prevent injury or death of either or both the dam and fetus. The Basic Causes of Dystocia The basic causes of dystocia may be divided into the following categories: hereditary, nutritional and mana- gerial, infectious, traumatic, miscellaneous, or com- bined causes. Many cases of dystocia may have two or more basic causes. Hereditary Causes—The hereditary causes for dys- tocia may be divided into those that have produced de- fects in the dam which predispose to dystocia, or those hidden or recessive genes in the dam and sire which may produce a defective fetus. Those hereditary defects in the dam predisposing to dystocia are inguinal hernia; persistence of the median wall of the Mullerian duct with a large band in, or caudal to, the external os of the cervix; double uterus or uterus didelphys; hypoplasia of the vagina or vulva, such as rectovaginal constriction in Jerseys, twinning; and in- herited breed characteristics. Inguinal hernia as a cause of dystocia especially in the dog has been discussed pre- viously. Persistence of the median wall of the Mullerian or paramesonephric duct may cause dystocia by ob- structing the passage of the fetus if one leg should pass on one side and the other leg on the other side of this strong band. In a true double uterus in the cow the pla- cental area is limited to only one horn. A severe dystocia may result from overlooking a twin in the other horn. Hypoplasia of hereditary origin is only rarely a cause for dystocia, as the hypoplasia often affects the uterus and ovaries, and conception does not occur. Twinning in uniparous animals is usually associated with double ovu- lation. Monozygous twins are uncommon. The release of two or more ova at one estrum is usually predisposed by the dam’s hereditary constitution or may be associ- ated with cystic ovaries in cows and the nutritional status of ewes. Twinning may be influenced to a lesser degree by the season and the age of the dam. Twin bicomual pregnancy in cows and ewes often results in dystocia because the long extremities frequently cause wedging 277278 VETERINARY OBSTETRICS of the fetuses in the pelvis. In twinning, uterine inertia associated with unicornual twins, posterior presentation of one fetus, death of one or both fetuses, and premature twin birth or abortion also favor dystocia. Certain breeds of cattle, such as Brown Swiss and Charolais with a long gestation period and large fetuses; and certain brachy- cephalic or dwarf breeds of dogs, such as Bulldogs, and other breeds with a large, broad head and a relatively small pelvis and underdeveloped or weak reproductive systems, are more prone to dystocia. Scotch Terrier fe- tuses have a tendency toward premature hardening of the skull bones that may lead to dystocia. Most of the he- reditary defects of the dam resulting in or predisposing to dystocia, with the possible exception of the inherited breed characteristics, are favored by inbreeding or close breeding practices. The hidden and usually recessive genes in both male and female animals may produce a variety of patholog- ical conditions affecting the fetus or fetal membranes, thus causing dystocia. Most of these are lethal genes, as they usually result in the death of the fetus. The known genetic lethals for cattle and the other domestic animals have been outlined in Chapter III. Dropsy of the fetal membranes and fetus may be caused by mating hybrids such as the bison with the domestic cow or zebu. In- breeding in Dexter and Tux-Zillertaler cattle and others has resulted in achondroplastic calves and occasionally hydramnios. Certain types of muscle contracture mon- sters may be associated with hydrops of the amnion. If this condition should go to term it usually is associated with uterine inertia and a weak or dead fetus. Both of these conditions favor fetal emphysema and dystocia. Achondroplastic and “ankylosed” calves have been pro- duced without dropsy of the fetal membranes by inbreed- ing animals with the recessive gene for those conditions. Dystocia often results at parturition due to the increased size of the fetus or certain of its parts. Hereditary lethals causing amputated limbs of fetuses, Acroteriasis con- genita, hydrocephalus, and stillborn fetuses frequently may cause dystocia. Hydrocephalus in cattle is fre- quently associated with deformed limbs. The early death of these fetuses at the time of parturition, and abnormal postures more common in defective fetuses, increase the incidence of dystocia. An hereditary condition called congenital dropsy resulting in large, anasarcous fetuses or calves occasionally causes dystocia in Ayrshire or Swedish Lowland cattle when carried 200 days or longer. An autosomal recessive gene causing a prolonged ges- tation of 300 to 370 days in Holstein cattle and termi- nating in severe dystocia due to the oversized, giant calves has been described. In this case the fetuses were already dead, died at birth, or were killed during the difficult delivery. The dam’s life was greatly imperiled and a number of the dams died as a result of the dystocia. Mummified fetuses in cattle occasionally may be hered- itary. Dystocia may result at the time the mummified fetus is expelled, especially in cases of fetuses that mum- mify after the fifth month of gestation. Muscular hyper- trophy or “double muscling” in cattle is an hereditary condition that when present in fetuses, especially in pri- mipara, often causes severe dystocia. Muscular hyper- trophy has been described in Charolais, Holstein, South Devon, Hereford, Angus and Piedmont cattle. Fifty per- cent of oversized fetuses in Belgium causing dystocia were double-muscled.33 Some of these lethal conditions causing dystocia affect bone development. The so-called muscle contracture monsters are usually produced by general functional ankylosis with an abnormal develop- ment of muscles and tendons, causing an immobility and extreme rigidity of the affected limbs. In sheep inherited lethals of general ankylosis and amputation and in swine general ankylosis have been described. There are many other inherited lethal genes such as cerebral hernia, ep- itheliogenesis imperfecta, and short spine that might contribute to dystocia because the fetus is weak and usu- ally dies at the time of parturition. This factor of a dead or weak fetus at parturition favors abnormal postures of the fetus even though its size may be small, and its shape normal or nearly normal. A recessive hereditary condi- tion should be suspected when several similar abnormal fetuses or dystocias are seen in related animals, over a period of several years. Nutritional and Management Causes—The nutri- tion of a pregnant animal and its management at partu- rition are closely associated and may be the basic causes of many dystocias. Dystocia due to the small size of the dam is frequently observed in primipara. One study3 measured the area of the pelvic opening in 3-year-old heifers. As the pelvic opening increased in size from 200 sq. cm. to over 279 sq. cm. the incidence of heifers with a normal birth rose from 44 to 100 percent. Almost all severe dystocias were in heifers with pelvic areas of 200 to 240 sq. cm. or less. Improper nutrition of the growing heifers was the most important factor in retarding body and pelvic growth. This study was further confirmed by a similar one in younger heifers.27 This condition may be caused by breeding the female at too young an age or by breeding a poorly grown, under-fed female that may be old enough to breed but the body growth has been greatly retarded due to poor nutrition, parasitism, or disease. Most domestic animals reach puberty before their body growth is great enough for a normal gestation and parturition. Dairy calves may show estrum at 3 to 12 months of age. Range calves still nursing their dams may occasionally come into estrum and be bred by a bull that is running with the herd. Many cases of severe dys-DYSTOCIA—ITS CAUSES 279 tocia have been reported in cattle 13 to 18 months of age. Twenty-six percent of 2 year-old range heifers had dystocia as compared to 4 percent of the older cows.31 Well-grown, well-nourished heifers are usually not bred before 12 to 20 months of age, mares 3 years of age, gilts 6 to 8 months of age, ewes 1 to 1.5 years of age, and bitches 1 year of age. Dairy heifers should be bred by size or weight rather than age.7 Holstein or Brown Swiss heifers should be bred when they weigh 750 pounds; Ayrshire and Guernsey heifers when they weigh 600 pounds and Jerseys when they weigh 500 pounds. De- pending on the levels of energy intake these weights may be reached from 10 to 19 months of age. The optimum feeding levels produce heifers of these weights from 13 to 17 months of age. During the gestation period animals should be fed sufficiently well to maintain their rate of growth so that at calving Holstein and Brown Swiss heif- ers weigh about 950 to 1000 pounds, Guernseys and Ayrshires 700 to 725 pounds and Jerseys 670 to 690 pounds. Restricting growth by underfeeding frequently results in dystocia and other periparturient difficulties. The breeding of animals that are immature or otherwise unfitted for a normal parturition is usually the result of an accident or gross carelessness in management. If dis- covered soon enough steps may be taken to prevent or terminate pregnancy. Animals that are stunted frequently develop dystocia at parturition. This delayed development may be due to a low nutritive plane or to chronic diseases such as en- teritis, pneumonia, severe pediculosis, mange or internal parasites. Stunting of a young female animal’s growth is not permanent unless continued for a long period of time. In many young animals the stunting effects of a low plane of nutrition may be overcome by a high plane of nutrition for 6 months or more. Many farmers in dairy sections stunt the growth of their young stock by feeding milk substitutes improperly and by limited grain feeding, by feeding poor hay, pasturing the young stock on poor pastures, and by housing the young stock under unfa- vorable environmental conditions. Thus at the time of parturition the heifers are thin, small and weak. Dystocia is invited by the small pelvis and underdeveloped, ju- venile genital tract, the lowered resistance to disease, and the lack of strength to expel the fetus in a normal manner. Growth and development in young animals should proceed normally from birth to puberty, from pu- berty to conception, and during the gestation period, if parturition is to be physiological. A proper nutritive level and efficient management are necessary to secure this goal. High feeding levels may favor dystocia, especially in heifers, by excessive deposition of fat in the pelvic re- gion, predisposing to difficult parturition. The influence of over-and underfeeding of pregnant animals and its ef- fect on increasing or decreasing the weight of the new- born has been demonstrated.18 Many owners try to com- pensate for low levels of feeding and poor growth in their young stock by high feeding levels during the last third of pregnancy. This is particularly true in dairy cattle, in which lactation is of major importance. This practice is of questionable value and may even be harmful, as it is during this last third of pregnancy that the fetus grows rapidly and the high feeding levels may favor the de- velopment of a larger fetus while increase in body size and growth of the immature dam occurs much more slowly. The balance between fetal size and pelvic or genital tract diameters, fetopelvic disproportion, and dystocia is favored. Overly fat, under-exercised sows and bitches often develop dystocia possibly due to uterine inertia. Fetopelvic disproportion caused by the large size and weight of the fetus or the small size of the pelvis of the dam or both are the two greatest factors in dystocia of animals, especially beef cattle. Sires, especially those bred to young immature dams should be selected for the ease of birth of their offspring.21b Male calves because of their larger size, partly due to their slightly longer gestation period, are most often associated with dysto- cia. Immature females should be managed and fed so that at the time of breeding and parturition they are healthy, not overly fat or thin, are of sufficient size and with a pelvic area large enough to give birth without as- sistance.4b'37b Failure to keep animals approaching or beginning par- turition under close observation may not actually be a cause of dystocia but this neglect may cause a relatively early and simple dystocia to become more severe, with danger to the life of the fetus and the dam. During par- turition all animals should be watched closely but not disturbed. No reliable birth detection system has been developed (see Parturition). Prompt aid may thus be given if parturition is not normal. This aid may prevent sec- ondary uterine inertia, death of the fetus, rupture of the uterus or birth canal, fetal emphysema, septic metritis, retained placenta, and injuries, such as obturator paral- ysis. Feeding or grazing pregnant animals on plants that may damage the fetus such as ewes on Veratrum, should be prevented in an effort to control fetal losses and dys- tocia that may accompany such losses. Pregnant animals which are not exercised and are kept in close confinement are more prone to difficulties such as torsion of the uterus and uterine inertia than those kept under more natural conditions, as on pasture. Exercise increases body tone, strength, and resistance and results in stronger labor contractions, less fatigue, shorter du- ration of parturition, less uterine inertia, and more prompt280 VETERINARY OBSTETRICS recovery. Pregnant animals closely confined for long pe- riods are more prone to abnormalities in the function of smooth muscle including prolapse of the vagina and uterus, intussusception, torsion of the cecum and dis- placement of the abomasum. In the first stage of labor the limbs of uniparous animals are flexed while during the second stage of labor they are extended. The strong contractions of the myometrium initiated active fetal movements and righting reflexes resulting in extension of the limbs.1 Thus uterine disease as well as fetal dis- ease may greatly influence the incidence of dystocia.37 Infectious Causes—Any infection or disease affect- ing the pregnant uterus and its contents may cause abor- tion, uterine inertia, fetal death, and occasionally septic metritis of pregnancy. In any severe infection of the uterus the uterine wall may lose its tone or ability to contract— a condition resulting in incomplete dilation of the cervix and uterine inertia. In the latter instance the second stage of labor may be abnormally delayed. Death of the fetus prior to parturition or premature birth renders the fetal extremities prone to postural abnormalities, and may re- sult in a dorso-pubic position of the fetus in the mare. The relation of uterine disease to hydrops of the allantois and edema of the fetus has been cited and may be a cause for uterine inertia and dystocia. Infections may be the immediate cause of conditions that predispose to dys- tocia, or they may be responsible for chronic uterine damage such as loss of caruncles, or a nonfunctional uterine hom, either of which may result in abortion, uterine inertia, hydrops, torsion, rare transverse preg- nancies, and other abnormalities at subsequent pregnan- cies. All known infectious reproductive diseases such as brucellosis, leptospirosis, vibriosis, salmonella, viral, and other septicemic or infectious diseases should be con- trolled according to our best knowledge at the present time so that late abortions or premature births, in which dystocia is common, will be kept at a minimum. Traumatic Causes—Traumatic causes for dystocia are not common. Ventral hernia and rupture of the pre- pubic tendon late in gestation may occur from traumatic causes. These injuries predispose to dystocia by render- ing the abdominal wall incapable of strong contractions, with a resulting inability of the dam to force the fetus through the birth canal. Torsion of the uterus may be caused by sudden slipping, falling, or rolling in ad- vanced pregnancy. This is not the only factor but it is an important one in the etiology of torsion. Fractures of the pelvis with secondary deformity and exostoses is seen most commonly in small animals struck by motor ve- hicles. These may result in a stenosis of the birth pas- sage, resulting in a severe dystocia. Miscellaneous Causes—The causes of certain minor abnormalities in posture, such as a flexed knee or lateral deviation of the head and neck, resulting in dystocia with a live fetus and an apparently normal uterus, are difficult to explain except as an accidental catching of the nose or foot on the brim of the pelvis or in the soft structures of the birth canal during the early stages of parturition. A degree of uterine inertia or disease of the fetus may also be important factors. As the second stage progresses and more of the fetus enters the birth canal the deflection of the extremity is further increased. The causes of pos- terior presentation of the fetus, a relatively common cause for dystocia in uniparous animals, have not been satis- factorily explained. The exact causes or even satisfac- tory theories are not given to explain transverse preg- nancies in domestic animals. Previous uterine disease in mares may predispose to transverse pregnancy and dys- tocia.37 However another worker disagreed and reported that in 11 cases of bicomual pregnancy in mares there was no previous history of uterine disease.34 In multipara a fetus may be located transversely in the uterine body, with the two ends of its body in separate horns. This may occur in polytocous dams having only a single fetus or it may be due to a fetus being misdirected during birth into the opposite horn rather than the vagina. In multi- para with only about one-third the normal-sized litter the fetuses are often larger than normal due to increased nu- trition and available uterine space. This may result in dystocia at parturition. In swine the most important fac- tor determining the birth weight of pigs was the number of pigs in a litter, the larger the litter the smaller the pigs.18 Improper hormone balance of estrogens, proges- terone or relaxin, or failure of the normal release of ox- ytocin may result in delay of the first stage or second stage of parturition, and in uterine inertia.24 Uterine Inertia is defined as the lack of normal phys- iologic uterine contractions during or after parturition. Two types of uterine inertia are recognized, primary and secondary. Primary uterine inertia is seen most often in the bitch, occasionally in the cow and sow and rarely in the mare or ewe. The following conditions may be factors causing primary inertia or lack of uterine tone and feeble contractions at the time of parturition. It is observed more often in animals that are closely confined and hence lack exercise. It is more common in dairy than beef cattle. Obesity may be a possible factor in bitches and other species. Certain brachycephalic breeds of dogs tend to develop uterine inertia despite the size of the lit- ter.1516 Overstretching or overloading of the uterus in hydrops and twin pregnancy in cows, and a large number of fetuses in small bitches and sows may predispose to uterine inertia. It is observed more often in older dairy cows and bitches. It is frequently associated with nutri-DYSTOCIA—ITS CAUSES 281 tional debility or debilitating diseases. It may be asso- ciated with disease or degeneration of the uterine wall due to uterine infections or secondary to peritonitis such as traumatic peritonitis. It may be associated with an im- proper hormonal balance during the complex process of parturition or the response of the genital tract to the var- ious hormones. Further studies in this important area are needed. A primary uterine inertia in dogs associated with a small number of fetuses where symptoms of parturition are absent and the fetuses die has been described.6 This is probably due to a hormonal disfunction. A combina- tion of the above factors may be present. Secondary uterine inertia, which is seen in all spe- cies, is the result of or follows dystocia and is due to exhaustion of the uterine muscle. In multiparous animals it may follow dystocia with one fetus; the remaining fe- tuses may not be expelled when the fetus causing the dystocia has been removed. Certain “sensitive” dams will refrain from vigorous labor because of apparent pain or discomfort and secondary inertia may ensue. In other multiparous animals lacking body condition or strength several young may be bom and then the dam and also the myometrium appears exhausted. After several hours rest the birth process will again proceed or may fail and outside aid will be necessary. Secondary inertia is fre- quently followed by uterine infection, septic metritis, re- tained placenta, and a failure of the normal involution of the utems. In prolonged dystocia in unipara and pos- sibly multipara, the uterine muscle may become fatigued and produce contraction or retraction rings, also called Bandl’s rings, that contract tightly around the fetus or caudal to it. This may further complicate the relief of the dystocia or if not recognized it may result in rupture of the uterus if forced extraction is applied to the fetus. A condition in bitches—especially Scotch Terriers and toy Dachshunds and sows is described that is interme- diate in character between primary and secondary uterine inertia.6,28 In these cases the bitch may have 1 or 2 fe- tuses and then labor ceases with a number of fetuses still in the utems. There is no apparent cause for the dysto- cia. Many cases of secondary uterine inertia may be avoided by careful observation of the female during par- turition so that proper help can be given as soon as dif- ficulty arises. Fetal monsters other than those described under he- reditary causes for dystocia are considered accidental oc- currences at the present time. Many of these are double monsters, with doubling of parts or nearly all of the fe- tus. These double monsters apparently arise from incom- plete development or separation of monozygotic twins in the early embryonic period. Single fetal monsters may have a portion of the fetus that is too large to readily pass through the birth canal. Since these more extreme monsters occur sporadically as a cause for dystocia and since their origin is so early in the gestation period little is known of their basic causes. During the past 10 to 20 years many studies have been conducted on dystocia or calving difficulties in dairy and especially beef cattle because of the large economic losses in calves, cows, labor and infertility or delayed rebreed- ing produced by such difficulties. Although similar ex- tensive studies on the other species of domestic animals have not been conducted, probably because the inci- dence of dystocia in these animals is much lower than in cattle, there are common significant correlations and observations that apply to all species. 1,11,20,21,23,26,29 Fetopelvic disproportion is the most common cause of dystocia in cattle, particularly in primipara beef cattle. About 30 percent of all bovine dystocias are due to this cause, with an incidence of 50 to 75 percent in beef cat- tle and 15 to 30 percent in dairy cattle.29,32 In beef cattle practice in the midwest U.S. about 90 percent of dys- tocias are due to fetopelvic disproportion.2 The occur- rence of dystocia is primarily related to the size or weight of the fetus and the pelvic area of the dam. Fetal size, weight and conformation are dependent on: Genetic factors including sex—male calves at birth are 4 to 6 more pounds heavier and have larger body mea- surements of heart girth, pelvis width and length and head width.26 Length of gestation—this is a function of the gen- otype of the fetus. Male fetuses are carried several days longer than female calves and both the sire and dam contribute to the length of gestation. A positive cor- relation between gestation length and birth weight of the calf exists. The larger breeds have a longer ges- tation period.26 Breed or genotype of sire and dam—both parents contribute significantly to the size or weight of the fe- tus, dystocia and resulting calf mortality especially in heifers. Calves sired by the large breeds, Charolais, Simmental, Limousin, South Devon, Holstein and Brown Swiss bulls were larger and heavier than calves sired by the small breeds, Angus, Jersey and Hereford bulls.1,26,29 Heterosis or crossbreeding also contributes to increased calf birth weights. Conversely inbreed- ing, especially at high levels, decreases calf birth weight and also increases dystocia and calf mortality.26 Even within a breed there are genetic differences between bulls in the transmission of size or weight and viability of the calf at birth. Many artificial insemination cen- ters publish this information for bulls of the larger breeds so that farmers breeding heifers can select sires pro- ducing smaller calves and avoid sires producing large282 VETERINARY OBSTETRICS calves.8b,c’9,23,25'32 This reduces calf mortality, calving costs, reproductive failures and generation interval. Another genetic trait of double muscling seen in the beef breeds affects the conformation of the fetus and often results in severe dystocia even though the weight of the fetus is average. However crossbreeding be- tween mature Jersey or Guernsey cows and Charolais or double-muscled bulls resulted in only a slight in- crease in dystocia.19,22 Thus genetic effects between certain breeds crosses seem less hazardous and non- genetic factors including age of dam or degree of maturity and growth are reflected in the size of the pelvis and genital tract. Evidence was cited to indicate that the incidence of dystocia in cattle under 2 years of age was over 70 percent, and this decreased to 66 percent in 2 year-old and 44 percent in 5 year-old pri- mipara and to 13 to 20 percent in adult pluriparous cows.29 Birth weight of Hereford and Holstein calves increased up to 7 or 8 years of age and then decreased slightly.26 Nutrition—different levels of energy intake low, medium or high, for 90 days before calving affected calf weight with about a six pound differential be- tween the low and high levels.26 But there was no sig- nificant effect on dystocia.4 However excessively high energy intakes producing overly fat heifers caused an increased incidence of dystocia due to excess pelvic fat decreasing the size of the birth canal.23,29 Exces- sively restricted energy intake also resulted in an in- creased incidence of dystocia due to weakness and de- bility even though the fetus was not large.14 In the latter instance a delayed return to estrous cycling was a concurrent problem. Larger better grown heifers usually had larger pelvic areas but breed also had a significant effect on pelvic size. The larger the pelvic area the lower the occurrence of dystocia.20,21,26 With Hereford heifers with less than 200 cm2 having a 69 percent incidence of dystocia, heifers with pelvic areas of 200 to 229 cm2 and 230 to 269 cm2 had a 30 and 25 percent incidence, respectively. Miscellaneous factors—more dystocia is observed in the winter months possibly because the cows were in better condition in the summer or because more cows are confined and were observed and aided in calving in the winter.25 Confined heifers had a higher inci- dence of dystocia and stillbirth, often characterized by vulvar constriction,12 than did heifers in yards or pad- docks. Possibly excessive disturbance during parturi- tion influenced these results. Dystocia caused a 15 percent reduction in estrous recycling during the AI period postpartum and a 15 percent lower postpartum conception rate.21 Experiments using artificial insemination by which Shire horses and Shetland ponies were mated to each other—Shire stallions on Shetland mares and Shetland stallions on Shire mares—proved that foals by a Shire stallion out of Shetland mares were not appreciably larger than pure Shetland foals.18,36 Foals by Shetland stallions out of Shire mares were three times as large as pure Shetland foals but not quite as large as pure Shire foals. This difference in size was greater in horses and less in the other species because the length of ges- tation in horses was longer and thus the influence of the maternal environment was greater. The foal is bom in the most advanced state of physiological develop- ment while the pig is the most immature of the large domestic animals. At birth the foal weighs 9 percent and the pig less than 1 percent of their mature weight.18 The basic causes for dystocia are multiple, but by properly applying our knowledge its incidence may be kept at a minimum. In general all elements that lower resistance or otherwise unfavorably affect the general health and vigor of the dam or fetus increase the pos- sibility of dystocia. The Immediate Causes of Dystocia Attendant upon dystocia are many forms of interfer- ence with physiological birth. The veterinarian handling dystocia is largely concerned with correcting or relieving the immediate interferences to birth, which may be di- vided for convenience into maternal and fetal types of dystocia; some overlapping may occur in certain con- ditions. In 95 cases of dystocia in cattle 25 percent were due to maternal causes and 75 percent due to fetal causes.39 In 60 dystocia cases in goats 28 percent were maternal and 75 percent were fetal causes.278 The Maternal Causes of dystocia are largely those factors that produce a narrowing or stenosis of the birth passage or prevent the normal entrance of the fetus into the birth canal. These include: fractures and exostoses of the pelvis; small size of the pelvis due to breeding at too young an age, or due to improper rearing with re- sultant stunting of body growth; hereditary or congenital hypoplasia of the birth canal or vulva; compression or stenosis of the cervix, vagina, or vulva by indurations caused by scars and connective tissue usually from in- juries at previous parturitions; intrapelvic hemorrhage; excessive perivaginal fat; impaction of the colon or dis- tension of the bladder in bitches and sows; tumors such as chondrosarcoma of the pelvic bones, fibromas, lipo- mas or leiomyomas of the uterus, cervix or vagina, or lymphomas of the large pelvic lymph glands; torsion of the uterus; folding of the uterus just cranial to the pelvic brim, especially in deep bodied older sows;28 persistenceDYSTOCIA—ITS CAUSES 283 of the medial wall of the Mullerian duct; failure of the cervix to dilate or “ringwomb” in ewes; uterine inertia; hydrops of the fetal membranes, inguinal, diaphragmatic or ventral hernias; rupture of the prepubic tendon; trans- verse presentations; uterine infections resulting in uterine inertia, death, abortion, or emphysema of the fetus; and twinning. In uniparous animals twinning is considered a maternal cause for dystocia since it is usually due to dou- ble ovulation. The Fetal Causes of dystocia are more numerous and are due in general to abnormal presentation, position and posture and to excessive size of the fetus. (See Figure 86.) These include: certain posterior longitudinal presen- tations in uniparous animals and all transverse ventral and dorsal presentations; dorso-ilial or dorso-pubic po- sitions; flexion of the limbs beneath the fetal body in unipara and in large fetuses in multipara; ventral, lateral or dorsal flexing of the head and neck; fetal anasarca, ascites, large fetal tumors, distention of any hollow or- gan such as the brain, liver1 lb stomach, cutaneous sac in Schistosomus reflexus, kidneys and ureters; fetal giant- ism in prolonged gestation; and fetal abnormalities or monsters such as mummified fetus, general ankylosis, double monsters, achondroplastic fetuses, and others. The incidence of dystocia in posterior presentations of the fetus in unipara is high. In 800 births in Holsteins 4.5 percent were posterior presentations but 47.2 percent of these were accompanied by dystocia.5 A Hereford sire used on an inbred line of cattle produced a high inci- dence of posterior presentations suggestive of an hered- itary factor conditioning such a malpresentation.38 Up to 30 percent or more of the fetuses in multipara are com- monly expelled in posterior presentation without dysto- cia occurring. Some equine fetuses in longitudinal pre- sentations may develop a wry or ankylosed neck.34 It is possible but unlikely that an equine fetus that developed transversely in both uterine horns might rotate into a lon- gitudinal presentation. If a fetus is presented in a dorso- ilial or dorso-pubic position, torsion of the uterus may be present. Many of the abnormal postures resulting in dystocia undoubtedly arise during the first and second stages of labor, with the fetal extremities catching on the pelvic brim or soft structures in the birth canal. These abnormal postures may often be predisposed by a weak or dead fetus.6 Lateral deviation of the head and neck is seen occasionally in all species except swine. The Common Forms of Dystocia in Domestic Animals In the mare dystocia is most often caused by an ab- normal presentation, position or posture. The long ex- tremities of the fetus tend to predispose the mare to dys- tocia. Abnormal posture of the head and neck is one of the most common causes of dystocia in mares. At birth the equine foreleg from the fetlock to the elbow is 73 percent of its adult length.18 Dystocia due to monsters or to disproportion between fetal size and pelvic diam- eters is rare. Transverse ventral presentation is not un- common, whereas transverse dorsal and rotated bicom- ual or transverse pregnancies are very unusual. (See Figure 86.) The ratio of transverse to longitudinal presentations in mares at foaling was 1:1000.34 Dorso-ilial or dorso- pubic positions are occasionally found in the mare due to the fetus failing to rotate into the normal dorso-sacral position early in parturition. All forms of abnormal pos- ture may occur in the mare. One or both of the long forelimbs may become lodged over the neck of the fetus. Wry neck is seen most commonly in the equine fetus which may or may not be associated with transverse pregnancy. Wry neck is characterized by an ankylosis and atrophy and contraction of the neck muscles, thus causing the head and neck to be fixed in a lateral direc- tion alongside the body, similar to a severe, long-stand- ing case of torticollis. It cannot be straightened even after the fetus is delivered. The abnormal positions and pos- tures, together with violent labor contractions, fre- quently result in wedging of the fetus in the pelvis or in laceration of the vagina, rectum or vulva. Only a very small percentage of equine abortions are due to maternal causes such as torsion of the uterus.34 In the cow disproportion between the fetal size and pelvic diameters are common, especially in primipara.1 Fetal giantism, hydrops of the fetal membranes and fe- tus, and fetal emphysema are not uncommon. The in- cidence of monsters such as achondroplastic fetuses, Schistosomus reflexus, Perosomus elumbis, double monsters and fetuses with general ankyloses is higher than in other species. Transverse pregnancy is rare. Uterine inertia and failure of the cervix to dilate are oc- casionally noted. Twin dystocia and dystocia due to uter- ine torsion are common. Breech presentation, lateral de- viation of the head and neck, and postural abnormalities of the limbs are often observed. In the ewe and doe postural abnormalities and twin or triplet dystocias are common. Marked disproportion between fetal size and pelvic diameters are uncommon. About 70 percent of Romney ewes delivering lambs weighing over 10 pounds had dystocia.30 Fetal anasarca or emphysema are occasionally seen. Relative oversize of the head is seen as a cause for dystocia in certain crosses in sheep.1 In 50 cases of dystocia in goats 7 were triplet and 21 were twin births; 3.5 percent were in trans- verse presentation, 15.3 percent in posterior and 81.2 percent in anterior presentation. In the anterior presen-284 VETERINARY OBSTETRICS Figure 86. Normal and abnormal presentations, positions and posture in bovine and equine births. I Normal anterior presentation, II Posterior presentation, III Anterior presentation with the rear legs extended beneath the fetus (“dogsitting” posture), IV Posterior presentation with the rear limbs extended beneath the fetus (breech presentation), V Anterior presentation with the head and neck extended over the fetus, VI Transverse ventral presentation of a foal, (as adapted from Diseases of Cattle U.S.D.A., 1942, Harm’s Textbook of Veterinary Obstetrics, and Veterinary Obstetrics, 2nd Ed., G. H. Arthur).DYSTOCIA—ITS CAUSES 285 tation 31.5 percent had a deviated head and neck. In posterior presentations 80 percent of the single births had one or both hind limbs flexed.40 In 1200 dystocias in ewes 65 percent of the fetuses were in anterior presen- tation, many with a lateral deviation of the head or with one or both forelegs flexed; 27 percent were in posterior presentation and two-thirds of these were in breech pres- entation; and 8 percent were in a transverse dorsal pres- entation. Failure of the cervix to dilate occurred in 15 percent of the cases.1317 In the sow the incidence of dystocia caused by uterine inertia is about 40 percent.28 Small litter size tends to cause larger fetuses that may predispose to dystocia. Dystocia in immature or poorly grown gilts is occasion- ally observed. Abnormal fetuses such as cyclops and hermaphrodites are uncommon and seldom cause dys- tocia. Double monsters and hydrocephalus are rare, about 0.5 percent.28 Stillbirths are high in sows with dystocia.' (See Figure 46.) In the bitch disproportion between fetal size and pel- vic diameters is common in toy and achondroplastic breeds. In the latter the large size of the head is the prin- cipal cause of the dystocia. Oversized fetuses are oc- casionally seen when there are only one or two fetuses.1 Uterine inertia, either primary or secondary, is a fre- quent cause of canine dystocia. Nervous voluntary in- hibition of parturition may occur due to excitement, a strange environment or pain.16 A prolonged first stage of birth may occur in posterior presentation of the first fetus because of failure of the head to engage in the pelvis and stimulate uterine and abdominal contractions.15 Poll presentation and lateral deviation of the head and neck are causes of dystocia. Postural abnormalities of the limbs are of little importance. Dorso-ilial and especially dorso- pubic positions are seen as a cause of dystocia. Monsters are rare except for occasional cases of hydrocephalus.16 Transverse presentation is rare and usually occurs only with bicomual pregnancy with a single fetus. A com- plete review of the causes of canine dystocia have been listed.6b In the queen dystocia may be due to postural abnor- malities of the head and neck and to breech presentation. Only rarely are two fetuses wedged in the pelvis. Uterine inertia, hydrocephalus and a large calvarium in primi- parous Persians have also caused dystocia.10 References 1. Arthur, G. H. (1975) Veterinary Reproduction and Obstetrics, 4th Ed. Bailliere and Tindall, London, Williams and Wilkins, Baltimore. 2. Ball, L. (1981) Personal Communication. 3. Bellows, R. A. (1966) Improving Reproductive Efficiency in Beef Cattle, Veterinary Scope, Upjohn Co., Kalamazoo, Mich. 11, 3. 4a. Bellows, R. A. and Short, R. E. (1978) Effects of Precalving Feed Level on Birthweight, Calving Difficulty and Subsequent Fertility, J. An. Sci. 46, 6, 1522-1528. 4b. Bellows, R. A., Short, R. E., and Richardson, G. V. (1982) Effects of Sire, Age of Dam and Gestation Feed Level on Dys- tocia and Postpartum Reproduction, J. An. Sci. 55, 1, 18. 5. BenDavid, B. (1961) Obstetrical Problems in the Israaeli Frie- sian Cow II Observations on Abnormal Parturition, Refuah Vet. 18, 152. 6a. Bensch, F. and Wright, J. G. (1951) Veterinary Obstetrics, Wil- liams and Wilkins Co., Baltimore, Md. 6b. Bennett, David (1980) Abnormal Parturition (Dystocia) in Cur- rent Therapy in Theriogenology, edited by D. A. Morrow, W. B. Saunders Co., Philadelphia, 599-606. 6c. Bollwahn, W. (1981) Surgical Procedures in Boars and Sows, in Diseases of Swine 5th Ed., by A. D. Leman, Iowa State Univ. Press, Ames, Iowa., 782. 7. Bratton, R. W. (1957) Breeding Difficulties in Dairy Cattle, Cornell Univ. Agr. Exp. Stat. Bull. 924, Ithaca, N.Y. 8a. Burfening, P. J. (1981) Effect of Dystocia on Future Repro- ductive Performance, Proc. Ann. Mtg. Soc. for Theriog., Spo- kane, 96. (A Review.) 8b. Burfening, P. J., Kress, D. D., Friedrich, R. L. and Vaniman, D. (1979) Ranking Sires (Simmental) for Calving Ease., J. An. Sci. 48, 2, 293-296. 8c. Cady, R. A. and Burnside, E. B. (1982) Evaluation of Dairy Bulls in Ontario for Calving Ease of Offspring, J. Dairy Sci., 65, 2150. 9. Carpenter, B. (1978) Calving Difficulty in Sires, Eastern AI Co- operator 34, 10, 5 & 6. 10. Colby, E. D. and Stein, B. S. (1982) The Genital System, in Feline Medicine and Surgery, 3rd Ed., Amer. Vet. Publ. Inc., Santa Barbara, California. 11a. Dennis, S. M. (1980) Low Viability of Calves at Birth, Vet. Ann., K.S.U., Manhattan, Ks. lib. Divers, T. J. and White, N. A. (1979) Equine Fetal Ascites with Resulting Abortion and Dystocia: A Case Report., J. Eq. Med. Surg. 3, 331. 12. Dufty, J. H. (1981) The Influence of Various Degrees of Con- finement on the Incidence of Dystocia and Stillbirths in Heifers, N. Z. Vet. J. 29, 44-48. 13. Ellis, T. H. (1958) Observations on Some Aspects of Obstetrics in the Ewe, Vet. Rc. 70, 952. 14. Falk, D. G., Christian, R. E., Bull, R. C. and Sasser, R. G. (1975) Prepartum Energy Effects on Cattle Reproduction, J. An. Sci. 41, 167. Abstr. 15. Fox, M. W. (1966) Canine Pediatrics, C. C. Thomas Co., Springfield, 111. 16. Freak, M. J. (1962) Abnormal Conditions Associated with Preg- nancy and Parturition in the Bitch, Vet. Rec. 74, 1323. 17. Grommers, F. J. (1967) A Preliminary Study on the Actual and Potential Perinatal Lamb Mortality in Texel Sheep, Tijdschr.v. Diergeneesk. 92, 222. 18. Hammond, J. (1955) Progress in the Physiology of Farm Ani- mals, Vol. 2, Butterworth Scientific Publications, London, En- gland. 19. Hansen, L. H. (1966) Incidence of Dystocia and Postparturient Disorders in Jersey Cattle after Crossbreeding with Charolais Bulls, Brit. Vet. Jour. 122, 273.286 VETERINARY OBSTETRICS 20. Laster, D. B. (1974) Factors Affecting Pelvic Size and Dystocia in Beef Cattle, J. An. Sci. 38, 3, 496-503. 21a. Laster, D. B., Glimp, H. A., Cundiff, L. V. and Gregory, K. E. (1973) Factors Affecting Dystocia and the Effects of Dys- tocia on Subsequent Reproduction in Beef Cattle, J. An. Sci. 36, 4, 695-705. 21b. Martinez, M. L., Freeman, A. E. and Berger, P. J. (1982) Ge- netic Relationship between Early Calf Mortality and Calving Difficulty, (Abstr.) J. of Dairy Sci. 65 Suppl. 1, 87. 22. Mason, I. L. (1964) Genital Aspects of Breeding Cattle for Beef (Muscle Hypertrophy), Vet. Rec. 76, 28, 765. 23. Miller, Paul (1974) An Analysis of Calving Difficulty, the Profit Brand, 5, 6, Amer. Breeders Service, DeForest, Wise. 24. Osenga, A. (1978) Endocrine Aspects of Bovine Dystocia with Special Reference to Estrogens, Theriog. 10, 2 & 3, 149-166. 25. Poliak, E. J. and Freeman, A. E. (1976) Parameter Estimation and Sire Evaluation for Dystocia and Calf Size in Holsteins, J. Dairy Sci. 59, 1817-1824. 26. Price, T. D. and Wiltbank, J. N. (1978) Dystocia in Cattle, A Review and Implications, Theriog. 9, 3, 195-219. 27a. Rahim, A. T. A. and Arthur, G. H. (1982) Obstetrical Con- ditions in Goats, Cor. Vet. 72, 279. 27b. Rice, L. E. and Wiltbank, J. N. (1970) Dystocia in Beef Heif- ers, J. An. Sci. 30, 6, 1043. 28. Runnels, L. J. (1981) Obstetrics in Diseases of Swine, 5th Ed., A. D. Leman, Editor, Iowa State Univ. Press, Ames, Iowa. 29. Sloss, V. A. (1974) Clinical Study of Dystocia in Cattle, Aus- tral. Vet. J. 50, 7, 290-293. 30. Stamp, J. T. (1967) Perinatal Loss in Lambs with Particular Reference to Diagnosis, Vet. Rec. 81, 21, 530. 31. Stonaker, H. H. (1958) Breeding for Beef, Colo. State Univ. Exp. Stat. Bulletin 501-5, Ft. Collins, Colo. 32. Thompson, J. R., Freeman, A. E. and Berger, P. J. (1980) Re- lationship of Dystocia Transmitting Ability with Type and Pro- duction Transmitting Ability in Holstein Bulls, J. Dairy Sci. 63, 1462-1464. 33. VandenBussche, O., VandenBussche, P. and Vandeplassche, M. (1964) Dystocia in the Red Cattle of West Vlaanderen, Vlaams Diergeneesk Tijdschr, 33, 5, 205. 34. Vandeplassche, M. (1958) The Normal and Abnormal Presenta- tion, Position and Posture of the Foal-Fetus during Gestation and Parturition, Dept, of An. Abst. and Reprod., State Univ., Ghent, Belgium. 35. VanDieten, S. W. J. (1963) Stillbirth in Bovine Cattle, Thesis, Univ. of Utrecht, Utrecht, Holland. 36. Walton, A. and Hammond, J. (1938) The Maternal Effects on Growth and Conformation in the Shire Horse-Shetland Pony Crosses, Proc. Royal Soc. B, 125, 311. 37a. Williams, W. L. (1943) Veterinary Obstetrics, 4th Ed., Ithaca, N. Y. 37b. Wiltbank, J. N. and Remmenga, E. E. (1982) Calving Diffi- culty and Calf Survival in Beef Cows Fed Two Energy Levels, Theriog. 17, 6, 587. 38. Woodward, R. R. and Clark, R. T. (1959) A Study of Stillbirths in a Herd of Range Cattle, J. An. Sci. 18, 1, 85. 39. Wright, J. G. (1958) Bovine Dystocia, Vet. Rec. 70, 17, 347. 40. Wyssmann, E. (1945) Statistics on Dystocia in Goats (Trans.) Schweitz. Archiv. fur Tierheilk., 87, 57.Chapter VIII PROCEDURES PRELIMINARY TO THE HANDLING OF DYSTOCIA Dystocia cases are handled promptly as emergency calls but it is essential to a successful outcome that the animal be given a routine careful examination to establish the correct diagnosis so that a sound course of action can be outlined. The History of the Case As the preliminary examinations and preparations for handling the dystocia are being made, the history of the case as well as certain other information should be ob- tained from the owner or by observation. This infor- mation should include: the age of the female; the breed or information on the sire of the fetus; the dates of ser- vice and the duration of gestation; the previous breeding history; whether dystocia or any other abnormal condi- tion was present at previous parturitions; whether the an- imal had exhibited any illness or unusual symptoms dur- ing the two months to the last few hours prior to parturition; the length of time the animal has been acting uneasy and shown anorexia or restlessness, or the length of time the animal has been in active labor. What is the nature of the straining—strong or weak, intermittent or regular, increasing or decreasing in frequency? Has the allantoic sac ruptured, the amnionic sac appeared at the vulva, or has any portion of the fetus appeared? In mul- tipara have any fetuses been expelled and if so were they living or dead? Has any assistance such as traction been used by the owner, his neighbors, or even other veteri- narians? Is the animal primiparous or pluriparous? Has the animal been able to get up if recumbent? This in- formation is useful and necessary for the intelligent ex- amination and handling of a dystocia case. The answers to some of these questions may have been obtained at the time the veterinarian was called or can be gotten along with the general examination of the patient. The General Examination The general examination of the patient with dystocia should include its physical condition, whether it is thin and emaciated, too fat, or in good condition. If the an- imal is recumbent the veterinarian should determine the following: Is it able to rise or is it exhausted? If it is a heifer is it affected with obturator paralysis usually seen in hiplock conditions. In older dairy cows parturient pa- resis or other conditions causing paraplegia of pregnancy may be present. It is much better to diagnose the pres- ence of such conditions as obturator paralysis and inform the owner before the operation. Afterwards, if this has not been done, the owner often will blame the veteri- narian for having produced the paralysis during the relief of the dystocia. The pulse and temperature should be noted. In most dystocia cases the pulse is moderately elevated and the temperature may be slightly higher than normal due to the efforts at parturition. The degree of abdominal enlargement should be noted. Dystocia in dogs is often characterized by depression and futile laboring during which the bitch’s mouth is open and its head is repeatedly thrown back. In exhausted prostrate animals the color of the mucous membranes should be noted for evidence of internal hemorrhage or shock due to rupture of the uterine vessels or rupture of the uterus. The gen- eral appearance and attitude of the animal should be ob- served, since some cattle affected with rabies frequently show tenesmus that might be confused with labor. Par- ticular attention should be paid to the vulva. The nature of the vulvar discharge, whether it is watery, mucoid, bloody, or fetid will often indicate the condition of the fetus. If much fresh blood is present, injury to the birth canal has probably occurred due to the intervention of the owner or someone else. The character of the fetal membranes if hanging from the vulva are of further as- sistance in determining the condition of the fetus and the length of time the dystocia has existed. If a portion of the fetus protrudes from the vulva its condition and po- sition and posture should be observed. The vulva itself should be noted to gain information on the amount of edema or trauma present as an indication of the length of time the dystocia has existed and whether someone has already been trying to deliver the fetus. The Specific Examination and Restraint The specific examination consisting of the detailed ex- amination of the genital tract and fetus should be un- 287288 VETERINARY OBSTETRICS dertaken only after the animal has been properly con- fined and restrained, as the obstetrical operations usually follow immediately after this examination. If the animal is on pasture it is usually advisable, es- pecially at night, in rough country, or during inclement weather to advise the owner, at the time he calls, to take the animal to a box stall in the bam, or to a shed near the dwelling house. This will usually insure light, easy access to hot water, and fairly comfortable working con- ditions. These are definitely desirable if a clean, careful obstetrical procedure is to be followed. It may avoid chilling and exposure of the operator as well as the pa- tient. Aftercare and proper nursing are facilitated if the animal is near the owner’s residence. A clean pasture lot or even a well-bedded stanchion stall are better locations in which to work than is a dirty, dark, cramped or too- small box stall. These suggestions are only common-sense practices and precautions but often if the veterinarian does not suggest or insist upon them the owner will neglect to provide satisfactory surroundings for the patient and operator. Working in the hot summer sun, on “the north- side of a barbed wire fence” in winter, knee-deep in water or filth, or in a dusty, dark, low swine house is not con- ducive to proper surgical cleanliness or technique. If a good supply of hot water is not available the veterinarian should take it with him. If possible the animal should be standing at the time of the examination. A satisfactory examination and the handling of dystocia are much more difficult in the re- cumbent patient, with the viscera and fetus forced to- ward the pelvic cavity. Most animals rise promptly when urged. Others may be fatigued or may not wish to stand, and more vigorous methods are required such as; prod- ding them over the loins and rump with a sharp object, rolling the tail, sudden thumping of the ribs over the chest with the operator’s knees, the use of the electric prod, or the intravenous injection of central nervous stimu- lants. Occasionally a cow which has refused to rise will do so after a small dose of anesthetic epidurally has re- lieved the pain. If the animal fails to get up, its rear parts should be raised above the front by lowering the front parts; or the rear parts may be placed on bags of straw, or elevated on a door or a plank resting on blocks and the animal held in place by a breast-harness. The rear parts may be hoisted by means of a figure-of-eight knot of rope around the hocks, which places the animal on its back, or by passing loops of rope around each leg up to the crotch and hoisting the animal’s rear parts. If this latter method is used, the animal often falls sideways if it struggles. The judicious use of commercially available hip slings may be helpful in these cases. In nearly all cases of dystocia a standing position or the elevation of the rear parts is necessary in order that the veterinarian may work with relative ease and effect a prompt cor- rection of dystocia. It is therefore desirable that the an- imal be placed in this position prior to the examination. The animals should be properly restrained so that they do not injure the operator at the time of the examination or operation. In mares a twitch usually should be applied to the lip and one foreleg held up. In range cattle a well- constructed chute is desirable, or cows might be fastened securely with a rope halter in a comer of a large box stall. If they kick, a nose lead will often divert their at- tention. In sheep the rear parts should be elevated by an assistant straddling the ewe. This position minimizes straining, aids repulsion and the introduction of a lubri- cant.6 Sows can be fastened securely by a strong rope with a loop around the upper jaw and behind the canine teeth. The sows may be secured or placed in a farrowing crate. Restless sows may be restrained by a short ob- stetrical chain around the metacarpus of the left foreleg and above the hock on the left rear leg and laying the sow on her left side." Dogs should be muzzled or have their jaws tied together and cats should be held firmly by an assistant. The use of epidural anesthesia, tran- quilizers or slight or deep narcosis may be necessary to properly restrain some animals. In doing obstetrical work on large animals, the most satisfactory dress is: rubber boots, the type that slip on over the shoes; a pair of rubber pants or overalls; in warm weather a sleeveless cotton shirt or jacket and in cold weather a rubber jacket with no sleeves and the armholes cut or adjusted with elastic to fit tightly over the upper arm. Rubber or plastic gloves and sleeves can be worn, when indicated, to prevent infection and odors from con- taminating the arms of the operator. These rubber or plastic gloves and sleeves are often damaged by instruments if fetotomy is employed. The long obstetrical gown is gen- erally undesirable because it is extremely hot in the sum- mer and does not provide proper protection to the lower portion of the operator’s body when he has to kneel to work on the recumbent animal. The animal’s external genitalia and the surrounding structures should be washed thoroughly with warm water and soap. In sheep and long-haired dogs it is necessary to clip the wool and hair in the perineal area. The tail should be held to one side by an assistant or tied with a tail rope over the back to the opposite elbow. In the mare the tail should be bandaged or covered by a plastic sleeve. Adding a sanitizing detergent like the quaternary am- monium compounds and a wetting agent to the water used in washing the rear parts of the dam will aid in thoroughly cleansing the area. In cattle epidural anes- thesia is helpful in preventing frequent defecation of loosePROCEDURES PRELIMINARY TO THE HANDLING OF DYSTOCIA 289 feces that contaminate the perineal area as well as the operator’s arm. In some cases, however, epidural anes- thesia might not be desirable, as it would cause a ces- sation of straining or labor. This straining may be helpful in the withdrawal of a normally-presented fetus. During the examination and obstetrical operation the perineal area should be kept washed and clean at all times. The op- erator should wash and lubricate his arms with water and soap or other nonirritating lubricant before making an examination of the birth canal and fetus. In the queen and bitch, after giving an enema and catheterizing the bladder, the rear parts may be cleansed and covered with a sterile drape; the veterinarian should wear sterile rub- ber gloves. If the history of the case leads the veterinarian to know or suspect that others have been examining and attempt- ing to relieve the dystocia, it is extremely important that the birth passages and caudal portions of the uterus be examined very carefully for evidence of trauma. In the middle of an obstetrical operation it is highly embar- rassing to find a tear in the vagina or uterus which was present or had been produced before the operation was begun. If this injury causes the death of the animal, the owner might accuse the veterinarian of having injured the animal. The veterinarian would not be able to prove his innocence. The birth canal should be examined to see if it is dilated, twisted, moist or slippery, inflamed, swollen, dry, necrotic, contains pathological bands, stenotic areas or tumors, or contains gummy mucus in- dicating that parturition has not yet begun or is in the early stages. The degree of dilation or relaxation of the cervix should be noted as well as whether there is any evidence of torsion. The size of the pelvic inlet, vulva, and vagina in relation to the size of the fetus should be checked. Any other abnormalities of the birth canal should be noted. The canine or feline patient might benefit from radiography of the fetuses and pelvis of the dam to de- termine the fetal and pelvic sizes and if the fetuses are dead.7b The fetus should be examined to see if it is dead or alive as this will alter the prognosis and make a differ- ence in the manner in which the case is handled. If the fetus is alive, grasping the foot and pulling or pinching it will cause movement of the limb. Pinching the eye- balls will cause the live fetus to shake its head. Placing the fingers in the mouth of the fetus may cause sucking or movements of the tongue and jaw. Putting fingers in the anus in breech presentation will cause contraction of the anal sphincter. If the fetus is dead the degree of de- composition or autolysis should be accurately assessed by the amount of subcutaneous edema or emphysema, whether or not the hair is sloughing and whether or not a putrid, fetid odor is present. When fetal emphysema and sloughing of the hair is present the fetus has been dead for 24 to 48 hours or more depending on the degree of changes noted. After a dead fetus has been removed from the uterus, if no emphysema is present, the length of time death has existed may be approximately deter- mined by the degree of cloudiness, turbidity or greying of the cornea. After the fetus has been dead 6 to 12 hours the corneas are grey and opaque. The fetus should be carefully examined to determine any abnormality of presentation, position, and posture, or any teratologic defects. In a breech presentation the tail is often observed hanging from the vulva or lying in the birth canal. If the head is not in the birth canal in anterior presentation its location can be determined by finding the neck, the mane of the equine fetus, or the ears and head, by swinging the arm and hand around the cephalic part of the fetus. If the feet are lying in the birth canal it should be determined whether they are front or hind feet. Inexperienced students frequently confuse the front and hind legs by mistaking the hock for the elbow or the elbow for the hock. Front limbs have two joints, fetlock and knee, between the hoof and elbow, while hind limbs have only one joint, the fetlock, between the hoof and hock. If the feet are protruding through the vulva with the soles ventral then the fetus is in either anterior longitu- dinal, dorso-sacral position or posterior longitudinal, dorso-pubic position. The latter rarely occurs. If the soles of the feet are dorsal then the fetus is in either posterior longitudinal presentation, dorso-sacral position; or an- terior longitudinal presentation, dorso-pubic position. This latter condition is only rarely observed. In fetal monsters the differentiation into the various types may be quite difficult, as ankylosis and marked distortion are fre- quently present. Most of these abnormal fetuses have se- verely atrophied muscles of the limbs, making them feel thin, very firm, and rigid. If no part of the fetus is in the vagina of the mare the condition is probably a trans- verse dorsal or rotated bicornual pregnancy. In the latter condition the birth canal is very long and the fetus can be touched only at arm’s length. Occasionally the am- nion may not yet be ruptured, in which case if the birth passageway is dilated sufficiently the amnion may be ruptured with the fingers or a knife, so that palpation of the fetus may be facilitated. If more than two limbs are in, entering, or are near the pelvis, the condition should be examined carefully to differentiate between twins that are wedged in the pelvis, a Schistosomus reflexus, a double monster, an anterior presentation with the rear limbs of the fetus extended over or under the body, or in the mare a transverse ventral presentation.290 VETERINARY OBSTETRICS It may occasionally be necessary to repel the fetus out of the birth canal and into the uterus in order to diagnose accurately the cause of the dystocia. If the animal is straining severely, epidural anesthesia should be given at once so that the examination can proceed without in- terruption. Sometimes examination is difficult, espe- cially in a protracted dystocia in heifers, with swollen mucous membranes, a dry, dead fetus, and a uterus con- tracting tightly around it, making it impossible to repel the fetus. In mares and occasionally other animals, where the owner has applied traction, the fetus may become firmly wedged in the pelvis. A similar examination is made with a finger per vaginam in the bitch. Strict cleanliness is necessary, as in other species. If more than one fetus is palpated in the abdominal cavity and the bitch has suffered a prolonged dystocia, inertia has prob- ably developed and cesarean section may be indicated. The importance of this complete examination cannot be overstressed, as it is the basis of the prognosis and pro- cedures that follow in the handling of the case. It should be thorough and accurate to be professional, to save time and effort in useless and often harmful procedures, and to determine in severe cases whether or not outside help or consultation is needed. Prognosis The prognosis in dystocia varies widely between the different causes and species affected. For this reason the prognosis in the various types of dystocia will be con- sidered as each type is discussed. In general the more prolonged the dystocia, the poorer the prognosis. The greater the trauma, irritation and infection of the birth canal caused by inexperienced laymen attempting to re- lieve the dystocia, the graver the prognosis. The prog- nosis in horses is graver than other domestic animals be- cause the fetus usually dies within 30 to 40 minutes after the commencement of labor. The mare’s pelvis is longer, and the fetal extremities are longer, making correction of the dystocia more difficult. Labor contractions are vi- olent and powerful, predisposing to impaction of the fe- tus in the pelvis, lacerations of the birth passages or rup- ture of the uterine vessels. Lastly, the mare is more susceptible than other animals to trauma, irritation, in- fection, and inflammation of the birth passage and to peritonitis. It is difficult to save the life of a mare if she has been in labor for more than 24 hours and the fetus is emphysematous. The same is true of other animals but the prognosis is usually better, as other species are more resistant to infection. The fetus in the cow usually dies after 6 to 12 hours of labor and emphysema sets in about 24 to 36 hours after the onset of labor. In the bitch the first fetus usually dies within 6 to 8 hours3 after the onset of labor and may become emphysematous in 24 to 36 hours. But some of the other fetuses may still be alive. After 48 hours of labor no living canine fetuses are found. In sows the first pig usually dies after 4 to 6 hours of labor. The other pigs may survive for 24 hours. After 24 to 36 hours of labor all fetal pigs are invariably dead. The ewe is similar to the cow. Williams very aptly described the handling of dystocia as resembling a salvaging operation on a “ship on the rocks.” If it is possible, the following should be sal- vaged:15 1. the value of the surviving dam—its future breeding life, its food value for milk or meat, or its value for work. 2. the value of the newborn. 3. the sentimental value of the dam or newborn. In the prognosis of a case of dystocia these values or credits should be weighed against the: 1. veterinary fees 2. mortality risk of the dam and the newborn 3. cost of labor and feed until the dam has recovered her value for milk, meat, work or breeding. When these factors are considered and discussed with the owner after a careful examination of the patient, the prognosis and handling of the case will be understood by the owner. In the large farm animals whose value is usually entirely economic and not sentimental, the vet- erinary fees will then be paid more willingly. If the prog- nosis is correct these fees should not exceed the salvage or slaughter value. Many young veterinarians have la- bored diligently and corrected a severe dystocia, visited the animal several times subsequently to provide nec- essary care and drugs, and then presented the bill only to have the owner exclaim, “That’s more than the heifer is worth.” This embarrassing position would have been avoided if the above factors had been discussed fully with the owner before the veterinarian undertook the correc- tion of the more severe dystocia cases. Thus the prog- nosis should take into consideration more than just the life of the dam or fetus unless the sentimental value is of prime importance. Obstetrical Equipment and Anesthesia The best guarantee of the proper and satisfactory han- dling of dystocia is the operator’s correctly applied knowledge and experience. Good help and equipment may be available, but if the problem presented in each dystocia case cannot be perceived, the several methodsPROCEDURES PRELIMINARY TO THE HANDLING OF DYSTOCIA 291 of handling it are not evaluated, a practical and logical approach and procedure are not developed, and the abil- ity to follow the outlined procedure calmly and confi- dently to a successful termination are lacking, the case will probably end in failure, with a dissatisfied or dis- gusted owner. The best obstetrical equipment available should be used. Poor or makeshift equipment is not con- ducive to good surgical procedures. The instruments should be kept clean and sterile. Chrome or other types of plated or stainless steel instruments are desirable. During obstetrical operations surgical procedures of cleanliness should be followed in so far as this is pos- sible. A plentiful supply of hot water, soap and lubricant are usually necessary. If possible a table should be pro- vided and covered with a sterile sheet upon which the obstetrical instruments may be placed during the oper- ation. Since this is usually lacking a clean pail of water to which an antiseptic has been added can be used and in which instruments may be placed or kept to prevent contamination. If the operation must be performed in a bam on a recumbent animal a sterile rubber sheet placed under the rear parts of the cow may help reduce contam- ination. In practice these sheets are difficult to hold in place. Epidural anesthesia may be necessary to control defecation. If the surroundings are poor the animal should be moved to a more suitable place. It is not necessary to have all of the following ob- stetrical equipment for the handling of dystocias. Certain veterinarians become quite adept at using particular in- struments while others prefer different ones. The type of practice in the various areas of the country also deter- mines to a large extent the type of equipment that is ac- cepted and used (see Figure 87). Obstetrical Instruments for Traction on the fetus include: Chains and handles: Gibbons’ handles, while more bulky than the smaller Muir’s handles, are better as they provide a longer, wider hand hold and do not cut into the hands. Obstetrical chains are preferred to sash cord or baling twine because they may be recleaned and ster- ilized, provide easier attachment for handles than does cord or twine. They are more professional in appear- ance. Obstetrical chains are strong, easily applied, and do not cause injury to the fetus or the genital tract of the dam. They are made in 10-, 21-, 30-, and 60-inch lengths. Lengths of 1- or 2-inch wide sterile gauze may be used for traction in dogs and cats. Hooks may be long or short but should always be blunt. Sharp hooks are frequently the cause of injury either of the operator or the dam. Blunt hooks can do anything sharp hooks can, but without the added danger. The short hooks have an eye at their base, through which a cord is run. The long hooks have a handle on the end opposite the hook. In general the long hooks are easier to apply because they can be turned or pushed from outside the vulva, but they occupy slightly more room than do the short hooks. The hook should be at a 45° angle from the shaft so that when traction is applied the hook tends to sink deeper into the fetal tissues. Another hook that is useful is Krey’s hook or tongs. These may readily be applied to the orbits or other portions of a fetus when traction is desired during fetotomy operations. Krey’s hook does not require guarding with the hands, as do other hooks that might pull out of the fetus and injure the birth canal or uterus. A fetal extractor consisting of a mechanical hoisting or jacking device on the end of a long metal rod fitted into a broad metal breech plate, has proven very useful when used judiciously. When obstetrical chains are fas- tened to the fetus and to the hoist or jack, traction is applied and the fetus is gradually withdrawn. This in- strument has great advantages over the block and tackle and wire stretchers used previously, because it allows traction to be regulated and applied upwards, down- wards, or to either side. The older block-and-tackle method of traction allowed traction to be applied in only one direction and was much less professional than the fetal extractor. This device must be used with judgement and caution and with epidural anesthesia to control pain because of the great pressures it can produce on the fetus and dam. If the fetus is alive and breathing it should be used intermittently with periods of rest to prevent as- phyxia from excessive tension on the respiratory mus- cles. Forceps and snares of a wide variety are used to re- lieve dystocia in ewes and sows, bitches and queens. Knowles’ cervical forceps are very satisfactory in swine as are certain wire forceps or snares. These same snares work well in many dystocias in ewes. Snares made of thin twisted wire with a long thin handle are valuable in securing the lower jaw, the limbs or the head and neck since they tighten securely and are much less apt than are chains to slip off and injure the teeth or hooves. The author has found that in an emergency clean hemp twine used for baling hay may be used after disinfection as a snare for the lower jaw or limbs. If a large knot is tied in the cord outside the vulva an obstetrical handle may be used for traction. In dogs “clam shell” forceps, sponge forceps, Roberts’ snare forceps, or Hobday’s type of for- ceps are useful.3 The clam-shell type of forcep in which there is a small offset in the handles so that the hinge does not fit tightly and cannot pinch the mucous mem- brane was preferred.10 Forceps or snare delivery in mul- tipara is necessarily limited to those fetuses that are in292 VETERINARY OBSTETRICS Figure 87. Bovine and Equine Obstetrical Instruments 1. Head snare, 2. Guard’s chisel, 3. Fetal extractor, 4. Hoeblade castrating knife, 5. Krey’s hook or tongs, 6. Williams’ chisel, 7. Fetatome, 8. Threader for fetatome wire, 9. Crutch repeller, 10. Detorsion rod, 11. Williams’ bluntpointed cutting hook, 12. Williams’ long blunt hook, 13. Handles for wire saw, 14. Muir’s chain handle, 15. Moore’s obstetrical chains, 16. Gibbons’ chain handle. the pelvic canal or the body of the uterus just cranial to the pelvic inlet. Great care must be used in applying rigid metal forceps or snares to the extremities of living fe- tuses as lacerations or injuries to the fetus or birth canal are easily produced. Instruments for section are used in fetotomy to re- duce the size of the fetus. These instruments should be kept sharp and in good operating condition. The number and type of instruments are many and each veterinarian usually develops his preferences. Williams stated that there is no place in surgery in which familarity with an in- strument is more important to the operator than in fe- totomy. Knives—A heavy scalpel and a Bard Parker knife are useful in removing a portion of the fetus that may be outside of the body of the cow, as for example, in the operation of decapitation. The hoe or hook-bladed cas- trating knife is useful within the uterus, particularly the former as it does not cut so deeply into the fetus and is therefore easier to use. These castrating knives are easy to guard with the hand while in the uterus. Williams’ long cutting hook with a blunt point is very useful for cutting ribs. Long cutting chisels are of three types: Williams, with a slightly concave flat blade; Guard’s, with a V-shaped head; and the Ames chisel, resembling a nasal septumPROCEDURES PRELIMINARY TO THE HANDLING OF DYSTOCIA 293 chisel. The usefulness of chisels is limited. Fetatomes of many types, especially in Europe, are used to protect and guide the fetatome wire.1'3'5,12 The two most widely used in America are the Benesch Uni- versal and the Utrecht fetatomes. Fetatomes have the ad- vantage over most chain saws or wire saws in that they can cut at different angles and not just in one caudal direction. The fetatomes use a stiff wire threader or guide to place the wire through the fetatome. There are several types of handles for the fetatome wire. The best type is the one in which the fetatome wire is placed between two interlocking rows of “teeth” that firmly secure the crimped wire when the handles are closed. Large forceps are also satisfactory. Several types of heavy metal rings or an obstetrical chain can be used as a guide or leader to carry the fetatome wire around the fetus. The wire should be of the best grade obtainable; it should be kept clean and free from rust, and after having been used for one fetotomy operation should not be used again. Kink- ing of the wire should be avoided. In applying and using the fetatome, the fetatome wire should be securely fastened to the guide or an obstetrical chain unless a loop of wire is used. The guide or chain should always be introduced over the top of the fetus, or dorsally and then downwards or ventrally to take ad- vantage of gravity to help carry the weighted guide around the part of the fetus to be removed. If a chain is used a large handful should be coiled in the hand and intro- duced as far around or over the fetal part as possible before being released. Otherwise the chain may follow the operator’s hand and arm as it is pulled back, thus making it impossible to reach when the hand is passed under the fetal structure to pick it up and complete this phase of the operation. This procedure should always be done against the fetal hair, so that fetal membranes will not interfere with nor complicate the prompt placing of the wire. Occasionally the guide or chain will drop into the nongravid horn, making recovery of it impossible when the hand is passed under the fetus or fetal part. If the fetatome wire is already threaded in the fetatome and a loop of this wire is to be slid up and over an extremity, the head of the fetatome should precede and help guide the loop of wire into place. In sectioning the fetus with a fetatome, the head of the fetatome should be held tightly against the fetus, and the handle of the fetatome held or braced with the other hand and arm placed across the chest or hip as the sawing proceeds. The newer Utrecht or similar models of fetatomes have a chain fixation plate or hooks behind the handle for at- taching obstetrical chains fastened under tension to the fetus. The older Benesch universal fetatome can be mod- ified by welding a chain fixation plate or hooks for at- tachment of chains to the handle. With these fetatomes the head of the fetatome is located in its desired position and the wire is placed properly and tightened. Before cutting with the wire the head of the fetatome is held in place on the fetus by obstetrical chains, and Krey’s tongs if needed, attached to the fetatome handle under tension. This innovation greatly facilitates accurate positioning of head of the fetatome and reduces the expenditure of ef- fort by the operator. The operator performing the sawing should maintain a constant strong tension on the wire with both arms, and use long, smooth strokes. If bone is encountered the wire will become hot and may break; therefore the po- sition of the wire cutting through bone should be changed frequently, or sawing should be intermittent in order to allow the wire to cool. Breaking of the wire occurs most often on angular cuts. Care should be used in placing the fetatome, to see that the wires are not crossed be- tween the fetatome and the fetus, as this generally results in immediate breaking of the wire. The fetatome wire should be kept taut at all times to prevent coiling, kink- ing and breaking. If the progress of the sawing is to be investigated, the assistant who is manipulating the wire should be warned so that the operator’s hand or fingers will not be cut. Wire Saws—There are several wire saws that cost less than the fetatome but they usually cut only in one di- rection, that is caudally. The pipe or guard used to pro- tect the birth passage from the fetatome wire has no spe- cifically designed head or end of hardened steel. Many other types of wire saws protected by metal spiral tubes or tubular pipes have been designed in Europe. The spi- ral types may be used to cut in more than one direc- tion.3'12 Other more elaborate instruments for section have been devised and used in Europe.3 The widespread acceptance of the fetatome has made for infrequent use of the earlier long blunt-pointed cutting hooks, chisels, and wire saws. Instruments for Repulsion and Rotation—In repel- ling the fetus from the pelvic cavity, examining the fe- tus, or making room for manipulation of the fetus or its extremities, epidural anesthesia and the operator’s arm are most commonly used. Williams’ crutch repeller, with or without the re- movable spike, is very useful when the fetus is firmly impacted in the pelvic inlet. It allows the operator’s as- sistants to provide the strength to repel the fetus, and thus conserves the operator’s strength. By use of this crutch the fetus can be repelled downward and forward, upward and forward, or laterally and forward. Kuhn’s crutch is strongly advocated3 for the relief of dystocia but it has not become popular in America. Most of the294 VETERINARY OBSTETRICS operations performed by these repelling instruments can be performed with greater facility by the operator’s hand and arm. The fetal rotators or uterine detorsion rods are of a number of types and are used to rotate the fetus when it is in longitudinal presentation in an abnormal position. This abnormal position may be due to a mild to mod- erate, 90° to 240°, torsion of the uterus. As in repulsion the operator’s arms or proper direction of traction on the obstetrical chains will correct many torsions of the uterus or dorso-sacral or dorso-pubic positions of the fetus in large uniparous animals. The so-called Cornell detorsion rod is simple and requires only a 60-inch obstetrical chain and handle to make it complete. Other metal rotators, such as Erikson’s, resembling a long-handled twitch with snares and chains to fasten the leg to the handle of the instrument have been used to advantage. In Europe Cammerer’s torsion fork is popular and requires two canvas sleeves.3 It is highly desirable that all long-handled instruments, such as the long blunt hook, the blunt-pointed cutting hook, and chisels be solid and rigid, as they often have to be twisted within the uterus. If they are jointed the instrument can be twisted or rotated in only one direc- tion. In difficult or prolonged dystocia proper lubricants for the genital tract are essential. When the mucous membrane of the vulva and vagina is dry, mild, non- irritating soap, such as Ivory soap flakes, and water or bland liquid soap may suffice in cases needing slight lu- brication. In cases requiring much lubrication epidural anesthesia is necessary to prevent the animal straining and throwing out the lubricant, and to cause sufficient relaxation so that the lubricant can flow about and cover the fetus and uterine, cervical, vaginal and vulvar walls. Mineral oil, 1 or 2 quarts, is only fairly satisfactory. Older practitioners used linseed infusions or lard or more re- cently canned cooking-fat preparations like “Crisco.” A blended mixture of white vaseline and 10 percent boric acid has been recommended especially for fetotomy op- erations.5 To remove this tenacious greasy lubricant from the arms and hands a good detergent or mechanic’s soap is recommended. The newer commercial lubricants such as Lubrivet and other lubricating jellies in tubes or jars or carboxymethylcellulose solutions393 are good. These solutions or lubricants may be rubbed on the fetus and walls of the birth canal after being pumped in with a stomach pump and tube. In smaller animals the rear parts may be elevated so that the lubricant runs in by gravity. In severe, prolonged operations the lubricant may have to be applied 2 or more times or as frequently as the fetus or birth canal becomes dry. In rotation of the fetus on its long axis lubricants are essential. They help to protect the mucous membranes from irritation, infection, trauma, and even rupture, besides making obstetrical manipulations and operations easier in the prolonged “dry” cases of dystocia associated with a dead or emphyse- matous fetus. Other equipment for obstetrical operations should con- sist of two clean enamel, stainless steel or plastic pails, soap, several types of antiseptics, common surgical in- struments including syringes, needles, scalpels, scissors, forceps, suture needles, and various types of sutures, sterile drapes and towels, sponges, razor, cotton, oxy- tocin, anesthetics for local and epidural anesthesia, tran- qualizers and general anesthetics. Epidural Anesthesia or Analgesia Epidural anesthesia in the cow and mare is one of the most useful tools for aiding the operator and relieving pain in the patient suffering from severe dystocia. Prior to this useful tool straining was combatted by a noselead, twitch, sharp object pressed down on the back and even tracheotomy. The former pain-producing techniques are very imperfect or only shortlived. The technique of epi- dural anesthesia was introduced into the United States by Benesch in 1926.2 In obstetrical work epidural anes- thesia is used frequently because it stops abdominal straining and makes mutation of the fetal extremities, repulsion of the fetus, correction of breech presentation and uterine torsion much easier. It abolishes or reduces all pain and is therefore more humane and should be administered when great power is used as in some forced extractions. It greatly increases the speed, ease, and safety to the operator and patient in fetotomy operations. With proper epidural anesthesia the animal stands quietly without moving about or lying down, which is helpful to the operator. Often the cow that is down and refuses to stand will rise and stand normally following the administration of epidural anesthesia. Defecation is sus- pended. The animal does not rapidly expel lubricants pumped into the uterus. When used in cesarean section it controls straining and prevents intestinal prolapse through the operative incision. It is used to aid replace- ment of prolapse of the vagina, cervix, uterus, rectum, or bladder. By controlling straining, it may prevent pro- lapse of the uterus immediately after a difficult parturi- tion. It alleviates symptoms of straining caused by se- vere vulvitis or vestibulitis. The use of epidural anesthesia is nearly free of danger and is seldom if ever contrain- dicated. Normal involution of the uterus is not inter- ferred with and epidural anesthesia does not cause or fa-PROCEDURES PRELIMINARY TO THE HANDLING OF DYSTOCIA 295 vor retained placenta. Epidural anesthesia is not required in every dystocia case. In those cases in which a rapid and normal course of parturition is expected or a simple easy manipulation can correct the dystocia, it need not be used. The technique for administering epidural anesthesia, particularly in the cow, is simple and easily mastered. Most veterinarians use a 16- or 18-guage 1-1/4" to 2" needle. The site for insertion of the needle is determined by elevating and lowering the tail and feeling where the vertebral joints are located by the depression and move- ment between the vertebrae. The joint between the first and second coccygeal vertebrae is the most moveable in the cow. In palpating caudally from the sacrum, the first vertebrae joint in which movement can usually be felt is between the last sacral and first coccygeal vertebrae. After properly shaving and disinfecting this site, the needle is inserted in the cow between the first and second coc- cygeal vertebrae or the first coccygeal and last sacral vertebrae. The author prefers the latter site in the cow. The needle is introduced at a 10 degree angle caudally from the perpendicular, and strikes the bottom of the vertebral canal of the last sacral vertebra. This readily determines the depth at which the anesthesia should be injected. Between the first and second coccygeal verte- brae the needle may go entirely through the spinal nerves and joint. Inserting the needle in the mare is more dif- ficult. It is introduced at a slightly greater angle cau- dally, 30 degrees from the perpendicular, than in the cow, about one inch cranially to the long coarse tail hairs. The veterinarian should be careful to insert the needle di- rectly on the midline. In the cow the needle is inserted about 3/4 to 1-1/2 inches deep, depending on the size, amount of fat and the thickness of the tail. In the mare the needle is usually inserted 1-1/2 to 2-1/2 inches deep. If the needle is inserted carefully one can often feel the point of the needle “pop” through the thick connective tissue sheath covering the nerve. When the needle point has reached the proper location the anesthetic solution flows easily out of the syringe into the epidural space. If the needle is not at the proper site the solution is in- jected with difficulty. If the anesthetic does not contact the nerve the tail does not become flaccid, and anes- thesia of the perineum is not produced. If anesthesia of the motor nerves of the tail is not evident within 3 min- utes, the anesthetic was not injected properly. Occa- sionally the needle strikes the artery or vein ventral to the nerve, and blood will flow from the needle. This should be of no concern except that it indicates the needle is at the proper site for injection, or just below the nerve. It should be noted that this epidural injection is a nerve block and not a spinal anesthesia. The injection is out- side the dura mater caudal to the end of the spinal cord. The spinal cord, containing the spinal fluid, terminates between the second to fourth sacral vertebrae in the cow and the first to third sacral vertebrae in the mare.1 The amount of anesthetic solution to be injected varies with the type of solution, the weight or size of the an- imal, the species of animal, and the degree of anesthesia desired. In most obstetrical cases the solution should be injected in repeated small injections, so that the animal remains standing. If too much is given the animal will stagger, and possibly fall and injure itself. The author prefers to use a 2 percent lidocaine or procaine solution in 5 to 10 ml. amounts for 600-pound to 1300-pound cows and mares. Lidocaine produces a more rapid and deeper sensory anesthesia than procaine. If 1 percent procaine solution is used the amount of solution injected should be nearly doubled. This anesthesia will last about 1-1/2 to 2 hours. This time may be nearly doubled by adding 0.5 to 1 ml. of a 1:1000 solution of epinephrine. Two percent procaine penicillin in 5 to 8 ml. amounts produces satisfactory epidural anesthesia. When the an- imal is recumbent and the operator desires it to remain so, the animal should be placed on its sternum and as much as 20 to 50 ml. of 2 percent procaine or its equiv- alent may be injected epidurally without any adverse ef- fects and with good sensory and motor anesthesia of the rear quarters. The larger amounts of anesthetic solution are forced cranially to anesthetize the motor nerves to the rear limbs. Products containing benzyl alcohol, propylene and polyethylene glycol when injected into the epidural space produce a prolonged anesthetic effect lasting for 4 to 40 days or more by destroying the nerve fibers. In dairy cattle or horses this is very undesirable; as the animal’s rear parts and tail become covered with fecal material because the tail cannot be elevated at the time of defe- cation and micturition. In rare instances when prolonged destruction of the nerve is desired, 5 to 10 ml. of 70 percent grain alcohol may be injected epidurally. In these instances recovery may be delayed 6 months or more. During the summer months flies and maggots may be- come a problem if the perineal region is not cleaned reg- ularly. Epidural anesthesia in sheep and goats is practical but seldom used as the abdominal contractions are not strong enough to interfere greatly with manual manipulations of the fetus. Using an 18-gauge needle 1 to 1-1/2 inches long, the operator may inject 2 to 4 ml. of a local an- esthetic solution between the last sacral and first coc- cygeal vertebrae or between the last two sacral verte- brae. Epidural anesthesia is seldom used in multipara except296 VETERINARY OBSTETRICS for cesarean section because of the number of fetuses and the long period of parturition together with the re- sulting interruption of labor which would require a pro- longed period of observation and assistance for each fe- tus as it entered the pelvic cavity. Epidural anesthesia or analgesia is obtained in dogs and swine by entering the lumbosacral space with a short-beveled, 2 to 5 inch, 18 to 20 gauge, spinal needle with stylet. The space is lo- cated on the midline a short distance caudal to a line at right angles to the spinal column and at the level of the crests of the dorso-iliac spines.7'8,9 After proper shaving and disinfection of the site, local subcutaneous anes- thesia may be administered with a small needle. The spinal needle is passed perpendicularly into the lumbosacral space. When it penetrates the ligamentum flavum or the interarticular spinous ligament a distinct “pop” is felt as the point of the needle enters the epidural space. The stylet should be removed and aspiration applied on the needle to be sure the needle did not penetrate a blood vessel or the subarachnoid space containing the cerebral spinal fluid. This is unlikely as this space is small or not present at this level and is difficult to enter in bitches and sows. The dose of 2 percent lidocaine for epidural anesthesia in the dog is 1 ml per 7.5 to 10 pounds of body weight and for swine is 1 ml per 20 pounds of body weight. If 4 percent procaine is used in swine the dose is 1 ml per 10 pounds of body weight. In dogs 2 percent procaine at a rate of 1 ml per 5 pounds of body weight is recommended.7,8,9 In recent years European veterinarians have reported on the extensive use of sympathomimetic agents and blockers of parasympathomimetic receptors resulting in a tocolytic effect and relaxation of uterine muscle in a variety of obstetrical cases in all species of animals. These have included dystocias due to abnormal postures and positions of the fetus, uterine torsion, fetotomies and ce- sarean sections. The advantages in using these agents, clenbuterol (Planipart) or isoxsuprine (Hanigif) are es- pecially indicated in prolonged dystocias with dead fe- tuses. The nonsurgical management of dystocia was greatly facilitated with no increase in calf mortality re- tained placentas or adverse effect on postpartum uterine involution. These tocolytic agents act rapidly after in- jection with muscle relaxation lasting for several hours.Ia,8b It is hoped that these tocolytic agents will soon be avail- able to veterinarians in the U.S. Other Forms of Obstetrical Anesthesia General anesthesia is often indicated in the mare with severe dystocia when extensive mutation, fetotomy pro- cedures, rolling of the mare to relieve torsion of the uterus or a cesarean operation must be undertaken. General anesthesia is often begun by administering a tranquilizer, such as Rompun, followed by a short-acting intravenous anesthesia such as 5 to 10 percent dextrose solution to which thiamyl sodium or thiopental sodium have been added or ketamine HCL. After anesthesia has been in- duced additional amounts of the former may be given intravenously to maintain anesthesia.13 These products have largely replaced the older chloral hydrate and pen- tobarbital intravenous solutions for equine anesthesia. In the more modem equine clinics inhalation anesthesia of halothane may be used since this product is safe and rel- atively nontoxic even when given over a prolonged pe- riod of time. If the fetus is alive and saving it is desire- able, tranquilizers, epidural or local anesthesia should be used. On occasion the intravenous or inhalant anes- thetics may be used when the fetus is alive, even though the anesthetics cross the placenta, if the fetus is removed immediately after these anesthetics are administered. If the mare is to be given general anesthesia this should be done in a location large enough to work in with ease. With the mare anesthetized, its feet should extend away from the body in a normal manner so that no pressure is placed on the abdominal cavity. The mare may be rolled from one side to the other, to help the operator. For example, if the head and neck of the fetus is retained along the right side of the fetus in anterior presentation the mare should be laid on her right side so the head and neck of the fetus are located above and not beneath its body, where the weight of the fetus would make cor- rection of the deviated head and neck difficult or im- possible. Assistants may apply backward pressure to the fetal head through the relaxed upper flank of the mare. For cesarean section in the cow, tranquilization, epi- dural, paravertebral, or local anesthesia or combinations of these may be used. When rolling to correct torsion of the uterus in the cow, 1.5 to 2 ounces of chloral hydrate may be given orally in capsules or by stomach tube, or 0.5 to 1 ounce given intravenously to narcotize the an- imal is still useful. For cesarean section in the sow, a tranquilizer fol- lowed by local anesthesia of the operative site may be used.I2b Spinal anesthesia has been administered to sows and bitches by injection of procaine or lidocaine into the epidural space of the spinal cord at the lumbo-sacral ar- ticulation.7,8,9 Presently atropine is given as a premedi- cation followed by an ultra-short acting barbiturate and a light plane of halothane or methoxylflurane anesthesia. Innovar, a neuroleptanalgesic, has also been used and followed by naloxone after the cesarean operation to re- verse its action in the bitch and pups. Local anesthesiaPROCEDURES PRELIMINARY TO THE HANDLING OF DYSTOCIA 297 may be used in the bitch in either of the above proce- dures to reduce exposure to the anesthetic. Doxapram, a respiratory stimulant, may aid recovery of pups or foals with a small amount given under the tongue or paren- terally.13 In the bitch and cat an ether, morphine and atropine combination was formerly used as a general an- esthetic during cesarean operations. In general the long- acting barbituates are not desirable because of their de- pressing effect on live fetuses. The proper use of tranquilizers and local and general anesthetics in dystocia and other obstetrical operations is frequently necessary and results in easier, safer, and more rapid handling of birth-related problems, to the great benefit of both the animal and the operator. References la. Albeck, A. (1981) Experience in the use of Uterine Relaxants (Planipart) in Bovine Obstetrics, Tierartzl. Umschau 36, 718. lb. Arthur, G. H. (1975) Veterinary Reproduction and Obstetrics, 4th Ed., Williams, and Wilkins Co., Baltimore, Md. 2. Benesch, F. and Udall, D. H. (1926) Contributions from Vi- enna, Cor. Vet., 16, 3, 225. 3. Benesch, F. and Wright, J. G. (1951) Veterinary Obstetrics, Williams, and Wilkins Co., Baltimore, Md. 4. Bennett, David (1980) Abnormal Parturition (Dystocia) in Cur- rent Therapy in Theriogenology, edited by D. A. Morrow, W. B. Saunders Co., Philadelphia 599-606. 5. Bierschwal, C. J. and deBois, C. H. W. (1972) The Technique of Fetotomy in Large Animals, V. M. Publishing Inc., Bonner Springs, Kansas. 6. Ellis, T. H. (1958) Observations on Some Aspects of Obstetrics in the Ewe, Vet. Rec. 70, 952. 7a. Evers, W. H. (1968) Epidural Anesthesia in the Dog: A Review of 224 Cases with Emphasis on Caesarean Section, Vet. Med. 63, 12, 1121. 7b. Farrow, C. S. (1978) Maternal-Fetal Evaluation in Suspected Canine Dystocia: A Radiographic Prospective, Can. Vet. J. 19, 24-26. 8a. Getty, R. (1963) Epidural Anesthesia in the Hog—Its Technique and Applications, Proc. AVMA, 88. 8b. Horvath, Gy and Bacsfay, N. (1981) Experiences with the Use of a Uterine Muscle Relaxant Preparation (Hanegif), Acta Vet. Acad. Sci Hungaricae 29, 65. 9. Klide, A. M. and Soma, L.R. (1968) Epidural Analgesia in the Dog and Cat, JAVMA, 153, 2, 165. 10. Leonard, E. P. (1955) Personal Communication. 11. Railsback, J. (1956) Personal Communication. 12a. Richter, J. and Gotze, R. (1960) Tiergeburtshilfe, 2nd Ed., Paul Parey, Berlin, Germany. 12b. Runnels, L. J. (1981) Obstetrics, in Diseases of Swine, Edit, by A. D. Leman, Iowa State Univ. Press, Ames, Iowa. 13. Short, C. and Gleed, R. (1982) Personal Communications. 14. Walker, D. F. and Vaughan, J. T. (1980) Bovine and Equine Urogenital Surgery, Lea and Febiger, Philadelphia (Caesarean Section). 15. Williams, W. L. (1943) Veterinary Obstetrics, 4th Ed., Ithaca, N.Y.Chapter IX OBSTETRICAL OPERATIONS In handling dystocia there are numerous operations or procedures that the veterinarian should be able to per- form or use. Following a careful examination, the most conservative procedures should generally be undertaken in the interest of the owner, the veterinarian, the animal, and the fetus. The principal purpose of obstetrical op- erations is to deliver a viable fetus and to prevent injury to the dam. After a careful assessment of each obstetrical case the procedure selected should best achieve this pur- pose. Radical and heroic handling of dystocia is seldom necessary and then only when more conservative treat- ments have failed or when examination indicates the condition is such that ordinary routine methods or a com- bination of them will not effect relief. In most cases of dystocia one or more combinations of the major obstet- rical operations are performed. The plan of operation should be carefully made with alternatives in case one procedure is not successful. If assistance or consultation is needed it should be obtained as soon as possible. In performing obstetrical operations on large animals it is necessary for the veterinarian to conserve his strength by working with both arms and by using lay assistance whenever possible. If the fetal membranes interfere with the obstetrical operations the offending portions of the membranes should be removed manually. The obstetri- cal operations may be divided into four major classifi- cations: mutation, forced extraction, fetotomy and ce- sarean section. Laparohysterectomy is only performed in occasional instances in the bitch or queen. For excellent illustrations of various mutation and fetotomy techniques the student is referred to the following reviews.-"-’393 Sloss42 reported the incidence of bovine dystocia on 1600 properties involving 126,790 Australian dairy and beef cows as recorded by 13 country veterinary practices and the results of different methods of handling the 2480 dystocias. Mutation and forced extraction were most commonly employed in dairy cattle and comprised 77.8 percent of the cases of dystocia. While fetotomy and ce- sarean section were more commonly used in beef cattle and comprised 16.6 percent and 4.7 percent, respec- tively, of the total number of dystocias. These figures were nearly similar to those cited by other authors. The maternal death rate was 6 percent with a rate of 3.1 per- cent in operations involving mutation and traction, 16.6 percent after fetotomy and 17.9 percent after cesarean section. Thirty two percent of the dystocias in dairy cat- tle were in heifers while 70.6 percent in beef cattle were in heifers. Mutation Mutation is defined as those operations by which a fetus is returned to a normal presentation, position, and posture by repulsion, rotation, version, and adjustment or extension of the extremities. Normal birth will pro- ceed in uniparous animals only with the fetus in anterior or posterior longitudinal presentation, dorso-sacral po- sition, with the head, neck and limbs extended. Most multipara can have a normal birth with the fetal limbs folded alongside of or beneath the body, since the limbs are small and flexible. In multipara, fetuses may be in a dorso-ilial or dorso-pubic position and be bom without difficulty. In unipara only premature or very small fe- tuses may pass through the pelvis in dorso-ilial or dorso- pubic position or with a flexed limb or limbs. In ewes, the fetus may often be bom without assistance in anterior presentation with one forelimb retained beneath the body. After the veterinarian has brought each part of the fetus into its normal posture, the cause of dystocia is usually relieved and the fetus will be expelled normally, or par- turition aided or completed by traction. Repulsion, sometimes called retropulsion, consists of pushing the fetus out of the maternal pelvis or birth canal into the abdominal cavity and uterus, where space is available for the correction of the position or posture of the fetus and its extremities. In nearly all cases in which expulsion is used, epidural anesthesia is indicated since repulsion frequently produces violent straining on the part of the animal. When repulsion is used, the portion of the fetus engaged in the pelvis is pushed cranially. Because the fetus and uterus are in the form of an arc in the cow, the opposite end of the fetus may be pushed somewhat nearer the pelvis. Repulsion is usually necessary because the birth canal or pelvic cavity is so narrow and so con- fining that it is impossible to correct deviations in po- 298OBSTETRICAL OPERATIONS 299 sition or posture without providing more room in which to manipulate the fetus or its long extremities. Besides its common use for repelling a portion of the fetus out of the pelvis, repulsion may also be used to force a por- tion of the fetus—usually the proximal portion of an ex- tremity and the part of the body to which it is attached— cranially, dorsally, ventrally, or laterally in the uterine and abdominal cavity so that sufficient room is provided to extend the flexed extremity with facility. Repulsion may be accomplished by the operator’s arm, the arm of an assistant, or by a crutch repeller. If the latter instrument is used it should be guarded by having the operator’s hand on the crutch part of the repeller as force is applied, so that slipping of the crutch and pos- sible uterine laceration or rupture is avoided. In anterior presentation the crutch or hand of the operator is usually placed on the fetus between the shoulder and chest or across the chest beneath the neck. In posterior presen- tation it is placed in the perineal region over the ischial arch. Epidural anesthesia is of great value especially in large animals, because the fetus after being repelled is not immediately forced back into the pelvis by straining, and therefore it is easier for the operator to correct the abnormal posture or position. If the crutch repeller is used and left in place the person applying the outside force should be properly braced and balanced so if the crutch slips or becomes displaced it will not be forced cranially, possibly through the uterine wall. If it slips it should immediately be withdrawn or replaced. It is somewhat safer to use an assistant and under the oper- ator’s direction have him repel the fetus with one arm while the operator’s arm corrects the abnormal posture. The only disadvantage to this method is that in heifers with a small birth canal, room for two arms is restricted. In ewes, does, and sows, repulsion is performed by the arm and hand, or by the finger in bitches and queens. Having the animal standing or with its rear parts el- evated if it is recumbent, is essential to make room avail- able for repulsion. Repulsion is difficult or impossible in the recumbent animal resting on its sternum, as the abdominal viscera are forcing the fetus back toward the pelvis. If the animal is recumbent it should be laid on its side with its four legs extended. In ruminants the dam should be resting on the left side so the weight of the rumen does not press on the fetus and uterus. Excessive repulsion may be dangerous, especially in cases in which dystocia has existed for some time, because the uterine wall is often tightly contracted around the fetus. The uterine cavity thus nearly ceases to exist, and hence rup- ture of the uterus is liable to occur. In other countries uterine relaxants and spasmolytic drugs have been ad- vocated and used.- These have not been available for use in the U.S. In cases of neglected dystocia or of emphy- sema of the fetus, the repulsive force should be carefully controlled. Frequently satisfactory repulsion is impos- sible and this is the reason why the handling of pro- longed dystocia cases is difficult and the prognosis is guarded to poor. In large animals, early diagnosis of mi- nor abnormalities causing dystocia may preclude the need for epidural anesthesia and with the animal standing the fetus can be repelled and its posture or position corrected between abdominal contractions. Rotation is the turning of the fetus on its long axis to bring the fetus into a dorso-sacral position. This position is necessary in all but very small fetuses in uniparous animals and is the usual presenting position even in mul- tiparous animals. In the latter species an abnormal po- sition of the fetus seldom causes dystocia due to the small size of the fetus compared with the size of the pelvic cavity or inlet. In the cow the presence of the fetus in a dorso-ilial or dorso-pubic position frequently is accom- panied by a 90- to 180-degree torsion of the uterus.56 In 90-degree torsion of the uterus twisting of the birth canal is often not noticeable. It seems very unlikely that an 180-degree torsion with its accompanying marked twist- ing of the birth canal would go unnoticed by an expe- rienced veterinarian. In the dorso-pubic position of the fetus in the cow, a rectal examination and examination of the relation of the broad ligaments and the uterine arteries to the uterus, would reveal whether torsion of the uterus existed and indicate the direction for rotating the fetus in correcting the twisted uterus. In the mare and multiparous animals in which the fetus lies in the uterus in a dorso-pubic or dorso-ilial position during pregnancy with the navel cord extending laterally or dor- sally toward the uterine attachment of the broad ligament and uterine wall, the fetus must rotate 90 to 180 degrees before entering the pelvic inlet in a dorso-sacral position. If rotation is not complete by the second stage of par- turition, dystocia may result. In multiparous animals with the fetus in a dorso-pubic position the nose of the fetus may catch on the pelvic brim in anterior presentation, or the buttocks may catch on the brim of the pelvis in pos- terior presentation. These positions and postures are common causes for dystocia in dogs.25 To relieve dystocia in unipara by rotation of the body of the fetus, it should be repelled cranially out of the pelvic cavity. If this cannot be done, due to the con- tracting uterus, it indicates that the dystocia has existed long enough to also result in a dry mucous membrane of the birth canal. In this case much careful lubrication of the birth canal and fetus is necessary to make rotation of the fetus within the confining structures possible and easier without injuring the uterine or vaginal walls. In300 VETERINARY OBSTETRICS dorso-ilial positions repulsion is often not necessary but may be helpful. Lubrication of the fetus and birth canal, caudal and downward traction on the extremities, and rotation of the fetus with the operator’s arm in the birth canal, readily corrects this mild abnormal position. After the body of the fetus in anterior presentation, dorso-pu- bic position, is repelled out of the pelvis, leaving the fetal limbs in the pelvic cavity, chains are fastened to the fetlocks and cross-traction is applied by two assis- tants. Depending upon which way the fetus is to be ro- tated one leg is initially pulled upwards, then horizon- tally to the left or right and then downwards while the other leg is being pulled underneath the first leg down- ward and obliquely to the right or left. This type of trac- tion causes a rotation of the body of the fetus that is aided by the operator placing his arm and hand under the withers or body of the fetus and elevating it to the level of the pelvic brim, using the pelvis as a fulcrum, and then pushing the fetus obliquely to either the left or right. , To prevent the hip-lock condition in anterior or pos- terior presentation Ball3,398 recommended rotation of the fetus so that the fetal hips engaged the maternal pelvis in an oblique manner to take advantage of the widest pelvic diameter. (See Figure 1.) This could be accom- plished by applying moderate traction to the fetus and inserting the arm between the fetal legs, and over the neck in anterior, and between the rear legs in posterior presentation, and rotating the fetal body and pelvis the desired angle. The fetus is withdrawn by caudal and lat- eral traction, first one hip and then the other, through the pelvic girdle of the dam. In occasional prolonged cases of dystocia in anterior presentation, the head and neck may be an obstacle to rotation and have to be amputated before rotation can be accomplished. In posterior presentation the fetus is ro- tated in a like manner, with the operator’s hand and arm under the buttocks. This method of cross-traction is su- perior to placing traction directly backward on one limb and twisting the opposite limb around the fulcrum thus established. This latter technique causes the fetus to be- come impacted in the maternal pelvis and thus resist ro- tation, and a great strain is placed on the joints and lig- aments of the leg that is twisted around the one to which traction is being applied. In the former techniques im- paction of the fetus in the pelvis is reduced to a mini- mum, and elevating the body of the fetus makes correc- tion of the abnormal position rapid and easy. If correction of the position is difficult in one direction, torsion may be present, and the direction of traction may be increas- ing the degree of torsion. If this is the case, the fetus should be rotated in the opposite direction. In mild cases diagnosed early in parturition or where the fetus is small, the fetlock protruding from the vulva may be flexed and used as a means of exerting a moderate twisting action on the leg to assist rotating the fetus. In a few cases, rotation may require the use of the detorsion rod or Cammerer’s fork as described under tor- sion of the uterus. In these cases the rod is fastened to the two limbs after lubrication of the fetus and the birth canal and by repulsion and rotation the position is cor- rected. In ewes and sows the hand and in bitches and queens the finger applied to or alongside the chest or buttocks after lubrication will usually repel and then ro- tate the fetus into a normal dorso-sacral position. In these smaller animals forceps may also be used with care to rotate the fetus. Version is the rotation of the fetus on its transverse axis into an anterior or posterior presentation. This is done most often in the mare in transverse ventral presen- tation and in rare cases in the cow, ewe, doe and bitch in transverse presentation. Transverse presentation in the mare occurred about 1 in 1000 pregnancies.44 Version is usually limited to 90°. By repulsion on the cranial or caudal end of the fetus and traction on the other end, the transverse presentation is changed to a longitudinal pre- sentation. If possible the fetus should be turned into a posterior longitudinal presentation, as that prevents the head and neck from complicating the correction of the abnormal presentation or posture. In the mare partial fe- totomy is often indicated before version is attempted in transverse ventral presentation. Often version is only through a relatively small arc if the fetus is lying obliquely rather than in a true transverse presentation. In the tu- bular type of uteri in domestic animals, version through a 180° arc such as from posterior to anterior presentation is rarely possible and should not be attempted. Extension and Adjustment of the Extremities is the correction of abnormal postures usually due to flexion of one or more of the extremities causing dystocia. Flex- ion of the head and neck causes dystocia in all species. Flexion of the limbs usually results in dystocia in uni- parous animals but only rarely in multiparous animals. Corrective procedures are difficult and often impossible within the confines of the pelvic cavity. The fetus must usually be repelled out of the pelvis into the larger uter- ine and abdominal cavities to have sufficient room for the correction of abnormal postures. This is particularly true in the large uniparous animals, in which the fetal extremities are long. Many of these abnormal postures may be caused by the distal portion of the fetal extremity being caught on the pelvic brim, and are aggravated when the body of the fetus passes over this extremity, thereby resulting in greater flexion of the extremity and even its extension beneath the body. The act of repulsion of the fetus cranially into the uterine and abdominal cavitiesOBSTETRICAL OPERATIONS 301 tends to correct the deviated extremity or abnormal pos- ture. Three basic mechanical principles are necessary to effect a prompt, easy correction of a flexed extremity (see Figure 88). (1) Repulsion of the Proximal Portion of the Ex- tremity such as the shoulder or chest is performed in anterior presentation in the correction of a flexed fetlock, carpus, elbow, or shoulder joints with the forelimb ex- tended beneath the body; or the head and neck flexed alongside, beneath or over the body of the fetus. In pos- terior presentation repulsion is performed on the but- tocks, stifle, or tarsus when the hind limbs are flexed at the stifle, tarsus, fetlock, or hip. In the latter condition the legs extend beneath the fetus, a breech presentation. (2) Lateral Rotation of the Middle Portion of the Extremity, Carpus, Tarsus, or Neck—Lateral rotation and repulsion of the flexed tarsus, carpus or neck into the cranial and lateral flank region provides adequate room in most cases for the medial extension of the fetlock or nose into the pelvic cavity. In small equine or bovine fetuses, if the operator firmly grasps the metacarpus or metatarsus, he can with the same motion perform both repulsion and lateral rotation as well as extension of the fetlock into the pelvic cavity. In larger fetuses the op- erator may require a crutch repeller, or even better an assistant’s arm, to force the tarsus or carpus laterally and cranially while the operator brings the fetlock medially and caudally into the pelvic cavity. This latter procedure allows the operator to cup or flex the pastern in his hand so that as the limb is extended the hoof of the fetus will not catch, tear, or lacerate the wall of the birth canal as the foot is drawn into the pelvic cavity. (3) Traction on the Distal Portion of the Extremity such as the pastern, the lower jaw or, until these distal structures can be reached, the structures between the body and the distal portions of the extremity, is applied to ex- tend the limbs or head and neck. This traction may be applied by the hands and arm, a chain, Krey’s tongs or a snare. When the fetus is in breech presentation with the legs extended beneath the body, the fetus is repelled cranially out of the pelvic cavity and into the right or left flank. The hand and arm is slid down the tibia on the opposite leg and by traction the leg is pulled into a hock-flexed posture and then handled as described. In cases in which the head and neck are deviated alongside the anteriorly presented fetal body the fetus is repelled cranially and laterally into the flank of the cow on the side opposite to the head so that as much space as pos- sible is provided in the other flank to allow correction of the deviated head and neck. By traction with the fin- gers in the orbits, around the lower jaw, in the angle of the mouth, by a snare around the lower jaw or small hooks in the orbits, the head can usually be pulled lat- erally back to the pelvic inlet without twisting the neck. The head is then returned to its normal posture by man- ual traction, elevation or rotation of the head, and lateral repulsion on the neck. During these procedures the muz- zle of the fetus should be guarded to make sure the lower incisor teeth do not lacerate the uterus, or the lower jaw catch on the pelvic brim of the dam, especially if the type of traction applied causes the mouth to gape. When the dam is recumbent the deviated fetal head should be located in the upper flank before mutation procedures begin. Otherwise the weight of the fetal body resting on the head and neck would make correction nearly impos- sible. The combined use of these three mechanical principles will relieve almost all abnormal postures. In rare cases, in order to obtain more room in which to perform these maneuvers when the uterus is contracted tightly around the fetus, a partial fetotomy may be necessary, such as amputation of a forelimb. In multipara, mutation of the fetus is not generally required except in deviation of the head and neck in anterior presentation, impaction of a large fetus in the pelvis in breech presentation or in dorso- pubic position when the nose or buttocks of the fetus may catch on the pelvic brim of the dam as the fetus enters the pelvis. By using the finger in the vagina and manipulating the canine or feline fetus through the ab- dominal wall and floor with the opposite hand these ab- normal postures may usually be corrected. Occasionally forceps or snares may be indicated. In a few cases dys- tocia in cattle is observed due to the impingement of the elevated tail on the dorsal border of the pelvic inlet in posterior presentation. Repulsion of the fetus, holding the tail against the perineum and applying traction to the rear limbs corrects the dystocia. Kuhn’s crutch was very useful in various mutation operations in the mare and cow.- Although the theoretical uses of the instrument are many, it has not proved useful in the author’s practice. Mutation of the fetus must be performed carefully, cautiously, and in a gentle manner in all animals. These manipulations can take place only at the level of or just below the pelvic brim. The earlier the dystocia is diag- nosed, the easier is mutation of the fetus accomplished; conversely, the longer aid is withheld or delayed, the more difficult or impossible it is for mutation to be suc- cessful. This is true, but to a lesser extent, in the other major obstetrical operations. Forced Extraction Forced extraction is defined as the withdrawal of the fetus from the dam through the birth canal by means of the application of outside force or traction. Traction should302 VETERINARY OBSTETRICS Figure 88. Procedures followed in mutation of deviated fetal extremities: A. Laterial view of a breech presentation of a bovine fetus. B. By repulsion on the buttocks and traction on the tibia the leg is drawn into a hock-flexed posture. C, D and E. caudal and lateral views show how, by upward repulsion and lateral rotation on the hock and medial and caudal traction on the fetlock and pastern, the leg is extended into the pelvis.OBSTETRICAL OPERATIONS 303 be applied only when the abdominal muscles of the dam are contracting and pulling the pubis cranially to provide the greatest pelvic diameters for the passage of the fetus. If traction on the fetus is applied when the abdominal muscles are relaxed the pelvic floor is pulled caudally reducing the size of the pelvic opening.3,398 This inter- mittent traction may prevent asphyxiation of the fetus if he should be breathing and it is also less stressful for both the fetus and the dam. Since the widest diameter of the bovine fetal pelvis is between the greater tro- chanters and the widest portion of the maternal bony pel- vic inlet is the dorso-pubic, not the bisiliac, diameter (See Figure 1), this information is used to assist with- drawal of a large fetus through the birth canal by rotating the fetus so the greatest diameters of the fetal and ma- ternal pelvis coincide.398 Manner and Dangers of the Application of Trac- tion Instruments to the Fetus—In anterior presentation obstetrical chains may be applied to the pasterns or above the knee or elbow. If the fetal membranes prevent the prompt application of the chains or snares they should be broken, ripped away, or pushed to one side. The chain should be tightly fastened around the pastern before ap- plying traction or it may slip down over the coronary band of the hoof and when traction is applied the hoof may be pulled off. Applying the chains above the fetlock may be satisfactory in almost all cases but in rare cases excessive traction and tightening of the chain over the epiphysis or “break joint” may fracture the leg. For these reasons many veterinarians place the noose of the ob- stetrical chain above the fetlock and place a half-hitch around the pastern. This prevents the chain from sliding down over the coronary band and distributes the force over the two sites. Some place the large terminal link in the obstetrical chain ventral to the pastern and pass the chain between the claws of the bovine fetus. This raises and extends the toe and may avoid its catching on the brim of the pelvis. In anterior presentation a snare may be applied around the lower jaw and tightened firmly so that with traction it will not slip and fracture the dental plate. Obstetrical chains around the lower jaw will not tighten sufficiently, and generally slip off, often damaging the incisor teeth. Excessive traction on the jaw should be avoided, as the jaw bones are not strong and fracture may occur. Mod- erate traction applied by one man is all that can safely be used on the lower jaw of a bovine fetus. A loop of obstetrical chain around the neck behind the head is used occasionally for traction when the fetus is dead; but the head and muzzle must be directed with the hand so that they will not become deviated. This technique is dan- gerous to a live fetus as it may cause injury to the spinal cord and vertebrae in the occipital region. A loop of ob- stetrical chain is more commonly used around the poll, under the ears and through the mouth in the manner of a “war bridle” for applying traction to the head. This causes the mouth to gape when traction is applied; the operator should therefore watch for this and protect him- self and the birth canal from injury by the sharp incisor teeth. Pinching the large link in the end of the obstetrical chain noose in a vise in such a manner that it catches on the chain, thus preventing the chain noose from tight- ening when traction is applied has been recommended.54 A commercial head snare is available that also over- comes gaping of the mouth. By the use of blunt or knobbed Krey’s hooks or short obstetrical hooks on a loop or cord in the orbits, traction may be applied to the head.- - This technique is safe unless excessive traction causes fracture of the facial bones. A technique in which an incision is made in the floor of the mouth anterior to the tongue, extending through the skin between the man- dibles has been described. A loop of obstetrical chain is then passed over the lower jaw, behind this incision, and the opposite end of the chain is passed through the in- cision and tightened.56 This provides a firm, solid hold on the lower jaw that will not slip and by means of which a large amount of traction may be applied. It is used most satisfactorily in dead fetuses, but even in live fe- tuses the wound heals quite rapidly after birth. The long or short blunt hook placed between the rami of the man- dibles is not satisfactory because it frequently slips, or with moderate traction may cause a separation of the symphysis of the mandible. In a dead fetus the long blunt hook may be passed through the mouth into the pharynx, turned dorsally, and then traction may be applied fixing the hook in bones dorsal to the pharynx. The long blunt hook may be used to advantage in the hiplock condition in anterior presentation. The hook is passed over the top of the fetal croup and turned ven- trally to engage the posterior border of the ischium or sacrosciatic ligament. In this position much traction may be applied. By raising the fetal pelvis and pulling the fetal hips at an oblique angle through the maternal pel- vis, the veterinarian can often relieve the dystocia. In ewes, does and sows the obstetrical chains are too large to be of value. In anterior presentation snares or forceps are applied to the ovine or porcine fetal head, around the neck, or to the forelegs. In small sheep and swine, in which the hand cannot be passed through the pelvis into the uterus, forceps of various types, as well as obstetrical snares, may be used to advantage.35 When- ever forceps, snares or chains are applied, the wall of the genital tract should be examined before traction is applied, to make sure it is not caught. In bitches and304 VETERINARY OBSTETRICS queens forceps may be applied to the head of the fetus after the head is repelled out of the pelvis into the uterus; but great care should be used to prevent tearing an ear or lacerating the skin, fracturing the mandible, or crush- ing the skull. Excessive traction or twisting of the head should be avoided, since injury or dislocation of the ver- tebrae may occur in the occipital region in these small species. Forced extraction in multipara is limited to those fetuses which have entered the uterine body or pelvis. Snares of gauze may be used on the limbs of canine fe- tuses. The use of forceps in dystocia in dogs has been described.14,25 In posterior presentation in large animals traction may be applied to the fetal pastern or above the hock by the use of obstetrical chains. The same danger exists as in the anterior presentation whereby excessive traction with chains fastened above the fetlocks or that slide down over the coronary band of the hoof, may cause fracture above the fetlock or removal of the hoof. In ewes and sows, snares may be fastened around the hind legs of the fetus. In bitches and queens snares or gauze around the hind legs or grasping the hocks with sponge forceps will assist traction. If forceps are used in multipara they should be fastened securely around or across the fetal pelvis, after the fetal hips have been repelled out of the maternal pel- vis. In bitches, forceps are generally preferred to apply- ing excessive traction to the hind legs with the accom- panying possible danger of dislocating the fetal hips. Excessive twisting of the fetal pelvis by the means of forceps may injure the lumbo-sacral articulation; or if the fetus is emphysematous excessive traction may pull it apart. Dislocation of the first cervical joint may occur in posterior presentation in the bitch when the occiput be- comes impacted in the pelvis and traction is continued. In this instance abdominal pressure by the operator’s hand will raise the chin of the fetus and help force the fetal head through the pelvis. Technique of Withdrawing Fetus Through the Ma- ternal Birth Canal—In anterior presentation of the fe- tus in uniparous animals, traction should be applied at three points, the two legs and the head. After the limbs followed by the head have passed through the vulva, traction may be applied to the legs only. At the begin- ning of labor the main portion of the fetus is below the level of the brim of the pelvis. Traction when applied in either anterior or posterior presentation should be dor- sally and caudally to lift the fetus up and over the brim of the pelvis into the birth canal. At this stage, with the fetal extremities approaching the vulva, the direction of traction should at first be caudal and slightly dorsal; and as the fetal legs and head engage in the vulva the direc- tion of traction should be obliquely ventral. After the head in anterior presentation or the hips in posterior pre- sentation pass through the vulva, the direction of traction should be more and more ventral until when the back of the fetus is passing through the vulva the direction of traction is perpendicular to the spinal axis of the dam or parallel to her hind legs. Thus the direction of traction and that of the fetus as it passes through the birth canal is in the form of an arc. The ventral structures of the fetus are relaxed and concave, and the dorsal structures of the fetus are stretched and convex. This arc-like ap- plication of traction results in the fetus assuming the physiologic curved shape that facilitates its removal through the birth canal; by producing the smallest pos- sible diameters of the fetal body stalling of the fetal pel- vis, or the hiplock condition, is prevented. By applying traction to the legs, head, and spine the abdominal wall of the fetus is relaxed and the fetal pelvis is forced back- ward and upward reducing its sacro-pubic diameter and causing it to pass through the greatest diameter of the maternal pelvis. If traction is applied in a straight caudal direction and not in the form of an arc, both the linea alba as well as the spine are stretched, and the fetal pel- vis is pulled ventrally and cranially thus increasing its sacro-pubic diameter and predisposing to hiplock. As described previously the rotation of the fetus in the birth canal into the dorsoilial position to cause the fetal pelvis to enter the maternal pelvis at an oblique angle corre- sponding to the greatest diameter of the maternal pelvis combined with lateral traction often prevents the hiplock condition.3,39a After the fetal hips have been withdrawn through the maternal inlet in an oblique or dorso-ilial position, the fetus should be rotated back to a dorso- sacral position before further traction is applied. When the head enters the vulva, if traction is applied dorsally or caudally instead of ventrally the fetal head jams against the dorsal commissure of the vulva and may cause severe stretching or laceration. At this point it is important to place ventral traction on the head. When the vulva is small, especially in primiparous cattle, ven- tral traction on the head alone together with insertion of the hands over the top of the head; stretching of the vulva with the wrists, arms or hands; and ventral and caudal traction with the hands over the occiput or with the fin- gers in the medial canthus of the orbit helps to pass the head through the vulva and prevent lacerations. Often, if this process is prolonged, lubrication of the head and vulva is helpful. Pushing or pulling cranially on the vulva if the vulva is tight while traction is applied on the fetal head will further aid dilation. When abdominal contractions in the dam occur during parturition the linea alba pulls the pubis forward, in- creasing the pelvic diameters. When strong traction isOBSTETRICAL OPERATIONS 305 applied to the fetus and the pelvic ligaments are relaxed the maternal pubis is pulled caudally and the pelvic di- ameters are lessened. A rope or breeching around the buttocks of the cow in lateral recumbency fastened se- curely to the manger so that when traction is applied to the fetus the maternal pubis is pulled forward by this rope or breeching was recommended.56 The metal breech device used with fetal extractors provides this same ad- vantage. Preventing the maternal pubis from extending caudally, and applying ventral traction on the fetus, will usually prevent impaction of the fetal hips in the mater- nal pelvis. Improper traction such as that produced by a block and tackle pulling directly caudally will in many instances cause severe impaction of the fetus in the ma- ternal pelvis. When traction is applied the operator should con- stantly watch, examine, and direct the progress of the fetus by instructing his assistants when to apply traction, when it should cease, and in what direction it should be applied. If the progress of the fetus through the birth canal should cease, traction should be discontinued and the fetus and the birth canal should be carefully exam- ined to determine the cause of the obstruction. This should be overcome or corrected before exerting further trac- tion. The operator should conserve his strength and di- rect the operation and not join his assistants in applying traction except when necessary. If the patient is strain- ing, traction should be applied principally during ex- pulsive efforts. This both aids the withdrawal of the fetus and to some extent prevents the fetus dragging portions of the uterus and vagina along with it, thereby causing possible rupture or prolapse of the uterus. Traction should be applied in a steady, even manner. Jerky, irregular ef- forts at traction are ineffectual, painful and dangerous to both the fetus and dam. In most instances traction should not be applied in a hasty manner. To avoid lacerations or ruptures of the soft structures of the birth canal time should be allowed for dilation of the birth canal as the fetus advances. This frequently requires 30 minutes or longer in heifers. The same general technique of remov- ing fetuses by traction in ewes, sows, does, bitches and queens is followed with traction caudally and then down- ward as the fetus passes through the vulva. In the bitch and queen pressure of the operator’s hand upward through the abdominal wall will help the passage of the fetus into the pelvis and through the birth canal. In uniparous animals traction may be greatly facili- tated by lubrication if the fetus and birth canal are dry. Traction on one extremity at a time in an alternate man- ner is also of assistance in withdrawing a fetus. This is especially true in posterior presentation, in which trac- tion should be applied to one limb at a time so that the fetal pelvis is pulled through the maternal pelvis in an oblique manner, thus reducing the possibility of hiplock. Even in anterior presentation, after the forelimbs and head have passed through the vulva, pulling the bovine fetus laterally and ventrally around the dam’s hips first to one side and then to the other may aid in withdrawal of the fetus and produce an oblique angle to the fetal pelvis, so that one greater trochanter will slip through the ma- ternal pelvic inlet and then the other will follow, pre- venting or reducing the chances of hiplock or impaction. As traction is applied, rotating of the fetal body from side to side may aid withdrawal of the fetus. Indications for Forced Extraction of the Fetus— Forced extraction is indicated when uterine inertia is present and the fetus does not engage in the birth canal and stimulate straining. It is indicated when epidural anesthesia has been administered and after mutation has corrected the cause for dystocia. Forced extraction is used most often when the fetus is relatively too large to be expelled through the birth canal without assistance, fe- topelvic disproportion, and when traction offers greater prospect of success than a fetotomy or cesarean. It is used in many cases in primipara with a small birth canal, as a means of withdrawing the fetus and dilating the canal. It may also be used when the birth canal is compressed by tumors or fat or other pathological conditions. It may be indicated in posterior presentation of the fetus to has- ten delivery and prevent the death of the fetus when the umbilical cord is compressed between the fetal abdom- inal wall and the brim of the pelvis. Within 5 to 10 min- utes after the umbilical circulation is cut off the fetus may die if its cranial extremities remain in the uterus and it cannot breathe. Hasty application of forced extraction may occasionally be indicated in mares with dystocia in which the cause for the dystocia has been corrected and the fetus is still alive. Thus it may effect removal of the fetus before separation of the placenta and death of the fetus occur. Forced extraction may occasionally be used to save time or in order to avoid fetotomy or cesarean section where working conditions are extremely poor. It is indicated in dystocia due to emphysematous fetuses after thoroughly lubricating the birth canal and fetus to avoid fetotomy or a cesarean, which are more hazardous to the dam than is forced extraction under such condi- tions. In many fetotomy operations, forced extraction is used as an aid. Forced extraction by forceps or snares in the multi- parous animals, sow, bitch, and queen, should not be used when one is short of time or patience as it may require a number of hours of intermittent work to com- plete the delivery of all the fetuses. It is, however, in- dicated when the owner is not interested in saving the306 VETERINARY OBSTETRICS fetuses; when only one or two fetuses are present and secondary uterine inertia has set in; when the fetuses are dead and emphysematous; and when in the opinion of the operator the delivery of one fetus will result in the unaided delivery of the rest of the litter. The veterinarian may even decide to use forceps and forced extraction in cases of primary inertia where the litter is small. Young primiparous bitches may force the fetal head through the pelvis and then rest. This pup becomes cyanotic and must be delivered immediately. Since the vulva is small and tight it is necessary to force the pup’s head through by means of outside pressure on the vulvar lips. Then by applying manual traction on the head and placing a fin- ger under the pup’s chest, the pup can be eased through the vulva.25 To prevent the fingers from slipping, a gauze pad may be used. Forced extraction should be limited strictly to cases in which the presentation, position and posture of the fetus are normal and in which, in the opinion of the operator, forced extraction is in the best interests of the fetus, the dam and the owner. Forced extraction is contraindicated or should only be undertaken with great care when ab- normal presentation, position or postures are present, when the fetus is excessively large or defective, when the birth canal is obviously small, when the animal is affected with obturator paralysis, when the birth canal has been severely lacerated, when secondary uterine inertia is present with the uterine walls strongly contracted around the fetus, and when the cervix is stenotic or has failed to dilate. In these latter conditions uterine relaxants and spasmolytic drugs might be recommended.- However, these products for use in dystocia in animals in the U.S.A. are not currently available. The Amount of Traction to Apply in Forced Ex- traction of the Fetus will vary greatly with the species of animal and the condition causing the dystocia. Al- though forced extraction appears simple and quick it is potentially dangerous to the fetus and to the dam. In the dam, excessive traction or traction in an improper man- ner or with the fetus in an abnormal presentation, po- sition, and posture may result in trauma, laceration, rup- ture to the soft structures of the birth canal or uterus or wedging of the fetus in the dam’s pelvis. It may predis- pose to prolapse of the uterus, or result in trauma to the obturator or gluteal nerves. However it is remarkable how seldom paralysis occurs even when excessive traction has been applied. In the mare, abdominal contractions are so violent that if the fetus is in the proper presentation, position and posture, forced extraction is seldom necessary. Aid with obstetrical chains by one or two men may help dilate the birth canal and vulva gradually in old or young primi- parous mares. Care should be exercised to avoid lacer- ating the vulva or the perineal region. If the mare is re- cumbent and much traction is applied, she will usually get to her feet. If the cow is standing and strong traction is applied to the fetus, the cow will usually fall and may injure itself or the attendants. In the cow, as in the mare, traction under certain circumstances should be moderate and intermittent; for example, if the fetus is alive and the cow already exhibits some obturator paralysis due to a hiplock condition. In normal circumstances the force of 2 to 3 men apparently causes no harm and may be indicated. The introduction of the fetal extractor with which one can exert great force in the proper manner, if necessary, has been received enthusiastically by many veterinarians because often sufficient manpower is not available and the block and tackle or wire stretchers pre- viously used applied traction in only one direction and in an improper manner, that is, directly caudally. Since excessive power can easily be applied by the fetal ex- tractor, judgment, caution, and care must be exercised in its use. Where great amounts of traction are used, epidural analgesia is strongly recommended to avoid ex- cessive pain in the dam. The amount of traction to be applied will vary from case to case and with the judg- ment of the veterinarian. Following forced extraction of large fetuses of beef cattle including Charolais, Charo- lais-cross and Simmental-cross calves, both hard and soft tissue injuries have been reported.173,30 The hard tissue injuries include; fractures of the proximal end of the fe- mur and slipped capital femoral epiphysis,173 fractures of the ribs, costo-chondral junctions, lumbar vertebrae and metacarpal or metatarsal bones. The soft tissue injuries include: femoral nerve paralysis and quadriceps femoris muscle damage and atrophy due to hyperextension of the femur.43 The author has observed that the above injuries to the newborn are much more common with the recent increased breeding of the exotic beef crossbreds and the introduction of the fetal extractor often employed by farmers or ranchers to relieve dystocia. Traction if prop- erly applied seldom results in injury to the fetus or to the genital tract of the mare and cow. However, to quote Williams,56 “Application of great force in improper po- sition, presentation or posture of the fetus is constantly to be condemned.” The use of a tractor or horses to ap- ply traction to the fetus, or tying the fetus to a tree and driving the parturient mare away, are definite examples of malpractice if performed by a veterinarian. In the ewe, doe and sow the same principles in regard to the degree of traction may be applied. In all cases, however, the force exerted by one man is sufficient for the relief of dystocia in these species. In the ewe and doe, before applying traction one should make certainOBSTETRICAL OPERATIONS 307 the snare is attached to one, not two, fetuses. In bitches and queens traction should be applied carefully and never excessively. Twisting of the fetus should be avoided. Occasionally in emphysematous fetuses traction may pull the fetus apart. In these small species traction should be used with care, especially if secondary uterine inertia has set in, to avoid laceration of the uterus or birth canal at the pelvic brim. This will result in herniation of the vis- cera through the birth canal or discharge of the fetuses into the abdominal cavity. Fetotomy Fetotomy is defined as those operations performed on the fetus for the purpose of reducing its size by either its division or the removal of certain of its parts. In most cases these operations are performed within the uterus of the dam. Partial fetotomy is most commonly per- formed. Total fetotomy is performed infrequently. In fe- totomy the life of the fetus is sacrificed if it is not already dead as is usually the case. In Germany attention has been paid to humane methods of killing the fetus, before fetotomy is begun.4 These authors indicate the fetal re- flexes and threshold for pain are of a very low order. For this reason incising the carotid artery or rupturing the umbilical cord before fetotomy is not necessary. The injection of a rapid-acting drug to produce euthanasia or an anesthetic state in the fetus has not been investigated but any such agent might well be transferred by the pla- centa to the dam. If the fetus is dead and the birth canal is not reduced in size, fetotomy should be given primary considera- tion.59 The advantages of fetotomy are: It reduces the size of the fetus. It avoids a cesarean operation. It re- quires little assistance. It will prevent possible trauma or injury to the dam through the use of excessive trac- tion.---59 The disadvantages of fetotomy are: It may be dan- gerous, causing injuries or lacerations to the uterus or birth canal by instruments or sharp edges of bone. It may take a long time, exhausting both the dam and the op- erator and is conducive to trauma and pressure necrosis of the birth canal. It offers certain dangers to the veter- inarian by wounds from instruments, and if the fetus is emphysematous there is a possibility of infection of the skin of the operator’s arms. The advantages outweigh the disadvantages, however, and fetotomy in large animals is a practical and suc- cessful way of relieving dystocia. It is used, and rightly so, many more times than is cesarean section, which is more costly and time consuming, and requires more help and more aftercare than do most fetotomy operations. Cesarean section is indicated over fetotomy only if the fetus is alive and the owner desires that it be saved; or when total fetotomy under difficult conditions, such as a small narrow birth canal, would probably cause greater trauma to the dam, take longer, and be more fatiguing to both the dam and veterinarian than would cesarean section. If there is little prospect of a successful fetotomy operation and forced extraction is impossible, the owner should be advised to have a cesarean operation per- formed or to slaughter the dam. Since cesarean section is more difficult to perform successfully in the mare than in the other domestic an- imals, fetotomy or forced extraction are methods of choice in this species. Because the genital tract of the mare is more easily traumatized, and with more serious conse- quences than that of the cow, fetotomy should be per- formed carefully and gently. For more than a simply fe- totomy in the mare, a general anesthesia should probably be administered. The mare should be restrained in a suit- able location large enough for the operation to be per- formed with the mare lying on her side. Simple fetotomy techniques using a guarded obstetri- cal wire- may be performed in the ewe and doe if the hand can be passed through the pelvis into the uterus. By threading a loop of the obstetrical wire through a pipe of small diameter, portions of the fetus, such as the head and forelimbs, may be removed with safety to the dam. Fetotomies are not performed in the sow, bitch, and queen because cesarean section is easier and safer. In rare cases in the bitch the skull of the fetus may be crushed inten- tionally by means of forceps in order to permit removal by traction. Vandeplassche and his associates48,49,50 compared the results of 239 fetotomies and 150 cesarean operations in cattle and came to the conclusion that fetotomy was still the more important and practical of the two methods in bovine veterinary practice. In summarizing the data on these 239 cases it was found that in 3 to 5 percent of them fetotomy was impossible. Six percent of the cows died, 6 of them from septic metritis, 2 from malignant edema, 3 from necrotic vaginitis, 1 from a ruptured uterus, and 1 from hemorrhage. Thirteen percent of the cows had retained fetal membranes and 82 percent conceived within 10 months after the fetotomy operation. A more reent review of the literature reported on many hundreds of fetotomy and laparohysterotomy (Cesarean) opera- tions and indicated that both procedures have their place in veterinary obstetrics.59 The fetotomy operation may involve any portion of the fetal body and presents many variations and possi- bilities. It may be performed in any normal or abnormal308 VETERINARY OBSTETRICS presentation, position, or posture of the fetus. In many cases it is employed in relieving dystocia due to fetal monsters in which the usual anatomical arrangement of pails may not exist. The operational procedure must be decided upon for each case. Fetotomy operations should be planned and carried out carefully, so that there will be no wasted effort. Generally, by careful planning and by using mutation or forced extraction, only one feto- tomy operation, instead of two, may be necessary. It should be borne in mind that the aim of fetotomy is to reduce the size of the fetus so it may be removed from the birth canal. The veterinarian therefore should, de- pending upon the particular conditions and circum- stances, plan the operation and procedures using one or more of the standard fetotomy operations or their vari- ations. At the present time the fetatome is standard equipment for the practitioner working with large ani- mals; therefore many of the older techniques56 using in- struments such as the knife, chisel, and blunt-pointed cutting hook are not often used. These older techniques, using simple instruments, involved some operations which were difficult to perform, requiring patience, strength, and extreme effort, placing a severe strain on both the operator and the animal. Veterinarians who have become adept through practice may perform many obstetrical op- erations with the knife, chisel, and hook and seldom use the fetatome. The author has for many years been a staunch advocate of the fetatome primarily because it is easier and safer to use. Except for minor simple obstetri- cal operations, he prefers it to the older instruments and their accompanying techniques. Some of the simpler older techniques are still practical, however, and will be de- scribed. In dairy cattle practice in New York State 90 percent of the fetotomy operations performed include: bisecting the pelvis in anterior presentation, (hiplock) or in pos- terior presentation, (breech presentation), amputation of the head and neck, and decapitation. In some cases evis- ceration is used prior to bisecting the pelvis in anterior presentation. Presently many of the subcutaneous fetotomy tech- niques advocated by Williams and others56 are rapidly declining in popularity. The newer percutaneous tech- niques pioneered by the Utrecht clinicians with their modification of the fetatome are being rapidly accepted and utilized because of their ease and safety of appli- cation.-4,59 Fetotomy Operations in the Anterior Presentation Decapitation, or Amputation of the Protruding Head is indicated when one or both forelimbs are retained and the head has passed through the vulva and become swol- len, edematous, or emphysematous so that it cannot be repelled or can be repelled only with great difficulty. In such cases the fetus is usually dead, and amputation of its head allows the fetus to be repelled, so that the ab- normal posture of the forelimbs may readily be corrected by mutation, without the interference of the head. Decapitation is easily accomplished by fixing a snare on the lower jaw, or eye hooks in the orbits, and exerting traction in any direction desired by the operator. With a scalpel or sharp knife a transverse incision is made be- hind the jaw through the skin, muscles, pharynx, larynx and esophagus to the cervical vertebra. This incision is continued through the skin ventral to the ears and across the frontal bones. The skin over the head, including the ears, is separated from the underlying muscle and bone to the occipital region, where another transverse incision is made ventrally through the ligamentum nuchae and muscles to the cervical vertebra. The head is grasped firmly and twisted, rupturing the articular ligaments. The remaining soft tissues are cut and the head removed from the neck at the occipital atloid articulation. The flap of skin, including the ears, should be firmly secured by an obstetrical chain or snare which pulls the skin over the exposed cervical vertebra. A small incision in this flap of skin distal to the loop of obstetrical chain and through which the free end of the chain is drawn will secure the chain so it cannot slip off even if strong traction is ap- plied. The fetus is then repelled, and the abnormal pos- ture of the limbs corrected by mutation. Traction on the neck and two front legs usually results in relief of the dystocia. In making the incisions the operator must guard against the knife accidentally slipping and cutting the vulva. The fetatome could also be used in this operation, but the technique just described saves time as well as aftercare of equipment. Cephalotomy or craniotomy is indicated only rarely when fetal hydrocephalus or other cranial deformity is the cause for dystocia. Cephalotomy is accomplished by fixing the head with a snare around the lower jaw or chain attached to Krey’s tongs inserted in the orbits. In hydrocephalus sometimes simply incising the distended cranium causes a sufficient reduction in size to permit delivery. In most cases, how- ever, it is necessary to separate the enlarged cranium from the rest of the head by passing the wire of the fetatome around its base. With the fetal head fastened under ten- sion to the chain fixation plate on the handle of the Utrecht fetatome and its head against the base of the enlarged cranium it is readily severed. Then the collapsed cranial bones and skin may be removed. The rest of the fetus can be withdrawn unless this is prevented by ankylosisOBSTETRICAL OPERATIONS 309 of the joints, a common characteristic of the hydroce- phalic fetus. Amputation of the Head and Neck is indicated when the head and neck are retained alongside, beneath, or above the body of the fetus or when performing a com- plete fetotomy.- Correction of this abnormal posture by mutation may be impossible or extremely difficult or dangerous, due to such conditions as wry neck, a uterus contracted tightly around the fetus, or to a dry, emphy- sematous fetus. Amputation may possibly be indicated when, due to a juvenile or hypoplastic pelvis or to a large fetal head, there is not room in the birth canal for the simultaneous presence of the head and neck and the two limbs. If this condition is present, one should de- termine accurately the relative size of the fetus and the birth canal because, if after removal of the head and neck further operations such as a total fetotomy are necessary, cesarean section might be preferable. Amputation of the head and neck may be performed by the wire saw or fetatome. The latter is preferred be- cause if the operation is performed properly the neck is amputated close enough to the body so that traction of the forelimbs will pull the scapulas and shoulder joints over the exposed stump of the neck vertebrae. Occa- sionally in a large mare it may be necessary to remove the forelimb opposite the side to which the head and neck are flexed, and to apply traction to the fetus in order to enable the operator to reach the neck and pass the fe- tatome wire around it. With the aid of the fetatome wire guide or obstetrical chain the fetatome wire is threaded over the base of the flexed neck and drawn around it. The head of the fetatome is held forcibly between the shoulder joint and neck of the fetus and the neck is sev- ered as close to the body as possible. The neck and head are then withdrawn by means of the hand, a snare, or Krey’s hooks. Traction on the forelegs of the fetus will deliver the fetal body unless further operations must be performed. If the cervical stump is long, it must be guided with Krey’s tongs and guarded with the hand to prevent possible laceration of the birth canal as the fetus is with- drawn. Amputation of the Forelimb is indicated to provide space so that amputation of the head and neck may be possible or easier. If the foreleg is retained or extended beneath the body and mutation is not possible due to fetal emphysema or contraction of the uterine wall, am- putation of the foreleg is necessary. It is indicated in large or emphysematous fetuses to reduce their size and expose the ribs for evisceration. In rare cases it may be indicated in transverse ventral presentation in the mare in which after amputation of the two hind legs at the tarsus, and the underneath foreleg at the humeroradial joint, the upper front leg may be removed in the manner described below and evisceration performed, if neces- sary, before the fetus is corrected by version into a pos- terior presentation. Amputation of the forelimb is initiated by means of constant traction applied to the leg with a snare or ob- stetrical chain. By making a crescent-shaped incision through the skin of the fetus and its trapezius and rhom- boideus muscles dorsal to the scapula with a hoe-bladed castrating knife or other knife, the dorsal end of the scapula is separated from the body. A loop of fetatome wire is placed around the limb and moved up the limb as the head of the fetatome is placed in the pectoral region. The wire loop is then moved upward and placed in the in- cision under the cartilage of the scapula, and the limb removed. This technique is particularly adapted to the cow; it is more difficult to perform in the mare due to the longer limbs of the equine fetus. Another technique is that of placing the loop of fe- tatome wire around the limb to be removed while the head of the fetatome is placed just dorsal and caudal to the top of the fetal scapula. The limb is extended tautly, by traction by a chain to the chain plate on the handle of the Utrecht fetatome. By means of acute-angled saw- ing the limb is removed. The wire usually passes through the dorsal part of the scapula. On occasion one forelimb as well as the head and neck can be removed in a like manner by proper placing of the wire to include the head and neck. The removal of the forelimb extended beneath the body is easily performed by passing the fetatome wire behind the elbow and beneath the arm. By placing the head of the fetatome on the withers of the fetus, the en- tire limb can be removed rapidly. The above two methods of amputation of the forelimb removes the skin over the chest wall, so that if eviscer- ation is performed the broken ends of the ribs are not covered. The older techniques of subcutaneous am- putation of the forelimb with a knife and chisel are rel- atively simple and rapid, especially when the fetus is emphysematous.2,37a’56 They are seldom performed how- ever because the use of the fetatome is more rapid and less stressful to the dam and operator. In fetal emphy- sema the muscles are greatly weakened. In many such amputations the fetal extractor is useful. For example one may girdle the skin above the knee, apply the ex- tractor and rapidly remove the entire limb. Amputation of the Anterior Limb at the Humero- Radial Articulation is indicated in the removal of the forelimbs in rare transverse ventral presentations in the mare prior to version of the fetus into a posterior presen- tation. Amputation of the entire forelimb is difficult or impossible in this presentation. Amputation at the hu-310 VETERINARY OBSTETRICS mero-radial articulation is accomplished by exerting traction on the limb. A loop of fetatome wire is placed around the leg and the head of the fetatome is pushed ahead of the wire loop to the pectoral region and held there firmly while the wire loop is passed up the leg and over the olecranon and tightened around the leg. The handle of the fetatome may be fastened by a chain or held securely to the extended leg in the metacarpal re- gion, preventing the head of the fetatome from slipping downward as the leg is amputated through the distal end of the humerus. The other limb is removed in a similar manner. Evisceration in Anterior Presentation is indicated to reduce the size of a large or emphysematous fetus and make it less inflexible, or to release ascitic fluid in fetal ascites. It may be indicated to assist the operator in put- ting his arm through the birth canal to thread the feta- tome wire around the pelvis in hiplock in anterior pre- sentation. It is also helpful in rare cases if the ribs are to be broken down for further reduction of the size of the thoracic or pectoral girdle. When the fetus is within the birth canal or uterus, evisceration in anterior presentation may be performed by amputation of the forelimb including the scapula with a fetatome which exposes the ribs. The intercostal mus- cles between the first, second, third, fourth, and fifth ribs are separated by the finger or knife from the spine to the sternum. In order to gain free access to the tho- racic and abdominal cavities, the second, third, and sometimes the fourth ribs are removed by cutting the costal cartilage just above the sternum with a knife, chisel, or cutting hook and bending the rib dorsally to break it off next to the spinal column, or with a cutting hook or chisel cutting the rib loose as near the spine as possible. If the cutting hook and chisel are used they should be carefully guided and guarded by one hand of the operator while controlled traction or thrusting motions are provided by the other arm, so that the uterus or birth canal are not injured by slipping of the instrument. The ribs should not be broken in the middle as it is difficult to remove both ends, especially the ventral part, and the broken ends are likely to lacerate the operator’s hand or arm. The heart and lungs are removed by manual traction after grasping the heart at its base and clasping the fingers firmly around the large vessels. By grasping the lungs in the region of the bifurcation of the trachea first one and then the other or both lungs can be removed. After the thoracic viscera have been removed the fingers are thrust through the diaphragm in the region of the large vessels and the opening enlarged. The stomach and in- testines are easily removed by wrapping them around the hand. The liver, the largest organ to be removed, is pulled loose from the diaphragm and withdrawn, usually in sev- eral pieces. The kidneys are small and therefore need not be removed. Destruction of the Rib Cage—On uncommon occa- sions, to further reduce the size of the thorax, the re- mainder of the ribs may be broken down with the cutting hook or the chisel. If the blunt-pointed cutting hook is used, the hook is pushed caudally between the skin and ribs about midway between the spine and the sternum until the end of the hook passes beyond the last rib. The point of the hook is turned medially through the abdom- inal wall and by short, firm pulls the hook is drawn through one to two ribs at a time until only one rib re- mains to be broken. To avoid cutting this rib suddenly and having the hook tear out of the fetus and possibly injure the uterus or the operator’s hand, this last rib may be broken by twisting the hook instead of applying trac- tion. If necessary the ribs on the other side of the thorax may be broken down by introducing the cutting hook through the body cavity to the last rib turning the point outward through the abdominal muscles and pulling the hook back through the ribs in the manner described above. Since the point of the hook is under the skin and might catch it or cut through a fold of skin, the operator’s hand outside the skin should guard and follow the progress of the hook. Another technique is to make a 3- to 4-inch vertical incision through the skin cranial to the opposite shoulder and push the cutting hook along the outside of the ribs beneath the shoulder and skin to the last rib and, turning the point of the hook medially, cut through the ribs as was done on the first side after the foreleg had been removed and the fetus eviscerated. A chisel instead of the blunt cutting hook may be used for breaking the ribs in a fetus fixed in the birth canal by traction. Complete percutaneous Fetotomy in the Anterior Presentation—Since evisceration and breaking down the fetal ribs is difficult especially in a cow with definite fetopelvic disproportion, a complete percutaneous feto- tomy in anterior presentation as described by Bierschwal and de Bois and others using the Utrecht model fetatome may be easier.-'4,59 This technique requires amputation of the head; amputation of both forelimbs, including the scapulas; transverse division of the anterior chest or trunk; transverse diversion of the posterior portion of chest through the abdominal wall caudal to the last rib; and bisection of the fetal pelvis through the sacrum and pubis. If the posterior portion of the chest or rib cage is of too great diameter to be withdrawn easily, the ribs are sev- ered longitudinally by the fetatome near their vertebral attachment. Detruncation in Anterior Presentation is indicated in rare instances when the fetus is in a “dog sitting” pos-OBSTETRICAL OPERATIONS 311 ture with the hind limbs extended alongside or beneath the body and wedged into or against the maternal pelvis. If repulsion and mutation are impossible due to pro- tracted dystocia, or if the head and forelegs are outside the vulva, fetotomy is usually necessary. To perform detruncation by means of the fetatome, a loop of fetatome wire is passed around the body of the fetus and the head of the fetatome is inserted into the birth canal over the lumbar region of the fetus. After the wire is manipulated back of the last ribs, detruncation is rapidly accomplished. On occasions two cuts through the trunk of a large fetus may be necessary. Using Krey’s tongs on the exposed vertebrae for traction further re- duction of the fetal body is facilitated. Evisceration would make this operation safer and easier if the fetus is large or emphysematous, or if the birth canal is swollen, small, or dry. Lubrication to prevent trauma to the birth canal is essential. Following detruncation, chains are applied to the two hind limbs and by traction on the limbs and repulsion on the spine the hind quarters of the fetus may be turned to a posterior presentation dorso-pubic posi- tion. After the hind quarters have been rotated to a dorso- sacral position they are removed by traction. If the pelvis of the fetus is large, its bisection with the fetatome should be considered without attempting mutation. Bisection of the Pelvis in Anterior Presentation is commonly indicated when the fetal pelvis becomes wedged in the maternal pelvis. In these cases the bisiliac diameter of the maternal pelvis is smaller than the dis- tance between the greater trochanters of the fetal hips thus causing hiplock. When this has existed for a number of hours as a cause of dystocia one should examine the cow carefully, since symptoms of obturator paralysis are present in many such cases. If symptoms of obturator paralysis are present, bisection of the fetal pelvis is in- dicated in preference to forced extraction to prevent fur- ther trauma to the obturator nerve. When the hiplock condition cannot be relieved by lubrication, mutation and traction, fetotomy is necessary. This may be performed with the fetatome. In using the fetatome, the wire is passed over the top of the fetal pelvis and as far down as possible behind the ischial arch. By passing the hand under the fetus and fetal pelvis the introducer, threader or obstetrical chain which is at- tached to the wire is pulled between the hind legs. After placing this end of the wire through the fetatome, the head of the fetatome is placed alongside the body of the fetus opposite the ribs. If the loop of the wire is on the right side of the tail the head of the fetatome should be on the left side of the fetus so the fetatome wire passes through the middle of the pelvis and not through the head of the femur. After the pelvis is bisected, the fetus minus one hind leg can be removed; then if the operator grasps the exposed pelvic bones the other hind leg can be with- drawn. This operation is made easier by evisceration, which allows the operator more room in the pelvic cavity for placing the wire and the fetatome in position. A simple procedure combining forced extraction, evisceration, and bisection of the pelvis is frequently used by the author to relieve dystocia in heifers with fetopel- vic disproportion. By means of forced extraction with the fetal extractor, the well-lubricated fetus is pulled through the birth canal until the hips approach the ma- ternal pelvis. In rare instances it may be necessary to amputate the head and neck or the head, neck and one forelimb in order to accomplish this. The forequarters outside the vulva are pulled dorsally, exposing the um- bilical region of the fetus. The abdominal wall is cut transversely and evisceration is easily completed through this wide incision. In many cases this incision extends dorsally through the intercostal muscles of one of the last 2 to 4 ribs, but these are short and cause no problem. If the difference between the size of the maternal and fetal pelves is not relatively great, traction is once more at- tempted. The long blunt hook is passed over the top of the pelvis and hooked on the ischial arch or into the cau- dal border of the sacro-sciatic ligament, providing a firm hold for traction and for elevation of the fetal pelvis. This also causes the fetal pelvis to be turned obliquely, thereby facilitating delivery. Since the abdominal wall has already been cut, and evisceration has greatly re- duced resistance in the birth canal and all the traction is on the fetal spine, correction of the dystocia in many such cases can be accomplished without bisecting the pelvis. Mutating the fetus into a dorso-ilial position be- fore applying traction may assist in the removal of the fetus by traction without bisecting the pelvis with the fetatome. Fetotomy Operations in the Posterior Presentation Fetotomy in Normal Posterior Presentation is in- dicated when the diameter of the fetal pelvis is relatively larger than the diameter of the pelvic inlet and wedging or hiplock occurs. This condition is seen usually in im- mature or stunted heifers and may be complicated by an emphysematous fetus. Under these conditions cesarean section or slaughter may occasionally be advisable. Fetotomy consisting of the amputation of one leg, or preferably one leg and part of the pelvis, may be ac- complished by means of the fetatome. A transverse in- cision just cranial to the external wing of the ilium is made in the fetus through the skin and muscle. A loop312 VETERINARY OBSTETRICS of fetatome wire is carried up the hind leg and placed in this incision. The head of the fetatome is placed between the hind legs. One hind leg and a portion of the pelvis are removed. A variation in this technique consists of passing the loop of fetatome wire around both legs and over the hips to the lumbar region of the fetus. With the head of the fetatome on one hip a cut is made with the wire halfway through the lumbar region just cranial to the fetal pelvis. The head of the fetatome is pulled out- side the cow and reinserted to rest between the two legs of the fetus and the rest of the cutting is completed, bi- secting the fetal pelvis longitudinally. Another technique is that of acute angle sawing with the fetatome.-- The loop of wire is placed around one leg and the head of the fetatome is placed dorsal to the wings of the ilium or even in the caudal lumbar region. The leg is tautly extended and fastened to the handle of the fetatome out- side the dam to insure a portion of the fetal pelvis being included with the amputated limb. Often, the leg is am- putated through the hip joint because it is difficult to hold the head of the fetatome in place. Bisection of the Pelvis in Breech Presentation is in- dicated in posterior presentation in uniparous animals with the hind limbs of the fetus extended or retained beneath the body, when dystocia has been present for some time, the uterus is contracted, the fetus emphysematous, and the uterus and birth passages are dry and swollen, so that mutation is difficult or impossible. The fetatome may be used in this operation. The heavy metal guide, introducer, or obstetrical chain is securely fastened to the fetatome wire and then introduced through the birth canal and over the thigh of the fetus between the leg and abdomen. It is pushed as far as possible ven- trally and caudally. The hand is then passed beneath the fetal pelvis and between the legs and the wire is drawn out through the vulva. The threaded fetatome is placed on the hip opposite the leg to be removed; that is, if the wire loop is around the right leg of the fetus the head of the fetatome should be on or just behind the greater tro- chanter of the left leg to insure a large portion of the pelvis being removed with the leg. If the head of the fetatome is not firmly held in place it will pull directly caudal to the perineal region and the leg will be removed at the hip joint or proximal end of the femur. After the leg and portion of the pelvis is removed the rest of the fetus can usually be withdrawn by traction on the pelvic bones with the long blunt hook or Krey’s hooks, with the opposite leg still extended alongside the body. If this is not possible, the operation may have provided enough room to correct the posture of the remaining limb by mutation. In rare cases evisceration may be performed to assist in the removal of the fetus. Another method of reduction of the pelvis in breech presentation is to place a loop of fetatome wire in a fe- tatome around the presenting buttocks. The head of the fetatome is placed in the region of the fetal lumbar ver- tebrae and held in place by an obstetrical chain tightly fastened to the handle of the fetatome and by Krey’s tongs to the fetal sacrosciatic ligament or sacrum. By acute angle sawing, this removes most of the pelvic bones and tail and may permit withdrawal of the fetus with both limbs alongside the body. Amputation of the Rear Limbs at the Tarsus may be indicated in rare instances in the mare in order to obtain additional room for removal of the forelegs in transverse ventral presentation, in cases in which the metatarsal bone is wedged into or across the pelvis, or when mutation of a hock-flexed posture in a mare is im- possible. It may occasionally be necessary in monsters with ankylosed hind limbs, such as Perosomus elumbis. The operation is easily performed by slipping a loop of fetatome wire around the leg. The head of the feta- tome is placed on the lower row of tarsal bones or the head of the metatarsal bone, and the leg is cut off in this region. Thus the lower portion of the limb is removed and the os calcis is left attached. The obstetrical chain will find secure lodging above this point when traction is applied. Evisceration and Breakdown of the Ribs in Poste- rior Presentation is indicated when further reduction in the size of the trunk is desired in order to effect removal of the fetus. After removal of one or both of the posterior limbs the opening into the abdominal cavity may be enlarged and the viscera removed as described under evisceration in anterior presentation but in a reverse manner, remov- ing first the abdominal and then the thoracic viscera. The ribs may be broken down in the manner described pre- viously, using the blunt-pointed cutting hook or chisel, but in the reverse order. In certain cases in which it is necessary to break down the thoracic cage after eviscer- ation, the fetatome wire might be passed cranial to the shoulder and between the front legs, thus bisecting the thorax. Other Fetotomy Operations There are many other fetatomy operations that may occasionally be used to relieve dystocia. Some are vari- ations of those just described. In fetal monsters causing dystocia, fetotomy operations must be designed to fit the individual case, using the basic operations and principles as a guide. In these cases fetotomies should be plannedOBSTETRICAL OPERATIONS 313 carefully and in a manner to reduce the number of cuts to a minimum. Double monsters or those single monsters that are sharply bent, such as Schistosomus18 and Cam- pylorrhachis, should be divided as nearly as possible into two equal sections so that removal may be prompt and easy. One should not attempt to start a fetotomy op- eration without being quite certain that the dystocia can be relieved by the planned operation. In many cases con- sultation may be advisable. It should be borne in mind that a prolonged unsuccessful fetotomy will make the prognosis more grave if the operator finally attempts to perform a cesarean section. Ischio-pubic Symphysiotomy—A simple, rapid, technique for splitting of the maternal pelvis at the sym- physis pubis in immature or stunted beef heifers under 24 months of age suffering from dystocia due to a small pelvic inlet has been described.6'10'16'19 To facilitate se- curing a live calf, one could induce parturition within the last 2 weeks or gestation with dexamethasone (30 to 60 mg). It is interesting that a brief notation of this sym- physiotomy technique was described in a French book in the nineteenth century.6 This operation is preferably done on a standing heifer. Epidural anesthesia is admin- istered. One authority recommends passing a metal cath- eter into the bladder to monitor the location of the blad- der before, during and after the symphysiotomy and using a small hypodermic needle to punch through the vaginal floor to ascertain before the operation that there are no areas of ossification in the symphysis.- The area beneath the vulva is washed, shaved, and disinfected. In as asep- tic a manner as possible a 4 cm incision is made through the skin and down the exact midline to the ischial arch avoiding the perineal vessels which can bleed profusely if incised. A small, guarded obstetrical chisel* is driven slowly into the symphysis, guided by the operator’s hand in the vagina, and the pelvis is carefully split. The chisel should be pushed back and forth through the symphysis several times to separate any fibrous attachments. Trac- tion is applied to the fetus. Because at the time of par- turition the ligamentous structures are relaxed, the pelvis spreads 2 to 3 inches and allows the fetus to be with- drawn by manual traction or by the fetal extractor. Af- tercare consists of keeping the heifer quiet, isolated and confined for several days or longer. Although the heifer may show some stiffness and slowness of gait it is able to get up and walk. Mounting by other cattle should be avoided. If symptoms of obturator paralysis are present it is advisable to tie a bowline around each hind fetlock with about 18 to 20 inches of rope between them. This *Holmes Symphysiotomy Chisel, Holmes Serum Co., Inc., 1301 Knotts Ave., Springfield, 111. 62703. is removed in about 1 to 3 days if the animal can handle itself well. Parenteral antibiotics are given to control possible infection at the operative site. By this technique fetotomy and cesarean section are avoided. Although this practice may be acceptable for beef cattle in some of the range sections of the West, eastern dairymen and veter- inarians would be reluctant to accept it for dairy heifers. This operation should not be performed on fat heifers or older cows. This technique of symphysiotomy has also been used successfully in yearling ewes to avoid a ce- sarean section.16 Occasionally in heifers a large calcified callus will form if the pubis bone is damaged. This might interfere with subsequent calvings. Aftercare and Examination of the Dam after Mutation, Forced Extraction, or Fetotomy Following a dystocia operation the genital tract should always be examined for the presence of another fetus in the uterus or abdominal cavity. This can readily be de- termined in the mare, cow, doe and ewe if the hand and arm can enter the uterus. It can be very embarrassing to a veterinarian to apparently relieve a dystocia only to be called back again in 2 to 4 hours or later for another dystocia in the same cow. Occasionally the second fetus may not be found until 2 to 3 days later when the cow develops anorexia, tenesmus, or attempts are made to remove a retained placenta. In the sow the farrowing of the last fetus is usually followed by the sow becoming quiet and content, nursing her pigs, urinating, eating, and drinking. If the sow remains restless, uneasy, shows anorexia and intermittent tenesmus, the birth canal should be examined for the presence of another fetus. Similar symptoms are exhibited by the bitch and queen. In rare instances, in large breeds of dogs, such as the Great Dane, St. Bernard and Newfoundland, the bitch may exhibit every outward sign of having finished whelping. Several days later the bitch may develop anorexia, depression, elevated body temperature, pulse and respiration, and a green, possibly fetid vaginal discharge due to a decom- posing fetus. Careful palpation, or preferredly a radio- graph, of the abdomen after whelping would have avoided leaving a fetus in the atonic uterus. After every dystocia operation the genital canal, in- cluding the uterus, should be examined for the presence of an invaginated uterine horn, lacerations, or ruptures. Small superficial tears of the cervix, vagina, or vulva are of little importance or significance unless retention of the placenta favors infection. In the region of the vulvo- vaginal border these lacerations may lead to infection314 VETERINARY OBSTETRICS and necrosis with secondary swelling, pain, and tenes- mus. Parenteral antibiotic therapy and local treatment with healing protective ointments are indicated. Lacerations of the cervix if extensive may lead to cervical induration and chronic cervicitis. Any tears in, or ruptures of, the uterus should be noted, inasmuch as the prognosis in these latter cases is poor. In large tears in the vulva, vagina, cervix, or uterus, suturing might be attempted by work- ing through the birth canal. Pulling the cervix and uterus back to or outside the vulva, if possible, would make suturing easier. A small uterine rupture especially of the dorsal wall of the uterus may heal spontaneously; but the uterus should be stimulated to contract by the use of oxy- tocin. Antibiotic therapy and letting the genital tract strictly alone may save a few cases. In extensive ruptures of the uterus, especially where infection exists, slaughter is ad- vised. In less severe cases laparotomy and hysterectomy or suturing of the uterine tear may be indicated. The placenta and placentomes should be examined in cows and mares. If the placentomes are firm and hard, retention of the membranes generally follows. If uterine infection is obviously present, preventive steps may be taken to control infection by parenteral antibiotic ther- apy, local treatment of the uterus with antiseptics or tet- racycline or other antibiotic compounds and possibly oxytocin to stimulate uterine involution and prevent uter- ine sepsis. In the bitch if placentas are still present in the uterus they may be withdrawn by the use of a gauze sponge on a forcep. Twisting the instrument in the uterus may catch and hold the placenta to be withdrawn. If re- tained placenta is suspected the owner should be in- structed about subsequent aftercare of the case. In most obstetrical cases involving forced extraction or fetotomy a dose of 3 to 5 ml., 30 to 50 units, of oxytocin in large animals; 1 to 3 ml., 10 to 30 units, in ewes, does and sows; and 1/2 to 1 ml., 5 to 10 units, in bitches and queens is indicated to prevent possible prolapse of the uterus and aid involution of the uterus and dropping away of the fetal membranes. If the animal is unable to rise, further examination should be made to determine whether obturator paraly- sis, dislocation of the hips, pelvic, or spinal injuries are present, and if so the degree of severity. Hypocalcemia in the cow may be masked by the dystocia. Occasionally the administration of oxytocin without a concurrent in- jection of a calcium product may precipitate milk fever or hypocalcemia in a dairy cow. The cow’s udder should be examined to make certain no pathology is present, or that teat wounds and lacerations did not occur during the dystocia. If the operator has been working with his bare arms in an infected uterus he should wash his arms and hands very carefully and thoroughly with soap and water and apply an antiseptic in order to prevent skin infections. If any infectious material has adhered to his clothes they should be changed before he goes to another farm. Boots and equipment should be washed and disinfected. Cesarean Section Cesarean section is the delivery of the fetus, usually at parturition, by laparohysterotomy. This operation is performed when mutation, forced extraction, and feto- tomy are deemed inadequate or too difficult to be em- ployed to relieve the impending or present dystocia or when it is desired that the fetus be delivered alive. The word cesarean is said to derive either from an edict by Julius Caesar that women about to die in advanced child- birth should have this operation performed to save the child, or from the Latin caeso matris utera, cutting of the mother’s uterus. It is a misconception that Julius Caesar was bom in this fashion, as his mother survived his birth in an era when this was impossible.21 John Field in 1839 was the first to report this operation in the English literature.57 He operated on two bitches. The next year J. B. Carlisle reported on a cesarean sec- tion in a sow. Cesarean operations on cows, mares, sows, and bitches were reported soon after. Later, with the ad- vent of anesthesia, suturing techniques, aseptic tech- niques, and antibiotic therapy, this operation became in- creasingly common. Cesarean section in the domestic animals has been well-described.----’38'47-52,53 Cesarean section in the Mare may be indicated in pelvic fractures with exostosis, transverse dorsal or transverse rotated bicomual pregnancies, anterior lon- gitudinal presentation with the rear limbs extended be- neath the body (dog-sitting posture), torsion of the uterus, fetal monsters such as hydrocephalus, and possibly em- physematous fetuses. In rare dystocia cases in mares where mutation, forced extraction or fetotomy procedures do not offer promise of successful delivery, cesarean sec- tion should be considered. In one large clinic 15 feto- tomies were performed for each cesarean section.48-50 In many instances the equine fetus is dead because the se- verity of the parturient problem is not recognized early enough, preferably before parturition, and the time from the onset of labor to the death of the fetus from placental separation or other causes is only 30 minutes to a few hours. The prognosis for a successful equine cesarean operation is poor if prolonged attempts at forced extrac- tion or fetotomy precede the decision to operate. With modem surgical techniques, asepsis, anesthetics and an- tibiotics successful terminations of this operation on maresOBSTETRICAL OPERATIONS 315 are being reported with increasing frequency. It is no longer necessary to sacrifice the life of the dam to save the fetus. A number of cases have been reported in which the mare conceived following the operation. The first successful equine cesarean was performed in Hungary in 1908.20 Since then many reports and reviews on equine cesarean section have appeared.47b In 1972 one study made a comparison between 129 equine fetotomy and 63 cesarean operations.473 In the fetotomy cases there was a 10 percent mortality rate, 28 percent retention of the placenta and of those mares rebred a pregnancy rate of 42 percent with an abortion rate of 10 percent. In the cesarean cases there was a mortality rate of 20 percent of mares and 70 percent of foals, 50 percent retention of the placenta and of those mares rebred a pregnancy rate of 50 percent with an abortion rate of 30 percent. In 71 equine cesarean operations 82 percent of the mares survived but only 28 percent of the foals as 64 percent were stillborn. Of 27 mares bred after cesarean section, 50 percent became pregnant but 6 of 14 aborted at 7 to 10 months of gestation.47b Thus, if at all feasible, vaginal delivery in mares is preferable to cesarean section. General anesthesia is indicated when the fetus is dead. This usually consists of epidural anesthesia and tran- quilizers prior to induction by a 5 to 10 percent glycer- ylguaiacolate in a 5 percent glucose solution to which an ultra-short acting barbiturate such as thiamyl sodium may be added. This is given intravenously to effect. In modem clinics halothane inhalation anesthesia may be used. These general anesthetics may have an adverse af- fect on the fetus if it is alive. Tranquilizers and local anesthetics in the form of epidural analgesia and local blocks of the abdominal area, or infiltration of the in- cision sites have been used when the fetus is alive. One clinic recommends using epidural anesthesia, glyceryl guaiacolate and local infiltration anesthesia.47 The mare should be restrained in a recumbent position on the left or right side or back depending on the site of the inci- sion. Various incision sites have been successfully used in the mare and the site should be determined on the basis of the nature of the dystocia, and the presentation or po- sition of the fetus particularly the location of the head of the fetus. The most popular incision site is the Mar- cenac approach in the left flank starting at the middle of the last rib and extending caudal and ventrally toward the stifle. The incision is usually 25 to 40 cm. in length.47 Other reported incision sites have been in the upper left flank or the left paramedian or midline abdominal areas.-53 Herniation is less common with the flank incision sites. Operations in the right flank area are complicated by the large cecum and its dorsal attachments. When incising the peritoneum care should be taken not to injure the viscera. The equine uterus is more difficult to bring to the in- cision than is the uterus in cattle, but if the proper in- cision site, the Marcenac site in the lower left flank is probably the best, has been selected this can probably be done. Excessive manipulation of the viscera or con- tents of the abdominal cavity should be avoided as this may precipitate shock symptoms and death. If the uterus is infected great care should be used to avoid contami- nation of the abdominal cavity. The incision of the uterus should be on its greater curvature over a fetal promi- nence. Because of the long fetal extremities, mutation, forced extraction and even partial fetotomy may be nec- essary to remove the fetus. If the foal is alive when de- livered the umbilical cord should be left intact for a few minutes until respirations have been established. If the placenta comes away easily it should be removed, other- wise the uterus should be promptly sutured. A complication of the equine cesarean operation is the rather diffuse bleeding that occurs from the submucosal area of the uterus after it is incised. To prevent severe intrauterine bleeding a continuous lock stitch suture of catgut should be placed through the endometrium, sub- mucosa and serosa completely around the uterine inci- sion for a depth of 1 cm being careful not to include the placenta. This suture was inverted into the uterine cavity by a double row of Lembert or Cushing sutures used to close the uterus after the fetus had been removed.47'53 The peritoneum, muscle and fascial layers of the abdom- inal wall should be sutured separately with #2 Dexon or strong #4 chromic catgut to obliterate dead space and subsequent seroma development. The modified Mayo or overlapping mattress suture for closure of the wound on the ventral abdomen was recommended.28 The skin in- cision was closed with a nonabsorbable nylon suture. They also recommended the use of quill sutures. The use of a tightfitting canvas or elastic support bandage may be indicated.40 Severe edema of the incision area with oc- casional rupture and gaping of the skin wound are not unusual following surgery in the horse. Aftercare should include stall confinement, feeding limited amounts of laxative feed, administering tetanus antitoxin, oxytocin and broad range antibiotics both lo- cally and systemically. The latter should be continued for 7 to 10 days. Retained placenta was a common prob- lem in equine cesarean operations.46,47 To correct this condition 40 units of oxytocin in 1/2 to 1 liter of saline was administered by a slow intravenous drip method over a period of 1 to 2 hours to produce more normal phys- iologic contraction of the uterus. Colic was avoided, and the afterbirth dropped away promptly in about 80 percent316 VETERINARY OBSTETRICS of the cases. Complications occurring in the postopera- tive period are shock that occurs within a few hours after the operation due to manipulation of the uterus and vis- cera, peritonitis that may cause illness and death 2 to 5 days later, and fatal colic due to strangulation of the gut that may develop one to three weeks or more after the operation due to fibrinous adhesive peritoneal bands sec- ondary to a non-fatal peritonitis.22 Four to 5 days after the operation a rectal examination may be performed to break down any adhesions forming around the involuting uterus.47 Hysterectomy, as in the cow, is extremely dif- ficult to perform.28 Cesarean Section in the Cow has been performed in increasing numbers by practitioners in the United States since 1940. Prior to that period it was performed only sporadically. Since 1942 the clinic at Kansas State Col- lege has performed between 50 to 100 cesareans each year. ’ • • Many more cesareans are performed in the western range states, where immature beef heifers are bred on pasture, than in the northeastern dairy states, where bulls are closely confined and artificial insemi- nation is widely used. Indications for cesarean section in the cow are as fol- lows.--3042 In the United States immaturity and growth retardation or stunting of heifers resulting in fetopelvic disproportion are by far the most common causes. It is seen particularly in beef cattle when the bull runs on pas- ture with heifer calves. Some young cattle come into es- trum and conceive at 4 to 15 months of age with preg- nancy resulting in a severe dystocia due to a very small pelvis and genital tract. In these cases the difference be- tween the size of the fetus and the birth canal is marked. Performing fetotomy operations through such a narrow birth canal is very difficult and the fetus is always lost. Incomplete dilation or relaxation of the cervix may be associated with secondary uterine inertia with advanced involution of the cervix and uterus secondary to torsion of the uterus, or fetal dystocia and emphysema in which the onset of parturition was not observed, or the cow was neglected for 36 to 48 hours. In other cases it may be observed, without a known predisposing cause, due to a primary uterine inertia, or it may be caused by sclerosis of the cervix. In such cases the fetus may still be alive; oxytocin might be given, and the condition of the cervix observed in 3 to 4 hours or more to make certain that parturition was not in its initial stages. An abnormally large living fetus may be a cause for cesarean section. Apparently normal healthy fetuses may occasionally be too large for birth without total fetotomy excessive traction or cesarean section. If the forefeet but not the head can enter the pelvic inlet or in posterior presentation if the hips are much too large to enter the pelvis, cesarean section should be considered, as it is frequently easier, safer, and faster than total fetotomy and in many such cases the delivery of a live calf is possible. These large-sized fetuses are most frequently seen in the large breeds, such as Holstein, Charolais, Simental, Brown Swiss, Shorthorn, and Herefords. They are usually male. The cause of the dystocia may appear to be a large normal fetus; actually, however, the cause may be an abnormal or relatively small pelvis; or both conditions may be present. In breeds of cattle with mus- cle hypertrophy or double muscling, affected calves fre- quently require cesarean section for delivery. In other cases the oversized condition of the fetus may be due to emphysema or to anasarca. In rare cases an excessively large fetal giant may be caused by a greatly prolonged gestation period exceeding 300 days. The prognosis in these latter pathologically oversized fetuses is grave be- cause of the overdistention of the uterus, the uterine in- ertia, and the high incidence of septic metritis and re- tained afterbirth following the relief of the dystocia. Other causes for oversized fetuses include fetal monsters such as Schistosomus reflexus, general ankyloses, and dou- ble monsters. At times, certain of these may be more safely and easily removed by cesarean section than by fetotomy. Other cases where cesarean section is indicated in- clude: a torsion of the uterus that is difficult or impos- sible to correct by other means; a juvenile hypoplastic genital tract due to poor growth and development; hy- drops amnii and allantois when the life of the dam is imperiled by great distention of the uterus and other methods have failed to relieve the condition; marked ste- nosis of the vagina in prolonged dystocia in heifers due to perivaginal hemorrhage compressing the genital tract; fetal mummification when ordinary treatments fail, or in heifers or young cows with a 6- to 8-month fetal mummy too large to be expelled through the undilated birth canal; when the dam is unable to rise, is exhausted, debilitated, diseased, or near death; and stenosis of the birth canal due to tumors or extensive scar tissue in the pelvic birth canal. In rare cases in cattle with prolonged dystocia the uterine wall contracts tightly around the emphysematous fetus, producing a contraction or retraction ring dysto- cia. Since forced extraction may cause rupture of the uterus and fetotomy would be difficult, cesarean section may be indicated. Fracture of the maternal pelvis in cattle is rare and therefore cesarean section due to this cause for dystocia is only seldom indicated. Prognosis—A review of cesarean opera- tions,2,31'34’37b-49-57:58'59 indicates that in cattle that are good surgical risks, and are operated on within 6 to 18 hours after the onset of labor, in cases where the fetus is stillOBSTETRICAL OPERATIONS 317 alive or very recently dead and the cow is in good con- dition physically and has not been damaged by excessive manipulation, injury, or infection of the birth canal or uterus, the mortality rate should be less than 10 percent, and possibly only 5 percent. Under field and actual prac- tice conditions the mortality rate might reach 15 percent. The mortality rate is about 10 to 30 percent in cases where the cesarean section is performed from 18 to 36 hours after the onset of the second stage of parturition. The fetuses are generally dead and occasionally slightly emphysematous; the cow is in poorer condition for the operation, and the genital tract is usually injured or trau- matized. In cases in which dystocia has existed for 36 hours or more, the fetus is emphysematous, the cow is usually in poor physical condition, and the uterus is atonic and infected, the mortality rate may reach 30 to 50 per- cent or more. In 103 cesarean operations where emphy- sematous fetuses were removed, the recovery rate was over 80 percent in a college clinic.51 In 121 bovine ce- sarean operations, mainly in primipara, 93 percent of the dams survived, 60 to 70 percent of the calves survived but the subsequent pregnancy rate was 52 percent com- pared to the herd average of 80 percent.34 In 340 cesar- ean and 80 fetotomy operations; the maternal mortality rate for each series was 5 and 9 percent, retained pla- centa was 33 and 20 percent and conception rates in cows rebred after the operation were 80 and 73 percent, re- spectively.8 In field cases on ranches the death rate after 117 bovine cesarean sections was 17.9 percent but it was 38.4 percent in cows with purulent decomposition of the fetus while in 412 cases of fetotomy the mortality rate was only 8.4 percent.42 In this latter study of nearly 2500 dystocias, 2.6 percent of all dystocias terminated in ma- ternal deaths and of these 44.5 percent were slaughtered after the initial diagnosis was made or after unsuccessful treatment was attempted. The decision therefore as to which procedure to use should be based on a careful evaluation of each case. The more common causes of maternal death are: shock, secondary to exhaustion; toxemia; excessive ma- nipulation of the abdominal viscera as in torsion of the uterus, or when abdominal pressure is released rapidly, as in removal of a large fetus or excessive amounts of fluids as in hydrops; septicemia, pyemia, and toxemia secondary to septic metritis; uterine inertia in prolonged dystocia; retained placenta; peritonitis; or severe necrotic vaginitis due to excessive manipulation and injury prior to the cesarean section. Hemorrhage and ventral hernia are occasional causes of death. In rare cases hemor- rhage, especially from the stalk of a tom or lacerated camncle, may occur in atonic uteri. Ventral hernia may be prevented by proper suturing technique and suture material. Most maternal deaths occur 1 to 8 days after the operation. In recent years improved surgical tech- niques, asepsis, antibiotics and supportive therapy have greatly improved the prognosis for recovery even in cases offering great surgical risks. It is generally stated that from 60 to 80 percent of cows having cesarean section should be fertile and con- ceive subsequently. Failure to conceive may be due to peritoneal adhesions or to severe endometrial damage secondary to septic metritis. Of 48 cows without adhe- sions after cesarean section 81 percent conceived, while in 47 cows with adhesions only 51 percent conceived.8 The incidence of retained placenta following cesarean section is high, between 20 and 35 percent, and the in- cidence of metritis may vary from 20 to 50 percent. Fifty to 80 percent of recovered cows conceived after the ce- sarean operation.-7,52 About 80 percent of the cattle op- erated upon had an abnormal puerperium due to retained placenta, uterine infection and delayed involution of the uterus. Uterine infections should be expected and pre- ventive treatment given. The reason for this high rate of placental retention after cesarean section is not known. According to the authors cited above, the incidence of live calves produced by cesarean section is from 30 to 60 percent. This varies with the promptness with which dystocia is observed, the veterinarian summoned, and the operation performed. Fetotomy in cattle with dead fetuses should be carefully considered before performing cesarean section, since cesarean section requires more trained assistance, is more costly, and results in a higher percentage of subsequent sterility. If it appears that a fetotomy is going to be difficult, prolonged, or danger- ous to the dam or operator especially in cases in which the birth canal is small or the birth canal is swollen, compressed, or dry making it difficult to perform a fe- totomy; or in cases in which the fetus is emphysematous cesarean section should be considered. It should give promise of being a safer, easier means for relieving the dystocia than does fetotomy or forced extraction. Fewer than 1 percent of the dystocias cannot be relieved by cesarean, while 3 to 5 percent will end in failure if fe- totomy is employed.49 Selection of the Operative Site, Means of Restraint, and Anesthesia—These will and should vary depending upon the case. The operation has been performed in the upper left and right flank, with the animal standing. This site makes the operation easier for the veterinarian as he can perform it standing; the incision can be smaller be- cause the muscle tissues can stretch into a circular shape when the fetus is removed; subsequent herniation is less likely, and many veterinarians are experienced in oper- ating in the flank site because of frequently having per-318 VETERINARY OBSTETRICS formed rumenotomies. The upper right flank approach may be desired when torsion of the uterus is present, as the standing position is of assistance in correcting the torsion. The disadvantages of the right flank incision are that the cow may be more difficult to restrain and con- trol. It is difficult to bring the uterus to the incision, and abdominal contamination with the uterine contents is nearly unavoidable. This is of no consequence when the fetus is alive and little or no infection is present in the uterus; but it is a major disadvantage with a dead fetus and an infected uterus. If during the operation the inci- sion is extended too far ventrally it is difficult to hold the small intestines within the abdomen. If the cow strains, coughs, or struggles intestines may be expelled through the laparotomy incision. The operation may be performed in the left flank, at which site intestines usually are not present to offer a problem. The operation can be performed more ventrally on this side if it is desired, but the same advantages and disadvantages apply as for the right flank incision. A large full rumen may make it quite difficult to bring the uterus from the right side of the abdominal cavity to the left. Since these upper flank operations are performed with the cow standing, anesthesia consists of a small dose of epidural anesthesia to control straining; a tranquilizer to quiet the animal; local infiltration, an inverted L-block or paravertebral nerve block anesthesia of the flank re- gion. Some veterinarians prefer to perform the cesarean op- eration on a recumbent animal by an oblique abdominal incision in the lower left or possibly right flank region below the fold of skin in the flank and above the at- tachment of the udder on a line between the stifle and the umbilicus, parallel the ventral borders of the ribs. This site allows easy access to the gravid uterine horn. The muscles in this region stretch easily. It is easier to prevent contamination of the abdominal cavity by uter- ine fluids. There is less possibility that hernia will de- velop than when the incision is on the ventral aspect of the abdomen. The disadvantage of this site on the right side is that it is necessary to control the small intestines during the operation so that they do not prolapse. In most cases intestinal prolapse may be prevented by making the cow lie on her left side, a position necessary for per- forming the operation. The lower-left flank as a site for the incision requires the cow to be laid on her right side. On the left side the incision is more caudal than on the right side, and the apex of the uterus can be brought to the incision behind the rumen. Control of the intestines is only occasionally necessary when the incision is on the left side. In these lower-flank incisions the cow is restrained or stretched in lateral recumbency by tying the two rear legs together and the two front legs together. Anesthesia may consist of an epidural of 40 to 60 cc. of 2 percent procaine or lidocaine solution, which will pro- duce sensory and motor paralysis of the perineum and rear limbs. This will cause the standing animal to stop straining and to go down. If the cow is laying on her side when epidural anesthesia is administered, sensory loss may be incomplete because the uppermost nerves may not be properly blocked. Paravertebral nerve block or local infiltration of the operative site is usually nec- essary. In some cases a tranquilizer may be desirable. Other clinicians prefer the ventral median or para- median approach, with an incision through the ab- dominal floor. The site between the linea alba and the right subcutaneous abdominal vein has been recom- mended.12'13'31 Others6'46’57 preferred to operate 4 to 10 cm. lateral but parallel to the left subcutaneous abdom- inal vein. In all ventral abdominal incisions the cow is placed on her back and the incision starts at or slightly lateral to the fore udder and extends forward as far as necessary, usually 24 to 32 cm. In this region the apex or ventral portion of the gravid horn can be brought to and outside of the incision, thereby preventing uterine contents being released into the abdominal cavity. This is a great advantage in cases in which the uterus is in- fected. The abdominal wall is not as thick in this area as in the flank. There is less muscle tissue and fewer blood vessels, especially in heifers, and the abdominal wall is composed mainly of fibrous connective tissue, the abdominal tunic. The presence of the uterus in the abdominal incision usually keeps the intestines within the abdominal cavity. The main disadvantages to this ap- proach is that the abdominal wall at this site is composed of largely fibrous tissue tunics and will not stretch as does muscle tissue. Thus the incision must be longer than in the flank. If the proper suture material and technique are not employed herniation is more common. The choice of operative site and mode of anesthesia should fit the amount of help available, the nature of the dystocia requiring cesarean section, the type of cow, the nature of surroundings, the location of the fetus and uterus, and the preference of the operator.- -'30'53 It is desirable to have one skilled assistant to aid the operator, and two lay assistants to control the cow, especially if the cow is in lateral recumbency. To perform the operation in lateral recumbency the operator should place the animal down by using the rope squeeze method after heavy tranquilization or should ad- minister a large dose of epidural anesthesia, 40 to 60 cc. of 2 percent procaine or lidocaine solution. The cow should not be dropped suddenly, as there may be danger of uterine rupture. Local anesthesia may be used on theOBSTETRICAL OPERATIONS 319 incision site, or if the incision is lateral to the mammary veins an L-block or paravertebral anesthesia is satisfac- tory. The innervation of the abdominal wall in cattle has been described.2 In operations on the ventral abdominal floor the hind limbs should be tied together and the front limbs tied together. They should be stretched apart and sufficient help should be available to roll the cow on her back at certain times during the operation. The cow should not be left on her back for a protracted length of time. The Operation should conform to all other surgical operations on the abdomen with regard to preparation and draping of the operative site. An approach to asepsis should be attempted. Hemorrhage from the incision should be controlled but in the ventral approach hemorrhage, especially in heifers, is slight. The upper flank operation is performed like the laparotomy incision in a rumeno- tomy, except that the incision is about 30 cm. long. The author believes that the ventral paramedian approach13 and the oblique lower left flank or ventrolateral abdom- inal approach-’1,27'33 are most satisfactory for the majority of cases. The former technique will be described in de- tail. After the skin is incised the cow should be rolled on her back and the rest of the incision completed. After incising the abdominal tunic the fascia of the transverse abdominal muscle and peritoneum is opened and the in- cision completed with scissors. In about 7 out of 8 cows the omentum is observed covering the uterus and ab- dominal viscera. This can be incised, but it is better to pull the omentum cranially as it helps to hold the intes- tines from the incision. One or both arms are inserted into the abdominal cavity and the fetus is grasped through the uterine wall, and the apex of the uterine horn con- taining the fetus is pulled into or through the abdominal incision as the cow is returned to lateral recumbency. The gravid uterine horn fills the incision and prevents the escape of the viscera. The uterine horn and fetal membranes are incised longitudinally over the greater curvature, avoiding the cotyledons. Incising of the ca- runcular stalk may result in persistent hemorrhaging. Chains are applied to the limbs of the fetus and by ex- erting traction in a ventral and caudal direction the fetus is removed. If necessary the incision in the abdominal wall and uterus should be enlarged to prevent tearing. If the fetus is in posterior presentation the head should be fastened by a snare and the two forefeet secured before the fetus is withdrawn. In rare cases fetotomy may be required on the fetus to assist removal. If uterine torsion is present the direction of torsion should be accurately ascertained before the cow is forced down. This is not so important when the standing cow is operated upon. The torsion should be corrected, if possible, by grasping the fetus through the uterine wall and rotating the uterus. If this is not easily accomplished, the fetus may be re- moved before the torsion of the uterus is corrected. In cases in which the uterus is greatly distended due to an emphysematous fetus or hydrops it may be difficult or impossible to draw the apex of the uterus through the incision. If the uterine contents are infected the uterus should be pulled tightly against the abdominal incision and the lips of the incision and the abdominal cavity carefully packed off to avoid contamination when the uterine contents are released. The normal noninfected al- lantoic and amniotic fluids cause no trouble in the ab- dominal cavity. After a live fetus has been removed the fetal mem- branes are left in the uterus. If the fetus is dead the fetal membranes are removed manually if they drop away readily. Otherwise, they are left within the uterus. Some of the excess fetal membranes may be trimmed away with scissors so that they do not interfere with the su- turing of the uterus. Because of the high incidence of uterine infections and retained afterbirths following ce- sarean section it is advisable to place 1 to 2 grams of tetracycline in the uterine cavity whether or not the fetal membranes are removed. The uterine incision is closed with a double row of Lembert or Cushing sutures of No. 1 or 2 chromic catgut. A long straight intestinal needle should be used. The assistant can greatly facilitate the suturing by holding the edges of the uterine incision to- gether. The cow is then rolled on her back, the uterus replaced, and the omentum pulled caudally over the uterus so that when the abdominal incision is sutured the omen- tum will lie against it. If torsion was not corrected before the fetus was removed it should be corrected after the uterine closure is completed. The uterus should always be examined for the presence of twins, although these are rarely encountered in conditions requiring a cesarean section. The ventral abdominal incision may be closed in sev- eral ways. Good success using a continuous overlapping mattress suture of heavy nylon (Vetafil), #2 Dexon, or umbilical tape through the abdominal tunic, muscle, and peritoneum was reported.-13,53 This is left in place to prevent eventration or herniation. Interrupted double mattress sutures of No. 4 to 5 chromic catgut with a supplementary continuous suture of doubled catgut along the muscle incision after the peritoneum had been se- curely closed was recommended.46,50 Until this second suture line was used occasional cases of herniation oc- curred. After its use no cases of herniation developed in 48 consecutive cesareans. In the ventral incisions just described, the tough abdominal tunic provides a firm an- chorage for the sutures. The superficial muscles and fas- cia may be pulled together with catgut. Mattress, inter-320 VETERINARY OBSTETRICS rupted, figure 8, or lock stitches of nylon, silk, linen, or umbilical tape are placed in the skin and underlying fascia or muscle. The peritoneal and muscle layers in the upper flank incisions are sewn with catgut or if preferred the stronger figure-eight sutures of umbilical tape or nylon through all layers including the skin. The skin sutures are usually removed in 7 to 10 days. This operation generally takes from 30 to 60 minutes to perform if complications are not encountered. Three to 5 ml., 30 to 50 U.S.P. units of posterior pituitary extract or oxytocin is given to stim- ulate uterine contraction and involution. This should not be given until after the operation, because if given ear- lier, it may complicate the suturing by contracting the uterus and pulling it away from the abdominal incision. Postoperative Care—Most cases should receive 3 to 6 million units of penicillin or 1 to 2 grams of the tet- racycline compounds parenterally after the operation. This should be repeated daily for 3 to 7 days. The cow should be observed closely for the first 24 hours for evidence of shock especially if large amounts of fluid or a large fetus were removed or if there was much manipulation of the uterus or abdominal contents. If shock develops it should be combatted immediately with intravenous in- jections of blood, saline, and glucose. In rare cases hy- pocalcemia, and straining due to vulvar irritation or other causes, may occur, requiring prompt attention. If the calf survives it should receive some colostrum soon after birth. If the afterbirth is retained and metritis develops the con- dition should be handled conservatively by allowing the afterbirth to drop away by itself. It is dangerous to re- move the placenta manually, since little can be gained by the attempt, and much lost by injury to the uterus. The cow should be kept quiet and away from contact with other animals after the operation, in order to avoid possible injury to the operative site. The skin sutures may be removed in 7 to 14 days. Cesarean Section in the Ewe and Doe—This oper- ation has been performed successfully by many veteri- narians in recent years but it requires a careful, aseptic technique oftentimes difficult to achieve under farm con- ditions.-- Sixty nine ovine cesarean operations to relieve dystocia with a 77 percent recovery were reported.11 Most deaths were due to infection. For this reason the oper- ation is best performed in a veterinary hospital to which the ewe can be transported easily. The operation is in- dicated in the ewe when the cervix fails to dilate, “ring- womb,” or when the ewe is bred too young or is poorly grown and the birth canal is too small to permit the op- erator to relieve the dystocia by forced extraction. In rare instances monster fetuses, fetal emphysema, fetuses with a large head, torsion of the uterus, and other conditions similar to those in the cow may necessitate cesarean sec- tion. Prolapse of the vagina is a common cause for the cesarean operation in ewes.9 However, this may be treated by the induction of parturition with the corticosteroids.- Another indication for a cesarean is in pregnancy tox- emia or ketosis in ewes, in which dead twin fetuses are usually present. Under usual circumstances the severely affected ewe would die before the dead fetuses were aborted despite glucose and cortisone therapy and other supportive treatments. The valuable ewe may be saved by cesarean section. The prognosis should be more guarded than in the cow. The operation is similar to that in the cow and is per- formed through the flank, through the ventrolateral ab- dominal wall, through the ventral abdominal wall be- tween the linea alba and the subcutaneous abdominal vein, or through the midline.'1 Tranquilizers and epidural, lo- cal, inverted L block, or paravertebral anesthesia can be used. If bicomual twins are present in the uterus an in- cision should be made in each horn. No. 4 chromic cat- gut is satisfactory for suturing the abdominal wall. Aftercare of the ewe is similar to that of the cow. If pregnancy ketosis is present glucose injections, propyl- ene glycol orally and cortisone may help promote ap- petite and recovery in the convalescent ewe. Cesarean Section in the Sow—has been performed successfully for many years. The sow is more resistant to infection and peritonitis than is the ewe and cow. Ce- sarean is indicated in the sow when because of being bred too young or of being poorly grown, the resulting small pelvis and genital canal prevent normal farrowing. The canal is usually too small to permit the introduction of the hand in order to apply traction. Cesarean may be indicated in primary uterine inertia that fails to respond to oxytocin or in secondary uterine inertia in which the second stage of labor has been prolonged and lay or vet- erinary assistance failed to correct the dystocia. In this latter type of dystocia the genital tract is usually swollen and may occasionally be severely traumatized. Cesarean may be indicated occasionally due to monster fetuses or to pelvic fractures with exostoses or other abnormali- ties.?'?'38 Cesarean section in the sow is 85 to 90 percent suc- cessful when performed soon after the onset of the sec- ond stage of parturition, when the fetuses are still alive and the sow or gilt is still strong and vigorous. Mortality in the sow rises when the operation is not performed un- til 18 to 24 hours after the onset of straining. By this time the pigs are usually dead and the sow is in poorer shape for the operation. If the operation is delayed more than 24 hours the fetuses are usually emphysematous, the uterus infected, and the sow exhausted and toxic.OBSTETRICAL OPERATIONS 321 Although some sows may survive surgery at this stage the prognosis is guarded to poor depending upon the condition of the genital tract. As in the ewe, the operation should be performed in a veterinary hospital if possible inasmuch as the average hog farm is rather unsanitary and inconvenient for sur- gery. If it must be performed on the farm the sow’s legs and body may be strapped to a panel and the panel placed across two supports, to form a satisfactory operating ta- ble set up in a clean, dust-free location. Many veteri- narians prefer to use heavy tranquilization and to sup- plement it with local anesthesia along the incision line. Epidural anesthesia with 2 to 4 percent procaine or 2 percent lidocaine solution injected in 8 to 10 ml amounts into the epidural space at the lumbo-sacral articulation has been recommended.13,15'38 The operator should make sure that the sow’s foreparts are kept elevated or level, so that the anesthetic solution does not gravitate forward. Surgical preparation and procedures similar to those in the cow and ewe should be carried out in preparing the operative area and maintaining near asepsis during the operation on the sow. For this purpose a large sterile rubber or plastic shroud to drape over the sow’s body is very helpful. A vertical incision, 17 to 20 cm., in length in the up- per flank region13,38 or a horizontal flank incision parallel to but 1 to 3 inches above the mammae have been rec- ommended.26 A midline abdominal incision site is not recommended for obvious reasons. The large amount of fat between the peritoneum and the body wall may cause some confusion unless it is recognized. One entire horn may be drawn through the incision to the outside before incising and removing the fetuses; or one fetus can be brought to the outside and removed, then the next fetus brought out and removed through the previously-made incision; and so forth until all the fetuses in the one horn have been removed and the horn is completely outside the abdomen. The fetuses may be pulled from the inside of the horn or forced toward the incision by pressure on the outside of the horn or a combination of both in order to facilitate their rapid removal. The pelvic portion of the canal should be examined to be certain a fetus is not left there. If the fetal membranes are expelled with the fetus they are removed. If not expelled with the fetuses they are left in the uterus to be expelled later—usually within 12 hours. The incision is sutured with a single or double row of Lembert or Cushing sutures of No. 1 chronic catgut and that horn replaced. The same tech- nique is followed on the other hom. In exceptional cases, if the uterus is well-involuted it may be necessary to in- cise the hom in several sites. If the uterus is severely infected, introduction of antibiotics—especially the tet- racycline derivatives—is indicated prior to closure of the uterine incisions. The peritoneum and muscle layers are sutured separately with chromic catgut or Dexon by con- tinuous sutures; and the skin with silk, nylon, Vetafil, or umbilical tape. For aftercare of the sow administration of oxytocin and antibiotics are indicated, as in the cow. The sow should be confined in a clean, quiet place for 8 to 10 days, at which time the skin sutures may be removed. Cesarean Section in the Bitch and Queen is very common and useful in the correction of dystocia in these species. It is performed most commonly in primary uter- ine inertia that fails to respond to “feathering,” or va- ginal stimulation of uterine contractions, or to the injec- tion of oxytocin. This condition is seen most commonly in certain toy breeds such as the Dachshund. It is fre- quently required to relieve dystocia in the brachyce- phalic breeds of dogs with large heads and small pelves, such as the Boston and other bulldogs, Pekinese, Box- ers, Pugs, and even the Scotch Terriers and Sealyhams. There is no doubt that cesarean section has been a great boon to these breeds of dogs. The discussion that centers around the fact that this operation has been conducive to the perpetuation of such abnormal breeds is a subject of importance, but is not discussed here because it is not appropriate to this text. Cesarean section may be indi- cated in Cockers, in which for apparently psychotic rea- sons whelping does not progress normally. It is indicated when pelvic fractures, tumors, rickets, or the rearing of a young dog under unfavorable conditions has resulted in dystocia due to a small pelvic canal. It is indicated in secondary uterine inertia in which more fetuses are still in the uterus and dystocia has been prolonged so that even if 1 or 2 fetuses could be removed by traction, the rest would not be expelled, because of uterine atony and fatigue. It may be indicated with 1 or 2 excessively large fetuses, or when a fetus is transversely located in the uterine body and cannot be removed manually. In rare instances it may be indicated for uterine torsion and for retention of one fetus in the uterus following apparently normal parturition, as is seen occasionally in the large breeds, such as the Great Dane and St. Bernard. The cesarean operation may also be used to remove mum- mified fetuses from the uterus and in cases of inguinal hernias containing a portion of the pregnant uterus.- It may be indicated when general debility and inanition make normal parturition impossible. When a greenish-black discharge appears at the vulva it is an indication that the placentas are disengaging, and cesarean might be indi- cated even though probably one fetus or more are dead. The same general indications for this operation apply to the queen. In the queen the most common cause for322 VETERINARY OBSTETRICS dystocia is deviation of the fetal head and neck, and if mutation per vaginam is not successful a cesarean op- eration is indicated. Many veterinarians perform cesarean operations when possibly mutation or forced extraction could be used be- cause they are surer of their results with this operation. They are better acquainted with it than with the other techniques in which fetuses might be injured by im- proper or unskilled use of instruments per vaginam. The operation is frequently employed because it requires much less time and patience of the busy practitioner. Other- wise the veterinarian might have to observe and assist the bitch at intervals for 4 to 6 hours or more. Besides this inconvenience to the veterinarian, it would be more costly to the owner. Lastly, many owners, expecting the bitch to be in dystocia because of its breed or past his- tory, request and expect the veterinarian to perform a cesarean operation. Prognosis—Cesarean section in the bitch when per- formed during the first stage of labor or within 12 hours after the onset of the second stage of parturition when the fetuses are still alive, should result in less than a 2 to 3 percent mortality rate. In many hospitals this may be less than 1 percent. If the operation is not performed until 12 to 24 hours after the onset of labor some of the fetuses may be dead, but the results nevertheless are usu- ally quite good. If the operation is delayed beyond 24 hours after the onset of labor the maternal mortality rate may be 50 percent or more due to shock, toxemia, septic metritis, and exhaustion. In these neglected cases the fe- tuses are usually dead, the uterus diseased and atonic, and hysterectomy may be indicated. In general, bitches should be examined if they have labored for 3 to 4 hours without delivering a fetus. The cause of the dystocia should be determined and if ce- sarean is decided upon it should not be delayed too long by efforts to remove fetuses by other means. Fetotomy is rarely possible in the bitch or cat due to the small birth canal. In cases in which dystocia, relievable only by ce- sarean, is expected on the basis of the previous breeding history or examination, the bitch should be observed closely for signs of beginning parturition. Body temper- ature readings may be made 2 or 3 times daily and when the temperature drops 1 degree or more below normal or goes below 100° F. the bitch is either in the first stage of labor or beginning the second, and a cesarean oper- ation should be performed immediately. Cesarean sec- tion apparently has little effect on the subsequent fertility of the bitch; many bitches have had from 4 to 8 cesarean operations performed without becoming sterile, even though slight to severe adhesions may form at the op- erative site. After 3 cesarean operations adhesions are common and the number of pups per litter decrease and operations are more difficult to perform.- The Operation should be performed in a skillful, aseptic manner under hospital or clinic conditions. Com- plications should be anticipated and prevented or han- dled. Extra aid should be present for receiving the pups as they are delivered. An incubator that provides warmth, 85 to 90° F, and oxygen may save many pups.23 Pre- medication for the canine cesarean operation consists of a small dose of atropine. After the operative site has been prepared an ultra short acting barbiturate is administered followed by a light plane of halothane or methoxyflurane or ether anesthesia. Innovar, a neuroleptanalgesic has been used and followed by naloxone to reverse its action in the bitch and pups after the operation. Local anes- thesia may be used in the bitch in either of the above procedures to reduce exposure to the anesthetic. Dox- apram, a respiratory stimulant, may aid recover of the pups. In the queen the above anesthetics may be used with the exception of Innovar. If local anesthesia is used in the queen diluting 2 percent lidocaine to 0.5 percent is indicated to avoid overdosing.41 In the queen a com- bination of zylazine and Ketamine have also been used but since these drugs also affect the intrauterine live fe- tuses, delayed recovery after birth is to be expected. Ep- idural analgesia is the method preferred in the bitch by some veterinarians.24 The incision may be made through the flank at an oblique angle parallel the last ribs. This site reduces the possibility of eventration but may leave a noticeable scar in shorthaired dogs. The approach takes more time, the horns are harder to reach, and an incision must be made in each horn. A left-flank incision 7 to 12 cm long par- allel to the spine and beginning 3 cm. behind the costal arch and 3 cm above the mammary glands provided bet- ter access to the uterus, and the scar is less noticeable.4 Many other veterinarians prefer the midline, or linea alba, as an incision site. The greatest disadvantages to this site, which are not serious, are possible eventration or injury to the wound by the pups. It has the advantage of easy access to the uterus. Because the withdrawal of the gravid uterus through the incision might predispose to shock, pressure should be applied to the abdomen after removal of the gravid uterus, and then gradually released. To pre- vent shock some veterinarians bring the uterus and a fe- tus to the incision, pack the incision with towels and incise each horn, removing the fetuses by pressure and traction, and keeping the uterus within the abdominal cavity. Because this procedure might result in peritonitis from uterine fluids, it is not desirable unless the fetuses are alive and the uterus not infected. This technique is also more time-consuming. Most veterinarians removeOBSTETRICAL OPERATIONS 323 one horn of the uterus at a time through the abdominal incision. The horn is incised near the bifurcation. The fetuses may be removed from one or even both horns through the same hysterotomy incision. The uterus is in- cised longitudinally on the side opposite the attachment of the broad ligament, care being exercised not to incise through a placental area. After the fetus is removed the placenta will come away by pressure on the outside of the uterine hom over the placental area of attachment. This can be aided by tension on the umbilical cord. As the fetuses are removed the umbilical cord is clamped with forceps which should not be allowed to dangle as this might predispose to hernia. The placenta is cut or tom away. The pups are rubbed with a towel to stimulate respi- rations. The pup’s head is held down, to facilitate drain- age of mucus from the nostrils and throat. If respirations are delayed, the pup should be dipped alternately into hot and cold water, or its umbilical vein injected with a respiratory stimulant like Doxapram. This may also be placed under the tongue and absorbed there.41,55 The pups should be kept warm, 80° F. or higher, until placed with the bitch for nursing. Each hom should be carefully checked to be sure all fetuses are removed. If a fetus should be in the birth canal it should be removed by traction through the vagina or drawn cranially through the incision in the uterine body. The uterine incision is closed by a single or double row of Lembert sutures of catgut. The flank incisions are sutured with several rows of catgut or Dexon with nylon or silk in the skin. The peritoneum on the midline incision is sutured with continuous catgut, the fascia of the linea alba with nylon, and the skin with interrupted nylon or silk sutures. The skin wounds are covered with adhesive if surgery was aseptic. If the wound is likely to be infected it should be left open for daily dressing and bandaging. Gauze or other dressing may be wrapped around the body between the breasts, but not so tightly as to cause discomfort. This is difficult to hold in place. After the operation all pups, especially those of the brachycephalic breeds, should be checked for abnor- malities such as cleft palate, hydrocephalus, and so forth, and deformed pups destroyed. Aftercare of Bitch and Pups—After the bitch has recovered from the anesthesia the pups are placed with her. If she does not encourage their suckling or ignores them she should be restrained or tranquilized while they suckle for the first several days until she “adopts” them. If the bitch should succumb, orphan pups may be raised on rich cow’s milk or goat’s milk, 1 to 5 parts of evap- orated milk and water, or “Esbilac” (Borden’s). A for- mula for feeding pups of 8 ounces of homogenized milk containing 2 egg yolks may also be used. About 1/2 to 3/4 oz. is given every 8 hours for the first week or two and by the third and fourth week about one ounce, 80 to 100 calories per lb. of body weight, is given every 8 hours.2b’39 Pups should be dryed after they are fed. De- fecation in the pups will be stimulated after they have eaten by their being rubbed beneath the tail with cotton dipped in olive oil. In a week or so some pablum may be given. Later they can be fed milk from a dish or pan. Ground meat, cereal and ordinary cow’s milk can be given when they are 3 weeks of age. Pups can be completely weaned at 4 to 5 weeks after birth. The aftercare of the bitch following cesarean operation is similar to that given the cow, in that a small dose of oxytocin 1/2 to 1 cc., 5 to 20 units, or ergonamine is given to aid contraction of the uterus. The bitch should be placed on parenteral antibiotics for several days or more and observed closely for symptoms of shock, peri- tonitis or sepsis the first 6 to 48 hours. If this is sus- pected or occurs, prompt administration of blood and sa- line is indicated, along with keeping the bitch warm. The abdominal wound should be observed for any evidence of infection or breakdown or evidence that the incision has been licked or chewed. If it has, muzzling or other restraint of the bitch may be necessary. If the fetuses are dead, the size and congestion of the mammary glands may be reduced by massaging them with camphorated oil. It is advisable to send the bitch home, where she will be in a familiar environment, as soon as possible after the operation. The stitches may be removed about the seventh day after the operation. Hysterectomy Occasionally hysterectomy may be indicated due to prolonged dystocia, in which much trauma, injury, and even rupture of the uterus has been produced by unsuc- cessful fetotomy, mutation, or forced extraction opera- tions, or the fetus is emphysematous and the uterus is atonic, severely infected and diseased.- In severe uterine torsion in which the uterine circulation is obviously com- promised hysterectomy is indicated. The dam is usually toxic and exhausted, with a subnormal temperature, an- orexia, and a rapid, weak pulse. It may be obvious be- fore the operation or at least at the time of the laparot- omy that cesarean section alone, without hysterectomy, will not save the life of the dam. In cases where there is a severely diseased uterus, hysterectomy offers the only hope of saving the dam. The prognosis is always very guarded to poor, since shock and peritonitis generally cause death in these already poor operative risks. In cases324 VETERINARY OBSTETRICS such as severe rupture or laceration of the uterus during fetotomy or forced extraction, hysterectomy might oc- casionally be considered. In mares, cows, ewes and sows hysterectomy is usu- ally of questionable value as the economic value of the animal does not generally warrant the expense and effort of surgery and aftercare because the mortality is high. Because of the large size of the uterus and fetus or fe- tuses it may be necessary to remove the fetuses first in order to remove the uterus. Contamination of the ab- dominal cavity is difficult to avoid when tying the uter- ine and ovarian arteries and removing the uterus. After removal of the uterus, eversion of the cervix or uterine or vaginal stump offers further severe difficulties. Shock frequently develops. Successful hysterectomy has been reported only occasionally in cows and sows and rarely in mares.28 In bitches and queens hysterectomy is more often suc- cessfully employed because working conditions are good and the animals and their uterus and fetuses are relatively small.- Hysterectomy is often considered in bitches and queens with a prolonged dystocia of 24 to 36 hours or more.- In 52 cesareans and 52 hysterectomies the re- covery rate was 82 percent and 67 percent, respectively. The recovery rate was only 50 percent when the fetuses were putrid.29 The prognosis in cases in which hyster- ectomy is necessary in bitches and queens is therefore guarded. Prior to and during surgery, proper attention should be paid to preventing shock and the contamina- tion of the abdominal cavity. A plentiful supply of in- struments should be available. Because the animal is a poor surgical risk anesthesia should be selected and used carefully. A relatively small dose of a tranquilizer with local anesthesia of the incision site is often used in these cases. A midline incision is favored in a hysterectomy operation. If possible the fetuses should be removed within the intact uterus to avoid contamination of the abdominal cavity or incision. Care must be used in exteriorizing the uterus so that tearing of a vessel and subsequent hem- orrhage does not occur. Double ligatures should be fas- tened securely around the utero-ovarian, uterine and cau- dal uterine arteries. At times excessive fat complicates the placing of tight ligatures around the large vessels in the broad ligament. Forceps are placed across the body and cervix of the uterus after the broad ligament has been incised and the ovaries and uterus are free. The uterus, fetuses, and ovaries may be removed by incising the body of the uterus between the forceps. The serosa of the stump of the uterus should be inverted by a Parker-Kerr stitch as the forceps are removed. After surgery the bitch should be kept warm and given blood and fluids to prevent the shock that sometimes follows the removal of such a large organ. Antibiotics and corticosteroids should be admin- istered to control possible abdominal contamination and necrosis of the liver associated with shock. Careful con- tinuous aftercare and nursing of these cases should be given. References General I- Archibald, J. (1965) Canine Surgery, American Vet. Publ. Inc., Wheaton, 111. 2. Arthur, G. H. (1975) Veterinary Reproduction and Obstetrics, 4th Edit. Bailline and Tindall, London & Williams & Wilkins, Bal- timore. 3. Benesch, F. (1952) Lehrbuch der Tierartzlichen Geburtshilfe and Gynakologie, Urban and Schwarzenberg. Wien-Innsbruck, Aus- tria. 4. Benesch, F. and Wright, J. G. (1951) Veterinary Obstetrics, Wil- liams and Wilkins Co., Baltimore, Md. 5. Bierschwal, C. J. and DeBois, C. H. W. (1972) Fetotomy in Large Animals, V.M. Publ. Co., Bonner Springs, Ks. 66012. 6. Richter, J. and Gotze, R. (1960) Tiergeburtshilfe, 2nd Ed., Paul Parey, Berlin, Germany. 7. Sloss, V. and Dufty, J. H. (1980) Handbook of Bovine Obstetrics, Williams and Wilkins, Baltimore. 8. Tavernier, H. (1955) Guide de Pratique Obstetricale chez les Grandes Femelles Domestiques, Vigot Freres Editeurs, 23 Rue De L Ecole- De-Medicine, Paris, France. 9. Tillman, H. (1965) Cesarean Section in Veterinary Obstetrics, 2nd Ed., Paul Parey, Berlin, Germany. Specific 1. Aehnelt, E., Konerman, H. and Grunert, E. (1962) Verglei- chende Untersuchungen uber die Schnittenbindung am Liegen- den Rind Ventrolateral Links and am Stehenden Rind in der lin- ken Flanke, Wien. Tierarztl. Monatschr. 49, 1, 61. 2a. Arnold, J. P. and Kitchell, R. L. (1957) Innervation of the Ab- dominal Wall of Cattle, Amer. J. Vet. Res. 18, 229. 2b. Baines, F. M. (1981) Milk Substitutes and The Hand Rearing of Orphan Puppies and Kittens, J. Sm. An. Pract. 22, 555. 3. Ball, L. (1979) Personal Communication. (Cornell Conference) 4. Bierschwal, C. J. (1976) The Use of Fetotomy in Large Animal Practice, 9th Ann. Conv. A.A.B.P. San Francisco, Cal. 56-57. 5. Bogedda, G., Lepori, S., Muzzetto, P. and Corta, S. (1966) The Cesarean Operation in Horses, Personal Contribution and Review of the Literature, Veterinaria (Milano) 15, 1, 6. 6. Bracken, F. (1972) Personal Communication. 7. Brone, Debruyne, Boeckx, and Vandeplassche, M. (1966) In- fertility of Cows Following Cesarean Section, Vlaams Dierge- neesk. Tijdschr. 35, 2, 87 (Abstr.). 8. Debackere, M., Vandeplassche, M. and Paredis, F. (1959) Eco- nomic Results of a Study on Cesarean Section and Fetotomy in Cattle, Vlaams Diergneesk. Tijdschr. 28, 1, 1. 9. De Bois, C. H. W. (1958) Cesarean Section in Sheep, Tijdschr. v. Diergeneesk 83, 7, 248. 10. Eden, E. L. (1952) Dystocia in Young and Underdeveloped Cat- tle, Allied Veterinarian, July-Aug. 17.OBSTETRICAL OPERATIONS 325 11. Ellis, T. H. (1958) Observations on Some Aspects of Obstetrics in the Ewe, Vet. Rec. 70, 47, 952. 12. Frank, E. R. and Roberts, S. J. (1940) Cesarean Section in the Bovine, N.A. Vet. 21, 9, 546. 13. Frank, E. R. (1964) Veterinary Surgery, 7th Ed., Burgess Pub- lishing Co., Minneapolis, Minn. 14. Freak, M. J. (1962) Abnormal Conditions Associated with Preg- nancy and Parturition in the Bitch, Vet. Rec. 77, 1323. 15. Getty, R. (1963) Epidural Anesthesia in the Hog—Its Tech- nique and Applications, Proc. 100th Ann. Meeting AVMA, 88. 16. Harsch, J. (1971) Pubic Symphysiotomy, Proc. 4th Ann. Mtg, A.A.B.P., Denver, 21-23. 17a. Hamilton, G. F., Turner, A. S., Ferguson, J. G. and Pharr, J. W. (1978) Slipped Capital Femoral Epiphysis in Calves, JAVMA, 172, 11, 13-18-1322. 17b. Heath, J. S. (1963) Indications and Complications in Cesarean Section in the Bitch. J. Sm. An. Pract. 4, 289. 18. Herr, S. (1979) Techniques for Fetotomy on Schistosomus Re- flexus Calves, Vet. Med/Sm. An. Clin. 74, 7, 1009-1012. 19. Hird, J. J. (1954) Pelvis Splitting as an Aid in Dystocia of Heif- ers, AVMA, Proc. 91st Ann. Meeting, 384. 20. Goldberg, M. A. (1970) Cesarean Section in the Mare, A Re- view of the Literature, Paper for Senior Seminar, N.Y.S. Vet. Col., Ithaca, N.Y. 21. Johnston, D. R. (1963) History of Human Infertility, Fert. and Steril. 14, 3, 261. 22. Juhler, H. (1956) Cesarean Section in Cattle, Nord. Vet. Med. 8, 165. 23. Kirk, R. W. (1958) Canine Pediatrics, Mod. Vet. Pract. 39, 3 and 4, 37 and 52. 24. Klide, A. M. and Sonna, L. R. (1968) Epidural Analgesia in the Dog and Cat, JAVMA, 153, 2, 165. 25. Leonard, E. P. (1950) Canine Obstetrics, N. A. Vet., 21, 9, 590. 26. Mather, E. C. (1966) Lower Flank Incision for Swine Cesarean, Vet. Med. 61, 9, 890. 27. Merkt, H. (1957) Die Schnittenbindung beim Rind in der Neuz- eitlichen Geburtshilfe, M. and H. Schaper, Hannover, Ger- many. 28. Milne, F. J. and Homey, F. D. (1960) Abdominal Surgery in the Horse, Canad. Vet. Jour. 1, 12, 524. 29. Nooder, H. J. (1952) De Operatieve Verlossing van Honden, Tijdschr. v. Diergeneesk 77, 18, 655. 30. Noordsy, J. L. (1979) Selection of an Incision Site for Cesarean Section in the Cow, Vet. Med/Sm. An. Clin. 74, 4, 530-537. 31. Oberst, F. H. (1954) Personal Communication. 32. Oberst, F. H. (1962) There is Still a Place for Surgery in Large Animal Practice, Vet. Med. 57, 3, 219. 33. Oehme, F. W. (1967) The Ventro-lateral Cesarean Section in the Cow, Vet. Med. 67, 889. 34. Patterson, D. J., Bellows, R. A. and Burfening, P. J. (1981) Effects of Caesarean Section, Retained Placenta and Vaginal or Uterine Prolapse on Subsequent Fertility in Beef Cattle, J. An. Sci. 53, 4, 916-921. 35. Railsback, L. T. (1950) Dystocia in the Sow, JAVMA, 116, 874, 27. 36. Rasbech, N. O. (1957) Cesarean Operation in the Cow, Nord. Vet. Med. 9, 721. 37a. Roberts, S. J. (1971) Veterinary Obstetrics and Genital Dis- eases, 2nd Ed., Woodstock, Vt. 37b. Roberts, S. J. and Frank, E. R. (1942) Further Observations on the Cesarean Operation in the Bovine, Cor. Vet., 32, 4, 395. 38. Runnells, L. J. (1981) Obstetrics in Diseases of Swine, 5th Ed., Edit, by Leman, A. D., Iowa State University Press, Ames, Iowa. 39a. Schuijt, G. and Ball, L. (1980) Delivery by Forced Extraction and Other Aspects of Bovine Obstetrics, in Current Therapy in Theriogenology, D. A. Morrow, Editor, W. B. Saunders Co., Philadelphia, Pa., 247. 39b. Sheffy, B. E., Baker, J. A. and Gillespie, J. H. (1961) A Dis- ease-Free Colony of Dogs, Proc. Animal Care Panel, 11, 4, 208. 40. Sherrod, W. W. (1967) Cesarean Section in a Mare, Mod. Vet. Pract. 48, 13, 60. 41. Short, C. E. and Gleed, R. (1982) Personal Communication. 42. Sloss, V. (1974) A Clinical Study of Dystocia in Cattle, I Treat- ment. Austral. Vet. J. 50, 290-293. 43. Tryphonas, L., Hamilton, G. F. and Rhodes, C. S. (1974) Peri- natal Femoral Nerve Degeneration and Neurogenic Atrophy of Quadriceps Femoris Muscle in Calves, JAVMA, 164, 801-806. 44. Vandeplassche, M. (1957-1958) The Normal and Abnormal Presentation, Position and Posture of the Foal-Fetus during Ges- tation and at Parturition, Mededelingen der Veeartsenijschool van de Rijksunivsiteit te Gent. 45. Vandeplassche, M. (1958) Public Lectures on Obstetrics and Gynecology, Cairo Univ. Press, Cairo, Egypt. 46. Vandeplassche, M. (1969, 1970) Personal Communication. 47a. Vandeplassche, M., Bouters, R., Spincemaille, J. and Bonte, P. (1972) Some Aspects of Equine Obstetrics, Eq. Vet. J. 4, 105-108. 47b. Vandeplassche, M., Bouters, R., Spincemaille, J. and Bonte, P. (1977) Caesarean Section in the Mare, Proc. 23rd Conv. A.A.E.P., Vancouver, 75-80. 48. Vandeplassche, M., Ide, M., Vanheuverswijn, A., Paredis, F. and Sierens, G. (1953) Is Foetotomie bij Dystokie van Runderen nog Aktueel?, Vlaams Diergeneesk Tijdschr., 22, 7-8, 1. 49. Vandeplassche, M. and Paredis, F. (1953) Cesarean Section in the Bovine, “Standard Boekhandel” Antwerp-Amsterdam, Neth- erlands. 50. Vandeplassche, M. and Paredis, F. (1953) Cesarean Section in the Bovine, “Erasme,” Paris and Standard-Boekhandel, Ant- werp. 51. Vandeplassche, M., Paredis, F., Bouters, R. and Spincemaille, J. (1963) Cesarean Section for Emphysematous Fetuses, Die Blauen Hefte fur den Tierarzt, Heft 3/4. 52. Vandeplassche, M., Paredis, F. and Debackere, M. (1956) Fer- tility of Cows after Cesarean Section, Proc. Ill Intemat. Congr. on Animal Reprod., Cambridge. 53. Walker, D. F. and Vaughan, J. T. (1980) Bovine and Equine Urogenital Surgery, Lea and Febiger, Philadelphia. 54. Wendt, D. O. (1949) Personal Communication. 55. Wester, R. F. (1961) Respiratory Stimulation of Newborn Pups, JAVMA, 139, 4, 448. 56. Williams, W. L. (1943) Veterinary Obstetrics, 4th Ed., Ithaca, N.Y. 57. Wright, J. G. (1953) Further Observations on Cesarean Section in the Bovine, Jour. Comp. Path, and Therap. 63, 3, 211. 58. Wright, J. G. (1958) Bovine Dystocia, Vet. Rec., 70, 17, 347. 59. Youngquist, R. S. and Bierschwal, C. J. (1981) Percutaneous Fetotomy for Relief of Dystocia in the Cow, Comped for Cont. Educ. II, 4, 67-71.Chapter X DIAGNOSIS AND TREATMENT OF VARIOUS TYPES OF DYSTOCIA In previous chapters the causes, equipment, and op- erations for the handling of dystocia were outlined. In this chapter the various conditions which produce dys- tocia and the practical handling of these problems will be discussed under the headings of: dystocia due to path- ological presentation, position, and posture of the fetus; abnormal size of the fetus; postmortem changes in the fetus; uterine displacements; stenosis of the birth canal; and uterine inertia. Dystocia Due to Pathological Presentation, Position, and Posture of the Fetus Pathological presentations, positions, and postures are apparently due to a combination of uterine inertia and a reduced viability and activity in the fetus especially dur- ing the first and second stages of parturition. Uterine in- ertia may be caused by hormonal or disease factors caus- ing a lack of, weak or irregular contractions of the uterine wall. If the fetus is diseased, deformed, lacks vigor, or is dead, its movements and righting reflexes are weak or absent, and postural abnormalities in such cases are common. In the mare, bitch, and sow these factors when combined with a normal dorso-ilial or dorso-pubic po- sition prior to parturition may result in the failure of the fetus to rotate into a normal dorso-sacral position at par- turition. As the fetus is forced through the birth canal the catching or impinging of an extremity at the pelvic inlet causes a progressive flexing of that extremity as the remainder of the fetus passes beyond it. Transverse preg- nancies caused by uterine disease, abnormal attachment and development of the fetus and its membranes, or in the case of multipara a single fetus developing in both horns transversely across the body, usually result in dys- tocia. (See Figures 86, 89, 90.) Dystocia in Anterior Presentation may result from the following types of abnormalities: Dorso-ilial or Dorso-pubic Positions are observed in all species as a cause of dystocia, especially in unipara, particularly when the fetus is of normal or large size. In rare cases small or premature fetuses are expelled in these abnormal positions. In these dystocias the fetus should be rotated into a normal dorso-sacral position before being removed. (See Figure 90.) Before doing this, one should carefully observe and examine the uterus and genital canal to make certain that torsion of the uterus is not the cause of the abnormal fetal position. If torsion is present the fetus should be rotated in the direction which will reduce the torsion. Many of the fetuses found in this position are weak or dead. Lubrication of a dry birth canal prior to rotation of the fetus is of great assistance. Deviations of the Head and Neck are common types of abnormal posture in anterior presentation causing dys- tocia in all species. In swine, because the neck is so short, this type of dystocia is very rare. The deviation of the head and neck may be in any direction. Lateral deviation of the head is seen most often in unipara. The deviation may be directly lateral, with the head along- side the thorax in the bovine fetus, or alongside the flank of the equine fetus. This lateral deviation may also be obliquely upward or downward, and occasionally the head may be rotated 45 to 90 degrees on the neck. Diagnosis in the cow is easily made by finding the two forelimbs in the birth canal, but not the head. By passing the hand and arm as far alongside the fetal body as possible and then carrying it around the body, the head and neck are found and the direction of the deviation noted. In the mare this may be more difficult because the head is usu- ally out of reach of the hand. By locating the withers and mane or the trachea of the equine fetus these may be followed to the left, right, downward or upward and the direction of the deviation determined. If the bovine fetus is alive and labor has not been in progress more than 4 to 12 hours the deviation may be corrected with the least amount of difficulty by means of mutation. This is best performed under epidural anesthesia with the an- imal standing. If the animal is down it should be placed in lateral recumbency with the rear parts higher than the foreparts and with the fetal head in the upper flank of the dam, above the fetal body. Repulsion on the fetal chest in an oblique manner is performed. The body of the fetus is pushed away from the fetal head and neck so that room is produced to allow correction by traction on the fetal head. The incisor teeth should be guarded to prevent laceration of the uterus. If the dam is recum- 326DIAGNOSIS AND TREATMENT OF VARIOUS TYPES OF DYSTOCIA 327 Figure 89. Dystocia due to a transverse presentation of a single fetus in a Pomeranian bitch. This was relieved by a Cesarean operation. bent it is helpful, particularly in the mare under general anesthesia, to have an assistant exert caudal pressure on the fetal head through the mare’s flank, helping to force it back toward the operator’s hand. In the mare caudal traction on a loop of chain passed around the neck or the use of a detorsion rod to push the chain loop toward the head before applying traction may aid in bringing the fetal head near enough the pelvis to grasp with the hand, hook or snare and thus correct the deviated posture. If the neck and head are twisted this is corrected in the uterus by grasping the muzzle or the orbits with fingers and rotating the head in the proper direction as traction is applied to the jaw, drawing the head and the forelimbs into the birth canal. In the bitch and queen lateral de- viation is corrected by vaginal manipulation with the fin- ger, and pressure applied through the abdominal wall. Forced extraction should never be applied to these cases of deviation of the fetal head and neck without first cor- recting the abnormal posture. If mutation fails because the fetus is emphysematous or because the uterine wall is contracted tightly around the fetus, fetotomy and am- putation of the head and neck with the fetatome is in- dicated. Occasionally it may be necessary to amputate the opposite forelimb at the elbow joint or to remove the entire limb in order to move the fetus nearer the vulva so that the wire can be placed around its neck. In the bitch and queen cesarean section or in exceptional cases hysterectomy may be indicated. Wry-neck is seen occasionally in equine and bovine fetuses. It usually occurs in transverse bicomual preg- nancy in the mare in which movement of the fetal head and neck is restricted or prevented during most of the gestation period. It may occur in a longitudinal preg- nancy with the fetus in one horn and the body. The outer bones of the face become convex while the facial bones lying against the fetus are concave, due to the pressure applied by the uterine wall. The cervical vertebrae are curved and the articulations and atrophied muscles pro- duce a sharply-bent “muscle contracture” condition of the neck resembling torticollis that cannot be straight- ened, even outside the dam, without fracturing the cervi- cal vertebrae. A bicornual or transverse pregnancy with a wry-necked fetus may rarely at the time of parturition undergo spontaneous version into an anterior or posterior presentation.42 In posterior presentation dystocia seldom if ever occurs. The extreme bend in the neck, the stiff, firm neck, and the fact that the head and neck move with the fetal body and cannot be straightened, aids in con- firming the diagnosis. Fetotomy is indicated and am- putation of the head and neck is simple and practical Figure 90. Normal dorso-pubic position of an equine fetus late in gestation. The fetus must rotate into a dorso-sacral position during the early stages of parturition or a dystocia will result.328 VETERINARY OBSTETRICS with the fetatome. Removal could also be effected by the removal of the opposite forelimb and evisceration. With forced extraction the fetus could then be withdrawn with the head occupying the space of the removed vis- cera. Downward deviation of the head between the fore- limbs is occasionally seen in all species except swine. In mild cases, only the nose of the fetus is caught on the brim of the pelvis with the forehead entering the pelvic inlet, “vertex presentation.” In more severe flexing of the head and neck the ears and the top of the head are presenting, “poll presentation.” This is usually corrected by mutation by repelling the fetus and grasping the muz- zle of the fetus and raising it into the pelvic cavity. In the more severe cases the neck extends between the fore- limbs, “nape presentation,” and the head is against the fetal sternum or abdomen. This latter condition is more difficult to diagnose but by means of careful palpation the operator will notice that the forelimbs do not come together, and that in the mare the mane of the fetus may be felt between the legs, and the head found beneath the fetal body. In cases which are diagnosed early, mutation may correct the deviation. As an aid in relieving this type of dystocia, after the fetus is repelled a forelimb may be flexed alongside the body and the abnormal pos- ture of the head and neck corrected by moving them lat- erally beneath this leg. The abnormal position of the limb is then corrected and the fetus removed by traction. In the mare, or in bovine cases diagnosed after prolonged dystocia, fetotomy is necessary. Removal of one fore- limb and then correction of the deviation by mutation has been recommended.42 It may be advisable to am- putate the head and neck and one forelimb by a single cut with the fetotome when the fetus is emphysematous or the uterus strongly contracted. In some cases cesarean section may be indicated in the bitch and queen. Upward deviation of the head is rare in the cow and mare but occasionally it is found as a cause for dystocia in bitches and queens. The handling is the same as in lateral de- viation of the head and neck. Deviations of the Forelimbs are relatively common causes for dystocia in uniparous animals. They are rarely a cause for dystocia in multipara because their forelimbs are short and flexible. In unipara, especially the cow and mare, normal birth cannot occur, unless the fetus is very small or premature, with one forelimb extended or re- tained alongside the body. Forced extraction should not be attempted. In ewes normal birth can occur with one forelimb retained. If dystocia is present with this posture and the ovine fetus is not too large, dystocia may be relieved by forced extraction without mutation. During birth the shoulder and large shoulder joint are displaced forward alongside the neck when the forelimb is ex- tended in the normal manner. This is made possible by a lack of a clavicle in these species. Pathologically when a portion of the forelimb is caught at the pelvic inlet or in the birth canal the leg is forced backwards toward the body, flexing the shoulder and the elbow joints. Dys- tocia results from the shoulder being pushed back over the chest, and thereby increasing the pectoral diameter of the fetus. In mild, early dystocia the toe may be caught on the pelvic brim or by a fold in the genital tract, and the fetlock then becomes flexed. The head is present in the birth canal or at the vulva, with one or no forefeet. Mutation by repulsion of the fetus and traction on the retained limb corrects the dystocia. The fetal toe or claw should be cupped in the operator’s hand or handled care- fully so that a fold of uterus or birth canal is not caught, causing a laceration or rupture of the genital tract. A more severe dystocia is present when the knees are flexed, knee-flexed posture, or the forelimbs are extended be- neath the fetal body. In these cases if the fetal head is not extending through the birth canal the condition may be corrected by mutation. The fetus is repelled under epidural anesthesia. The knees are grasped and repelled cranially and laterally into the cow’s flank as the feet are extended medially and caudally into the birth canal. If possible the body of the fetus should be repelled into the flank of the dam opposite the side where the abnormal posture of the forelimb is being corrected. In dystocia cases when the head is outside the vulva repulsion is very difficult or impossible unless the fetus is small, because the head rapidly becomes very edem- atous. Decapitation should be performed especially if the fetus is dead or emphysematous. Following decapitation the fetus is repelled and the abnormal posture of the fore- limbs corrected. If the forelimb is extended beneath the body traction on the forearm and repulsion of the body cranially and dorsally will bring the leg to a knee-flexed posture. In a very few cases it may be necessary when the fetus is emphysematous and the uterine wall closely invests the fetus to remove the forelimb extended be- neath the body by a fetotomy operation. Once the legs have been brought into the birth canal they should be extended by traction and the fetus removed by traction on them and on the head or stump of the neck vertebrae if decapitation has been performed. In rare cases to avoid fetotomy a small bovine fetus may be withdrawn with one leg retained, when the head is outside the vulva and the thorax is in the pelvic cavity. Dystocia due to the one or both forelegs being crossed over the neck is rare except in the mare. This abnormal posture increases the chest diameters as the elbows are forced against the pubis. It may also result in the dor-DIAGNOSIS AND TREATMENT OF VARIOUS TYPES OF DYSTOCIA 329 sally-directed hooves engaging the roof of the vagina and causing rupture of the vagina, rectum, or perineum. This condition is readily diagnosed. Traction by the opera- tor’s hand or with a snare or chain by an assistant should be placed on the uppermost pastern or foot, if both legs are crossed over the neck, and this leg should be pulled upward and then laterally and downward and medially so the leg is brought beneath the neck and head and fully extended. Elevation of the head helps in placing the legs beneath the head. Repulsion and epidural anesthesia usu- ally are not necessary unless the foot is engaged in the dorsal vaginal wall. Flexion of the anterior limbs at the elbow is a rela- tively common cause for dystocia particularly in young cattle. It is caused by the olecranon catching on the brim of the pelvis with the leg not fully extended as the fetus passes into the birth canal. In many instances both el- bows are impacted. The elbow and shoulder joints are flexed, greatly increasing the pectoral diameters of the fetus. This condition is diagnosed by the fact that the nose of the fetus is resting on or below the fetlock joints while in the normal extended position the nose rests on the middle of the metacarpal bone. By feeling along the fetal leg the operator finds the olecranon firmly wedged against the pelvic brim. This condition is easily cor- rected by traction first on one limb and then on the other; or the operator can place his hand under the olecranon and raise it as traction is applied to the limb extending it into its proper posture. Interlocking of the Maternal and Fetal Pelves or “Hip lock” in Anterior Presentation is commonly ob- served as a cause for dystocia in heifers. The major tro- chanters of the fetal femurs are the structures that fail to pass through the bony pelvis of the dam. The tuber coxae in calves are small and rarely if ever are the cause of dystocia. Dystocia due to hip lock may be caused by an improper direction of traction putting tension on the lin- ea alba and increasing the pelvic diameter of the fetus and by traction causing the maternal pelvis to tip cau- dally and dorsally, thereby reducing the diameter of the pelvic inlet of the dam. In most of the naturally occur- ring longstanding cases of interlocking of the maternal and fetal pelves, obturator paralysis is observed and al- ways should be looked for before relieving the dystocia. This type of dystocia is easily diagnosed by the fact that the head, forelimbs, and a portion of the thorax extend through the vulva. In dystocia due to fetal ascites, or the hind limbs extending alongside the body or against the pelvis as in the Perosomus elumbis monster, the thorax seldom extends through the vulva. There should be a careful examination of the relative sizes of the maternal and fetal pelves. If traction is decided upon, the fetus and birth canal should be well-lubricated. Traction should be applied by assistants or by the fetal extractor, pulling the fetus in an arc-like curve, first backward and then downward and if the dam is down even exerting leverage with the handle of the extractor between the rear legs. In other cases lateral traction around the dam’s hips may aid by pulling the fetal pelvis through the maternal pelvis at an oblique angle or in a dorso-ilial position. Some veterinarians rotate the fetus by placing the arms be- tween the fetal legs and over the neck as gradual traction is applied to rotate the fetal pelvis so it can pass through the greatest diameter of the maternal pelvis in an oblique manner. Others tie the forelimbs of the dead fetus to- gether and by placing a long handle between them will rotate or twist the fetus as a traction is applied. The use of the long blunt hook placed over the fetal ischial arch or into the caudal border of the sacro-sciatic ligament aids in placing traction on the pelvis, lifts the fetal pelvis in the maternal pelvis, and pulls the fetal pelvis in an oblique manner aiding in the relief of the dystocia. If the fetus is dead an extensive transverse incision in the ab- domen of the fetus caudal to the xiphoid region followed by evisceration, insures traction being applied not to the linea alba or fetal pubis but only on the spinal column. This produces extension of the fetal pelvis on the spinal column and facilitates withdrawal of the fetus. If judicial traction fails to relieve the dystocia, fetotomy should be performed by bisection of the fetal pelvis with a feta- tome. This is made less difficult by evisceration after transversely incising the abdomen. Forward Extension of the Hind Limbs beneath the Fetal Body or the “Dog Sitting” Posture is observed uncommonly in the mare and cow. The reason for the dystocia may not at first be obvious. The cranial extrem- ities are usually presented normally and pass into the birth canal before dystocia results. Passing the hand forward along the fetus, the operator can feel the hind feet and limbs entering the pelvic cavity alongside the fetal ab- domen. This examination will serve to differentiate the condition from twins, fetal ascites, or a fetal monster such as a Perosomus elumbis. This condition is seen most commonly in the mare because it is possibly a ver- tical form of the transverse ventral presentation in which the anterior portion of the fetus became dislodged and entered the pelvis. The prognosis in the mare should be guarded to poor. Traction by laymen or veterinarians not recognizing this condition may cause severe damage es- pecially if the hind feet are caught beneath the brim of the pelvis instead of extending into the pelvic cavity. This operation may be handled by mutation only in large mares with a small fetus, or in the cow by repelling the hind limbs into the uterine cavity as the fetus is pulled330 VETERINARY OBSTETRICS from the vulva. Forced extraction should never be used. Fetotomy is often the method of choice and consists of detruncating the fetus with the fetatome through the pos- terior thoracic or anterior lumbar region. Sometimes evisceration is helpful if performed before detruncation. Often it is necessary to make two cuts through the trunk in order to remove enough of it so that the rear quarters can be manipulated. Krey’s tongs placed into the ex- posed vertebrae assist greatly in drawing the lumbar por- tion of the trunk toward the vulva, in placing the feta- tome wire and in removing more of the trunk of the fetus. After detruncating, chains are placed on the hind pas- terns, the rear quarters are repelled into the uterus as the hind feet are drawn into the birth canal and the hind quarters are rotated from a dorso-pubic to a dorso-sacral position and then removed by traction. If necessary the pelvis may be bisected with a fetatome. In some in- stances cesarean section may be preferred for the cor- rection of this serious type of dystocia. Dystocia in Posterior Presentation is relatively much more common than dystocia in anterior presentation. Posterior presentation is considered pathological in all except the multiparous animals. The frequency of phys- iological birth in posterior presentation in the mare and cow is quite low. The fetal mortality in posterior presen- tation is high. Most authorities advise rather prompt re- moval of the live fetus in posterior presentation to pre- vent asphyxiation following pressure on or rupture of the umbilical cord. Most fetuses are usually dead at the time of the examination. Dystocia due to Dorso-ilial or Dorso-pubic Posi- tions in Posterior Presentation is similar in nature to, and handled by rotation in the same manner as patho- logical positions in anterior presentation. They are usu- ally less difficult to correct, because the head and neck are not present to offer obstruction to rotation as in an- terior presentation; and, because the rump is more rounded than the withers, rotation is easier. Occasionally, in the mare in posterior presentation, the hind feet may engage the roof of the vagina and cause lacerations of the va- gina, vulva, and rectum. Lifting the fetal buttocks up- ward and to one side or the other aids rotation of the fetus by opposite traction on the two rear limbs. Prior to correcting the abnormal position, the operator should de- termine if the birth canal requires lubrication and whether torsion is present. Deviations of the Hind Limbs in Posterior Presen- tation are common in uniparous animals. They are un- common as a cause for dystocia in multiparous animals because of the latter’s small, flexible limbs. These are caused by failure of the hind limbs to extend into the pelvic cavity or by the foot or fetlock catching on the birth canal or pelvic brim, causing the hind limb or limbs to become flexed. When one joint becomes flexed all joints in the hind limb flex except when the hind leg is extended beneath the body. The flexion of the limbs at the tarsus or “hock-flexed posture” causes the flexing of the rest of the articula- tions, followed by dystocia. It may be diagnosed by pal- pation of the perineal region and tail and then below these the point of the flexed hock either in or just below and cranial to the pelvic cavity. This condition should be dif- ferentiated from ankylosed rear limbs seen in Peroso- mus elumbis. Correction of this dystocia is easily ac- complished by mutation when dystocia has not existed too long. After epidural anesthesia is administered the fetal buttocks are repelled cranially and to one side. The flexed hock is grasped and repelled forward and laterally into the opposite flank while the foot is drawn caudally and medially and extended through the birth canal (see Figure 88). The hoof or claw should be guarded or cupped in the hand as it is brought back over the pelvic brim so that it does not catch and lacerate the soft structures of the uterus or birth canal. If the dam is recumbent the rear parts should be elevated above the fore parts and the flexed fetal limb should be in the upper flank of the dam so that room is available for mutation and so that the weight of the fetus does not rest upon the flexed limb. In cases of a very large or an emphysematous fetus, or a contracted uterus that will not allow repulsion and room for mutation, or in recumbent cases in which mutation is very difficult, fetotomy with amputation of the rear limb at the tarsus may be necessary and is simple to per- form with the fetatome. Rarely in the mare the flexed rear limb may become wedged in the pelvis with the hock impacted against the sacrum and the fetlock against the floor of the pelvis. Amputation of the tarsus is the safest procedure to follow as it prevents further lacera- tion or contusion of the birth canal. Occasionally the rear limbs will have the stifles flexed with the tibias impacted against the pelvic brim. Repulsion of the fetus, lifting the femorotibial joint upward with the hand, as traction is exerted on the pastern, will remove this cause for dys- tocia. Complete Retention or Extension of the Rear Limbs beneath the Body, or Breech Presentation is observed frequently as a cause for dystocia in animals. This is a more advanced case of retention of the rear limbs than the hock-flexed posture. The rear limbs are usually com- pletely extended beneath the fetus. The buttocks and tail are in the pelvic cavity and occasionally the tip of the tail is hanging from the vulva. In many cases no part of the limb can be reached until the fetal buttocks are re- pelled cranially out of the pelvic inlet. Epidural or gen-DIAGNOSIS AND TREATMENT OF VARIOUS TYPES OF DYSTOCIA 331 eral anesthesia is very helpful or necessary. By grasping the cranial aspect of the tibia with the hand or passing a chain around the tibia the operator can pull the fetal leg back into a hock-flexed posture as the fetal hind quarters are repelled forward and upward. If this is pos- sible the procedure is the same as outlined previously (see Figure 88). If, however, the fetus is dead, emphy- sematous, or large, and the uterine wall has contracted around the fetus so that room for mutation is not avail- able, fetotomy is indicated. Forced extraction is seldom indicated, warranted, or necessary. Bisecting the fetal pelvis in breech presentation in posterior presentation is easily performed with the fetatome by passing the feta- tome wire around one hind leg, placing the head of the fetatome on the opposite hip and making a diagonal cut through the fetal pelvis. In multipara forceps may be ap- plied across the fetal hips after lubrication and the fetus removed by traction; or the hind limbs may be extended into the birth canal and traction applied by a snare, or manually with gauze wrapped around the rear legs of the fetus. Excessive traction in multipara is to be avoided. In severe or prolonged dystocia in multipara, cesarean section or hysterectomy may be indicated. Hip Lock in Normal Posterior Presentation is oc- casionally a cause for dystocia, especially in heifers. In posterior presentations, uterine inertia or delay in the second stage of labor are commonly observed. For this reason, in many cases traction is applied successfully by laymen, or the veterinarian may be called to effect a sim- ple delivery with the fetus in posterior presentation, and its hind limbs lying in the birth canal. This should not be termed, or confused with, true hip lock, where, as in anterior presentation, the width of the fetal pelvis at the level of the greater trochanters is greater than the bisiliac diameter of the maternal pelvis. In hip lock in the pos- terior presentation, the fetus should be repelled and lu- bricated, if necessary. Traction should be applied to only one rear limb at a time. Some veterinarians will tie the two rear limbs together, place a long handle or their arms between them and rotate and twist the hips as traction is applied. This causes the fetal pelvis to pass through the maternal pelvis at an oblique angle or in a dorso-ilial position necessary to effect a correction of the condition. If this fails, because of the large size of the fetus or the small size of the maternal pelvis, or both, then cesarean section or fetotomy should be considered. If the fetal hips can pass through the pelvis, little difficulty will be encountered with the chest and pectoral girdle. In rare cases fetal ascites may cause dystocia in posterior pre- sentation, simulating a hip lock condition. In dystocia due to severe hip lock, if the fetus is alive and the birth canal small, cesarean section should be given serious consideration. If the birth canal is relatively large and the fetal size not excessive, fetotomy may be the pro- cedure of choice. This is accomplished by amputation of the rear limb at the hip joint or preferably by bisecting the pelvis with the fetatome, as previously described un- der fetotomy. Dystocia due to Bicornual Pregnancy or Trans- verse Presentation is rare and is seen most commonly in the mare. In rare instances it may occur in all species except swine, in which it has never been reported. The incidence of this type of pregnancy was reported as 1 in 1000 equine births.35 This author believes it may be even more rare. Some bicornual pregnancies might possibly undergo spontaneous version at the time of parturition into an anterior or posterior presentation,41,42 but this is questioned. For a transverse presentation to occur it is essential that either a bicornual pregnancy be present or that a fetus in a normal longitudinal pregnancy become deflected at parturition across the pelvic inlet into the opposite horn. The former condition, a primary bicomu- al pregnancy, has been described most commonly in mares, bitches, and cows (see Figures 86 and 89). It is possible for it to occur also in ewes and queens. Sec- ondary bicornual pregnancy may occur occasionally in multiple or bicornual pregnancy in ewes, does and cows or in bitches and queens. When a fetus is wedged in the birth canal, the next fetus may be forced across the uter- ine body into the opposite horn; when both horns are large one fetus may fail to enter the birth canal in a proper manner and be forced into the opposite horn. In bitches bicornual or transverse pregnancy is seen most com- monly in conceptions with a single fetus that develops across the body of the uterus with the fore quarters in one horn and the rear quarters in the other horn and the dorsum toward the pelvic canal. It is suggested that this is a natural attempt of physiological forces to equalize the load of pregnancy between the two horns. Usually this single canine fetus is large. Transverse pregnancy has not been reported in swine because of the very acute angle at which the horns meet the body and the short compact body of the porcine fetus, making transverse pregnancy a near impossibility. In the cow the trans- versely developing fetus must assume a U-shape, with portions of the fetus in both horns. It is necessary that the dorsum of the fetus becomes convex and lies against the cervix. In cattle this condition is extremely rare. In sheep it has been observed occasionally in cases where triplets or quadruplets cause a great distention of the uterine horns, and a transverse presentation of one fetus may develop at the time of parturition. In rare cases an equine body pregnancy may occur with the fetus in transverse presentation, with only a small portion of the332 VETERINARY OBSTETRICS cranial and caudal parts of the fetus in each horn. Transverse Ventral Presentation is the transverse presentation most commonly observed in the mare. The limbs are extended into the uterine body. The occurrence of wry neck is common in equine fetuses developing transversely. Thus at parturition the four limbs are wedged across each other in the pelvis. The head is usually out of reach alongside the fetal body. Expulsive efforts by the mare or traction by laymen result in failure to relieve the dystocia. Due to the nature of the transverse presen- tation little or no damage of the birth canal or uterus usually results from these efforts. It is necessary to care- fully examine the limbs to differentiate the fore and hind legs, so tightly are they impacted and wedged across each other. In certain cases the feet may protrude from the vulva. The prognosis in transverse ventral dystocia in the mare is fair to good depending upon the condition of the mare and her genital tract. Occasionally the transverse ventral presentation is somewhat oblique in presentation, with no portion of the fetus extending into the pelvis. Possibly these are partially rotated bicomual pregnan- cies. In these cases it is difficult or almost impossible to relieve the dystocia and save the mare without resorting to cesarean section. To correct the usual transverse ven- tral pregnancy, mutation alone—by repelling the fore parts and applying traction on the rear limbs as the forelegs are flexed and repelled along with the fore parts—can be accomplished only when the fetus is small and the uterus and birth canal are relaxed and large. Epidural analgesia or general anesthesia is usually necessary. The generally accepted manner of relieving this type of dys- tocia is to remove the forelimbs by amputation at the humero-radial joint with the fetatome. It may be nec- essary or advisable to amputate the rear limbs at the tar- sus in order to provide room for amputating the fore- limbs. By applying traction with rotation of the rear limbs and repulsion on the fore quarters or sternum, the fetus is turned by version and rotated into a posterior dorso- sacral position. With the fetus in a posterior presentation the fetal head and usually wry neck do not cause diffi- culty for the operator. Aftercare of these bicomual preg- nancies in the mare is important, as metritis and vaginitis are likely to develop. The Compound or Rotated Bicomual Pregnancy is of rare occurrence in the mare. It is basically a bicomual pregnancy, usually ventral, that during the latter stages of gestation rotates so that the fetus comes to rest be- neath the elongated vagina and uterine body. The dor- sum of the uterine horns is ventral and the ventral por- tions of the horns lie dorsal to the fetus, with the legs of the fetus pointing cranially and dorsally. This rotation of the two horns may be nearly a complete 180 degrees. At the time of parturition the birth canal is very long and the elbow may be the only portion of the fetus that can be reached by the operator. The rest of the fetus may be palpated through the long narrow birth canal, below the hand and arm. For this reason it may occasionally be confused with an extrauterine fetus. Occasionally the ro- tation may not be through 180 degrees, and the fetus may be resting on its back, as the uterine horns have rotated only 90 degrees; but here too the birth canal is long and narrow, offering a serious obstacle to birth. In the author’s limited experience on only 6 to 10 of these rotated bicomual pregnancies, the mare in most in- stances had a history of dystocia or retained placenta the previous year. Another report did not confirm this as- sociation.35 The symptoms of dystocia in these rotated bicomual transverse presentations are mild, resembling the first stage of labor. Tenesmus or straining is absent or slight because the fetus does not enter the pelvic canal and stimulate labor. In this respect it resembles torsion of the uterus. By the time the veterinarian is summoned to examine the mare, in many instances 24 to 48 hours after the onset of parturition, the uterus is well-con- tracted and the fetus is often emphysematous. A cesar- ean operation offers the only hope for saving the mare with this type of dystocia. The prognosis is usually guarded. In many cases consultation may be desirable whether the mare is destroyed or a cesarean operation performed. Fetotomy is impossible because of the stretched narrow, long birth canal. Transverse Dorsal Presentation is very rarely ob- served in the mare but usually occurs in the rare trans- verse pregnancies in ruminants and carnivora because of the sharp angle at which the two horns leave the body. In cases which have had an early diagnosis, mutation may be performed by repelling one end of the fetus— preferably the cephalic portion—and by putting traction on the opposite, or caudal extremities of the fetus by means of chains, Krey’s hooks, or a blunt hook inserted through an incision in the skin. If version of the fetus into a posterior presentation cannot be brought about then version into an anterior presentation should be at- tempted. When mutation fails fetotomy is often suc- cessful in the large animals and is accomplished by pass- ing a fetatome wire around the fetus in the lumbar region and bisecting the fetus so each half may be removed sep- arately. If this cannot be done with the fetatome then the skin over the lumbar region should be incised trans- versely, the back bone broken with a chisel, and the fe- tus eviscerated. The fetatome wire may then be passed around the collapsed body of the fetus and the body di- vided and removed. In the bitch mutation is usually im- possible and cesarean section is the method of choice.DIAGNOSIS AND TREATMENT OF VARIOUS TYPES OF DYSTOCIA 333 This may also be decided upon the the cow and mare. Dystocia Due to the Umbilical Cord and Pla- centa—Dystocia caused by the cord being wrapped around a portion or extremity of the fetus does not occur in domestic animals. Occasionally the umbilical cord may be found around a leg, especially a rear leg, of the fetus. In this position it will usually rupture before causing dys- tocia. Thus it may be the cause for the death of the fetus by asphyxia. The belief that amputation of the fetal limbs can be caused by the umbilical cord being looped around them is erroneous. A bovine dystocia due to a very thick amnion that required incising to deliver a normal live calf has been described.21 This appeared to be a vascular lesion involving the entire amnion as little edema was present. Dystocia Due to Abnormal Size of the Fetus Dystocia may occur as a result of fetal giantism, ex- cessive volume of parts of the fetus, excessive volume of the fetal fluids (hydrops), fetal monsters, and multiple births in uniparous animals. Fetal Giantism is observed only in rare instances in domestic animals. True fetal giantism is seen most com- monly in the cow and occurs only as a result of a pro- longed gestation period of over 300 to 310 days. True fetal giantism with prolonged gestation has been re- ported only very rarely in other domestic animals. In mares that carry foals 365 days the foals are not excessively large. An inbred herd of Holsteins and an Ayrshire herd have been described,18'23,43 in which fetal giantism was due to a simple recessive hereditary factor. This condi- tion has been described in other breeds of cattle.1617 The cows carried their fetuses over 310 days. The fetuses were excessively large and the cows showed no signs of pelvic relaxation and little or no mammary development prior to parturition or at the time that normal parturition was expected. All the calves died shortly after birth even when a cesarean operation had been performed. These calves had possible anterior pituitary gland abnormali- ties, hypoplastic adrenals and an abnormal glucose me- tabolism.22 Most fetal giants have long hair, long hoofs, and the incisor teeth are well-erupted. In many cases hairballs may be found in the amniotic cavity. Fetal giants are poorly viable and often male. When a bovine fetus weighs over 130 lbs. it may be termed a fetal giant. Pro- longed gestation does not necessarily indicate the pres- ence of fetal giantism. In cases of excessively prolonged gestation in Guernsey cattle 19 (See Duration of Gesta- tiona and Initiation of Parturition) most fetuses are small, immature and pathological and in some cases mild hy- drops of the amnion and allantois may occur. Dystocia in these cases is uncommon and not severe. Prolonged gestation may also rarely occur in cattle and other species associated with congenital defects of the head such as hydrocephalus,17 with cerebral hernia, or a Catlin mark, with a reduced size of the cranial cavity and in ewes grazing on Veratrum californicum result- ing in fetal cyclopia and often associated giantism. These animals have an abnormal or hypoplastic pituitary gland and hypoplastic adrenals. As mentioned previously nor- mal or increased amounts of glucocorticoids are neces- sary in these species to initiate parturition. When this does not occur gestation is prolonged and the fetus con- tinues to grow in size. Oversized lambs weighing more than 20 pounds are occasionally described.15 Prolonged gestation and oversized lambs were reported in Karakul sheep in Southwest Africa.8 In these cases of prolonged gestation and fetal giantism in sheep and those in cattle the fetus in many cases dies after a variable period and then a number of days later the dam attempts to expel it. In many cases the pelvic cavity and genital tract is not properly relaxed, there is a lack of fetal fluids, udder development is often lacking and severe dystocia occurs. In a few cases beginning mummification of the large fe- tus may begin before the fetus is expelled. In cows and ewes the mortality is high due the severe dystocia, uter- ine inertia, septic metritis, and retained placenta. The condition of fetal giantism should be carefully dif- ferentiated from a large fetus, especially in the large breeds of cattle, causing dystocia due to fetopelvic dispropor- tion at the end of a normal gestation period when the relatively small size of the birth canal makes the large fetus seem a “giant.” This latter condition, resulting in dystocia, may occasionally be handled in a mature cow by forced extraction. Percutaneous total fetotomy might be considered in selected cases.6 44 If the birth canal is small and underdeveloped or not relaxed, and the fetus emphysematous, fetotomy is extremely difficult or im- possible to perform. Cesarean section should be consid- ered. Under certain conditions slaughter might be rec- ommended. If fetal giantism is discovered or suspected at 280 to 300 days of gestation, and parturition does not seem im- minent, a daily dose of 15 to 20 mg. estradiol alone or together with 20 to 40 mg. of dexamethasone or 5 to 10 mg. of flumethasone repeated daily or every third day and possibly combined with 25 to 40 mg of prostaglan- din F2a might be indicated to induce parturition or abor- tion. Farge repeated doses of estrogen, such as 60 to 240 mg. of stilbestrol every 24 hours, resulted in 13 to 16 cows calving within 2 to 5 days.37 These were cases of334 VETERINARY OBSTETRICS prolonged gestation, where the fetuses had been carried 9-1/2 to 12 months. Lactation was not affected in most of these cattle so treated. (See Artificial Induction of Abortion.) When parturition is artificially produced the cow should be observed carefully so that aid may be given if necessary. Cesarean section might be used to terminate the prolonged pregnancy; however, metritis and retained placenta invariably complicate the treatment. Slaughter should be seriously considered in dairy cattle since milk production is greatly reduced. Dystocia Caused by Excessive Size of Parts of the Fetus may be due to rare instances of hypertrophy of any gland; a tumor such as a melanoma, sarcoma or oth- ers (see Tumors of the Newborn); a pathological enlarge- ment or cystic dilation of any hollow or secreting organ or structure due to an anomaly in development causing a stenosis or an obstruction to the release of fluid. Re- ports show that dystocia may be due to an enlarged fetal thyroid, thymus or kidney, polycystic kidney, cystic di- lation of the ureter,30 hydrocephalus, distention of the rumen in a Schistosomus reflexus monster or fetal as- cites. If forced extraction is not successful, incision of the abnormal glands or cystic enlargements to allow the escape of the soft parenchyma or fluid will usually re- lieve dystocia due to these causes. Except in cases of hydrocephalus and ascites further fetotomy is seldom re- quired. In a few unusual cases cesarean section might be indicated. Dystocia caused by a Disparity between the Size of the Normal Fetus and the Maternal Pelvis, Fetopelvic Disproportion. These dystocias occur usually in pri- mipara in which the fetus may be slightly larger than normal or the pelvis may be slightly smaller than nor- mal, or both causes may be present. Male calves are carried slightly longer and weigh 5 to 10 pounds more than female calves. Thus male fetuses are frequently present in these dystocias. As discussed under the basic causes for dystocia, crossbreeding of certain breeds and breeding heifers to certain bulls may predispose to dys- tocia. If primiparous animals are not grown well by proper feeding and management practices or are bred too young, the size of the pelvis at parturition may not be adequate. In these mild to moderate disparities between fetal size and maternal pelvic diameters, application of moderate forced extraction is indicated when the fetus is in a nor- mal presentation, position and posture for birth and the genital tract, especially the cervix, has dilated to its full- est extent. Delaying assistance by traction for too long may result in a dead fetus or an exhausted dam. In some cases added lubrication may be desirable. Traction should be in the proper direction. Alternate traction as well as lateral traction should be used. Twisting or rotation of the fetus may be helpful. If excessive traction is to be used epidural anethesia should be given. If traction is not successful, early consideration of cesarean section should be given in order to save a living fetus. Fetotomy is less commonly indicated in animals with a narrow birth canal and a large fetus. But percutaneous total fetotomy might be considered if the birth canal is not too small.6,44 Dystocia may be caused by Dropsical Conditions, such as Fetal Ascites, Fetal Anasarca, Edema of the Allantois Chorion, and Hydrops of the Amnion or Al- lantois or both. Fetal ascites is seen as an occasional cause for dystocia in any species but occurs most often in the cow. It is occasionally associated with a dropsical condition of the uterus, mesotheliomas of the fetal ab- domen, and has been observed associated with brucel- losis. The fetus is usually fairly small but the distended abdomen causes it to become wedged in the pelvic inlet. (See Figure 91.) It might be confused, therefore, with the hip lock condition. Close examination of the fetus in the birth canal will readily reveal the cause for the dys- Figure 91. Ascites and mild anasarca of a 6-month bovine fetus that caused dystocia.DIAGNOSIS AND TREATMENT OF VARIOUS TYPES OF DYSTOCIA 335 i .■ Figure 92. An anasarcous bovine fetus that caused dystocia at the time of abortion. tocia. To release the fluid from the abdomen the fetus must be sacrificed but this is no great loss as these fe- tuses are usually dead or weak or would fail to survive if delivered alive. The easiest method is to reach in alongside the fetus and with a castrating knife make a liberal incision through the abdominal wall. In anterior presentation a foreleg could be removed and evisceration would release the ascitic fluid. The other dropsical conditions of fetal anasarca (see Figure 92), edema of the allantois chorion, hydrops am- nii and allantois, and hydrops allantois were discussed in Chapter 5. In removing large anasarcous fetuses, forced extraction is usually successful. If the fetus is too large, fetotomy including amputation of the forelimb and evis- ceration may occasionally be necessary. This is easily performed because of the soft, friable, edematous fetal tissues. Rarely cesarean section might be indicated. In these dropsical uterine conditions uterine inertia and a weak or dead fetus frequently occur and favor abnormal postures, emphysema and dystocia that can usually be relieved by mutation and forced extraction. Twinning in Uniparous Animals is a Common Cause of Dystocia. This is produced by portions of bicornual fetuses becoming wedged in the maternal pelvis. Dys- tocia is predisposed in unicomual twins because of the inertia of the long, distended uterine horn bent at a 180- degree angle at the diaphragm. Uteri containing multiple fetuses in unipara are prone to develop uterine inertia and uterine disease. The fetuses are less viable. These latter factors usually produce abnormal postures. In many cases one fetus presents anteriorly and the other poste- riorly, the latter often in breech presentation. Dystocia due to twins is most common in dairy cows, and less common in beef cattle. Twin dystocia is uncommon in the mare inasmuch as twins almost always are aborted. Sheep have adapted themselves to two fetuses and twin dystocia is uncommon by comparison with the incidence of twins in that species. Twin dystocia usually may be diagnosed readily on examination of the birth canal by finding three or more limbs attached to two separate fe- tuses. Diagnosis should differentiate between this con- dition and double monsters, Schistosomus reflexus, campylorrhachis, or dystocia in anterior presentation with the hind limbs extended alongside the body. If twins are wedged in the birth canal usually traction is placed on the twin nearer the vulva. The other fetus is repelled at the same time. Since twin fetuses are small, mutation is invariably successful. Conditions of twin pregnancy and dystocia may be followed by metritis and retained pla- centa. In cases of unicomual twin dystocia it occasion- ally happens that one twin is removed and the other overlooked. The same may happen in triplet pregnan- cies. Thus following all dystocias the uterus should al- ways be examined carefully to be certain no fetus is left in the uterus. Dystocia due to Fetal Monsters. The relative inci- dence of fetal monstrosities by species is reported as fol- lows: Table 15. Relative incidence of fetal monstrosities. Craig (citing Gurlt) Williams Roberts Cow 239 15 92 Ewe 179 1 2 Sow 87 1 2 Bitch 78 Cat 71 Mare 56 3 Goat 24 2 Total 734 17 101 According to other authors, out of 2340 foals in one stud, only 9 were monstrosities; in cattle about 0.5 per cent; and in sheep 1 in 768 lambs were anomalous.7 Not all anomalous fetuses or monsters cause dystocia. The monsters that are characterized by an increased size of the fetus include: hydrocephalic, anasarcous, or as- citic monsters; monsters with marked skeletal defects such as Schistosomus reflexus, Campylorrhachis scoliosa, Perosomus elumbis; monsters due to conjoined twins or double monsters; monsters due to pseudo-ankylosis of the limbs or neck; achondroplastic fetuses with short, broad bodies; and mummified fetuses that died late in gestation. Other anomalous fetuses that are weak or dead at birth may cause dystocia due to abnormal positions and postures because of their lack of movement and muscle tonus. If these latter defective, malformed, non- viable fetuses cause dystocia they can usually be re- moved by mutation and forced extraction unless emphy-336 VETERINARY OBSTETRICS sema or marked contraction of the uterine wall has resulted. Among the author’s cases the incidence of dystocia in cattle due to excessive size of the fetus was as follows, in order of frequency: Schistosomus reflexus, 14 cases; Perosomus horridus (Gurlt) with ankyloses of the limbs and a short S-curved spine 13 cases; Perosomus el- umbis, 5 cases, double monsters, 3 cases (two Thoraco- abdomino-pagus, one Dicephalus); fetal anasarca, 2 cases; Achondroplasia, 2 cases; and Hydrocephalus, 2 cases. Hydrocephalus is occasionally seen also in equine, pro- cine, canine and feline fetuses. Most single fetal mon- sters weigh less than normal fetuses, so they are easily handled. In a dystocia case a careful examination of the fetus should be made for signs of a monster such as: deformed limbs, ankylosed thin limbs with prominent joints, im- proper placement or location of extremities, atrophied muscles and small fetal size. This examination is partic- ularly important in differentiating between twins and double monsters. When traction or repulsion is placed on one portion of the fetus and the opposite part also moves, either a double monster or a sharply-bent single monster is present. In other cases of dystocia when proper and normal progress toward the correction of the dys- tocia ceases the fetus should be carefully reexamined for the possible presence of a monster or an anomalous con- dition. In the handling of dystocia due to monsters each case is an individual problem. The operator must rely on a careful examination of the fetus and birth canal and on his own ingenuity and ability to plan a procedure that assures a satisfactory outcome. If the condition is severe and complicated extra assistance and even consultation should be obtained. Double monsters occur most com- monly in the cow, sow, bitch, and queen, and only very rarely in the mare. Fetotomy, including evisceration, is usually indicated to reduce the size of the monster to the point where the fetatome wire may be placed around conjoined twins at the point of attachment and separate them for removal. A cesarean section to relieve dystocia due to excessive size of the fetus requires a large ab- dominal incision that may complicate the operation and aftercare. Hydrocephalus is seen most often in the cow, bitch, queen and mare and when it is severe enough to result in a dystocia that cannot be relieved by mutation and forced extraction the soft portion of the distended crani- um should be reduced in size by an incision to release the fluid. An excessive bony enlargement of the craniun may require that a cephalotomy be performed with the fetatome, by placing the wire around the base of the en- larged skull, amputating and withdrawing the collapsed cranial bones and tissues. An achondroplastic calf generally can be removed by traction with a chain looped around its neck. Lubrication is of vital importance in severe cases. The limbs are quite short and small and cause little trouble. In cases asso- ciated with fetal emphysema, removal of the foreleg and evisceration of the fetus may be indicated. This applies also to anasarcous calves (see Figure 92). The latter are usually aborted prematurely and their tissues are soft and easily mutilated for the purpose of releasing fluid in or- der to reduce the size of the fetus. Fetal ascites often is associated with this condition. Schistosomus reflexus (see Figure 43) is seen in cat- tle and occasionally the sheep, goat, and pig but never in the other species. It may be presented in the birth canal in a ventral manner, with the viscera easily palp- able. When examining these monsters in this presenta- tion, the operator may be startled to feel viscera and even a beating heart. The fetal viscera might be mistaken for the dam’s viscera, and a diagnosis of a ruptured uterus may follow. This mistake will be avoided by a careful examination of the fetus. The dorsal presentation of the Schistosomus monster consists of the head and the four feet extending into the pelvic cavity. Since many of these monsters are small they may be removed by careful trac- tion especially from adult dairy cows with a large pelvis. In the ventral presentation hooks or Krey’s tongs may be used for traction. In dorsal presentation alternate trac- tion on the legs is sometimes successful in relieving dys- tocia. In many cases, however, fetotomy is indicated. It is desirable to cut the body in half at the point of the greatest ventral curvature of the spine. Every effort should be made to place the fetatome wire around the middle of the fetus and between the front and hind limbs before the actual cutting operation. In some large fetuses after removing the head, forelimbs, and part of the thorax, it may be necessary to bisect the pelvis before the dystocia can be relieved. In rare cases a sac of skin may com- pletely enclose the limbs and must be incised and the enclosed fluid released before starting the fetotomy (see Figure 43). Cases of dystocia in this type of monster associated with a greatly distended rumen have been ob- served by the author and others.14,41'42 Campylorrachis scoliosa is rarely observed but is handled similarly by cutting the body into two halves with the fetatome. Perosomus elumbis if in posterior presentation may be mistaken for a breech presentation. This abnormality is seen most often in cattle and pigs. In anterior presentation the rigid ankylosed hind limbs may obstruct the passage of the caudal portion of the fetus through the maternal pelvis. Since the fetus, es-DIAGNOSIS AND TREATMENT OF VARIOUS TYPES OF DYSTOCIA 337 pecially the rear quarters, are small, atrophied, and loosely attached to the trunk, correction of the dystocia by mu- tation and careful traction can be accomplished in many instances. Occasionally amputation of the rear limbs at the tarsus or hip with the fetatome may be necessary in order to remove the fetus without endangering the dam. Perosomus horridus with general ankylosis or muscle contractures of the fetus is an occasionally observed anomaly in cattle in New York State. The monster, usu- ally a Holstein, is small and very short due to an S-shaped multiple bending of the spine from the occiput to the sacrum. The vertebrae are definitely abnormal, short- ened, and ankylosed. The limbs, neck, and tail are an- kylosed and deformed. Due to the small size of the fetus, however, the dystocia is usually relieved by traction. In any of the above types of dystocia due to monsters with the exception of the achrondroplastic or anasarcous calves, pseudo-ankylosis of one or more joints or limbs is common. If fetotomy does not give promise of suc- cess, cesarean section would be indicated; but the ab- dominal incision will necessarily be large unless feto- tomy can be performed on the fetus in utero before its removal through the abdominal incision. Most of these animals will conceive on subsequent breeding and pro- duce normal young unless complications following the dystocia cause pathological conditions that delay or pre- vent conception. In the sow, bitch, and queen cesarean section is the method of choice and often is necessary in order to relieve dystocia due to a fetal monster. Dystocia Due to Uterine Displacements Dystocia may be caused by uterine displacements such as uterine torsion, displacement of the uterus in inguinal or ventral hernias, rupture of the prepubic tendon, fold- ing of the uterus cranial to the pelvis in older deep bod- ied sows and possibly vagino-cervical prolapse. Uterine torsion as a cause of dystocia is uncommon in the mare, however one report indicated that 5 to 10 per- cent of all serious dystocias in mares were due to torsion of the uterus.36 Dystocia due to Uterine Torsion is frequently ob- served in cattle, especially dairy cattle confined for long periods in the stable. It is occasionally observed as a cause for dystocia in ewes, does, mares, bitches and queens and in rare instances in the sow (See Figure 93). As noted in Chapter 5, in which the etiology, symptoms, and diagnosis of torsion of the uterus in the preparturient animal were discussed, about 90 percent of torsions of the uterus in cattle are observed at parturition and cause dystocia. Whereas in the other species, except possibly the occasional ewe or doe, most uterine torsion occurs with symptoms during the latter third of the gestation period prior to parturition.3,25 Torsion of the uterus as a cause of dystocia was present in 7.3 and 7.0 percent of 1555 and 998 cases of bovine dystocia observed in the Ambulatory Clinic of the New York State Veterinary College from 1943 to 1953 and 1963 to 1968, respec- tively. Records from the same clinic from 1925 to 1945 showed that of 1703 cases of bovine dystocia, 225, or 13.2 percent, were due to uterine torsion.42 In other countries the incidence varies from 1 to 12 percent.34 About 70 percent of torsions occur in cows and 30 per- cent in heifers. This is probably a reflection of the num- bers of pregnant cows at risk. Uterine torsion is appar- ently rare in Bos indicus type cattle due to the anatomical attachment of the uterine ligament.34 The condition is observed most frequently in stabled cattle during the spring months. Apparently most cases of torsion occur during the first stages of labor. Torsions to the right are usually associated with fetuses in the left horn and viceversa.3,34 Most twisted uteri are outside the omentum that usually encloses the uterus. The degree of torsion varied from 90° to more than 720° with 80 percent of the cases be- tween 180° and 270°3,34 or more. Uterine torsion is rare in twin pregnancies. The symptoms of uterine torsion of the cow occurring at the time of parturition and resulting in dystocia are frequently so mild that the owner thinks the cow is still in the first stage of labor. The cow is uneasy, restless, may show colic by treading, kicking at its abdomen, and switching its tail. Moderate anorexia is present. Tenes- mus, or abdominal straining characteristic of the second stage of labor, is either absent or mild and intermittent because the twisted birth canal prevents the entrance of the fetus into the pelvis—a necessary prerequisite to the initiation of normal abdominal straining. The history given by the owner is usually that the cow had acted as if calv- ing was imminent for the past 8 to 18 hours or more, but true labor or straining has not occurred. This history of a prolonged first stage of parturition is usually ob- served in uterine torsion causing dystocia and is signif- icant when an owner observes his parturient cows closely. Examination of the cow reveals increased respirations, and the heart rate is usually elevated to 80 to 100 per minute. In advanced cases with complications of uterine gangrene, uterine rupture, or fetal emphysema, the an- imal may be toxic, with a very rapid, weak pulse, severe depression, weakness, prostration, low body tempera- ture, cold extremities, and possibly a fetid diarrhea. Hemorrhage from ruptured uterine vessels, occasionally occurs in uterine torsion and causes the cow to exhibit symptoms of anemia, weakness, rapid breathing, rapid338 VETERINARY OBSTETRICS pulse rate, and prostration. In some severe 270° to 360° torsions in cattle it may be noticed that the dorsal com- missure of the vulva is pulled forward and to the left or right, depending upon which direction the uterus rotated. An accurate diagnosis of uterine torsion may be made by vaginal and rectal examination of the uterus, broad ligaments, vagina, and fetus, as described in Chapter 5 (see Figure 93). Whenever the birth canal is narrow and stenosed in the region of the cephalic portion of the va- gina or the cervix at the time of parturition, torsion should be suspected. If the torsion is greater that 180° to 240° it is usually impossible to pass the hand through the twisted portion of the birth canal. This twisted portion usually includes the cephalic portion of the vagina, the cervix, and occasionally the body of the uterus. Frequently in the mare, but rarely in the cow, the torsion may be en- tirely cranial to the cervix so a vaginal examination is not as highly diagnostic in the mare as it is in the cow.25,36 Epidural anesthesia is usually necessary, as oftentimes this examination initiates severe straining. The fetus is usually in a dorso-ilial or dorso-pubic position as most torsions in cattle are 180° to 240°. The fetal membranes may have ruptured. The fetus is likely to be dead, and long-standing neglected cases of dystocia may show evi- dence of emphysema or maceration. In all cases of dorso- ilial or dorso-pubic positions of fetuses in unipara the birth canal should be carefully examined for the presence of a torsion. The incidence of uterine rupture is fairly high in cases of uterine torsion and therefore an exam- ination for this should be made prior to treatment. The direction of the torsion should be carefully ascertained. Torsions in the mare and cow of 180° or less during the gestation period may recover spontaneously. The symptoms in the mare and ewe are similar to those in the cow. In the mare the foal is usually dead and often the symptoms are mistaken for colic or indigestion. Tor- sions of the uterus greater than 180° are fairly common in the mare. In the ewe the fetus cannot be directly pal- pated, due to the twisted narrow birth canal. In multi- para, such as the bitch, parturition progresses with the fetuses being expelled from the normal horn and in some cases from the caudal or patent portion of the horn in which torsion may have occurred. Unless the abdomen is palpated fetuses in the twisted or rotated hom or por- tion of a hom that may be still attached to the rest of the uterus or rarely separated from it will not be noted. Transverse rupture of this uterine segment may release the fetuses into the abdominal cavity. In 24 to 48 hours, the bitch will show depression, anorexia, elevated tem- perature, and rapid pulse, with symptoms of abdominal involvement by a tense, firm abdomen, arched back, and a slow, painful gait and attitude. The extrauterine fetuses may be diagnosed by radiographs or palpated through the abdominal wall. In rare instances, especially in the queen, the twisted segment of the uterus containing one or two fetuses, isolated or separated from the rest of the uterus due to torsion of the uterus, may be walled off in the abdominal cavity by connective tissue causing the fetuses to macerate or mummify. The prognosis of uterine torsion causing dystocia is usually fair to good when the condition is diagnosed early, before the occurrence of fetal emphysema, secondary contraction of the cervix, uterine ischemia, necrosis, rupture and peritonitis. In the 113 cases of bovine uterine torsion occurring in the Ambulatory Clinic from 1943 to 1953 there was an 11 percent mortality of the dams. In 70 cases of uterine torsion treated from 1963 through 1968 in the same clinic there was only a 4.3 percent mortality. A series of 225 cases of uterine torsion were reported42 from 1925 to 1945, in which an 18 percent mortality resulted. In 42 cases of equine uterine torsion, 5 to 10 percent were associated with serious dystocias but more than 50 percent occurred before the end of gestation.36 Most equine cases of torsion were 360° or more, usually to the left. Thus the prognosis is guarded for the dam and fetus with 40 percent mortality in the dams and 70 percent in the foals. Correction was best accomplished in the standing mare by rotation of the fetus and uterus through the gen- ital tract. If this was not possible, correction through a laparotomy rather than rolling was preferred.36 In very serious cases cesarean section was the method of last resort. In an excellent recent review of 26 cases of equine uterine torsion, the mean duration of gestation at the time of diagnosis was 9.6 months with a range of 8 months to term.25 Torsions were clockwise in 59 percent of cases and 23 percent had torsions of 360° or more. Uterine rupture was diagnosed in 4 cases. Correction was by left or right flank laparotomy in the standing mare. Of the foals alive at surgery 70 percent were bom alive. Of the 26 mares operated on 73 percent survived, 7 died from peritonitis, shock, or hemorrhage. The prognosis in the other smaller species is guarded to poor because an early diagnosis is difficult or impos- sible to make without an exploratory laparotomy oper- ation. The prognosis in respect to the life of the fetuses is poor, since in most cases veterinary aid is not sum- moned until too late and the fetuses, having a reduced oxygen supply, are less viable and die due to asphyxia. In torsion of the uterus with an extensive rupture of the uterus, hemorrhage from the uterine vessels or severe uterine edema and gangrene secondary to thrombi in the large uterine vessels, the prognosis is poor, especially when the latter condition is present in large animals. InDIAGNOSIS AND TREATMENT OF VARIOUS TYPES OF DYSTOCIA 339 L Rectum R Figure 93a. Diagram of a normal and twisted bovine uterus and vagina. (Upper center) Normal position of broad ligaments and vagina. (Lower left) 180° right torsion of the uterus. (Lower right) 180° left torsion of the uterus. Figure 93b. The Schaffer method for the correction of right uterine torsion. A. The cow is cast on the right side corresponding to the direction of the 180° right uterine torsion, note the position of the right mesometrium. A plank and weight of 75 to 100 kg (black arrows) are applied over the abdomen. B. The cow is rolled slowly to the right in the direction of the uterine torsion. C. Rolling is completed, with the correction of the uterine torsion.31 Courtesy of the Cornell Veterinarian.340 VETERINARY OBSTETRICS the bitch and queen hysterectomy may be successful if shock and peritonitis can be controlled. Most cases of unrelieved uterine torsion of greater than 180° result in the death of the dam. In rare cases the fetus remains in the uterus and macerates, with extensive adhesions de- veloping around the uterus; and the condition may not be diagnosed for several months. Uterine torsion in cat- tle is likely to be followed by retained placenta, metritis, perimetritis, and delayed conception. Only rarely does torsion recur at the following parturition. The handling or treatment of dystocia caused by uterine torsion in large animals includes several tech- niques, such as cesarean section, rolling the dam, and rotation of the fetus and uterus through the birth canal or through a laparotomy incision. These treatments and the modifications thereof are designed to correct the tor- sion of the uterus and to remove the fetus. The tech- niques of laparotomy, cesarean, and rolling are indicated when the birth canal is so twisted usually more than 240° and the hand cannot be passed through it to grasp the fetus, or when the cervix is not dilated, as may occur in torsion during the gestation period. Rolling the dam is one of the oldest and simplest of the various methods used to relieve torsion of the uterus. Its principal drawback is that it requires the assistance of 2 to 4 men depending on the size of the cow or mare. If possible, rolling should be done out-of-doors, on a grassy, gentle slope with the cow’s head lower than the rear quarters. In the winter months the bam floor, litter alley, or large box stall that are well-bedded or covered deeply with straw or hay may be used. The cow, es- pecially if large and vigorous, should be given a large dose of tranquilizer intravenously or intramuscularly, or 0.5 to 1.0 ounce of chloral hydrate intravenously or 1.5 to 3.0 ounces orally, as a sedative 20 minutes prior to rolling. After the direction of the torsion has been de- termined accurately, the cow is laid down in lateral re- cumbency on the same side as the direction of the tor- sion. The squeeze method, with half hitches around the thorax and abdomen; or the Alabama technique, with ropes crossed over the back and between the hind legs, is used to force the cow to lie down. The hind leg on the side on which the cow is to be cast is pulled cranially and underneath it by a rope attached to the pastern and passed to the other side at the same time the body ropes are tightened. Occasionally this procedure of dropping the cow suddenly on the same side as the direction of the torsion relieves, or partially relieves, the condition. The hind legs of the cow are fastened together and the front legs are tied together, leaving an 8- to 10-foot end on each rope. The cow’s head is held extended by a halter and rope and if necessary a nose lead. The front and hind feet should not be tied together, because this compresses the abdominal cavity and tends to make the gravid uterus rotate with the cow. It is better not to tie the front legs in a flexed position to the body, as the cow will throw her knees apart and brace herself, thus making it difficult to roll her. The object in rolling the cow when relieving torsion is to rotate the body of the cow in the same di- rection as the torsion of the uterus, rapidly enough to rotate the body around, or faster than, the inert uterus and fetus. The rapidly rotating body of the cow thereby overtakes the more slowly rotating inert gravid uterus. The cow should be rapidly rotated in the same direction as the torsion, by strong coordinated pulling on the ropes attached to the forelegs and hind legs. If because of a lack of assistance, rolling cannot be done rapidly, some other method should be selected to relieve the torsion. Since this is often the case, the rolling technique of Schaffer may be utilized. After the cow has been rapidly rolled 180 degrees her body must then be either rolled back slowly to the original position or be pushed, usually slowly, over her legs and sternum so that she is once more in lateral recumbency on the same side as the di- rection of the torsion, ready to be rapidly turned over again. Although some authors advise the operator to keep the hand in the vagina or even to grasp the fetus, in order to hold the gravid uterus in place, this is very awkward position to assume or maintain as the animal is being rolled, and is unnecessary unless the operator is uncer- tain as to the direction in which the uterus is rotated. Placing the hand in the cranial portion of the vagina as rolling is performed will reveal at once, by the tightening of the spiral folds in the vagina, if the rolling is in the wrong direction. After each two or three rapid rotations of the cow’s body the birth canal should be examined to determine if the torsion is corrected. If so, the spiral folds and stenosis of the birth canal have disappeared and if the cervix is dilated the fetus may be palpated with ease. Occasionally there may be a rush of fetal fluids from the uterus as the torsion is relieved. If the torsion is not re- lieved, this procedure should be repeated 4 to 5 more times before failure is admitted and another technique attempted. Rolling mares with torsion of the uterus often results in correction of the torsion as in cattle.I2b Rolling might result in rupture of the uterus or cause a rupture of a uterine vessel especially if the uterus was edema- tous.10'36 A modification of this rolling technique, called Schaffer’s method has been described3’31 (See Figure 93b). This method requires less assistance because the cow or mare with torsion is rolled slowly instead of rap- idly. The mare should be anesthetized with a short-act- ing narcotic. The cow is cast on the same side as theDIAGNOSIS AND TREATMENT OF VARIOUS TYPES OF DYSTOCIA 341 direction of the torsion and tied in a manner similar to that described for the previous rolling technique. A plank 9 to 12 feet long and 8 to 12 inches wide is placed on the cow’s abdomen with the lower end of the plank on the ground. An assistant stands on the plank and the cow is slowly rolled in the same direction as the torsion by pulling on the ropes around the front and hind feet. This creates pressure first on the upper abdominal wall, then the floor and finally the opposite side of the abdomen resulting in a correction of the torsion that can be de- termined by examining the genital tract. If there is any question concerning the direction of the torsion, the op- erator, by placing his hand in the genital canal, can read- ily determine whether the torsion is being relieved or not as the cow or mare is slowly rolled. As in the initial rolling technique if the torsion is not relieved the first time the animal is rolled, the procedure may be repeated several times. In most cases the torsion is corrected on the first rolling. In the Schaffer method the uterus and its contents are held in place by the plank and the weight of the man or a similar weight placed on it while the animal is rolled. Laparotomy for the intra-abdominal correction of tor- sion is especially valuable during the gestation period or when the cervix is closed. It is usually performed on the standing cow or mare through the left or right para- lumbar fossa. This technique has the advantage of re- quiring less assistance than does rolling. In most cases tranquilizers or a small dose of chloral hydrate, 0.5 to 1.0 ounce intravenously and light epidural anesthesia are given to control tenesmus at the time of the operation. The right flank in the cow is anesthetized by paraver- tebral, inverted L block, or local anesthesia and a 6- to 8-inch vertical laparotomy incision is made. The omen- tum is pulled cranially if it is over the uterus. If torsion of the uterus is to the right the hand and arm are passed downward between the uterus and abdominal wall until the bottom or ventral surface of the uterus can be felt. A portion of the fetus, usually the leg, is grasped through the uterine wall and by alternately lifting and lowering the uterus it is made to rock up and down in an arc of 10 to 12 inches and finally by strongly lifting the uterus and pushing it toward the midline and downward, cor- rection of the torsion is accomplished. If torsion is to the left the hand and arm are passed over the top of the uterus and down between the rumen and uterus. The same pro- cedure of rocking and then rotating to the right or lat- erally and downward is carried out to correct the left torsion. A left flank incision is preferred in mares. The laparotomy incision then is closed securely. In rare cases in which laparotomy alone is unsuccessful because of chronic adhesions or a very large distended uterus or ru- men, making correction impossible, cesarean section may be indicated. If at the time of parturition the cervix is not dilated sufficiently and the operator does not wish to lose a living fetus by delay, a cesarean may be per- formed. This may be done by enlarging the laparotomy incision. Although the torsion may be corrected before or after the fetus is removed, it is easier to relieve torsion after cesarean section. If a cesarean section in a cow is decided upon before making the right flank incision, an- other laparotomy site may be chosen since correction of the torsion is usually easily accomplished, even in the recumbent cow after the fetus has been removed. Tor- sion in the ewe and goat may be relieved by laparotomy if elevation of the animal by hanging it by the rear legs or by rolling it is not successful. The relief of uterine torsion in two sows after a laparotomy operation has been described.40 One sow died due to hemorrhage from a vessel in the broad ligament; the other recovered follow- ing correction of the torsion and removal of the pigs. Rotation of the fetus and uterus through the birth canal is probably the most common way of relieving dystocia due to torsion of the uterus in the cow and may be used in the mare. Since most bovine torsions, about 90 percent, are discovered at the time of parturition when the cervix is relaxed and dilated, and since most torsions are less than 240 degrees, the hand may be passed through the twisted portion of the birth canal and the fetus grasped and rotated in the standing cow. Manual rotation of the fetus and uterus through the birth canal is very difficult to perform with the cow lying down. In the mare with a 180° torsion of the uterus the cervix may be dilated and the fetus grasped. It is advisable, and in many cases necessary, to have the cow on its feet or its rear parts elevated, and enough epidural anesthetic injected to pre- vent straining. If the birth canal is dry, lubrication is necessary. If the fetal membranes have not ruptured and released the fluids this should be done to reduce the size and weight of the uterus. Depending on the position and posture of the fetus and the direction of the torsion, the left or right arm is used for manually rotating the fetus. The leg of the fetus is grasped in the metacarpal or meta- tarsal region and the knee or hock joint flexed. By re- pelling the fetus and twisting the leg in rotating manner at regular intervals the fetus and uterus are rocked back and forth through an arc of 10 to 12 inches; and then with a sudden strong twist they are lifted and then pushed downward to the side opposite to the direction of the torsion, thereby in many cases relieving the torsion. Some veterinarians pass the hand alongside the body of the fe- tus, start it rocking and then lift it upward, over, and downward, in a like manner, opposite to the direction of the torsion. This manual technique is easier in the smaller342 VETERINARY OBSTETRICS breeds of cattle with the smaller and lighter calves. It is also easier for the stronger, taller operators. In the larger breeds of cows when correction of the torsion is not possible by manual rotation of the fetus and uterus the detorsion rod described by DeMott and Roberts,9 or a similar instrument such as Erickson’s de- torsion rod or Cammerer’s fork is of great value. Mod- ification of these detorsion rods to permit the tight at- tachment of obstetrical chains to the handle is desirable. The DeMott detorsion rod is made of 3/8-inch steel rod, 30 inches long, has an eye at either end with 1-1/4 inch inside diameter. After making an 8- or 9-inch loop in a 60-inch obstetrical chain the end of the loop is passed through one eye of the detorsion rod and the rod and loop of chain are carried into the uterus. The free end of the loop is passed around one leg of the fetus and the rod is pushed up to that leg. The other end of the loop, on the opposite side of the eye of the rod, is passed around the other leg. Both ends of the loop around the legs should be placed around the pasterns or just above fetlocks and the free end of the chain drawn tight. If the loops of chain are passed up the leg to the knees or above the knees of the fetus, the hoofs and feet may be forced into or through the uterine wall as the detorsion rod is rotated unless they are carefully held by the operator. A short piece of broom handle or Gibbon’s obstetrical handle is then inserted into the eye of the rod and the tightly drawn chain wrapped several times around the handle. There is another method of applying this instrument, but it is not as safe inasmuch as it may injure the fetal limbs. If, however, the fetus is dead this aspect is un- important. A loop is made in the long obstetrical chain. It is carried into the uterus and placed around one or preferably both legs of the fetus. The free end of the chain is placed through one eye of the rod and the rod is pushed into the uterus so that the eye fits tightly on the loop around the leg or legs. The chain is drawn tight and the free end of the chain wrapped around the handle. Before and during rotation of the fetus and uterus, the hand should be inserted into the vagina and uterus to make certain that no portion of the mucous membrane is being pinched by the chain and that the claws of the feet do not engage or rupture the uterine wall. Vaginal examination during the reduction operation is helpful in making certain that the fetus and uterus are being rotated in the proper direction and in determining when the tor- sion is corrected. When rotating the fetus, repulsion by means of the rod is definitely helpful. In most cases, rocking the fetus and uterus back and forth a few times before starting reduction of the torsion makes the oper- ation easier. Then the handle is rotated slowly in the di- rection opposite to that of the torsion, and the torsion is relieved. Rotating a fetus in anterior presentation a quarter of a turn beyond the normal position and then returning the fetus to the normal position will bring the head into the proper posture. If the torsion and stenosis of the birth canal are not severe and both fetal limbs are lying in the vagina, rotation of the fetus and uterus is simplified; but the torsion should not be overlooked. Other techniques may possibly be used to correct tor- sion or to assist in the previous procedures. Abdominal ballottment is recommended5 and may be of use in aid- ing manual correction of the torsion through the birth canal, or in rolling the cow. In right torsion an assistant on the right side pushes downwards and inwards in the upper right flank while an assistant on the left side pushes upwards and inwards on the lower left flank. In left tor- sion the upper left flank and the lower right flank are pushed strongly with the fists. These two assistants push alternately, at intervals of about one second. This causes the uterus to roll back and forth, aiding the operator who is working on the fetus and uterus through the birth canal. When the cow is on her back during the rolling, alternate pressure through the relaxed abdominal walls may aid in reducing the torsion. If the fetus cannot be palpated per vaginam it is very doubtful that rectal palpation and ma- nipulation would be of much value in aiding correction of the torsion. The stimulation of vigorous fetal move- ment is an aid to correction of early cases of torsion.5 If the hand can be passed into the uterus, the eyeballs of the fetus should be pressed firmly. This results in strong reflex movements of the fetus that may aid manual cor- rection of the torsion. A technique that may be useful in correction of torsion when manual correction of the tor- sion is to be accomplished by rotation of the fetus and uterus through the birth canal or through a laparotomy incision was illustrated.29 One end of a wide board about 8 feet long is placed on the ground under the abdomen and at a right angle to the body of the standing cow. An assistant pushes upward on the other end of the board into the right flank if right torsion is present or into the left flank if left torsion is present. The operator can lift the twisted gravid uterus and fetus from 4 to 6 inches; the board is pushed into the flank and the uterus rests on the board until the operator can get another hold on the uterus or fetus and lift it higher, where pressure up- wards and inward on the board again holds it until the process can be repeated. The gravid uterus is thus “walked up” the board until it is in a position to be pushed over and downward, and the torsion corrected. Another old technique, rather crude and not recommended for cows but useful in ewes is that of suspending a ewe’s body by her hocks, until only the ewe’s shoulders remain on the ground. The gravid uterus rotates more easily intoDIAGNOSIS AND TREATMENT OF VARIOUS TYPES OF DYSTOCIA 343 its normal position when the viscera fall forward. Ab- dominal ballottment or manual rotation of the fetus through the vagina or rectum, or both, may be necessary to effect correction. Cesarean section may be indicated in uterine torsion when correction by laparotomy or other means fails; when the cervix is not dilated or only slightly so and it is de- sired to save the live fetus; when the cervix has under- gone a secondary constriction after prolonged dystocia and an emphysematous fetus is present; when uterine rupture has occurred and the fetus is partially in the ab- dominal cavity; or when torsion of the uterus is sus- pected in multiparous animals such as the bitch, queen and sow. In these latter species cesarean section should not be delayed. In the ewe and doe as in the cow, ce- sarean section may be used whenever ordinary means of handling fail or are not indicated. Before performing ce- sarean section under these complicated conditions the prognosis should be discussed with the owner, as slaugh- ter may be preferable. In the mare, rolling usually results in correction of this condition, although some veterinar- ians indicate that rolling may be more hazardous for the mare than reduction by a laparotomy incision in the left flank. Manual or instrumental rotation of the fetus might be attempted but is more difficult and dangerous than rolling. The rotation of the uterine horns in the mare in rotated bicomual pregnancy has been discussed under transverse presentations. In severe uterine torsion, es- pecially in the bitch and queen, in which the uterus is severely damaged and necrotic, hysterectomy is indi- cated and is usually successful if shock or peritonitis do not present severe complications. When hysterectomy is indicated in the cow, the prognosis is very grave. In rare cases in which torsion has become chronic with many adhesions between the involved horn and uterus and the rest of the abdominal viscera, the cow should be slaugh- tered. In bitches and queens this encapsulated mass con- taining macerated or mummified fetuses may be re- moved if necessary. After the torsion has been corrected by the above methods, with the exception of cesarean section, the fe- tus may usually be removed by traction after correction has been made of any abnormal posture of its head, neck, or limbs. Before the fetus is removed the uterus should be examined carefully to make certain a rupture, which is usually located transversely in the uterus just cranial to the cervix, has not occurred. In some cases the cervix is not completely dilated. If the fetus is alive, this may be because the stage of parturition has not progressed sufficiently. The treatment indicated in these cases is to administer 20 to 50 units of oxytocin and wait 2 to 4 hours for further dilation or normal parturition to occur. A slow intravenous drip of the same amount of oxytocin over a period of several hours may produce a more phys- iological dilation of the cervix. In most cases, however, the cervix is only partially dilated due to an atony or inertia of the cervix and uterus caused by the torsion of the uterus and interference with normal circulation and the fetus is dead. Due to unrelieved dystocia during the period corresponding to the first and second stages of parturition the cervix may partially contract with the fe- tus still in the uterus. This latter condition is usually ob- served with a dead fetus and occasionally fetal emphy- sema is present. The condition of the fetus is an important factor in the decision whether to wait for the cervix to dilate more or to exert moderate, continuous traction with lubrication at once and gradually dilate or, if necessary, even slightly lacerate or incise the cervix, cervicotomy,34 in order to remove the fetus. When the cervix is poorly dilated great traction is not indicated, since it may cause severe cervical laceration or rupture of the uterus espe- cially when the fetus is dead, or dry and emphysema- tous. Under these circumstances cesarean section, using one of the ventral abdominal laparotomy sites, is indi- cated. After the fetus has been removed, the uterus, birth canal, and the cow should be carefully inspected. Rup- ture of the uterus with peritonitis, internal bleeding due to rupture of the large uterine vessels, retained placenta, septic metritis, and perimetritis are common sequelae to torsion of the uterus. There should be proper treatment or preventive treatment of these complications. Dystocia due to Abdominal Hernias, such as in- guinal hernias in the bitch and rarely in the queen; large ventral hernias in the mare, cow and ewe; and extensive ventral hernias due to rupture of the prepubic tendon in the mare (see Figure 80) and cow, were described in Chapter 5. Dystocia might be possible but would be of great rarity, due to diaphragmatic, umbilical, or perineal hernias. Inguinal hernias causing dystocia must be re- lieved by a cesarean section; in some neglected cases hysterectomy might be necessary.3 In rupture of the pre- pubic tendon in the mare, traction should be provided as soon as the first stage of labor is completed. Induction of parturition might be considered. Cows and ewes may give birth normally even with large ventral hernias but aid should be available if it is needed. Dystocia due to Vagino-Cervical Prolapse is rarely observed in domestic animals. In most cattle affected with vagino-cervical prolapse that carry their fetuses to term, parturition is usually uneventful. Occasionally abortion with a secondary dystocia may be associated with va- gino-cervical prolapse. The vagina or cervix might be severely diseased, atonic, edematous, and traumatized344 VETERINARY OBSTETRICS and cause dystocia that might have to be relieved by lu- brication and gentle traction. In rare instances vagino- cervical prolapse might be severe enough to indicate ce- sarean section as an aid to relieving the condition. A cesarean might be necessary if cervical stenosis is pres- ent, associated with cervical prolapse (see Chapter 5). Dystocia Due to Stenosis or Obstruction in the Birth Canal The immediate causes for dystocia due to stenosis or obstruction of the birth canal may be divided into several groups according to the structures affected—the pelvis, the cervix, the vagina, or the vulva. Dystocia due to Abnormalities or Injuries of the Pelvic Bones resulting in a stenosis or narrowing of the pelvic inlet is seen commonly in domestic animals. In all animals, especially in the cow and sow, the females may be bred too young and the pelvis at the time of parturition be too small and juvenile to allow passage of the fetus. Primiparous animals, especially the cow and sow, may also commonly have dystocia due to a dis- parity in the size of the maternal pelvis and the size of the fetus even though bred at the proper age, when they have been grown poorly or stunted, usually due to a lack of the necessary nutrients for normal growth, or have suffered chronic disease processes that prevented or re- tarded normal growth and development. (See Chapters VII and IX.) Dystocia is common in achondroplastic dwarf cattle. In certain breeds of dogs especially the brachy- cephalic breeds, with a large broad head, dystocia is common due to the relatively small, narrow flattened pelvis. Pelvic fractures and exostoses as a cause for dys- tocia are uncommon in the large domestic animals but are occasionally seen in bitches and queens that are struck or injured by moving vehicles. Fortunately most females with fractures and exostoses of the pelvis are not bred. Occasionally in the cow, rarely in the mare, a large or sharp bony prominence may be found on the cranial por- tion of the symphysis pubis. This prominence may pro- ject into the pelvic canal and cause lacerations or con- tusions of the vagina or cervix when traction is applied to the fetus. It is unlikely that an owner would breed any animal affected severely enough to have pelvic deform- ities. Correction of this type of dystocia may be overcome in most cases with steady, moderate traction in the proper direction or directions on a well-lubricated fetus. When there is a bony prominence on the cranial part of the symphysis pubis care should be taken not to rupture or lacerate the vagina, cervix, or uterus. In most cases of severe dystocia due to pelvic stenosis, in which there is a great difference between the size of the fetus and the pelvic diameters cesarean section is indicated. Fetotomy may be indicated only in selected cases. If the head of the fetus cannot enter the pelvic cavity at the same time as the forelimbs in anterior presentation, or if the fetal pelvis is much larger than the maternal pelvic inlet in posterior presentation, cesarean section is indicated. Es- pecially if the dystocia is severe, the fetus is alive, and mutation and forced extraction offer little hope of suc- cess, cesarean section is the method most often selected. If in anterior presentation the fetal extractor can with moderate traction draw the thorax through the birth canal, sometimes after amputation of the head and neck, evis- ceration through a transverse abdominal incision is per- formed and the impacted fetal pelvis is bisected with a fetatome. This procedure may be simpler and safer than a cesarean operation. Fetotomy through a narrow birth canal is often difficult, prolonged, and usually must be total rather than partial. The newer percutaneous total fetotomy techniques in selected cases may be indi- cated.6'44 The possibility of severe trauma to the birth canal by prolonged fetotomy operations through a small pelvic inlet is great. In severe cases, even those com- plicated with fetal emphysema, cesarean section may be more desirable and easier for the operator and the cow than a prolonged, difficult fetotomy operation. Pelvic symphysiotomy might be indicated in certain cases in heifers in range areas. In the bitch, queen, sow, and probably the ewe, cesarean section should be resorted to immediately as soon as dystocia develops. With the ex- ception of young animals which have been on a low nu- tritive plane, or been bred at too young an age, or pos- sibly brachycephalic dogs, these females should not be rebred after dystocia. Dystocia due to Failure of the Cervix to Dilate is seen occasionally in the cow and the ewe and very rarely in other domestic animals. In England and Australia this condition is spoken of as “ring-womb,” especially in ewes. Failure of cervical dilation is due to a number of causes— cervical induration, primary uterine and cervical inertia, secondary uterine inertia with cervical involution—and in the early stages of normal parturition this condition might be diagnosed erroneously. In ewes this condition has been associated with prepartum prolapse of the va- gina lending further credence to the hypothesis that “ring- womb” is of an endocrine etiology.3 The cervix may fail to dilate because of severe fibrous induration or sclerosis of the cervix. This is observed most often in older cows with a history of cervical lac- erations and uterine and cervical infections. The inci- dence of true cervical induration or sclerosis producingDIAGNOSIS AND TREATMENT OF VARIOUS TYPES OF DYSTOCIA 345 dystocia is rare and this diagnosis should only be made after a careful clinical examination. In other cases the diagnosis of stenosis or atresia of the cervix may be erroneous, because the animal may not yet have entered the first or second stage of labor. If the animal is left alone for a number of hours cervical dilation will often take place physiologically. In these animals the uterine tone is good, the fetus is alive, the uterine artery is very large and has the typical whirring feeling, the tenacious cervical seal is loosening and the fetal membranes are intact. There have been rare cases in which for some undiagnosed reason the animal began to strain intermittently a day or more prior to parturition. Rabies in cattle, because of the frequent occurrence of tenesmus in this disease, may resemble approaching par- turition in a cow in advanced pregnancy. Stenosis or atresia of the cervix may be associated with dystocia when, in abortion or at term, the cervix does not dilate completely, or relaxation of the cervix fails to take place. This condition is probably caused by hor- monal factors that fail to produce a normal relaxation and dilation of the cervix. It is often associated with uterine inertia. This may be due to a failure of the usual or nec- essary hormones to be secreted or their receptors to de- velop or possibly more frequently due to disease of the cervix and uterus that renders the cervical and uterine muscles incapable of responding normally to the hor- monal stimulus that relaxes the cervix and produces di- lation by contraction of the uterine muscles forcing the fetal membranes and fluids, and the fetus into the cervix. The estrogenic hormone, relaxin, and prostaglandins are considered to play important roles in this process by re- leasing collagenase causing a breakdown of collagen in the cervix and its relaxation (See Chapter VI, Parturi- tion). The exact mechanism requires further study. Fail- ure of the cervix to dilate properly at the time of par- turition is associated with or observed in: uterine inertia, uterine torsion, metritis, placentitis, death of the fetus, septic metritis of pregnancy, diffuse peritonitis due to traumatic gastritis, hydrops of the fetal membranes, a terminal condition in severe septic or toxic diseases, mummified fetus, in certain abortions, preparturient pa- resis, ketosis in ewes, and twin pregnancies in unipara. The history, evidence of uterine inertia, lack of uterine tone, evidence of a diseased fetal membrane or fetus, possible rupture of the fetal membranes and results of attempted treatment will aid in making a diagnosis. A further condition resulting in a cervical stenosis is involution of the genital tract. In neglected cases of abor- tion or dystocia, characterized by a dead and usually em- physematous fetus, ruptured membranes, loss of fluid, and a dry birth canal, a stenosis of the cervix may be observed. It is seen after correction of uterine torsion, a breech presentation or other prolonged type of dystocia, especially one in which no part of the fetus enters the birth canal. As a result there is a contraction or invo- lution of the cervix with the dead fetus still in the uterus. It may be difficult to differentiate this type from failure of the cervix to dilate when uterine disease results in uterine atony and death of the fetus. The handling of these cases will depend on the cause of the cervical stenosis, the condition of the fetus and uterine contents, and the uterus. In rare cases due to cervical induration and sclerosis the prognosis is guarded and cesarean section is probably indicated if cervical di- lation is slight. Dilation of the cervix by mechanical means such as the operator’s hands and arms, instruments, a heavy rubber balloon inserted into the cervix and then inflated, or steady, moderate traction on the fetus, will often result in success in selected cases but the cervix may be severely traumatized. Incision of the cervix, va- ginal hysterotomy or cervicotomy3,34 might be tried through the dorsal and dorso-lateral portions of the cer- vix. Such an operation is of questionable value and is dangerous and not recommended for valuable breeding animals. In cases in which normal parturition is ap- proaching or the animal is in the first stage of labor no treatment is indicated; often however, verterinarians will give estrogens and oxytocin and wait for normal birth to occur. As described previously in Chapter VI, parturi- tion in mares may be induced more physiologically by 30 to 50 units of oxytocin in saline given by an intra- venous drip technique over a period of several hours. In the type of case in which the cervix fails to dilate due to uterine inertia, diseased uteri, metabolic diseases, and others, the prognosis is guarded and a careful di- agnosis should be made if possible. If sufficient time is available a large dose of estradiol, 20 to 30 mg. and/or 20 mg. of dexamethasone administered intramuscularly possibly with prostaglandin F2a, and repeated every other day if necessary, may aid relaxation of the cervix and initiation of parturition. Injections of oxytocin and cal- cium gluconate may improve the tonus of the uterus and aid or hasten cervical dilation. Uterine relaxants and spasmolytics have been used in other countries.34 Grad- ual traction on the fetus along with lubrication massage and stretching of the cervix of the cow may relax the partially dilated cervix sufficiently after one-half to one hour to remove the fetus. Strong, forced traction on the fetus is to be avoided, since it pulls the stenosed cervix caudally toward the vulva, narrowing its lumen. Strong traction may cause a transverse rupture of the uterine wall just cranial to the cervix. Occasionally, however, forced extraction, even though it produces a slight to346 VETERINARY OBSTETRICS moderate laceration of the cervix, is indicated over fe- totomy or cesarean. Good lubrication is essential. Fetotomy is very diffi- cult because of the small diameter of the cervix. Cesar- ean section may be indicated especially if the fetus is alive and the uterus free of infection. In cases of par- turient paresis occurring during parturition, an intrave- nous injection of 250 to 750 cc. of a 20 percent solution of calcium gluconate usually results in parturition within 4 to 6 hours. In ketosis in ewes the fetuses are usually dead and the ewe will die unless the fetuses are aborted and removed promptly; cesarean section therefore may be necessary. In neglected dystocia cases with cervical stenosis due to involution of the cervix, the prognosis is poor because the fetus is usually emphysematous. The uterus may al- ready be ruptured or may easily be ruptured if forced extraction is applied. Fetotomy, moderate careful forced extraction with much lubrication, or cesarean section, may be attempted depending upon the conditions and the judgment of the operator. Following the correction of the dystocia, the aftercare of the animal is important, as sep- tic metritus, retained placenta, perimetritus, necrotic va- ginitis, metritis, and cervicitis are common. In the bitch and queen cesarean section or hysterectomy are usually performed in cases where there are conditions associated with uterine inertia. Dystocia due to Stenosis or Obstruction of the Va- gina may be found in all species. It may be due to tu- mors such as fibromas or leiomyomas. In rare instances in the mare, ewe, sow or cow dystocia may be due to compression of the vagina by a massive intrapelvic he- matoma often following rough intervention by laymen. This may develop during forced extraction or a fetotomy operation. In rare cases a pelvic abscess, excessive fat around the vagina, or possibly a perineal hernia may cause dystocia because of compression of the vagina. A high incidence of fat necrosis was reported in beef cattle graz- ing on heavily fertilized fescue pastures in northern Georgia.39 In some cattle the fat necrosis was extensive enough to cause a stenosis of the birth canal. In occa- sional instances a severe necrotic vaginitis may heal and the resulting scar tissue cause a marked stenosis of the vagina and dystocia at the next parturition. A persistent hymenal band may cause stenosis of the birth canal. A persistent median wall of the Mullerian duct, usually found as a fibrous band from 0.5 to 2 inches in diameter just caudal to the cervix, may cause dystocia if the limbs of the fetus straddle this band. This condition is seen most commonly in the cow but may rarely occur in other spe- cies.13 Either rearing the heifer under unfavorable con- ditions, or breeding the heifer at too young an age, may cause dystocia due to vaginal infantilism. Occasionally, however, in abortions or premature births in heifers, the normal relaxation of the birth canal does not occur and dystocia results, due in many instances to lack of normal dilation of the cervix and vulva rather than to underde- velopment of the vagina. The handling of vaginal stenosis will vary with the cause. If a tumor is present it often can be repelled cra- nial and lateral to the pelvic inlet as the fetus is with- drawn. In dystocia due to a persistent wall of the Mul- lerian duct, the fibrous band can be located and cut with a knife or scissors. In mild cases of vaginal stenosis steady moderate traction on the fetus, together with good lu- brication, will usually dilate the vagina and allow the fetus to be removed. Occasionally if excessive traction is applied, rupture of the vagina may occur with prolapse of fat or the bladder. In most severe cases of vaginal stenosis, obstruction, or compression, especially in mul- tipara, cesarean section is the method of choice for relief of dystocia. Fetotomy is of very limited or no value be- cause the small size of the vagina makes manipulations and operations very difficult and conducive to postpar- tum necrotic vaginitis. Dystocia due to Stenosis or Constriction of the Vulva and Vestibule is occasionally seen in the heifer or mare and less commonly in the other animals. It is usually oserved in heifers with genital hypoplasia due to im- proper growth of the heifer because of chronic disease or poor nutrition or due to a genetic recessive such as anovestibular stenosis or rectovaginal constriction (RVC) in Jerseys.20 Dystocia due to a small vulva may be ob- served sometimes in heifers that abort or calve prema- turely before the vulva is properly relaxed. About 55 percent of dystocias in two-year-old Angus heifers was due to stenosis of the vulva or vestibule.28 This incidence seems too high unless mild stenosis predominated or the heifers were too fat. In exceptional instances it may be hereditary in nature or be secondary to extensive scarring from lacerations following previous parturitions or dys- tocias. In anterior presentation the nose and head, and in posterior presentation the thighs or stifles stall at the vulva or vestibule. This condition will also occur when large mummified fetuses are expelled by injections of prostaglandins because the genital tracts are not relaxed by estrogens or relaxin. The treatment or handling of stenosis of the vulva is best performed by gradual, steady, moderate traction over a period of 1/4 to 2 hours, in order to dilate the vulva slowly. The use of lubrication is essential. Prolonged at- tempts to dilate the vulva, especially if care and lubri- cation are not used, may result in an extensive necrosis and cellulitis of the vulvar and vestibular tissues. Stretching the vulva by pulling it over the fetal head and pushing outward on the vulva from the inside with theDIAGNOSIS AND TREATMENT OF VARIOUS TYPES OF DYSTOCIA 347 hands and wrists, helps to dilate it. Moderate traction on the fetal head alone, with the feet released, will help draw the head through the vestibule and aid dilation be- cause of the triangular- or wedge-shape of the fetal head. Patience is essential, since excessive or too-rapid trac- tion will rupture the vulva, vestibule or perineum, caus- ing laceration, severe hemorrhage or contusions. Exces- sive traction on the fetal jaw may fracture it. Excessive rotation of the fetal head should be avoided. Placing the hand over the poll and pulling the head ventrally and caudally and the vulva cranially and dorsally helps slide the dorsal commissure of the vulva over the top of the fetal head. Severe laceration of the vestibule and vulva rarely occurs, even in the mare, when parturition pro- ceeds unassisted; but if traction is applied, even by one man, laceration may be severe because normal, gradual dilation was not permitted. If the vulva and vestibule fail to dilate within a rea- sonable length of time, if haste is imperative or if it is obvious that vulval dilation will not occur, an episi- otomy may be performed under epidual anesthesia or lo- cal infiltration of the incision sites,12'34 With the vulva under tension an incision should be made on either side of the dorsal commissure in a dorso-lateral direction. This is done to prevent a recto-vaginal laceration or a “gill flirter” in the larger domestic animals, in which the dor- sal commissure of the vulva is near the rectum. In mul- tipara the vulva is a greater distance from the rectum and an episiotomy is made in a dorsal direction toward the rectum. After removal of the fetus the episiotomy inci- sions should be sutured together immediately with in- terrupted deep vertical mattress sutures of catgut and/or nylon and the animal treated with antibiotics for several days. Fetotomy is not indicated in these cases for the same reasons as in vaginal or pelvic stenoses. In rare cases cesarean section may be the method of choice particu- larly in multiparous animals or if the live fetus is to be saved. Gradual, moderate traction is the most satisfac- tory method, inasmuch as dilation of the vulva is nec- essary or advisable in order that the dam may give birth without assistance at subsequent pregnancies.42 In mares and cows in which the vulva has been su- tured to prevent pneumovagina, this band of tissue should be cut just before parturition in order to prevent uneven or irregular tearing of the scar between the two vulvar lips. This thin band of tissue will not cause dystocia. Dystocia Due to Uterine Inertia For convenience in discussing this problem it will be divided into two parts: primary inertia and secondary in- ertia. Both are characterized by a weakness or absence of uterine contractions during the first or second stage of labor that usually persists into the third and involution stage after parturition. Dystocia due to Primary Uterine Inertia is observed most frequently in the bitch, cow—especially the older dairy cow—and sow. It is uncommon in the other spe- cies. It is produced by a lack of tone or failure of the uterine muscles to contract. The failure of the uterine muscles to contract normally at parturition may be due to a primary failure of the muscles to respond to hor- monal stimuli due to disease of the muscle; or it may be due to an actual lack or failure of release of hormones or the development of receptors such as estrogen, oxy- tocin and possibly prostaglandins that initiate uterine contractions in normal muscles (See Chapter VI, Par- turition). In bitches it is observed more frequently in cer- tain small breeds such as the Dachshund. In a few Cock- ers it may be associated with psychotic abnormalities and nervous voluntary inhibition of parturition due to pain. Primary uterine inertia was common in infertile dogs with 3 or fewer fetuses.3'11 Lack of exercise, excessive fat- ness, debility, and senility are all causes of weakness of uterine contractions at parturition. Overdistension of the uterus in fetal giantism, hydrops of the fetal membranes, fetal anasarca, twins in unipara—especially unicornual twins—and an excessive number of fetuses in small bitches are other conditions conducive to primary uterine inertia. Undoubtedly uterine disease, or pathology as- sociated with uterine infections and placentitis during gestation, also play a role in the production of uterine inertia. Apparent bovine uterine inertia is observed in parturient paresis due to a hypocalcemia. A type of pri- mary uterine inertia in dogs, especially Chows, Retriev- ers, Bull Terriers and Spaniels, associated with a small litter, with slight or absent mammary development, and with no signs of parturition at the proper time has been described.5 The fetuses apparently succumb and by 70 to 80 days after service a dark green viscid fluid escapes from the vulva. This was probably due to a hormone disfunction. The animals affected with primary uterine inertia are usually and obviously parturient and in the first stages of labor, as shown by relaxation of the soft structures of the pelvis, marked mammary development, and dis- charge of mucous from the vulva. The animals show no distress and eat and drink nearly normally but the second stage of labor does not occur for 6 to 36 hours or more, if at all. On examination, the cervix is usually relaxed and dilatable but the fetus and fetal membranes are not being forced into the cervix or birth passage. In some cases in cattle the cervix fails to dilate normally due to a lack of hormones or to a failure of the uterus to con-348 VETERINARY OBSTETRICS tract. What may be diagnosed as a failure of the cervix to dilate may in reality be a manifestation of a primary uterine inertia. One or both membranes may have rup- tured. There is usually no abnormality in presentation, position, or posture of the fetus. The uterus apparently fails to contract normally, and consequently does not force its contents through the cervix and into the birth canal. Usually in 24 to 48 hours the second stage of labor may set in but in many cases by then the fetus is dead and occasionally infection of the fetal membranes and fetus is apparent. The prognosis is favorable in most cases that are diagnosed early. In the cow or ewe this condition is rather easily han- dled if the cervix is relaxed and open by rupturing the membranes, correcting any abnormal posture, and re- moving the fetus by moderate or slight traction. In cer- tain cases in the cow as well as in multiparous animals in which the condition is diagnosed early, intramuscular injections of oxytocin, 2 to 10 ml (20 to 80 units) for large animals, or 1 to 2 ml (10 to 20 units) for small animals, may stimulate uterine contractions and normal birth of the young. Giving this injection in saline by an intravenous drip technique over a period of several hours may be a more physiologic procedure. Others state that the intravenous injection of calcium gluconate, 500 ml of a 20 percent solution in cattle and 10 ml of a 10 per- cent solution in bitches, is of value in these cases, es- pecially if calcium levels of the blood are low or if par- turient paresis is present. In the bitch as well as other species “feathering” the vagina by inserting a finger, and stroking the dorsal wall of the vagina, or in other similar ways stimulating the production of oxytocin by the an- imal’s own pituitary may be helpful. If this treatment does not result in the initiation of normal parturition in 1 to 2 hours the treatment might be repeated. After 3 to 4 hours with no response, cesarean section is indicated and should be performed at once in the multiparous an- imals. If according to the history primary uterine inertia has existed for 4 to 6 hours before the veterinarian ex- amines the case, cesarean section may be indicated at once rather than the use of the above techniques and waiting for uterine contractions to begin. Hysterectomy may be preferred if evidence of infection is present in the uterus of the bitch or queen. Morphine, 1/8 to 1/2 grain or tranquilizers may quiet nervous, psychotic Cockers sufficiently to permit normal parturition. Since this inertia extends into the third stage of par- turition and beyond, retained placenta, metritis, and de- layed involution of the uterus are common. Administra- tion of several injections of oxytocin or ergonovine accompanied by intrauterine and parental antibiotic ther- apy, may help prevent septic metritis and other compli- cations due to delayed involution of the uterus. Secondary Uterine Inertia usually follows a pro- longed dystocia and is characterized by exhaustion of the uterine muscle. This condition is seen in all species and is more common in large animals than is primary uterine inertia. In multiparous animals when prolonged labor or dystocia is relieved by removing the fetus causing the dystocia, it is quite common to find that secondary uter- ine inertia has occurred and consequently the rest of the fetuses are not expelled. This type of inertia can be pre- vented by correcting dystocias early. In certain breeds of dogs such as the Scotch Terrier or Dachshund sec- ondary uterine inertia may occur spontaneously early in the second stage of parturition. Usually one or two fe- tuses are expelled normally and then labor ceases even though more fetuses are present in the uterus. In cattle examined after prolonged dystocia the uterus is often contracted tightly around the fetus. In some cases this condition closely resembles the condition called re- traction, Bandl’s, or contraction ring dystocia, described in humans following prolonged dystocia.27 In retraction ring dystocia the uterine muscle just cranial to the cervix contracts tightly, so that normal expulsion of the fetus into the birth canal can not take place. A contraction ring may occur any place in the uterus and if it occurs around the fetus it can interfere with birth. These abnormal con- tractions of the uterine muscle are strong sustained te- tanic contractions caused by exhaustion spasms of the muscle which are a fatigue phenomena. Diagnosis of this condition may be based on the history of prolonged dys- tocia; in multipara on the birth of one or two fetuses with a cessation of labor, or the removal of the fetus causing the dystocia, not followed by the normal resumption of parturition. In large animals intrauterine examination re- veals the nature of the condition causing the dystocia— usually an abnormal position, posture, or presentation, and the contraction of the uterine walls upon the fetus. In some uteri in which contraction bands or rings are very strong and broad especially around or caudal to the fetus, this condition will complicate the primary cause for the dystocia. The prognosis in secondary uterine in- ertia is more guarded than in primary uterine inertia be- cause the fetuses may be weak, dead, or emphysema- tous, and rupture of the uterus is more common. Retained placenta and metritis are usual sequelae. In the handling or correction of this type of dystocia in large animals the condition causing the original dys- tocia should be corrected by mutation if possible and the fetus then removed by moderate, careful traction. Lu- brication of the fetus and birth canal is usually neces- sary. Excessive traction should be avoided if strong con- traction or retraction rings are present in the uterus andDIAGNOSIS AND TREATMENT OF VARIOUS TYPES OF DYSTOCIA 349 definitely retard removal of the fetus, since transverse rupture of the uterus may occur. This is a highly im- portant reason for examining the uterus carefully in pro- longed dystocia cases as occasionally ruptures occur spontaneously or due to previously applied traction. If contraction rings are not too strong, careful, slow, cau- tious mutation and traction may be successful in reliev- ing the dystocia. If they are severe and markedly reduce the lumen or diameter of the uterus it may be necessary to resort to fetotomy or cesarean section to relieve the condition. In other countries uterine relaxants or spas- molytic or tocolytic drugs, such as isoxsuprine lactate, are recommended in this condition.3’25,34 Since infection of the uterus is often present, the ventral abdominal ap- proach for the cesarean operation is indicated. In humans these contraction or retraction rings may be relaxed by intravenous administration of adrenalin or modem relax- ants and by general anesthesia; if this fails, a cesarean is necessary. The author in a limited number of bovine cases has had little success using adrenalin. Epidural anesthesia is not effective in relaxing the uterine muscle. In bitches, mild narcosis or anesthesia with morphine may be helpful. This marked contraction of the uterine wall in prolonged gestation is another reason for being very careful not to rupture the uterus by repelling the fetus in an attempt to gain room for mutation operations. In the sow it is common practice, when several pigs have been expelled before dystocia occurred, to remove by traction the one causing dystocia, lubricate the birth canal, and give 1 to 2 ml. of oxytocin, or 2 to 3 ml. of Lentin. If the rest of the litter is not expelled in 2 to 3 hours, another pig may be removed by traction and the injection repeated; or cesarean section may be decided upon as the method of choice. This decision should not be delayed too long. In bitches the situation is similar to that in sows, in that the handling of the case will depend upon the duration of labor, the number and condition of the fetuses, and the degree of uterine infection. Early cases in bitches may be handled in the same manner as in sows except that Lentin should not be used. If the dog appears exhausted but the fetuses are in good con- dition, 1/4 grain of morphine will relax the bitch and possibly the uterus and after one or two hours rest strong uterine contractions will commence again and whelping continue. In this condition of secondary uterine inertia, helping the bitch with forceps may be indicated if only one or two fetuses remain in the uterus. If, however, there are 3 or more fetuses and dystocia has been pro- longed, cesarean section is indicated. If the fetuses are dead and infected, hysterectomy may be desirable. Cats are quite resistant to infection. Oxytocin usually will reinitiate labor even after dystocia of 48 hours’ dura- tion.32 As in primary inertia, retained placenta, septic metritis, delayed involution, and pyometra are common following secondary uterine inertia. Dystocia Due to Postmortum Changes in the Fetus These dystocias may be caused by mummification of the fetus in cattle, and by fetal emphysema and fetal maceration in all species. Dystocia due to Fetal Mummification in cattle was described in Chapter 5. In some instances mummified fetuses may macerate. This is probably secondary to a relaxation of the cervix at the time of an unobserved, spontaneous, but incomplete abortion. Organisms en- tered the previously sterile uterus and start the macera- tion process. Hematogenous uterine infection may pos- sibly occur. Dystocia due to Fetal Emphysema is observed in all species and is usually associated with a prolonged dys- tocia of 24 to 48 hours’ duration. The fetus dies and organisms from the vagina pass through the open cervix, invade the uterus and cause rapid fetal emphysema. Fetal emphysema may complicate dystocia in incomplete abortions after the fourth month of pregnancy when the dead fetus is retained in the uterus (see Chapter 5). Al- though fetal emphysema usually occurs with the cervix open it may occur with a closed cervix in rare conditions such as a septic metritis of pregnancy in which the fetus dies, becomes emphysematous, and may even macerate before the cervix opens. Such a condition occurring late in pregnancy especially in a heifer with a small, under- developed, or unrelaxed genital tract may result in a se- rious and often fatal termination. Fetal emphysema is also observed in cases of neglected torsion of the uterus in which the fetus dies. It is commonly seen in rotated bicornual pregnancies in mares. In any type of condition causing uterine inertia, fetal death and emphysema may result if treatment is not given promptly. In bovine twin pregnancy one twin may be expelled and the other re- main in the uterus and become emphysematous or mac- erate. This is more commonly seen in unicomual twins. Dystocia due to any condition causing the death of the fetus may result in fetal emphysema if the fetus is not removed promptly. In bitches and sows fetal emphysema may occur in prolonged dystocia in a manner similar to that in other animals. It is also observed in the large breeds of dogs such as Great Danes, Afghans, Boxers, Newfoundlands, and St. Bernards. In these dogs birth proceeds normally until the last fetus.5 This remains in the uterus and goes undetected for one or two days; by350 VETERINARY OBSTETRICS this time the bitch shows a fever of 103°, there is a green, black, fetid discharge from the vulva, the bitch manifests no interest in the live pups, and exhibits symptoms of depression and toxemia. In these breeds a careful ex- amination should be made for the last fetus, if necessary by radiographs of the bitch, since usually this last fetus cannot be palpated through the abdominal wall or felt by forceps through the birth canal. Fetal emphysema can usually be suspected if dystocia has existed 24 hours or more. The animal is usually de- pressed, toxic, and shows anorexia. Labor is usually weak and intermittent. The temperature is frequently elevated early but may be normal or subnormal late in the con- dition or at the time the veterinarian is summoned. This is especially true in the cow. The heart and respiratory rates are elevated. The extremities are cold and the feces may be loose and fetid. Often a fetid, watery, reddish vaginal discharge is observed. The mucous membranes of the genital tract are dry, swollen, and inflamed. In some cases the cervix may be partly involuted or con- tracted. The uterine walls are contracted closely about the fetus. The fetus is dead and swollen because of gas, that can be felt as it crepitates beneath the skin. In early cases of fetal emphysema only that portion of the fetus nearest the vulva may be emphysematous, but in pro- longed dystocia cases the entire fetus is involved. In some cases of twins, the twin nearer the cervix may be em- physematous and the deeper twin may be normal. The fetal hair may be beginning to shed. Fetal meconium is often present on the fetus. The corneas of the eyes are grey; and the teeth usually loose. Rupture of the uterus may be present or be easily produced by traction due to the dry fetus and the tense, contracted uterine walls. Ex- amination is likely to result in violent straining. The prognosis is always guarded to poor as uterine disease, septic metritis, and retained placenta usually follow this condition. The future breeding life of the dam is in doubt. Complications such as rupture of the uterus are likely to arise in the handling of dystocia due to fetal emphysema, making the prognosis guarded to grave. The least difficult and the best method of correction of fetal emphysema in large animals is forced extraction after mutation, if the latter is necessary. Care should be used in repelling the fetus and in exerting traction of the fetus, so that rupture of the uterus or cervix does not occur. Lubrication of the birth canal and fetus is essen- tial. In bitches forced extraction is probably not indi- cated unless only the one fetus is present or is wedged in the birth canal so that it would have to be removed by traction before a hysterotomy or hysterectomy is per- formed. In some cases such a fetus may be pulled apart and a portion may drop back into the uterus and become difficult to remove by forceps. Occasionally in large an- imals fetotomy may be necessary. Extensive mutilation of the fetus and its evisceration greatly reduce the size of the fetus by releasing the gases present. The fetal tis- sues are soft and friable due to the emphysema and op- erations are performed with greater ease and speed than in normal fetuses if the birth canal is dilated. Frequent lubrication is essential to prevent trauma to the birth canal. Necrotic vaginitis or vulvitis or even metritis are likely to follow removal of an emphysematous fetus. In large animals cesarean section is indicated when the birth canal is involuting and is small, swollen, and dry, and when the uterine wall closely invests a greatly swollen and em- physematous fetus. If the cow’s life is to be saved a ce- sarean may be a last resort if fetotomy is not feasible or possible. A total fetotomy of an emphysematous fetus may be more exhausting and dangerous for the cow and operator than is a cesarean section. The prognosis should be guarded and the operation performed on the ventral abdominal wall so that contamination of the abdominal cavity can be avoided. In removing emphysematous fe- tuses in uniparous animals care should be taken not to leave a hoof in the uterus that might remain and act as a chronic foreign body, producing chronic pyometra. Another possible technique for relief of dystocia due to bovine emphysematous fetus is to make a long lapa- rotomy incision in the left flank, suture the uterus to the peritoneal and fascial tissues around the periphery of the incision. The uterine wall is incised and sutured with non-absorbable material to the musculature and skin. The fetus and membranes are then removed, by fetotomy if necessary, thus preventing contamination of the perito- neal cavity. The vaginal and uterine cavities are well ir- rigated and parenteral antibiotics administered. The cow may be slaughtered for beef several months later.38 In the bitch and other multiparous animals cesarean section may be indicated. Many veterinarians prefer to perform a hysterectomy in dogs and cats in order to pre- vent possible contamination of the abdominal cavity. In multipara with emphysematous fetuses, secondary uter- ine inertia, or associated uterine torsion, administration of oxytocin might result in uterine rupture and death due to peritonitis and shock. In these cases care should be taken to prevent shock and hemorrhage and to be certain a fetus is not left in the birth canal. The aftercare of cases of dystocia due to fetal emphy- sema should consist of antibiotics parenterally and into the uterus, and injections of oxytocin and ergonovine to stimulate uterine contractions, an increased blood supply to the uterus, and to hasten the overcoming of infection. Other supportive therapy such as blood, saline, and glu- cose may be given, inasmuch as septic metritis and re-DIAGNOSIS AND TREATMENT OF VARIOUS TYPES OF DYSTOCIA 351 tained placenta are common sequelae to the removal of an emphysematous fetus. Fetal Maceration as a Cause of Dystocia in incom- plete abortions was discussed in Chapter 5. It may de- velop in all species during pregnancy, as a sequela to abortion or mummified fetuses that were not expelled when the cervix dilated. In rare cases this condition may be observed following undiagnosed and untreated tor- sions of the uterus during pregnancy or at term. In all animals the uterus or a twisted segment of it containing the macerating fetuses may be walled off in the abdom- inal cavity; or if the uterus ruptures and the fetuses es- cape into the abdomen, they may become walled off there and macerate. In rare cases some fetuses may slough to the outside or into the alimentary tract. In uniparous an- imals uterine torsion can cause fetal death and macera- tion with adhesions between the uterus and the other ab- dominal viscera. Fetal maceration is often observed in animals at term when a dystocia or a twin fetus has been overlooked or neglected for 3 to 10 days. The symptoms are usually limited to a persistent, fet- id, vaginal or vulvar discharge often containing hair, hooves, or bones. The cervix is usually partially dilated and the fetus is in an advanced stage of emphysema, maceration and decomposition and pulls apart when han- dled. In chronic cases the cervix is only slightly open, and the animal fails to show estrus. On rectal exami- nation fetal bones can be felt to crepitate within the uterus. In some cases a perimetritis may be present. In undi- agnosed or untreated dystocias a history of constant but intermittent straining, generally considered by the owner as due to retention of the placenta, is noted, as is also a fetid, purulent discharge. The lack of general symp- toms shown in some of these cases is amazing. The au- thor observed a 7-year-old cow with macerating twins in the uterus. The owner believed the cow had calved 7 days before on pasture, although he had found no calf. The cow was eating normally and milking 30 lbs. a day. The fetuses were pulled apart in removal through the cervix, which was about 12 cm. in diameter. The uterine wall was about 3 to 5 cm. thick. Recovery was unevent- ful. A number of similar cases have been described in mares that subsequently conceived following the re- moval of the macerating fetus.24 The fact that other vet- erinarians have similar experiences suggests that in ex- tremely difficult dystocia cases it might possibly be advisable in certain cases to try only supportive treat- ment and antibiotics, for 4 to 6 days, until the fetus has macerated sufficiently to be removed easily. During this same period the uterine wall builds up its natural de- fenses against infection. The dangers might be uterine rupture due to fetal emphysema before the inception of maceration or further closure of the cervix which might be prevented by injections of estrogens. In certain cases exploratory laparotomy may be advisable. The prognosis in these cases, occurring more than three days to a week following dystocia, is guarded. In the more chronic cases, with the cervix nearly completely closed the prognosis is very poor. When these cases in large animals occur, they are han- dled in a manner similar to that of treating emphyse- matous fetuses. In the more chronic bovine cases the cervix cannot be dilated manually. Estrogens are usually ineffective in evacuating the uterus, as the bones are more or less imbedded or caught in the endometrium. Laparo- hysterotomy or hysterectomy in the cow is very difficult in chronic cases with only fetal bones and pus in the uterus because the uterus is so small it is difficult to bring to the abdominal incision even if no adhesions were present. The prognosis as far as the future breeding life is concerned is very poor. Since most of these animals are in fair to good health, slaughter is usually advised. In multipara, especially bitches, hysterectomy is advised in most cases. After handling cases of fetal emphysema or macera- tion in large animals, especially if fetotomy was per- formed, the operator should be careful to cleanse and disinfect his arms and instruments carefully, and then boil the instruments. This is done to avoid a severe in- fection on the arms or the introduction of infection into the next cow through the use of the contaminated in- struments. Aftercare of cases of fetal maceration in which the fetuses were removed is similar to that following fe- tal emphysema. References 1. Adams, Wm. M. (1969) The Elective Induction of Labor and Parturition in Cattle, JAVMA, 154, 3, 261. 2. Arthur, G. H. (1966) Recent Advances in Bovine Obstetrics, Vet. Rec. 79, 22, 630. 3. Arthur, G. H. (1975) Veterinary Reproduction and Obstetrics, 4th Ed., Bailliere and Tindall, London, and Williams and Wil- kins, Baltimore. 4. Benesch, F. (1952) Lehrbuch der Tierartzlichen Geburtshilfe und Gynakologie, Urban and Schwartzenberg, Wien-Innsbruch, Austria. 5. Benesch, F. and Wright, J. G. (1951) Veterinary Obstetrics, Williams and Wilkins Co., Baltimore, Md. 6. Bierschwal, C. J. and deBois, C. H. W. (1972) The Technique of Fetotomy in Large Animals, V. M. Publishing, Inc., Bonner Springs, KS, 66012. 7. Craig, J. G. (1918) Fleming’s Veterinary Obstetrics, 3rd Ed., Alex. Eger Co., Chicago, 111. 8. DeLange, M. (1961) Prolonged Gestation in Karakul Ewes in South West Africa, 4th Intemat. Congr. on An. Reprod., Neth- erlands, Vol. Ill, 590.352 VETERINARY OBSTETRICS 9. DeMott, A. R. and Roberts, S. J. (1945) A Simple Instrument for the Relief of Dystocia in the Bovine due to Uterine Torsion, Cor. Vet., 35, 4, 333. 10. Derivaux, J. and Dewalque, J. (1963) Notes on Equine Ob- stetrics, Annales De Medecine Veterinaire, 107, 4, 236. 11. Freak, M. J. (1962) Abnormal Conditions Associated with Preg- nancy and Parturition in the Bitch, Vet. Rec. 74, 1323. 12a. Friermuth, G. J. (1948) Episiotomy in Veterinary Obstetrics, JAVMA, 113, 231. 12b. Guthrie, R. G. (1982) Rolling for Correction of Uterine Torsion in the Mare, JAVMA, 181, 1, 66. 13. Herr, S. (1978) Persistent Postcervical Band as a Cause of Dys- tocia in a Bitch. Vet. Med./Sm. An. Clin. 73, 12, 1533. 14. Herr, S. (1979) Techniques for Fetotomy on Schistosomus Re- flexus Calves, Vet. Med/Sm. An. Clin. 74, 7, 1009-1012. 15. Hilton, G. B. (1967) An Oversize Lamb, Vet. Rec. 80, 10, 336. 16. Holm, J. W. (1967) Prolonged Pregnancy, Advances in Vet. Sci. Vol. II, Academic Press Inc., N.Y.C., 159. 17. Huston, K. and Gier, H. T. (1958) An Anatomical Description of a Hydrocephalic Calf from Prolonged Gestation and the Pos- sible Relationships of these Conditions, Cor. Vet. 48, 1, 45. 18. Jasper, D. E. (1950) Prolonged Gestation in the Bovine, Cor. Vet., 40, 2, 165. 19. Kennedy, P. C., Kendrick, J. W. and Stormont, C. (1957) Ad- enohypophyseal Aplasia, an Inherited Defect Associated with Abnormal Gestation in Guernsey Cattle, Cor. Vet. 47, 1, 160. 20. Leipold, H. W. and Saperstein, G. (1975) Rectal and Vaginal Constriction in Jersey Cattle. JAVMA, 166, 3, 231-232. 21. McEntee, K. (1969) Personal Communication. 22. McEntee, K., Roberts, S. J. and Sears, R. M. (1952) Prolonged Gestation in Two Guernsey Cows, Cor. Vet. 42, 3, 355. 23. Mead, S. W., Gregory, P. W. and Regan, W. M. (1949) Pro- longed Gestation of Genetic Origin in Cattle, J. of Dairy Sci. 32, 8, 705. 24. Milne, F. J. and Homey, F. D. (1960) Abdominal Surgery in the Horse, Canad. Vet. Jour. 1, 12, 524. 25. Pascoe, J. R., Meagher, D. M. and Wheat, J. D. (1981) Sur- gical Management of Uterine Torsion in the Mare: A Review of 26 Cases. JAVMA, 179, 4, 351-354. 26. Penny, R. H. C. (1958) An Alternative to Cesarean Section in Incomplete Cervical Dilation of Sheep, Vet. Rec. 70, 431. 27. Pride, W. T. (1938) Retraction Ring Dystocia—Its Cause and Correction, Surgery, Gynec., and Obstet., 66, 1047. 28. Rice, L. E. and Wiltbank, J. N. (1970) Dystocia in Beef Heif- ers, J. An. Sci. 30, 6, 1043. 29. Richter, J. and Gotze, R. (1960) Tiergeburtshilfe, 2nd Ed., Paul Parey, Berlin and Hamburg, Germany. 30. Roberts, S. J. (1955) Unpublished data. 31. Roberts, S. J. and Hillman, R. B. (1973) An Improved Tech- nique for the Relief of Bovine Uterine Torsion, Cor. Vet. 63, 111-116. 32. Sheppard, M. (1951) Some Observations on Cat Practice, Vet., Rec., 63, 44, 685. 33. Sloss, V. (1974) A Clinical Study of Dystocia in Cattle. 2. Complications, Austral. Vet. J. 50, 294-297. 34. Sloss, V. and Dufty, J. H. (1980) Handbook of Bovine Obstet- rics, Williams and Wilkins, Baltimore, London. 35. Vandeplassche, M. (1957-1958) The Normal and Abnormal Presentation Position and Posture of the Foal-Fetus during Ges- tation and at Parturition, Dept, of An. Obstet. and Reprod., State Univ., Ghent, Belgium. 36. Vandeplassche, M., Bouters, R., Spincemaille, J. and Bonte, P. (1972) Some Aspects of Equine Obstetrics. Equine Vet. J. 4, 105. 37. Vandevelde, A., Vandenberghe, J., Vandeplassche, M. and Pa- redis, F. (1952) Het Gebruik van Stilbestrol bij het Verwekken van Abortus en bij het Inleiden wan de Partus bij Overdracht van Runderen, Vlaams Diergeneesk. Tijdschr., 21, 5, 93. 38. Vorpahl, P. V. (1979) Uterine Fistula for Treatment of Emphy- sematous Fetus in the Cow, Vet. Med./Sm. An. Clin. 74, 3, 365-366. 39. Williams, J. (1968) Personal Communication. 40. Wensvoort, P. (1956) Two Cases of Torsion of the Uterus in the Sow, Tijdschr. v. Diergeneesk. 15, 711. 41. Williams, W. L. (1931) Studies in Teratology, Cor. Vet. 21, 1, 25. 42. Williams, W. L. (1943) Veterinary Obstetrics, 4th Ed., Ithaca, N.Y. 43. Wilson, A. L. and Young, G. B. (1958) Prolonged Gestation in an Ayrshire Herd, Vet. Rec. 70, 4, 73.Chapter XI INJURIES AND DISEASES OF THE PUERPERAL PERIOD The injuries and diseases of the puerperal period dis- cussed in this chapter include puerperal infections and metabolic diseases as well as hemorrhages, lacerations, contusions, ruptures, and prolapses of various organs, especially the genital organs that may occur during or following parturition. A summary of the causes of post- parturient paraplegia is included. In a study of 2,480 cases of dystocia43 in six dairy and four beef breeds reported by veterinarians in Australia in 13 country practices, a total of 528 dams, 21.3 percent, suffered parturient or post-parturient conditions with about one-quarter of the dams being affected with two or more complications. A partial list of the complications and their incidence were: paraplegia other than hypocalcemia 9.1 percent; retained placenta, 4.9 percent; septicemia and toxemia, 2.7 per- cent; injury to vagina and cervix, 2.2 percent; uterine rupture 1.0 percent; metritis, 1.1 percent; peritonitis, 1.0 percent, lameness and paresis, 0.9 percent; shock, 0.8 percent; prolapse of portions of birth canal, 0.6 percent and hemorrhage 0.3 percent. Maternal death was usually associated with a prior existing disease state or devel- oped as a result of it and aggravated the dam’s condi- tion.43 Postpartum Hemorrhages Hemorrhage or bleeding into the uterus or birth canal may occur postpartum due to trauma, lacerations, or rupture of the genital organs. Hemorrhage into the uterus may be due to bleeding from an incised or tom caruncle or caruncular stalk in the cow or ewe, from the incised or lacerated endometrium in the mare, or from premature removal of the fetal membranes or placenta. This accident may occur at the time of parturition, dur- ing a cesarean section or fetotomy, or may take place later due to improper or too early removal of a retained placenta in any uniparous animal. Severe intrauterine hemorrhage in rare cases occurring from several hours to a day or so after calving and dropping of the placenta, that resulted in a massive blood clot filling the gravid horn of the utems was described.59,60 Rarely death may occur. Slight bleeding may be observed, from the rup- tured end of the umbilical cord or from slight lacerations of the uterus, cervix, vagina, or vulva. A hemorrhagic discharge from the vulva in a bitch was due to an in- vagination of a portion of one horn not visible exter- nally.30 In severe lacerations or rupture—particularly of the cervix, vagina, and in rare instances, the vulva— hemorrhage may be profuse due to a rupture of a large vessel. Blood may flow in a stream from the vulva as soon as the fetus is removed. Most of these lacerations and injuries follow forced extraction. Intraperitoneal or extravaginal hemorrhage may occur. If severe enough the former may produce acute symptoms of anemia and rarely death, especially in the mare. This is ordinarily seen in cases of dystocia, rupture of the uterus and uter- ine vessels before, during, or after correction of torsion of the uterus, in prolapse of the uterus, and in trauma especially in fetotomy operations or forced extraction in young heifers. These hemorrhagic conditions would be greatly aggravated in cattle fed moldy sweet clover hay. In the treatment or handling of these conditions the usual surgical procedures to control the hemorrhage and supportive treatment are indicated. Most cases of slight bleeding from the genital tract at parturition are not se- rious and require no treatment. In more severe bleeding from the uterus of large animals oxytocin, 20 to 50 I.U., may help control hemorrhage by contracting the uterus and its vessels. Injecting 500 ml. of saline to which 10 cc. of formalin has been added, or 500 ml. of calcium gluconate may also aid in hastening the clotting of blood, and thus control the hemorrhage. If bleeding occurs from a large vessel through a laceration in the vaginal wall, the vessel may be clamped by forceps. These should be left in place for 24 to 48 hours, or the vessel should be ligated. If this cannot be accomplished, packing the va- gina to provide intravaginal pressure should be done promptly. In severe intrauterine hemorrhage the clot should not be disturbed. In several weeks or months the large clot will be reduced and absorbed by natural pro- cesses. Intrapelvic or perivaginal bleeding may cause a stenosis of the vagina during or after forced extraction or fetotomy but neither it nor the intrauterine hemor- rhage is usually fatal. In 12- to 21-year-old mares rup- ture of the uterine vessels and sudden death due to hem- 353354 VETERINARY OBSTETRICS orrhagic shock may occur before, during or after an apparently normal gestation and parturition. The middle uterine artery was most commonly involved but the iliac or utero-ovarian arteries occasionally were affected. Pre- partum rupture occurred most often in the latter vessel.41 Most fatal hemorrhages occur intraperitoneally due to rupture of the large vessels in the broad ligament caused by degenerative changes in the vessel wall, especially in mares or by torsion of the uterus or prolapse of the uterus. Definite symptoms of severe hemorrhage may be ob- served, indicated by weakness, depression, very rapid pulse and respiration rates, and pale mucous membranes and death within a few hours.34 If the operator promptly enters the peritoneal cavity through the abdominal wall in the flank region or through the uterine wall in pro- lapse, he may be able to control bleeding by ligating the ruptured vessels. The prognosis is very poor in these cases as severe hemorrhage, shock, and death may occur in rapid succession. In mares early signs of colic, sweating, pain, rapid pulse rate and moderate anemia may occur due to rupture of a uterine vessel with relatively slow loss of blood between the two layers of the broad liga- ment causing a large hematoma. If this ruptures intra- peritoneally within the next few weeks then severe acute signs of shock, rapid weak pulse, anemia, prostration and death follow. If hemorrhage is severe enough to cause clinical symptoms, blood transfusions of 2,000 to 8,000 ml. or more in large animals, saline injections, gelatin or other types of solutions designed to maintain blood pressure should be given, and repeated as often as nec- essary. The mare should be sedated with a large dose of a tranquilizer and closely confined. In lacerations or ruptures of the genital tract preven- tive treatments to control infection should be used, such as the administration of sulfonamides, antibiotics, or lo- cal mild antiseptics. Thrombosis of the larger uterine ar- teries and veins is occasionally observed or described in animals. Thrombi are seen most often in the veins fol- lowing prolapse of the uterus or uterine torsion when circulation has been restricted. Occasionally an aneurism of the middle uterine artery may be palpated on rectal examination after parturition in the cow, or a hematoma in the broad ligament of the mare. Adhesions between the genital tract and ovaries and other pelvic and abdom- inal organs and tissues may occur following postpartum hemorrhage. Subinvolution of the placental sites formerly called “persistent decidual reaction” and occasionally mistak- enly called uterine chorioepithelioma is observed infre- quently in bitches and is characterized by a persistent discharge of blood from the vulva for 30 to 60 or more days after whelping.2 6'31 Subinvolution of the placental sites should be differentiated from cystitis, uterine tu- mors, acute or chronic metritis, and cystic endometrial hyperplasia. This condition has been reported11 in Alas- kan Malamutes and in some cases causes a decline in the hematocrit. The bloody discharge was nonfetid and it ceased about two weeks before true estrum. Concep- tion occurred normally. Normal involution of the canine uterus requires about 12 weeks. In a study of 95 postpartum bitches’ uteri 20 had subinvolution of one or more placental sites indi- cating that hormonal influences or infection were prob- ably not causative factors.2 The lesions of subinvolution of certain placental sites include sites that are twice nor- mal size and hemorrhagic and on microscopic section several large collagen masses, dilated endometrial glands, and numerous “trophoblast-like (decidual) cells,” are usually seen.2,6,31 In the normal bitch these latter cells regress and disappear spontaneously within a month postpartum. The pathogenesis of subinvolution is un- known. Further studies are indicated. The discharge of blood in affected bitches is most noticeable about the time of weaning. Most bitches recover spontaneously without or despite various treatments including proges- terone.431 Occasionally a few bitches become anemic and ovariohysterectomy and blood transfusions may be nec- essary.^29 Most recovered bitches subsequently breed and whelp normally. Lacerations and Contusions of the Birth Canal and Adjacent Structures After each dystocia operation the operator should carefully examine the uterus and genital canal for evi- dence of contusions and lacerations. Minor lacerations and trauma are common especially to the vulva, vesti- bule and cervix in uniparous animals after forced ex- traction or fetotomy. Since the vagina is freely dilatable it is less often injured. Minor lacerations are of little im- portance and usually heal promptly without treatment. Although the more severe lacerations of the cervix in cows seldom result in rupture, a few veterinarians rec- ommended that these be immediately sutured through the vagina to prevent the healed cervix from gaping or being ectropic, and to prevent the formation of excessive con- nective tissue in the cervix. Mild lacerations of the en- dometrium heal promptly. These may be aided to heal by the injection of oxytocin which favors uterine con- traction. Vaginal lacerations generally occur near the vulvovaginal border. Lacerations of the vulva are usu- ally mild when parturition is normal. Occasionally the mare, especially if sutured by the Caslick operation, willINJURIES AND DISEASES OF THE PUERPERAL PERIOD 355 tear the vulva in a normal parturition. In the mare and cow vulvar and vestibular lacerations are quite common when strong traction is applied too rapidly to permit nor- mal dilation of the vulva. Mild lacerations need not be sutured. Deep lacerations or episiotomy incisions should be promptly sutured after parturition with deep vertical mattress nylon or catgut sutures to prevent gaping and scarring of the vulva and thereby predisposing to vulvitis and vaginitis. Parenteral antibiotics should be adminis- tered. Certain mares and cows with relaxed, flaccid, tipped or horizontal vulvas should have the dorsal half or two- thirds of the commissure sutured as described under the Caslick or vulva-suturing operation to control postpar- tum infection. Lacerations, if not sutured, commonly be- come infected especially if the tissue is traumatized or devitalized or if metritis and retention of the fetal mem- branes are present. Infected lacerations of the vulva and vestibule result in pain, swelling, and persistent straining or “wind sucking”—conditions which are particularly undesirable in the postpartum cow or mare. Recom- mended treatment consists of parenteral antibiotics and local treatment of lacerations by suturing early, or ap- plication of protective mild antibiotic dressings. Tetanus antitoxin or a booster injection of toxoid should be ad- ministered in the mare. Hematomas and Contusions of the Vagina or the Vulva are occasionally noted in all animals but most commonly in the mare and sow. They may be confused with or mistaken for tumors or prolapse of the vagina or bladder. Hematomas involving the vaginal wall are found on examination of the genital tract. In rare instances they may be observed protruding between the vulvar lips. A temporary Caslick’s operation closing the dorsal portion of the vulva will prevent the protrusion, contamination and irritation of the vaginal hematoma. Hematomas of the vulva are readily noted. If left alone they are usually absorbed within 1 to 3 weeks. In some cases they may rupture through the mucous membrane or the owner of the animal may request that they be removed; this can be done by incising, removing the clot and carefully su- turing to control further bleeding and to obliterate the area that contained the large blood clot. This should not be performed until after 3 to 4 days following parturi- tion. In occasional cases diagnosed early, ice packs or cold water spray might be indicated. Contusions of the vulva, vagina, and cervix resulting in swelling and edema, occur most frequently due to trauma during fetotomy op- erations or from external injuries. Occasionally in the sow hematoma of the vulva may rupture and cause serious or fatal hemorrhage. To con- trol or prevent such hemorrhage the labial branch of the internal pudendal artery should be ligated by inserting a heavy Vetafil or umbilical tape suture at the junction of the vulva and the semimembranosus muscle in the dorso- lateral quadrant of the vulva, at about 2 to 3 o’clock (9 to 10 o’clock) into lumen of vulva and out again through the dorsal mucosa and skin at about 12 to 1 or 11 to 12 o’clock. This ligature can be removed in 5 to 7 days. Mechanical protection of the vulva can be provided by placing a piece of plywood behind the sow at a 60 to 70 degree angle to the floor of the farrowing stall with the uppermost end nearest the sow.12a 27 Occasionally a blow or a kick in the region of the cli- toris will result in marked edema of the clitoris and vulva in the mare. In most cases these swellings subside fairly promptly and should not be confused with edema from the udder that may extend upward and involve the vulva in cattle. If edema is severe, alternate cold and hot ap- plications, massage, and in certain cases small punctures or incisions through the mucous membrane may release the fluid or reduce the edematous swelling of the vulva. Contusions of the Maternal Pelvic Structures by the fetus or by instruments used during fetotomy may result in intrapelvic hematomas and hemorrhages, or may cause obturator or gluteal paralysis by injury to those nerves at parturition. Gluteal paralysis is rare and is described only in the mare; it is brought about by contusions caused by a bony prominence on the fetus pressing on the glu- teal nerve as it passes over the bony portion of the lumbo- sacral articulation or ilium. This may be a bilateral or unilateral injury and usually occurs in mares that appar- ently give birth without difficulty. In this condition the mare will show some difficulty in rising and may require assistance in rising if the injury is bilateral. The gait is characterized by a definite lameness and weakness of the affected limb. After a few days to a week, a marked atrophy of the gluteal muscles on the affected side is very noticeable. After a few weeks the lameness or pa- ralysis of the limb becomes less observable but it may take 6 to 18 months for complete recovery. The prog- nosis is favorable. Treatment consists of good nursing and possibly nonsteroidal antiinflammatory drugs such as phenylbutazone. The mare should be in a large, well- bedded box stall with good footing. In some cases slings or assistance in rising may be necessary for several days or a week. Affected mares should not be allowed to struggle or exert themselves in rising. External appli- cations, massage, or other treatments are of no value. Calving Paralysis or Obturator Paralysis may occur in the mare or cow but is most common in the latter. It is much more prevalent in heifers than in cows. Injury to the obturator nerve and lumbar (L6) roots of the sciatic (ischiatic) nerves14 is observed so often in hip lock in the anterior presentation that before this type of dystocia is356 VETERINARY OBSTETRICS relieved calving paralysis should always be suspected. An examination is done to inform the owner of the pa- ralysis before the obstetrical operation so that later the veterinarian will not be blamed for the injury. The con- dition may affect one or both rear limbs. If the cow is down and laboring with a hip lock condition, the un- derneath leg and nerves is the one most commonly and severely affected. This contusion is usually caused by the bony tuberosities of the fetal hips, especially the greater trochanters, contusing the obturator and sciatic nerves as the nerves either pass over the bony prominence of the lumbo-sacral articulation, or as it passes down the shaft of the ilium before it enters the obturator foramen. Calv- ing paralysis in heifers is very common in the hip lock condition that has existed for several hours. Yet when strong forced extraction has to be applied manually or with the fetal extractor to draw a large fetus through a heifer’s pelvis, calving paralysis seldom occurs. Injury to the obturator and sciatic nerves causes a paralysis of the medial and caudal adductor muscles of the thigh and partial loss of tibial and peroneal nerve function. This seriously effects the total support of the pelvic limb.14 If the condition is unilateral the cow can stand on the un- affected limb and as it walks the affected limb is moved stiffly forward and is abducted so the foot is placed on the ground 8 to 24 cm. lateral from the normal position. The cow is unsteady and is likely to slip and fall. If both nerves are bilaterally contused and injured, both limbs are stiffly extended and abducted and the cow usually is unable to rise. If assisted to its feet and the hind limbs held together, the animal can stand but when it takes a step the affected limb is extended cranially and abducted and the cow falls to the ground. If paralysis is severe and bilateral the prognosis should be guarded. If the paralysis is mild and the animal can walk, even though with difficulty, the prognosis is good. In most cases the condition improves rapidly and in 2 to 7 days the animal is able to walk quite well. Other cases may take longer for recovery, even up to 4 to 8 weeks. In rare cases the damage to the obturator and L6 roots of the sciatic nerves may be severe and permanent. The chances for recovery after 2 to 3 weeks are poor, and slaughter may be recommended. The only treatments of any value are good nursing and tying the animal’s rear legs together in order to prevent excessive abduction, over 35 to 45 cm., and possible complications of a dis- located hip or fractured pelvis. The use of straps such as hame straps around the pasterns tied with a length of rope or chain aids in preventing abduction of the limbs and helps the animal to rise. Some veterinarians strap or tie the hocks together but it is difficult to fasten straps or ropes above the hocks tightly enough so that they do not slide down, and yet loosely enough to allow move- ment of the gastrocnemius tendon. In the mare and oc- casionally in the cow the use of slings may be of value in assisting the animal to rise to its feet and supporting it for a short period. The animal should be kept in a well- bedded large box stall or pen, preferably with a dirt floor. Under such conditions dairy cattle should be milked by rolling the cow first to one side and then to the other. Possibly treatment with the anterior inflammatory non- steroidal drugs such as phenylbutazone may be helpful. Peroneal paralysis due to injury or trauma to the per- oneal nerve as it passes over the dorsolateral condyle of the tibia and fibula is observed in cattle confined in stan- chions with their rear parts over the edge of the gutter. It occurs most often in cows with dystocia and hypo- calcemia that struggle to rise (See Figure 94). Injury to the peroneal or fibular nerve results in anesthesia of the cranial surface of the fetlock and metatarsus and paral- ysis of the muscles that extend the digit and flex the hock, namely the long and lateral digital extensors, the peroneus tertius and the anterior tibial muscles. This re- sults in knuckling of the fetlock and dropping of the hock and difficulty in rising, standing and walking.25 As with injury to the obturator nerve good nursing care and close confinement are essential. A rigid supporting bandage to the lower leg may prevent knuckling of the fetlock. Pe- roneal paralysis should be differentiated from rupture of the gastrocnemius muscle and posterior paresis due to Figure 94. Bilateral peroneal nerve injury and paralysis in a cow.INJURIES AND DISEASES OF THE PUERPERAL PERIOD 357 lesions in the spinal cord. Rarely other paralyses may be observed following dystocia or injury at the time of par- turition including brachial or radial nerve paralysis in stanchioned cattle in which the forelimb was caught in the manger and forcefully extended. These miscella- neous nerve paralyses have been well-demonstrated.62 Rupture of the gastrocnemius muscle is apparently secondary to Zenker’s degeneration of the muscle and usually follows considerable struggling or efforts to rise during dystocia, hypocalcemia or after epidural anes- thesia (See Figure 95). Zenker’s degeneration may be due to excessive muscular activity especially in cows that have been confined for long periods and provided very limited exercise. Furthermore it is seen more often in states where selenium is known to be deficient.42 Eleven cases of rupture of the gastrocnemius muscle were re- ported,36 in 3 high-producing Holstein herds in one year in south-central New York State where selenium is de- ficient. The condition may be diagnosed by the inability to support weight on the affected leg, the flaccid gas- trocnemius tendon and the hard swelling due to edema, hemorrhage and Zenkers’ degeneration in the gastroc- nemius muscle. Mild cases that can stand may recover in several weeks if they are confined and possibly a sup- port such as a metal brace or Thomas splint provided. In most advanced cases slaughter is indicated. Prophy- lactic injections of selenium or selenium provided as a trace mineral may be indicated in selenium deficient areas. Rupture of the Uterus, Cervix, Vagina, and Perineum Uterine or Vaginal Rupture may occur in any spe- cies.3’22,33,35'43’46,48’55 It may be due to prolonged dystocia Figure 95. Unilateral rupture of the gastrocnemius muscle in a cow during postparturient paresis. with fetal emphysema; torsion of the uterus, in which transverse rupture may occur in prolonged cases; to im- proper manipulations and traction on the fetus; to fatigue of the operators, or to an accident in fetotomy operations in large animals or to forceps removal of a fetus in bitches; to protruding bones of the fetus after fetotomy; or due to inexpert manipulations of the fetus by laymen. The author has observed a ewe with maternal intestines in the vagina due to a ruptured uterus caused by an owner with large hands attempting to relieve a dystocia. For this latter reason and others associated with prolonged dystocia, the uterus and vagina should be carefully ex- amined prior to any obstetrical operation to be certain that a rupture of the uterus, cervix, or vagina is not pres- ent. Rupture produced by the operating veterinarian even if due to his fatigue is extremely embarrassing and should be avoided. In 26 cases of uterine rupture in cows out of 1004 referred obstetric cases to a college clinic, 7 cows had uterine torsion, 7 had oversized fetuses, 4 had emphsematous fetuses, 3 had fetal monsters and 2 had an immature pelvis. Nineteen of the 26 cows recovered after surgery.35 In the birth of fetuses with long extrem- ities, such as the foal, vaginal rupture may be due to improper presentations, positions, and postures, espe- cially dorso-pubic positions, anterior longitudinal pre- sentations with the hind limbs extended beneath the body, transverse ventral presentations, and when the forefoot or feet are crossed over the neck. This latter presentation may result in rupture of the vagina, rectum and perineum (See Figure 96). Rupture of the uterus is common in the mare in rotated bicomual pregnancy if traction is applied to the fetus. Forced extraction of a bovine fetus in a nor- mal presentation may cause rupture of the uterus, cervix, or vagina by forcing these structures against a sharp bony prominence occasionally found on the cranial portion of the pubic symphysis. Transverse rupture of the uterus may be caused by retraction or contraction rings of the uterine wall; or rupture of the cervix if the cervix is poorly dilated; rupture of the vagina may occur if perivaginal fat is pushed caudally as the fetus is forcibly drawn to- ward the vulva. In this latter instance the vaginal wall near the hymenal ring or vestibular-vaginal border rup- tures to allow the escape of the fat. A similar tear or rupture of the vagina occasionally results in a prolapse of the bladder. Forced extraction with the fetus in ab- normal posture or position or in torsion of the uterus may cause a portion of the uterine or vaginal wall to be caught by a deviated extremity and folded upon itself to produce a rupture. A dry, emphysematous fetus and a swollen, dry birth canal are conducive to rupture of the vaginal, cervical, or uterine walls when strong traction or repul- sion is applied. In one cow rupture of the uterus occurred358 VETERINARY OBSTETRICS Figure 96. Rupture of the rectum, vagina and perineum of a mare caused by dystocia. This picture was taken 8 weeks after the accident. apparently due to extensive severe adhesions of the uterus to the adjacent viscera. Administration of oxytocin to dogs or other animals with dystocia and/or uterine tor- sion may cause uterine rupture.26 (See Figure 97.) In a few cases spontaneous uterine rupture may occur due to unknown causes. After each dystocia case the veteri- narian should carefully examine the uterus and birth canal for the presence of a rupture of the uterus or birth canal in order that it may be treated promptly or in hopeless cases the cow may be slaughtered and some value thereby salvaged. The symptoms and prognosis of rupture of the genital tract vary with the animal and the portion of the genital tract involved; the size of the rupture; the character of the rupture, whether regular or irregular, horizontal or vertical; the nature of the uterine contents; the amount of uterine contents that have escaped into the abdominal cavity; and whether or not intestines or bladder have pro- lapsed through the rent in the wall of the genital tract. In a mare unless the uterine rupture is small and no in- fection was present in the uterus, a fatal peritonitis usu- ally develops rapidly. In the cow or other domestic an- imal rupture of the uterus due to an emphysematous fetus rapidly produces a fatal peritonitis. A similar termination can be expected in a uterine rupture in any animal in which the uterine contents are severely infected. In rare cases in cows, a rupture of the uterus may occur which releases a live or recently dead fetus into the abdominal cavity. Occasionally the symptoms of uterine rupture in the cow may be slight, but usually anorexia, lack of ruminations and rumen contractions, restlessness, rapid pulse and respiration rates, and cold extremities are pres- ent. The body temperature is usually normal or subnor- mal but may occasionally be elevated. If infected fetuses and material are released into the abdominal cavity, acute, severe septicemia or shock symptoms develop rapidly. Prostration, and death usually occur in 1 to 2 days. In less severe cases peritonitis is less marked and the ani- mal may survive with the fetus becoming walled off, or death may occur in 3 to 7 days. The fetus may be re- moved through a laparotomy incision and the uterus su- tured. With proper technique and aftercare some of these cases will survive. In small ruptures of the uterus after parturition or dystocia when no infection is present and the rent is in the dorsal half of the uterus some cows have survived after repeated doses of oxytocin and with parenteral antibiotic therapy. In these cases penicillin (three to six million units), and streptomycin (4 to 5 gms.), or Aureomycin or Terramycin or tetracycline in 2- to 4- gm. doses or similar antibiotic therapy is given daily to the average 800- to 1000-lb. cow or mare. One to two grams of the latter broad-range antibiotics should be placed in the uterus to control intrauterine infection. The admin- istration of antibiotics and of sodium sulfonamides in concentrations of 5 to 10 percent, through the abdom- Figure 97. Transverse rupture at parturition of the isolated uterine horn containing canine fetuses—this condition apparently followed trauma or torsion of the horn at about midgestation resulting in the separation of the horn from the rest of the uterus, note the scarring.INJURIES AND DISEASES OF THE PUERPERAL PERIOD 359 inal wall into the peritoneal cavity might be indicated in some cases. Occasionally the uterine rupture is large enough to require suturing. This is difficult in cows, but may be performed by working through the birth canal, using continuous or mattress sutures to bring the serous surfaces of the uterus on either side of the rupture into apposition. Some veterinarians have recommended pro- lapsing the uterus or vagina by pulling it to the outside through the birth canal and then suturing the rent and replacing the organs. A few veterinarians have success- fully prolapsed the severely lacerated uterus through the birth canal and amputated it.13 In large animals suturing the uterus through a laparotomy incision may be suc- cessful or it may be sutured in this manner with assis- tance through the birth canal. The presence of a retained placenta, septic metritis, an atonic uterine wall, or pro- lapsed intestines results in a poor prognosis. In most se- vere cases of uterine rupture in the cow, ewe, or sow the prognosis is poor and slaughter is usually advised if the animal is in an otherwise satisfactory condition. Even if recovery takes place, the future breeding life of that animal is very questionable, as chronic perimetritis and peritonitis are the probable results. In the bitch uterine rupture, as in the larger animals, is usually characterized by anorexia, depression, weakness; in the early stages an elevated and in late stages a depressed body temper- ature; rapid pulse and respirations; cold extremities; con- stipation, or fetid diarrhea; pale mucous membranes es- pecially if there is internal hemorrhage or shock; followed by prostration and death in 1 to 3 days. In the bitch lap- arotomy and hysterectomy, if performed early, together with flushing of the abdominal cavity with warm saline solution and antibiotics, and treatment to prevent shock and infection, occasionally results in recovery of the bitch. In all species except the mare extrauterine fetuses may be walled off or encapsulated as described previously. Under no circumstances should fluids be injected into the ruptured uteri nor should manipulations of retained placentas take place. The latter should be allowed to drop from the uterus without assistance. Complete rupture of the cervix in large animals is similar to rupture of the uterus but because proper suturing of this structure is so difficult, the prognosis is poor if the rupture is extensive. Rupture of the vagina is usually not as serious as uter- ine rupture and the prognosis is much better unless the rupture extends into the peritoneal cavity. Simple rup- tures of the vagina especially of the lateral or dorsal wall need not be sutured unless the operator desires to do so. In most cases there is no need to suture small ruptures even on the floor of the vagina, but some veterinarians prefer to do so in order to prevent a possible perivaginal abscess if a retained placenta or metritis occurs. In rare cases these perivaginal abscesses, which may also occur secondary to an infected perivaginal hematoma, become large and finally after 2 to 6 weeks or more break out between the vulvar lips and the tuber ischii. Mild wounds of the vagina heal rapidly. Recto-vaginal fistulas due to rupture of the dorsal wall of the vagina and ventral wall of the rectum are occasionally observed, especially in mares in which parturition is violent. If these are noted promptly they should be sutured immediately, care being taken that the rectal wall is tightly sutured in a transverse manner. Suturing of the vaginal wall is not as essential. If 24 to 48 hours pass before this condition is noticed it usually is impossible to correct at that time and one must wait until the edema, swelling, granulation tissue, and wound edges have completely healed before surgical in- tervention is undertaken to correct the fistula.57b In these chronic cases some feces and a mucopurulent discharge are expelled from the vulva. If the fistula is small, the rectum may be packed with cotton and the vagina douched with saline before breeding. If pregnancy occurs the fis- tula may then be sutured without the loss of a breeding season. Due to straining, rupture of the uterus may be fol- lowed by prolapse of the intestines into the uterus or birth canal or through the vulva. If rupture of the vagina or cervix extends into the peritoneal cavity it may also re- sult in prolapse of the intestines. The bladder or fat may prolapse through a rupture in the ventral or lateral wall of the vagina. These conditions will be discussed later. Rupture of the Perineum and Vulva is observed chiefly in the mare but may occasionally be observed in cows and possibly ewes when excessive traction is ap- plied to rapidly remove the fetus. Thus the vulva and perineal region may be ruptured before it has time to dilate gradually. This condition has been rarely observed in dairy heifers; hemorrhage may be severe and in some cases fatal.59,60 More often it is observed in the mare in which the forelegs and even the nose in anterior presen- tation or in the dorsopubic position the long limbs of the equine fetus may be pushed dorsally into the vaginal roof and rectal floor. This sacculated portion, due to the vi- olence of parturition, is forced into the dilated anus. (See Figure 96.) The vagina and rectal floor rupture, the feet protrude from the anus, and as the fetus is expelled the vulva and anus are tom longitudinally. In rare cases the vulva and vestibule remain intact and the fetus is expelled through the ruptured rectum, anus and perineal tissues. The presence of the ruptured perineum or “gill flirter” condition causing the rectum and vestibule to be- come a continuous cavity or “cloaca” is readily noted. As in recto-vaginal fistula it is advisable to correct and suture the rupture immediately, paying particular atten- tion to suturing the rectal wall and anal sphincter. If the operation is not performed at once it must be postponed360 VETERINARY OBSTETRICS about 6 weeks until the swelling and granulation tissue has subsided and the wound has completely healed.57b If these mares are not operated upon the feces drop into the vagina, the vulva and vaginal mucous membranes are irritated, and the animal sucks air, pneumovagina, and there is a profuse discharge of mucus and feces that soil the rear parts. This condition is seldom observed in the cow but mild vulvo-anal lacerations and ruptures are seen especially in beef heifers and rarely in ewes. Proper use of episiotomy operations in cattle would prevent this condition. The prognosis for the life of the patient is good if hemorrhage or shock is not immediately fatal. If the condition is not corrected, the future breeding life of the animal is poor. Very rarely “gill-flirter” mares may con- ceive. The prognosis for this operation is usually guarded. For a discussion of this operation and that of the recto- vaginal fistula the author recommends the standard vet- erinary surgical texts the detailed anatomy of the peri- neal region of the mare,23 and a description of the op- eration in the mare and cow. 1,5,8’50’57b The author particularly commends the technique of a two-phase op- eration for the surgical repair of third degree perineal lacerations and rectal vaginal fistulas.1 The first opera- tion produces a firm shelf of tissue between the rectum and vagina by suturing the scarified tissues between the rectum and vagina and the vaginal mucous membrane but not placing sutures through the rectal mucosa. In about 2 weeks the second operation is performed that closes and reforms the perineal area, the anus and vulva. Rupture of the pelvic and abdominal organs other than the genital tract during birth or dystocia have been described rarely in the cow and mare. A rupture of the rectum in cows has been described.16,56 Four cases were reported20 where the free end of the cecum ruptured through the rectal wall. In all these cases the fetus was in posterior presentation. Rupture of the intestine of cows has been described.47,48 Rupture of the cecum and ventral colon have been reported during parturition in the mare.17,28,57a Death always occurred in mares after rup- ture of the intestine and usually occurred in cattle. A few cows operated on immediately after the rupture sur- vived. Rupture of the bladder may occur occasionally in the mare and cow.7,45,58b In very rare instances rupture of the diaphragm in a mare may result from violent straining. Prolapse of the Abdominal or Pelvic Viscera Prolapse of the Intestines may occur through a rup- ture or laceration in the uterus, cervix, or cranial portion of the vagina at the time of parturition. The intestines may only enter the uterus or may pass into the vagina and out the vulva. This condition should be differen- tiated from a Schistosomus reflexus or a ruptured um- bilical hernia of the fetus. The prognosis is invariably poor, since the dystocia causing the rupture usually is severe, contamination and infection of the intestines and abdominal cavity is probable, and it is difficult to control the intestines to prevent their injury during removal of the fetus. Slaughter of the animal is usually recom- mended. In occasional cases in which infection or trauma to the intestines is minimal, replacing the intestines, su- turing the rupture and removing the fetus might be pos- sible. Closure of the rupture wound in the uterus may be accomplished through the birth canal, or probably a better approach would be through the laparotomy inci- sion after a cesarean operation. If the intestine is trau- matized or severely contaminated resection of a portion of it may be necessary. Perforating lacerations or rup- tures of the cervix and anterior vagina are sutured through the birth canal.21,58 Aftercare consists of carefully sutur- ing the rupture, and administering local and parenteral antibiotic treatment to control peritonitis, as recom- mended for the handling of uterine rupture. Left dis- placement of the abomasum is a fairly common oc- currence after parturition in the cow. Prolapse of the rectum may occasionally occur in any animal in dystocia or other causes associated with per- sistent violent straining and a relaxed anal sphincter. Slight eversion of the rectum at parturition is common, but se- vere prolapse is rare. In the mare prolapse of 2 to 3 feet of rectum is usually fatal since rupture of the rectum or small colon often occurs secondarily. If prolapse of the rectum begins in the mare it should be controlled by holding the rectum in place forcibly with a towel over the anus until the fetus is expelled or withdrawn. In other species prolapse is neither as serious nor as extensive. It should be prevented if possible or replaced promptly before or after the fetus is removed. A purse-string su- ture of heavy nylon material around the anus is often indicated after replacement. If unnoticed until trauma and edema are present, surgery, including either the sub- mucosal resection reefing operation or amputation, to- gether with retaining sutures may be necessary to replace and maintain it in position. The different types of equine rectal prolapses and their correction was reviewed.52 Prolapse of the Bladder may occur in all species but it is seen most commonly in the larger domestic animals before or after parturition. Prolapse of the bladder usu- ally takes place through a rupture or tear in the floor of the vagina and the bladder is noticed hanging from the vulvar orifice after parturition. Due to the sharp bend in the urethra the prolapsed organ fills with urine. This con-INJURIES AND DISEASES OF THE PUERPERAL PERIOD 361 dition must be differentiated from eversion of the blad- der through the urethra, vaginal or vulvar tumors, cysts, a mass of fat protruding through a rupture in the floor of the vagina, or vaginal or vulvar hematomas.51 If the bladder is distended with urine it may be replaced and the urine forced out or it may be drained with a needle before replacing. The external surface of the bladder should be carefully cleaned, covered with an antibiotic solution, and the organ replaced. The rupture in the vagi- nal floor permitting the prolapse should be sutured and the animal placed on parenteral antibiotics. Eversion of the Bladder has been described mainly in the mare, in which the urethra is large and parturition violent. It has only very rarely been seen in the other animals such as the cow or sow.17b In rare and serious cases in the mare intestines may prolapse into the everted bladder and prevent reduction.24 55 Eversion of the blad- der may occur before or during parturition. It seldom if ever obstructs the passage of the fetus but occasionally the everted bladder and urethra may be severely trau- matized when the fetus passes through the vestibule. Eversion of the bladder is easily recognized, as this or- gan is attached to the area of the ventral floor of the vulva where the urethra orifice is normally located. The everted bladder is pear-shaped. The openings of the two ureters drip urine and the mucous lining of the bladder may be noted and felt. If the everted bladder is small it may not become exposed through the vulvar lips until the animal lies down. In handling eversion of the blad- der, the bladder should be thoroughly cleansed. If a tear or rupture is present it should be sutured or if a portion is damaged severely that portion might be removed and the edges of the incision sutured. Following the injection of epidural anesthesia, the operator should use both hands to compress the bladder and force it back through the urethra. The bladder should be massaged and pressed through the vagina floor until it is in its proper position. Aftercare consists of irrigating the bladder with saline solution and antibiotics and administering antibiotics parenterally so that the urine will contain a high con- centration of the antibiotic for a number of days. It is seldom necessary to place a stitch in the external urinary meatus to prevent another eversion once the fetus has been removed and labor has ceased. Prolapse of Perivaginal Fat may occur through a small rupture of the caudal portion of the vagina during forced extraction of the fetus especially in fat dairy or beef heif- ers. These masses of fat should be differentiated from prolapse or eversion of the bladder, as they are likely to resemble those structures. On examination, the vaginal rapture, which is usually quite small, may be found at the base of the prolapsed mass of fat. This fat may be cut off with a knife or scissors, as there will be little bleeding. The vaginal rupture may be sutured or left to heal without suturing. Sulfonamide powder or antibiotics are customarily placed in the wound before suturing. The prognosis is good as a perivaginal abscess seldom de- velops. Prolapse or Eversion of the Uterus may be called casting of the “wethers” or casting of the “calf bed.” It is observed most commonly in the cow and ewe, oc- casionally in sows,123 and rarely in the bitch, queen and mare. It occurs most often immediately after parturition and occasionally up to several hours afterward. In rare cases it may occur 48 to 72 hours after parturition. In bitches there may be rare cases of prolapse of one horn while fetuses are still in the other horn.10 Prolapse of the uterus is predisposed by long mesometrial attachments; violent or strong tenesmus; a relaxed, atonic, flaccid uterus; retention of the placenta especially at the ovarian pole of the gravid horn in cows and of the nongravid horn in mares; and by excessive relaxation of the pelvic and perineal region. In dairy cows it is commonly seen in confined or stabled cattle during the winter months that calve in a stanchion with their rear parts sloping downwards and hanging over the gutter. The use of great force in forced extraction of the fetus predisposes to te- nesmus after relief of the dystocia. If the uterus is not contracting it frequently prolapses immediately after re- lief of the dystocia. Prolapse of the relatively flaccid uterus in older cows is frequently associated with hypocalcemia at parturition.5,32 Dystocia associated with a mild hy- pocalcemia was present in 42 percent of 26 beef cows with uterine prolapse compared with only 6.7 percent of the control animals.38 In dystocia when the uterus is con- tracted tightly around a dry fetus, forced extraction is likely to result in prolapse of the uterus. Prolapse of the uterus is seen most commonly in pluriparous dairy cows but is not infrequent in poorly grown, thin, debilitated dairy heifers. Prolapse of the uterus was frequently ob- served in sheep in Australia due to a hyperestrogenism from eating clovers high in estrogenic hormones. Pro- lapse of the uterus is apparently not hereditary although occasionally it may be seen in dam and daughter. There was a probable hereditary basis for prolapse of the uterus and vagina in Hereford cattle.61 A low plane of nutrition may also be a factor. Prolapse of the uterus very rarely occurs following prolapse of the vagina prior to partu- rition despite the common belief among owners that if the cow prolapses the vagina prepartum it is apt to suffer prolapse of the uterus postpartum. Prolapse of the uterus rarely recurs at a subsequent parturition. In a Norwegian study32 of 955 cows treated by 171 veterinarians for prolapsed uterus, 27 percent occurred362 VETERINARY OBSTETRICS within 1 hour, 48 percent within 3 hours, 65 percent within 6 hours and 90 percent within 15 hours after calving. Numerically uterine prolapse was most common in pri- mipara but the highest incidences, 3 times higher than first and second calvings, occurred in cows at their fifth or greater calving where it was related to hypocalcemia. Of 506 cows that prolapsed, only 18 had prolapsed at 1736 prior calvings, an incidence of about 1 percent. About 1 percent of cows with vaginal prolapse prior to calving developed uterine prolapse after calving. At the time of uterine prolapse 56.6 percent of the fetal mem- branes were still attached. Of 955 cases 83 percent re- covered. Of those not surviving 35 percent died before or during treatment, 24 percent were slaughtered be- cause of uterine injury or irreplaceable prolapse, 16 per- cent died shortly after treatment and 24 percent died or were slaughtered later in the course of the illness. Deaths were highest in cows with both a prolapsed uterus and hypocalcemia. Of 407 cows with prolapse that were rebred 78.4 percent conceived. Breeding after 90 days post- partum resulted in normal conception rates. In only 6 cows did the prolapse reoccur within a few days. Thus suturing the vulva to prevent subsequent prolapse is not necessary.32 The symptoms of prolapse of the uterus are obvious. (See Figure 98.) The animal is usually recumbent but may be standing, with the uterus hanging to the hocks. Retention of the placenta is likely. The fetal membranes and/or mucous membrane of the uterus is exposed and usually covered with feces, straw, dirt, or blood clots unless of very recent occurrence. The uterus is usually enlarged and edematous especially if the condition has existed for 4 to 6 hours or longer. Excellent illustrations of the condition in various species of animals have been made.10 In the cow the gravid horn prolapses or everts sufficiently so that the cervix is usually present at the vulva. The nongravid horn is inside the peritoneal sur- faces of the prolapsed gravid horn and does not evert be- cause of the strong intercomual ligament. The opening of the nongravid horn may be observed as an oval or slit-like orifice near the vulva on the ventral or lateral side of the prolapsed gravid horn. Prolapse of the uterus in the ewe is similar to this condition in the cow. In the other species, horses and multipara, usually one horn— or rarely both horns—may be prolapsed or everted. Ninety percent of the uterine prolapses in sows were bicomual with the initial invagination occurring in the uterine body.54 In cows the initial invagination also occurred at this site. Prolapse or invagination also occurred at this site. Pro- lapse or invagination of the uterine horn should be dif- ferentiated from a prolapse of the vagina. In the bitch and queen palpation of the abdomen may reveal the Figure 98. Uterine prolapse in a Hereford cow. thickened invaginated uterine horn and abdominal pain. In the mare the uterine body may compose the major portion of the exposed everted uterus. In most animals prolapse of the uterus results in mild to moderate symp- toms of tenesmus, restlessness, pain, anxiety, anorexia, and an increase in pulse and respiration rate. In cases with complicating factors of internal hemorrhage due to rupture of one of the uterine vessels, shock, incarcera- tion and ischemia of intestines present in the peritoneal sac of the prolapsed uterus due to pressure obstructing the circulation of the intestines, or other diseases such as hypocalcemia may cause the animal to be recumbent. A very rapid, weak pulse, irregular, rapid respiration rates, pale mucous membranes, expiratory grunt, and prostra- tion with severe depression and inability to rise indicate serious complications. When intestines or excessive hemorrhage with a large blood clot are present in the peritoneal sac formed by the prolapsed uterus, the bo- vine uterus may be 30 to 45 cm. or more in diameter. In ewes, intestines frequently are present in the pro- lapsed uterine horn. The prognosis in uterine prolapse varies greatly. InINJURIES AND DISEASES OF THE PUERPERAL PERIOD 363 most cases in which the condition is observed early, the veterinarian called promptly, the cow able to stand and the uterus not severely injured, the prognosis for the life of the cow is good. In 158 cases of prolapse of the uterus in dairy cattle seen from 1943 to 1953 in the Ambulatory Clinic of New York State Veterinary College, the mor- tality rate was 18 percent. If cases obviously compli- cated by other conditions were eliminated the mortality rate in cows in good physical condition at the time of the operation would probably be 5 percent or lower. The prognosis is poorer in beef cattle on pasture, where the condition may not be observed as early and aid secured promptly.61 The animals’ future breeding history may be good or poor depending upon the severity of the uterine lesions, the promptness of treatment and the rate of in- volution. If the uterus is grossly contaminated, or dried due to exposure to the sun, or if lacerations are present, the prognosis is more guarded due to the possibility of a septic metritis, perimetritis or peritonitis developing, and the prognosis for the future breeding life of the an- imal is questionable. It is surprising how much trauma, irritation, and contamination the uterus can withstand. Upon replacement of the organ this infection is over- come, the traumatic lesions heal, and the animal re- covers. In other cases, with the animal prostrate, unable to rise and conditions complicated by shock, internal hemorrhage, or incarceration of the intestines, the prog- nosis is usually very poor to hopeless. In the author’s experience, mainly with dairy cattle, the percentage of cases of uterine prolapse that terminated fatally due to internal hemorrhage, shock, or incarceration of the in- testines was high when the cows were in stanchions and the prolapsed uterus had dropped into the gutter. This is further reason for having box stalls for calving cows or having them calve on pasture. If other diseases are pres- ent, such as hypocalcemia or obturator paralysis, the prognosis is based on the severity of those conditions as well. In cattle in which the uterus is so badly damaged or diseased that replacement cannot be considered and amputation of the uterus is the only recourse, the prog- nosis is poor although some of these cases may survive. In the ewe the prognosis for prolapse or eversion of the uterus is similar to that of the cow. In the mare the condition is more serious, but if the animals are treated promptly most will survive. Amputation of the uterus in the mare should seldom if ever be attempted since it is indicated only when the uterus is severely traumatized and lacerated, and then the prognosis is extremely grave. In the sow the prognosis is poor as extensive prolapse usually results in internal hemorrhages and shock. The author has observed 5 or 6 cases of prolapse of the uterus in the sow and all were either dead on his arrival at the farm or died with 15 to 30 minutes. A few cases of pro- lapse of the uterus in sows have recovered following a laparotomy or replacement.5'17 In the bitch and queen the prognosis is fair to good even though the condition is rather difficult to handle because of the length of the uterine horns and the inability of the operator to aid re- placement with his hand and arm as in the larger do- mestic animals. Laparotomy and replacement of the uterus in the abdomen may be necessary in the bitch, queen and sow. Ovario-hysterectomy is more frequently and successfully performed in the bitch and queen than in the larger animals.18 Following proper replacement of the prolapsed uterus very few cases recur in any species. The treatment or handling of prolapse of the uterus in the cow can be made much easier if the owner is in- structed to wrap the cow’s uterus in a wet towel or sheet or to place it in a plastic bag to keep it moist and clean until replaced. If the cow is standing the uterus should be raised and supported level with the vulva until assis- tance arrives. If the cow is recumbent in a stanchion the gutter should be built up to support the uterus and keep it from hanging. This prevents the uterus from becoming edematous and may possibly prevent rupture of the uter- ine vessels. If possible the cow should be in or near the bam, in a clean paddock or well-bedded stall to make the operation cleaner, more convenient, and less diffi- cult. Good light is essential. Proper restraint of the an- imal aids in prompt and easy replacement of the everted uterus. Epidural anesthesia should be used routinely in sufficient dosage to provide good anesthesia but at the same time to keep the animal standing. In fact some cows and mares that are down and refuse to stand may get up promptly after epidural anesthesia is given. Epidural anesthesia controls and prevents defecation during re- placement of the uterus. Elevation of the rear parts greatly facilitates replacement of the uterus. The ordinary stand- ing posture of the cow usually gives sufficient elevation of the rear parts. If replacement is to be made even easier the fore feet may be lowered or the rear parts elevated by making the animal stand on a slope. If the animal is recumbent and refuses to rise and cannot be stimulated to do so by prodding with a sharp object or an electric prod, by rolling her tail beneath the foot, or the intra- venous injection of calcium gluconate, benzidrine stim- ulants, or 20 to 40 ml or more of Pyribenzamine, even after giving epidural anesthesia, and since it is very difficult or harmful to elevate the rear quarters of a cow that is unable to stand either manually or mechanically, a practical effective procedure is to place ropes on the rear pasterns and draw both legs out behind the cow. This tips the pelvis ventrally and greatly facilitates re- placement of the uterus. Epidural anesthesia is not nec-364 VETERINARY OBSTETRICS essary in ewes because with the aid of one or two men grasping each hind leg the rear parts can be elevated high enough so that the uterus almost falls into place. In mul- tiparous animals, and possibly the mare, general anes- thesia may be indicated. The uterus of the cow should be carefully prepared for replacement. It should be held level with the ischial arch or vulva during these operations. The purpose of this is to relieve pressure on the broad ligament and uterine veins as they pass over the ischial arch, and to restore normal circulation in the prolapsed uterus. This avoids further edema of the uterine wall and aids in absorption and dis- appearance of the edema already present. This position of the uterus permits the bladder to resume its normal position and if intestines are present in the uterus they return to the abdominal cavity. The danger of possible rupture of the vessels in the broad ligament is greatly reduced and the cow is more comfortable when the uterus is held level with the vulva. This can be done by sup- porting the uterus in a towel or sheet held by a man on either side of the rear quarters of the cow, or it may be supported on a wooden or metal tray, or held in the arms of the veterinarian if he is suitably attired in a rubber apron, gown, or coveralls. The afterbirth, if present, should be gently removed. Only rarely is the afterbirth attached so securely it cannot be removed. If the re- moval of the placenta is impossible without severe trauma and hemorrhage resulting, it may be left in place. Fol- lowing replacement of the uterus, the placenta is handled in the same manner as retained placenta in a cow not affected with prolapse of the uterus. The uterus should be cleansed thoroughly with a warm physiological saline solution, or with water to which a small amount of mild antiseptic such as chlorine or qua- ternary ammonium compound has been added. To cleanse the uterus thoroughly may require 5 to 10 gallons of water. Usually if the farmer is warned at the time of the call to have plenty of hot water available, it will be ready, but if it is not available, the veterinarian should be equipped to take some with him. In some cases it may be nec- essary to use cotton to help clean and wipe the uterus. The adjacent vulva and perineal region should be care- fully washed and cleansed at the same time, particular attention being given to folds and creases in the skin. If the utems is lacerated, tom, or perforated, it should be carefully sutured bringing the serosal surfaces in appo- sition. If hemorrhage from the surface of the uterus is severe the vessel should be ligated. If prolapse of the uterus has been present for some time and edema is se- vere, the massage of washing the uterus and the holding of the utems level with the vulva may not be sufficient to readily reduce its size so that is can be replaced. Vig- orous massage of the utems with the palm of the hand, with the fingers extended but held tightly together, may be accomplished by wrapping a towel or piece of sheet- ing tightly around the utems and applying pressure through the towel without the danger or possibility of forcing a finger through the uterine wall or edematous mucosa. The author believes that the practice of applying sugar to the edematous utems on the theory that it removes fluid through the endometrium is cmde, unscientific, and not necessary. Probably most of the edematous fluid re- moved when sugar is massaged into the swollen utems is forced out through small fissures produced in the en- dometrium by the sharp granules. It may be well to pal- pate the bladder before replacing the utems, since in rare instances it may be distended and require catheterizing so that it will not interfere with the operation. Some veterinarians advise giving 30 to 50 units of oxytocin or pituitrin to contract the bovine utems when it is ready for replacement. The author does not advise this, inasmuch as it makes the uterine wall tense, con- tracted, and difficult to return to its normal position without a portion of the horn remaining invaginated. On several occasions when the prolapse occurred 36 to 72 hours after parturition and oxytocin was administered before replacement, the contracted, tense utems could not be replaced through the contracted cervix until the uterine walls had relaxed. Many veterinarians advise coating the prolapsed utems with oil or ointment con- taining a mild antiseptic or antibiotic. In replacing the utems it should be held above the level of the floor of the pelvis; the vulvar lips should be pulled apart, and first the ventral portion and then the dorsum of the pro- lapsed portion of the utems should be replaced, starting at the cervical end of the utems nearest the vulva. Since the utems is still more or less in the form of an arc, replacing 3 or 4 inches of the ventral or concave portion of the prolapsed hom is accompanied by replacement of 6 to 8 inches of the dorsal or convex portion of the hom. In replacing the utems, pressure should be exerted with the palm of the hand, with the fingers extended but held tightly together, to avoid perforating the utems. Finally the ovarian pole of the utems is pushed by the fist through the vulva, vagina, and cervix, into the uterine cavity. If the cervical rings are contracted, pulling them gently backward with one hand and working the utems through with the other is helpful. The ovarian pole is pushed through the vagina, cervix, and utems with the clenched fist and arm by a piston-like or shaking motion on var- ious parts of its perimeter until the hom is completely straightened out and no invagination is present. This is of great importance to prevent possible necrosis of the invaginated pole of the uterine hom. One should use careINJURIES AND DISEASES OF THE PUERPERAL PERIOD 365 not to tear or remove a caruncle and thus cause bleeding. If the uterus has been sutured no douching should follow replacement. If complete replacement of the ovarian pole is difficult the introduction of 2 to 3 gallons of very warm water or physiological saline solution into the uterine cavity is often of assistance, since it stimulates uterine contractions and helps to wash out uterine debris. This fluid should be siphoned out. Most cases do not require douching. After the uterus is replaced properly and completely, 30 to 50 units of oxytocin should be given intramuscu- larly or intravenously. If it is given by the latter method the uterine wall will contract tightly on the operator’s arm within 30 to 60 seconds. Following replacement, most veterinarians use a uterine antiseptic or antibiotic such as those described in treating retained placenta. Probably one to two gms. of a tetracycline or similar antibiotic is most efficient in controlling infection. In treating valuable cows another dose of oxytocin might be administered in 2 to 4 hours. If the cow is standing and not straining, a recurrence of the prolapse is very rare. Temporary suturing of the vulva with a figure of eight or mattress suture of umbilical tape into the hair line, or some other type of vulvar suture described under vaginal prolapse, or the application of a truss for 1 to 3 days is a placebo for the farmer. Very rarely does a pro- lapse recur if the uterus is properly replaced in a cow. If the owner has the cow under close observation for the next 3 days, as he should, a rare recurrence of the pro- lapse can be treated promptly. This is much better than having, as the author did in one cow, the prolapse recur into the vagina, and because of the vulvar sutures it went unnoticed for 3 days. It was impossible to replace at that time and the cow was slaughtered. A cow that failed to conceive following a prolapse of the uterus was exam- ined and on finding no evidence of the uterus on rectal examination, a small involuted uterus was present in the vagina protruding through the cervix.19 If vulvar sutures are used they should be removed in 24 hours. Pessaries are not recommended, as they tend to cause straining. If the cow continues straining following replacement of the uterus it may be due to invagination of the ovarian pole of the uterine horn or an irritation or inflammation of the vulva. The former should be corrected, and oily protec- tants or anesthetic ointments may be used for the latter condition, together with a long-lasting epidural anes- thetic. If the cow is recumbent the rear parts should be kept slightly higher than the fore parts for several days. If the cow can stand this is not necessary. In uncompli- cated cases it is generally found that within 24 hours the cervix is closed tightly enough so that recurrence is un- likely.5 Parenteral antibiotics are often indicated to help control uterine infection after replacement. In rare cases a severe or even fatal infection with metritis or peritoni- tis may follow prolapse of the uterus. In the ewe the same general replacement technique is applied as in the cow but it is less difficult, since the rear quarters can be easily elevated. Recurrence is pos- sible but vulvar sutures are also of questionable value. In these cases epidural anesthesia is valuable. Close con- finement of the ewe with her rear parts elevated may be indicated. In the mare replacement is similar to the cow except that general anesthesia may occasionally be nec- essary. In the mare the body of the uterus is the only visible portion of the prolapsed organ.512 Tetanus anti- toxin, oxytocin, antibiotics, and other supportive treat- ments are indicated to prevent secondary tetanus, me- tritis, and laminitis in the mare. In multiparous animals replacement of the uterus in the manner described in the cow is difficult, but may occasionally be possible if the rear parts of the animal are well-elevated. A laparotomy is usually necessary to accomplish the return of the uterus to its normal position. Some authors advise suturing the apex of the uterine horns to the body wall to prevent a recurrence. Occasionally in the sow and bitch one horn of the uterus prolapses and a few fetuses may still be in the other horn. Therefore in most cases in multipara a laparotomy is probably advisable. If the uterus is badly traumatized, amputation of the horn or hysterectomy is indicated in the bitch and queen and possibly rarely in the larger animals. Hysterectomy or amputation of the prolapsed uterus is undertaken only when replacement is impossible or when it is quite certain that replacement of a badly tom, lacerated, necrotic, infected uterus possibly would result in death. In some cases where the cow is unable to rise, chickens or hogs severely mutilate a prolapsed uterus. The prognosis is always guarded to poor because of the severity of the operation and the conditions preceding it. It is contraindicated in the mare, but is often the method of choice in the bitch and queen. Although the prognosis is poor there are many recorded cases of successful am- putations or hysterectomies. In the cow and ewe am- putation of the uterus may be accomplished by making a long longitudinal incision in the prolapsed uterus and cervix on the dorsal and caudal surface between the rows of caruncles starting at the vulvar lips (See Figures 99 and 100). Through this extensive incision the uterine ar- teries and veins can be seen in the tense mesometrium. These vessels are carefully ligated in 2 or 3 places and the broad ligament is severed from the uterus between the ligatures. The cranial portion of the vagina anterior to the prolapsed cervix is easily drawn out of the vulva and is carefully ligated with fixation ligatures. The utems366 VETERINARY OBSTETRICS Figure 99. A surgical technique for amputation of a prolapsed and part or all of the cervix is removed and the stump is replaced in the vaginal cavity. This technique pre- cludes the occurrence of hemorrhage from the uterine vessels, and insures the vagina and peritoneal cavity being closed tightly.40 In the bitch, queen and sow a similar technique can be used, but the incision is circular and the uterine stump can be closed by a Connell suture fol- lowed by a Lembert stitch. In the bitch a dorsal episi- otomy may be necessary in order to make the operation less difficult. In the bitch, queen and sow a laparotomy can be done, the prolapsed horn returned to the abdom- inal cavity, and an ovario-hysterectomy performed. In the cow or ewe the most common technique rec- ommended for amputation of the prolapsed uterus con- sists of making certain that neither the bladder nor any intestine is present in the prolapsed portion and then li- gating that portion close to the vulva, using a strong lig- ature or preferably a soaped or oiled cord or fine rope tightened by two men pulling on opposite ends of the cord or rope. Three or 4 separate ligatures are firmly tied around the neck of the prolapsed portion of the uterus allowing 15 to 20 minutes to elapse between the appli- cation of each ligature. This is necessary as edema is always present in such cases, and the enclosing ligatures I' must be tight enough so that when the uterus is removed 3 or 4 inches caudal to the ligatures the uterine vessels in the mesovarium will not withdraw into the abdominal cavity and cause fatal hemorrhage. Some veterinarians have successfully used a heavy elastic ligature made of long 2-inch-wide strips of rubber inner tube wrapped a number of times very tightly around the neck of the pro- lapsed portion in a manner similar to the cord method just described. After a lapse of 20 to 30 minutes to per- mit the edema to be forced from beneath the ligature, the uterus is amputated, leaving a fairly large stump to be replaced in the vagina. The ligatures or elastic tubing should be held in place by transfixing sutures through the enclosed vaginal wall. Following this operation the cow should be observed closely for evidence of shock, and saline solution, blood, glucocorticoids, and other stimulants should be administered at once. This is very important if the patient is to survive, as shock or hem- orrhage may be fatal. The stump replaced in the vagina will slough in several weeks, it is usually advisable to administer parenteral antibiotics for 4 to 6 days. Invagination of the Uterine Horn is occasionally noted in the cow and mare, but occurs only rarely in other species. In this condition the ovarian pole of the gravidINJURIES AND DISEASES OF THE PUERPERAL PERIOD 367 horn in the cow and usually the nongravid horn in the mare is everted but not far enough to be observed at the vulva. Ordinarily the invagination is completely within the uterus and is like an intestinal intussusception. It is more likely to occur during or after parturition and after replacement of a prolapsed uterus. It may be due to the pull or weight of the attached placenta on the ovarian pole of the uterus. Not infrequently it may be produced by traction on the fetal membranes at the time their re- moval is attempted. In a few cases the ovarian pole of the uterus may become incarcerated and necrotic with the cow showing symptoms of a septic metritis and peri- tonitis followed by death. In some mild cases the con- dition may correct itself spontaneously, while in others the invagination may progress until complete prolapse of the uterus occurs. This is another reason for careful ex- amination of the uterus after relieving a dystocia. The symptoms of an invaginated horn may be lacking, or there may be evidences of uneasiness, straining, or pain. In an occasional advanced case the invaginated portion of the horn may become necrotic; there may be symptoms of toxemia and septicemia; and a fetid, red- dish-black vulvar discharge similar to that in a septic me- tritis may appear. On rectal palpation the enlarged uter- ine mass may feel like a large intussusception, and the mesovarium will be tense and tight. On vaginal exami- nation if the hand can enter the uterus the invaginated horn is recognized as a dome-shaped, tumor-like mass projecting upward into the lumen of the uterus. This is noted most often in removal of an afterbirth in the cow when strong traction is placed on the placenta and the ovarian pole invaginates toward the cervix. In the mare this may also occur and in most cases involves the non- gravid horn. The prognosis is usually good unless the invaginated ovarian pole has been incarcerated by the contracting uterine muscle and becomes necrotic, in which case death usually occurs unless a hysterectomy is performed. The treatment of the condition in large animals consists of kneading the invaginated pole back into place with the fist, with piston-like shaking movements around the edge of the uterine lumen. Douching with 2 to 4 gallons of water may aid in replacing the invaginated pole. If one hand inserted in the rectum puts traction on the cranial portion of the broad ligament and the mesovarium at- tached to the invaginated pole, and the other hand pushes on the “tumor, ” this bimanual action may reduce the in- vagination. Ordinarily when the uterus is contracting strongly this condition cannot be relieved at that time. In cases where the invaginated horn cannot be replaced, when the animal’s uterus is examined again in 3 to 6 hours it will be found that the condition often was cor- rected spontaneously after the uterus relaxed. The at- tending veterinarian should closely follow and treat such cases of an invaginated uterine horn until the condition is corrected. 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(1981) Metabolic Abnor- malities Associated with Rupture of the Urinary Bladder in Neo- natal Foals (and a Mare), JAVMA, 178, 3, 263-266. 8. Bemis, H. E. (1930) A New Operation for Rectovaginal Fistula, N. A. Vet., 30, 2, 37. 9. Benesch, F. (1930) Die Graphische Darstillung der Normalen der Medikamentell Verstarkten und der Abgeschwachten Ute- rusbewegung an Lebenden Rind im Involutionsstadium, Proc. 11th Intemat. Vet. Congr., 351. 10. Benesch, F. and Wright, J. G. (1951) Veterinary Obstetrics, Williams and Wilkins, Baltimore, Md. 11. Berger, Charles (1966) Personal Communication. 12a. Bollwahn, W. (1981) Surgical Procedures in Boars and Sows, in Diseases of Swine, 5th Ed., A. D. Leman, Ed., Iowa State Univ. Press, Ames, Iowa, 782. 12b. Brewer, R. L. and Kliest, G. J. (1963) Uterine Prolapse in the Mare, JAVMA, 142, 10, 1118. 13. Carlson. A. (1960) Lacerated Uterus Technique, HaverGlover Messenger, Jan.-Feb. 14. Cox, V. S., Breazile, J. E. and Hoover, T. R. (1975) Surgical and Anatomic Study of Calving Paralysis, Amer. J. Vet. Res. 36, 4, 427-430. 15. Cox, V. S., McGrath, C. J. and Jorgensen, S. E. (1982) The Role of Pressure Damage in Pathogenesis of the Downer Cow Syndrome, Am. J. Vet. 43, 1, 26-31. 16. Danelius, G. (1941) Rupture of the Rectum in Connection with Calving in a Heifer, Cor. Vet., 31, 4, 393. 17a. Donelan, E. and Sloss, V. (1972) Rupture of the Large Intestine in the Mare Associated with Unassisted Parturition, Austral. Vet. Jour. 48, 7, 413. 17b. Ducharme, N. G. and Stem, E. S. Ill (1981) Eversion of the Urinary Bladder in the Cow, JAVMA, 179, 10, 996-998. 18. Egger, E. L. (1978) Uterine Prolapse in a Cat. Feline Practice, 8, (1) 34-37. 19. Fincher, M. G. (1954) Personal Communication.368 VETERINARY OBSTETRICS 20. Galvan, D. (1938) Rupture de la pointe du Caecum pendant le Velage, Rec. de Med. Vet., 114, 12, 788. 21. Godkin, G. T. (1959) Dystocia with Vaginal Rupture, JAVMA, 135, 4, 218. 22. Grunert, E. and Geyer, K. (1964) Beitrag zur Chirurgischen Be- handlung von Perforierenden Zervix and Uterusverletzungen beim Rind, Deutsche Tieraztl. Wochenschr. 71, 9, 241. 23. Habel, R. E. (1953) The Perineum of the Mare, Cor. Vet., 43, 2, 249. 24. Haynes, P. F. and McClure, J. R. (1980) Eversion of the Uri- nary Bladder: A Sequel to Third-Degree Laceration in the Mare, Vet. Surg., 9, 66-71. 25. Keown, G. H. (1956) Peroneal Nerve Damage, Canad. J. Comp. Med. and Vet. Sci. 20, 445. 26. Krichel, J. H., Jr. (1969) A Report of Six Cases of Uterine Rupture in the Dog, Vet. Med. 64, 10, 872. 27. Ladwig, V. D. (1975) Surgical Procedure to Control Hemor- rhage of the Porcine Vulva, JAVMA, 166, 6, 598-599. 28. Littlejohn, A. and Ritchie, J. D. S. (1975) Rupture of the Cae- cum at Parturition in the Mare, Jour. S. Afr. Vet. Assoc. 46, 87. 29. McEntee, K. (1982) Personal Communication. 30. McMullen, M. E., Nurse, W. H. and Nurse, H. G. (1964) Tele- scoping of the Uterus in a Boston Terrier, Vet. Med., 59, 2, 206. 31. Mosier, J. E. (1980) Disorders of the Postparturient Bitch, in Current Therapy in Theriogenology, edit, by D. A. Morrow, W. B. Saunders Co., Philadelphia, 611. 32. 0degaard, S. A. (1977) Bovine Uterine Prolapse, Acta Vet. Scand. Suppl. 63, 1-124. 33. O’Neill, A. R. (1961) Rupture of the Uterus in the Parturient Ewe, Vet. Rec. 73, 1041. 34. Pascoe, R. R. (1979) Rupture of the Utero-ovarian or Middle Uterine Artery in the Mare at or Near Parturition, Vet. Rec. 104, 77. 35. Pearson, H. and Denny, H. R. (1975) Spontaneous Uterine Rupture in Cattle: A Review of 26 Cases, Vet. Rec. 97, 240- 244. 36. Phillips, S. (1965) Personal Communication. 37. Raleigh, P. J. (1977) Reduction of Uterine Prolapse in a Sow by Laparotomy, Vet. Rec. 100, 89-90. 38. Richardson, G. F., Klemmer, A. D. and Knudsen, D. B. (1981) Observations on Uterine Prolapse in Beef Cattle, Canad. Vet. J. 22, 6, 189. 39. Richter, J. and Gotze, R. (1950) Lehrbuch der Tiergeburtshilfe, H., Laupp, Jr., Tubingen, Germany. 40. Roberts, S. J. (1949) Amputation of the Prolapsed Uterus, Cor. Vet. 39, 4, 438. 41. Rooney, J. R. (1964) Internal Hemorrhage Related to Gestation in the Mare, Cor. Vet. 54, 1, 11. 42. Schnautz, J. O. (1954) Postparturient Myorrhexis in Cattle, N. A. Vet. 35, 191. 43. Sloss, V. (1974) A Clinical Study of Dystocia in Cattle. 2. Complications, Austral. Vet. Jour. 50, 294-297. 44. Sloss, V. and Dufty, J. H. (1980) Handbook of Bovine Ob- stetrics, Williams and Wilkins, Baltimore and London. 45. Smith, J., Divers, T. J. and Lamp, T. M. (1982) Ruptured Uri- nary Bladder in a Post-Parturient Cow, Cor. Vet. In Press (1982). 46. Snoeck, M. A. (1962) Uterine Rupture in a Pony, Tijdschr. vor Diergeneesk, 87, 15, 1035. 47. Stauffer, V. D. (1959) Traumatic Resection of Intestine During Parturition, JAVMA, 134, 3, 122. 48. Steiner, H. (1962) Contribution to Enterectomy after Intestinal Rupture During Parturition in Cattle, Deutsche Tierarztl. Woch- enschr. 69, 13, 362. 49. Steiner, H. (1962) Spontaneous Rupture of the Uterus in the Sow during Farrowing, Deutsche Tierarztl. Wochenschr. 69, 10, 283. 50. Staub, O. C. and Fowler, M. E. (1961) Repair of Perineal Lac- erations in the Mare and Cow, JAVMA, 138, 12, 659. 51. Teige, J. (1956) Birth Injury of Vesica Urinaria in the Cow, Nord. Vet. Med. 8, 658. 52. Turner, T. A. and Fessler, J. F. (1980) Rectal Prolapse in the Horse, JAVMA, 177, 10, 1028-1032. 53. Vandeplassche, M. (1963) Cesarean Section in Complicated Cases in Cattle, Schweizer Archiv fur Tierhielkunde, 105, 1, 21. 54. Vandeplassche, M. and Spincemaille, J. (1963) Comparative Etiology and Pathogenesis of Uterine Prolapse in Domestic An- imals, Berl. and Munch. Tierarztl. Wochenschr. 76, 16, 324. 55. Vanderplassche, M. and Vanheuverswijn, A. (1953) Behan- dling van Dystokie door Omegekeerde Blaas met Darmen bij een Merrie, Vlaams Diergeneesk. Tijdschr., 22, 1, 8. 56. VanKruiningen, H. J., Fox, F. H. and Weber, W. T. (1961) Rupture of the Rectum, Cor. Vet. 51, 4, 557. 57a. Voss, J. L. (1969) Rupture of the Cecum and Ventral Colon of Mares During Parturition, JAVMA, 155, 5, 745. 57b. Walker, D. F. and Vaughan, J. T. (1980) Bovine and Equine Urogenital Surgery, Lea and Febiger, Philadelphia. 58a. White, J. B. (1961) An Unexplained Condition (Vaginal Rup- ture) in Pregnant Ewes, Vet. Rec. 73, 281. 58b. White, K. K. (1977) Urethral Sphincterotomy as an Approach to Repair of the Urinary Bladder in the Mare, A Case Report., J. Eq. Med. Surg. 1, 250. 59. Williams, W. L. (1943) Diseases of the Genital Organs of Do- mestic Animals, Ithaca, N.Y. 60. Williams, W. L. (1943) Veterinary Obstetrics, 4th Ed., Ithaca, N.Y. 61. Woodward, R. R. and Quesenberry, J. R. (1956) A Study of (Postpartum) Vaginal and Uterine Prolapse in Hereford Cattle, J. An Sci., 15, 1, 119. 62. Worthman, R. P. (1957) Demonstration of Specific Nerve Pa- ralysis in the Dog, JAVMA, 131, 4, 174. METABOLIC DISEASES OF THE PUERPERAL PERIOD Milk Fever, Parturient Paresis or Hypocalcemia is a metabolic nonfebrile disease of dairy cows usually four years of age or older, characterized by hypocalcemia oc- curring just before, during, or most often within 72 hours after parturition and the onset of lactation.19 Parturient hypocalcemia is an adaptation disease.11 Although dif- ficult to quantitate parturient hypocalcemia costs the dairy industry many millions of dollars each year.19 At the be- ginning of lactation when there is an increased demand for calcium, 2 to 5 times that of the gestation period, the cow is forced into a hypocalcemic state and partu- rient paresis ensues.1116'19'20'21’23 With the onset of lac- tation an adequate increase in dietary calcium intake andINJURIES AND DISEASES OF THE PUERPERAL PERIOD 369 absorption to meet the body demands is essential. In- appetance frequently associated with parturition, to- gether with the “lag period” of several days before bone tissue is activated to supply sufficient calcium retard the normal adaptation of the cow from the loss of calcium at the onset of parturition and lactation and results in a high incidence of parturient hypocalcemia and relapses following therapy.19 The blood serum calcium level drops from a normal of 8 to 12 mg. per 100 ml. to 3 to 7 mg., with symptoms of parturient paresis becoming progressively more pro- nounced as the calcium level declines. Hypocalcemic paresis is due to a depression of neuromuscular trans- mission of motor stimuli.6 Subclinical hypocalcemia, with calcium levels below 8 mg. per 100 ml. of serum may last for 11 to 32 hours in many parturient cows without paresis developing. Paralysis was usually associated with calcium levels below 5 mg. per 100 ml. serum.20 Hy- pophosphatemia, hyper- or hypomagnesemia and hyper- glycemia are other changes associated with parturient hypocalcemia.19 Parturient paresis is observed in all dairy breeds but most commonly in Jerseys. Recurrent attacks of milk fever may occur at subsequent parturitions. The symptoms of parturient paresis are anorexia, cold extremities, lowering of the body temperature, stiff gait, staggering, incoordination, inability to rise, an S-curve in the neck, failure of the pupil to contract on stimulation by light, suppression of urination and defecation, con- stipation, slight tympany of the rumen, cessation of par- turition if it develops during that period, coma, and fi- nally death usually occurring in 6 to 24 hours if treatment is not instituted. Only rarely does spontaneous recovery occur in the paretic cow. With proper care and prompt handling the prognosis is good, and the mortality should be less than 2 to 3 percent in uncomplicated cases that do not injure themselves in attempting to rise. Prolonged recumbency in parturient hypocalcemia frequently re- sults in pressure damage of ischemic necrosis of muscles and inflammation of sciatic and peroneal nerves leading to the downer cow syndrome and death.7 Early and prompt treatment of milk fever is necessary to avoid the latter syndrome especially in the larger heavier, often obese, cows of the Holstein breed. It has been demonstrated that 50 percent of normal healthy cows confined in re- cumbency for 6 to 12 hours developed extensive lesions leading to the downer cow syndrome and death or eu- thanasia.7 Treatment consists of administering 500 to 1000 ml. (depending on the size of the cow) of 20 percent calcium gluconate, one half of the amount injected intravenously and one half subcutaneously. In 100 cows recumbent with parturient hypocalcemia the overall relapse rate was 22 percent after treatment with calcium preparations either intravenously or intravenously and subcutaneously. The incidence of relapse was about 38 percent in the cows treated only intravenously while it was about 4 to 8 per- cent in the cows treated both intravenously and subcu- taneously.8 In these latter cows the serum calcium levels 12 hours after treatment were significantly higher than the cows only treated intravenously. Reduced amounts of milk should be removed from the udder for 2 to 3 days. Complete emptying of the udder should be avoided if possible. Udder insufflation to raise the plasma calcium con- centration by reducing milk secretion and transferring calcium in the udder back into the circulation was re- ported upon.21 This technique did not induce hypercal- cemia and was seldom followed by a relapse. Cotton- filtered compressed air from a cylinder introduced into the barrel of a syringe filled with an antibiotic udder in- fusion preparation to firmly distend the cow’s udder and teats was used. Following treatment the teats were tied with a tape for several hours to hold in the compressed air. Since 1930 many attempts have been made to pre- vent parturient hypocalcemia by administering large amounts of vitamin D either orally or by injection. These studies have been recently reviewed.19b Although various forms of vitamin D and D3 will produce a temporary hypercalcemia, their toxicity and the timing of the administration of these products with parturition have created serious drawbacks to their practical widespread acceptance and use.19a Recent preliminary studies on ad- ministering a large dose of a readily absorbed propri- etory calcium product containing other trace minerals and vitamins immediately after calving has shown some promise in reducing the incidence of parturient hypo- calcemia and retained placenta in dairy cows.9 Milk fe- ver or hypocalcemia has been described in the ewe, doe and sow mainly in Europe. The symptoms are similar to those in cows.3 To prevent the occurrence of parturient paresis which may reach an incidence of 80 percent or more in the pluriparous cows in certain dairy herds, the total dietary calcium intake late in lactation and during the nonlac- tating period should be greatly reduced by removing le- gumes such as clover and alfalfa from the diet as well as common mineral supplements used for lactating cows which are usually high in calcium. This practice causes a slight hypocalcemia and increased secretion of para- thyroid hormone. Timothy hay, straw and com silage are low in calcium content and may be fed.136,19 If too much of the com silage is fed the cows may become overly fat resulting in the “fat cow syndrome” in which the cows are more susceptible to milk fever, ketosis, digestive dis-370 VETERINARY OBSTETRICS orders as displaced abomasums, retained placentas and metritis, mastitis and foot problems. In certain areas and herds where some or all legume roughage must be fed, the addition of 2.5 to 5 percent monosodium phosphate to the grain ration, resulting in Ca. P ratio of 1:1 instead of a 3 to 7:1 may reduce the incidence of milk fe- Ver.5 ‘3b'19 However low calcium diets, regardless of di- etary phosphorus intake, prevent milk fever by the pre- partal activation of both bone and intestinal tract.13b Ketosis or Acetonemia is only rarely observed prior to parturition in cows.3,13 It may occur the first 7 to 10 days after parturition but by far the greatest number of cases occur from 10 to 60 days after parturition. Ketosis in dairy cows is a lactation disorder, with elevated levels of ketones in the blood, urine and milk, associated with high milk production and a negative energy balance.19 It is estimated that clinical and subclinical ketosis costs U.S. dairymen about 150 million dollars a year. Three types of ketosis in cattle may develop:24 (1) primary sponta- neous ketosis which may have an hereditary predispo- sition, (2) primary nutritional, which is the most com- mon and (3) secondary ketosis which occurs with reduced TDN intake due to metritis, displacement of the aboma- sum, traumatic gastritis and other diseases. Ketosis is characterized by hypoglycemia, ketonemia and ketonu- ria. The normal bovine blood levels of 40 to 60 mg. per 100 ml. of glucose drop to 40 to 18 mg. of glucose and the blood ketone levels rise from a norm of 2 to 15 mg. to 15 to 75 mg. per 100 ml. This condition is due ba- sically to a reduced intake of nutrients, especially car- bohydrates, in relation to the loss of energy by heavy lactation. Secondary conditions such as fatty changes in the liver may occur. There is a marked loss in weight due to the use of body fat, carbohydrates and proteins for milk and energy. The condition may develop in dairy cows at any age. The symptoms observed are of two types, digestive and nervous. In the more common digestive type, the symptoms are anorexia, constipation, gradual drop in milk flow and rapid loss of weight. In the less common ner- vous type the symptoms are more severe, and depression is marked; various nervous symptoms such as trembling, nervousness and licking may be present; paresis is not uncommon, and anorexia and drop in milk flow are also observed. At times it may be difficult to differentiate between acetonemia and metritis following parturition, and both may be present. By testing the urine or milk with Ross reagent, the development of a definite purple color is usually indicative of ketosis. Inasmuch as very few animals die of ketosis, the prognosis is good; but the loss in milk production and body weight can be of great economic importance to the dairy farmer. The av- erage incidence of ketosis in the United States is about 4 percent but in some high producing herds it may reach 20 to 50 percent. The condition is more common in the winter stabling period. The treatment of ketosis in cattle consists of raising the blood sugar level for a period, thereby restoring the cow’s appetite. Following the increased intake of addi- tional nutrients, especially carbohydrates, the cow will recover and a relapse is unlikely. The preparations used to raise blood glucose levels include glucose solutions of 500 ml. to 1000 ml. of 40 percent glucose injected intravenously, or continuous, slow intravenous drip of several thousand ml. of 25 percent glucose. Sodium pro- pionate, 1/3 to 3/4 lb. fed daily in small doses or given as a drench or a similar but more palatable product, pro- pylene glycol administered orally in 200 to 500 ml. amounts daily increase propionic acid in the rumen which is absorbed and used by the cow in place of glucose. This conserves and raises the blood glucose level. Glu- cocorticoids injected intramuscularly raise blood glucose levels rapidly and also improve appetite and lower milk production for several days. ACTH, 200 to 600 I.U. in- jected intramuscularly stimulates production of the glu- cocorticoids by the adrenal glands and thus raises the level of blood sugar. Ten to 30 gms. daily of chloral hydrate in divided doses given orally also raises blood sugar levels. If metritis, mastitis or other infectious pro- cess due to bacteria is present the glucocorticoids should not be given or they should be accompanied by paren- teral antibiotics. They are contraindicated in viral dis- eases. Relapses are likely to recur if the level and amounts of nutrients, especially carbohydrates, TDN or energy in the ration are not increased so that the cow will consume 1 lb. of 12- to 14-percent protein grain for 2-1/2 to 4 lbs. of milk produced, depending upon the quality and quantity of roughage. The level of energy intake must equal the work of milk production so that the cow main- tains a positive energy balance and does not relapse into ketosis. As nutrition and management of present dairy cows are improved to reduce ketosis, the genetic in- crease in future milk production of cows will ensure this disease remains a problem. Ketosis or Pregnancy Disease in Ewes is seen the last 2 to 4 weeks of pregnancy. Usually the dam is car- rying twin or triplet fetuses. It is caused by a hypogly- cemia produced by the rapid growth of the fetuses and insufficient intake of nutrients, especially carbohydrates in the ration.3 Ketosis is not due to an insufficiency of ACTH as hydrocortisone levels are elevated.10 The af- fected ewes are usually thin but ketosis may be observed in ewes in good condition. It is also predisposed by a lack of exercise. The liver shows fatty changes and theINJURIES AND DISEASES OF THE PUERPERAL PERIOD 371 ketone levels in the blood and urine are greatly elevated. In ewes the symptoms of ketosis are dullness, anorexia, paresis, or inability to rise without assistance, and ner- vous symptoms of mental derangement such as walking in a circle, pressing the head against some object, draw- ing the head backward and to one side. The nervous signs exhibited might be due to inability of nerve cells to uti- lize sugar.10 Urine obtained by a small catheter or by stopping respirations by squeezing the nose and mouth firmly shut can be tested by the Ross test, as in cattle, for the presence of ketones. In more advanced cases the fetuses die and if they are aborted promptly the ewe may recover. Ketosis may be differentiated from listeriosis by a lack of paresis of the lips or ears. In listeriosis the limbs are flaccid while in ketosis the limbs will resist flexion if upward pressure is applied to the toe. The course of the disease is 2 to 6 days. The prognosis is usually poor unless cases are diagnosed and treated early or abortion occurs before the ewe is severely affected. Treatment consists of any one or a combination of the following: the injection of 200 ml. of 40 percent glucose intravenously; administration of glucocorticoids or 50 to 100 I.U. of ACTH intramuscularly which may initiate premature parturition; an increase in the carbohydrate in- take of 1/2 to 1 lb. of grain, 1/4 to 1/2 lb. of molasses daily per ewe or 2 ounces of propylene glycol 2 to 3 times a day. Sometimes valuable ewes which are se- verely affected can be saved by cesarean section; the fe- tuses are often dead. The glucocorticoids and estrogens have been used to cause or hasten parturition or abortion in ewes with severe ketosis. The disease may usually be prevented in the rest of the flock by increasing the grain ration or by feeding molasses and increasing the amount of exercise. Ketosis in goats is similar to that in ewes but is observed less commonly. Grass Tetany, Lactation Tetany, Transport Teta- ny, “Wheat Poisoning” or Hypocalcemia, or Hy- pomagnesemia is a metabolic disease of beef and dairy cattle, and sheep and goats in Europe, especially those which are in advanced pregnancy or lactating heavily, grazing on lush, heavily fertilized grass or early wheat pastures or are transported or stressed in the puerperal or early lactation period. This disease complex is well- described.319 It occurs more commonly on certain types of soils and in certain regions. It is seen most often dur- ing the spring or fall months and less often during the summer months. Grass tetany is characterized by a hy- pocalcemia, occasionally a concurrent hypomagnese- mia, or hypomagnesemia alone. It is caused by the ex- cessive consumption of young lush grass on well-fertilized pastures. Some9a,n believe that the high potassium or trans- aconitate and citric acid content in grass causes a loss of calcium and magnesium from the body, accentuated in advanced pregnancy or during heavy lactation, when there is an increased drain on body calcium and magnesium. Hypomagnesemia may occur in stabled animals fed ra- tions low in magnesium. The symptoms of grass tetany are similar to those of milk fever when a simple hypo- calcemia with hyper- or normo-magnesemia is present. If, however, a hypomagnesemia is present with hypo- or normo-calcemia trismus, hyperesthesia, tachycardia, nystagmus, erect ears, tetany of the hind limbs, tremors, twitching of muscles that may progress into general spasms or convulsions, may be exhibited.17 Paresis is a common symptom. Unknown extrinsic or intrinsic factors appar- ently play a role in precipitating signs of hypomagne- semia when the serum levels of magnesium are low. A recent study indicates there may be a relationship be- tween age, renal function, magnesium antagonists and parathyroid hormone in the etiology of hypomagnesemic tetany.9a Decreases in magnesium levels in the cerebro- spinal fluid are more closely associated with clinical signs of grass tetany than are serum magnesium levels. Thus grass tetany may be due to alterations of central nervous system function possibly brought on by vascular lesions and hemorrhagic edema characteristic of pathologic le- sions of grass tetany.19 Often during the early stages of grass tetany the animal is excitable and may be aggres- sive. Some hypomagnesemic cows may act normally un- til handled when signs of tetany suddenly develop. This disease is more gradual in onset than is milk fever. The prognosis is usually good but sudden deaths are not un- common if the condition isn’t treated early. The treatment consists of injecting 500 to 1000 ml. of a calcium-magnesium solution intravenously and sub- cutaneously in a divided dose, removing the animal from the grass pasture, feeding good alfalfa hay, and supply- ing a mixture of bone meal or dicalcium phosphate, and magnesium oxide, sulphate or carbonate, up to 60 to 120 gms. daily, free choice, in a molasses block or prefer- ably in the grain ration. Since magnesium can’t be stored in large amounts in the body, a nearly daily intake is necessary. Magnesium may be combined with the cal- cium gluconate or 200 to 500 ml. of a 10 to 25 percent solution of magnesium sulphate may be given subcuta- neously. An outbreak of transport tetany or hypocal- cemia was described in which a flock of ewes kept on a stubble field low in calcium was driven 9 miles to a new pasture. The ewes near parturition or in early lac- tation showed depression, stiff gait, high pulse and res- piration rate and excessive salivation. Giving 150 ml. of 20 percent calcium gluconate subcutaneously resulted in recovery.1 Tetany or Eclampsia in the Mare is rare but has been372 VETERINARY OBSTETRICS described.3 Usually it occurs within several weeks after parturition, in a mare that has a normal foal, is lactating heavily, and is on a good, lush pasture. An attack may be precipitated by unusual handling, transport, or by a change in surroundings. It is probably a hypocalcemia similar to grass tetany in the cow or eclampsia in the bitch. In the early stages, symptoms of restlessness, rapid breathing, staring eyes, twitching, trembling and clonic spasms, especially of the diaphragm, are common. In later stages clonic spasms are followed by more tonic spasms, with trismus, marked restlessness, labored breathing, profuse sweating, and injected cyanotic mu- cous membranes. In advanced cases the animal is unable to stand. Tetany of most muscles is present; the animal becomes prostrate; convulsions are nearly continuous; and death results in 12 to 48 hours. The condition should be differentiated from tetanus. If treated promptly the prog- nosis should be good but deaths are not uncommon in untreated mares. Spontaneous recoveries have occurred at any time during the course of the disease. The treat- ment consists of intravenous injections of calcium glu- conate and possibly the administration of narcotics such as chloral hydrate, sodium pentobarbital or heavy tran- quilization. Puerperal Tetany or Eclampsia in the bitch and queen is a metabolic disease characterized by hypocalcemia.2,26 It is seen in heavily lactating bitches during the first 3 weeks after parturition, although it may occur prior to, during, or up to 6 weeks after parturition.4,18 The serum calcium level drops from a normal of 9 to 12 mg. to 5 to 7 mg. per 100 ml. It may occur in all breeds but is seen most commonly in small or medium-sized bitches. The disease is characterized by rapid breathing, a dry mouth and sclera, restlessness, nervousness, and whin- ing, followed by staggering, incoordination, stiffness of limbs, and an elevated body temperature. Later there is the development of symptoms of inability to rise, ex- tended legs, excessive salivation, champing movements, dilated pupils, clonic and tonic spasms and convulsions, congested mucous membranes, labored respirations and a rapid, hard pulse. The prognosis is good if treatment is instituted. Spontaneous recoveries may occur. Treat- ment consists of administering sodium pentobarbital or 5 to 10 ml. of a 10 percent calcium gluconate solution intravenously, intraperitoneally or subcutaneously. Re- currence of the condition is more common following the use of calcium gluconate than of sodium pentobarbital. If the pups are old enough they should be weaned. The bitch and queen should be fed added amounts of calcium lactate or gluconate in the ration. The administration of corticosteroid therapy, 5 mg. prednisolone or 25 mg. hy- drocortisone, daily will help prevent a relapse. If given for a week or more the steroid therapy should be with- drawn gradually.12 If the bitch has metritis, antibiotics should be given with the corticosteroids. If affected bitches are rebred the condition frequently recurs in the subse- quent lactation period.2 The disease is rare in the queen but symptoms and treatment are the same as in the bitch.10 Postparturient hemoglobinuria is an uncommon dis- ease of high-producing, older dairy cows occurring 2 to 4 weeks after calving and characterized by hemoglobin- emia, hemoglobinuria, and anemia.3 It is associated with rations deficient in phosphorus or rations high in rape, turnips, kale, beet pulp or cabbage. The affected cows show anorexia, weakness, dehydration, pale mucous membranes, rapid pulse and respiration, constipation and in the later severe stages, prostration and death after a course of 3 to 5 days. In mild cases or treated cases recovery occurs after several weeks. In severe cases there is a hypophosphatemia as low as 0.5 to 1.5 mg./100 ml. of serum; normal values are 4 to 6 mg./100 ml. Post- parturient hemoglobinuria should be differentiated from leptospirosis and pyelonephritis. Treatment consists of blood transfusions to effect; the intravenous injection of phosphorus containing compounds and oral supplemen- tation of the ration with monosodium phosphate or pos- sibly bone meal or dicalcium phosphate especially if cru- ciferous plants are in the diet.3 Puerperal Metabolic Diseases 1. Asbury, A. C. (1962) Hypocalcemia in Ewes—A Case Report, JAVMA, 141, 6, 703. 2. Austad, R. and Bjerkas, E. (1976) Eclampsia in the Bitch, J. Sm. An. Pract. 17, 793-798. 3. Blood, D. C., Henderson, J. A. and Radostits, O. M. (1979) Veterinary Medicine, Lea and Febiger, Philadelphia. 4. Bloom, F. (1954) Pathology of the Dog and Cat, Amer. Vet. Publicat. Inc., Evanston, 111. 5. Boda, J. M. and Cole, H. H. (1956) Calcium Metabolism with Special Reference to Parturient Paresis (Milk Fever) in Dairy Cattle; A Review, J. Dairy Sci. 39, 7, 1027. 6. Bowen, J. M., Blackmon, D. M. and Heavner, J. E. (1970) Neuromuscular Transmission and Hypocalcemic Paresis in the Cow, Amer. J. Vet. Res. 31, 5, 831. 7. Cox, V. S., McGrath, C. J. and Jorgensen, S. E. (1982) The Role of Pressure Damage in Pathogenesis of the Downer Cow Syndrome. 8. Curtis, R. A., Cote, J. F., McLennon, M. C., Smart, J. F. and Rowe, R. C. (1979) Relationship of Methods of Treatment to Relapse Rate and Serum Levels of Calcium and Phosphorous in Parturient Hypocalcemia, Bov. Pract. 14, 56-58. 9a. Deetz, L. E., Tucker, R. E., Mitchell, G. E., Jr. and De- Gregorio, R. M. (1982) Renal Function and Magnesium Clear- ance in Young and Old Cows Given Potassium Chloride and Sodium Citrate, J. An. Sci., 55, 3, 680. 9b. Dolge, K. L. (1982) Personal Communication. 10a. Forbes, T. J. and Singleton, A. G. (1964) Ovine Pregnancy Toxemia: A Review, Brit. Vet. Jour. 120, 56.INJURIES AND DISEASES OF THE PUERPERAL PERIOD 373 10b. Gray, S. J. (1975) A Case of Feline Eclampsia, Austral. Vet. Pract., 5, 182. 11. Jonsson, G. (1960) On the Etiology and Pathogenesis of Par- turient Paresis in Dairy Cows, Acta Agric. Scand. Suppl. 8. 12. Kallfelz, F. A. (1968) Current Veterinary Therapy III, Edit, by R. W. Kirk, W. B. Saunders Co., Philadelphia, 64. 13a. Kingrey, B. W., Ladwig, V. D., Monlux, W. S. and Ramsey, F. K. (1957) Pregnancy Disease of Cows, N. A. Vet. 38, 321. 13b. Kichura, T. S., Horst, R. L., Beitz, D. C. and Littledike, E. T., Relationships between Prepartal Dietary Calcium and Phos- phorus, Vitamin D, Metabolism, and Parturient Paresis in Dairy Cows, (1982) J. of Nutr. 112, 480. 14. Kronfeld, D. S. (1970) The “Downer” Problem, in “Bovine Medicine and Surgery,” W. J. Gibbons, E. J. Catcott and J. F. Smithcors Editors, Amer. Vet. Public, Inc. Wheaton, 111., 394. 15. Kronfeld, D. S. and Emery, R. S. (1970) Acetonemia in “Bo- vine Medicine and Surgery,” Amer. Vet. Public Inc., Wheaton, 111., 350. 16. Kronfeld, D. S. and Ramberg, C. F. (1970) Parturient Paresis in “Bovine Medicine and Surgery," Amer. Vet. Publ. Inc., Wheaton, 111., 382. 17. Kronfeld, D. S. and Simensen, M. G. (1970) The Hypomag- nesemic Tetanies, in “Bovine Medicine and Surgery,” Amer. Vet. Public Inc., Wheaton, 111., 339. 18. Lawler, D. C. (1963) Lactational Tetany in the Cat and a Re- view of the Literature, Vet. Rec. 75, 811. 19a. Littledike, E. T. and Horst, R. L. (1982) Vitamin D, Toxicity in Dairy Cows, J. Dairy Sci. 65, 749. 19b. Littledike, E. T., Young, J. W. and Beitz, D. C. (1981) Com- mon Metabolic Diseases of Cattle: Ketosis, Milk Fever, Grass Tetany, and Downer Cow Complex, J. Dairy Sci., 64, 1465- 1482. 20. Mayer, G. P., Ramberg, C. F. and Kronfeld, D. S. (1966) Hy- pocalcemia Without Paresis in Cows, JAVMA, 149, 4, 402. 21. Mayer, G. P., Ramberg, C. F. and Kronfeld, D. S. (1967) Udder Insufflation and its Physiologic Basis for Treatment of Parturient Paresis in Cattle, JAVMA, 151, 12, 1673. 22. Mayer, G. P., Ramberg, C. F., Kronfeld, D. S., Buckle, R. M., Sherwood, L. M., Aurbach, G. D. and Potts, J. T., Jr. (1969) Plasma Parathyroid Hormone Concentration in Hypo- calcemic Parturient Cows, Amer. J. Vet. Res. 30, 9, 1587. 23. Nurmio, P. (1968) On Plasma Calcium Regulation in Paresis Puerperalis Hypocalcemia in Cattle, Acta Vet. Scand. Suppl. 26. 24. Pehrson, B. (1966) Ketosis, Acta Vet. Scand. Suppl. 15. 25. Poulton, B. R., Anderson, M. J. and Dell, J. C. (1962) The Relationships of Various Hereditary and Environmental Factors to the Incidence of Milk Fever (Parturient Paresis) in Dairy Cows, Maine Agric. Exp. Stat. Bull. 604, Univ. of Maine, Orono, Me. 26. Toivola, B. E. and Mather, G. W. (1968) Puerperal Tetany of the Bitch, Norden News 43, 1, 16. Puerperal Infections, Uterine Infections and Diseases Retained Placenta or Retention of the Afterbirth or Fetal Membranes is one of the most common condi- tions occurring in animals following parturition. It is ob- served chiefly in the cow and less commonly in the other domestic species. Retained placenta in the cow. In physiological par- turition the afterbirth of the cow falls away within 3 to 8 hours following calving. If the placenta is retained longer than 8 to 12 hours the condition is considered patholog- ical. Etiology. Retention of the fetal membranes is basi- cally due to failure of the villi of the fetal cotyledon to detach themselves from the maternal crypts of the ca- runcle. After the fetus is expelled and the umbilical cord ruptures no blood is pumped into the fetal villi and they shrink in size. In the dam, uterine contractions continue and the large amount of blood formerly going to the uterus is markedly reduced. The maternal caruncles become smaller in size, due to a reduced blood supply, and the maternal crypts dilate. Although there is no muscle in the caruncle, during contractions of the uterine wall fol- lowing parturition the shape of the caruncles may change from oval to round.2 Detachment of fetal cotyledons from the maternal caruncle was much easier during these con- traction waves than between them. The weight of the fetal membranes assist in their normal dropping away from the caruncles and the uterus. Other workers 17'24,60 have stated that stimulating uterine contractions by the injection of oxytocin immediately after calving appar- ently lowered the number of retained placentas, by com- parison with control cows not thus injected. In a small trial oxytocin, 40 IU every 20 to 30 minutes for up to 6 treatments, was given to cows judged unlikely to pass their fetal membranes with a reduction of the incidence of retained placenta by 50 percent.17 Separation of buf- falo calves from the dams immediately after birth so that suckling could not stimulate the release of oxytocin from the posterior pituitary gland, resulted in 22.7 percent re- tention of the afterbirth in 189 calvings as compared with 4.9 percent retained placentas in 122 calvings on the same farms when suckling was allowed.68 Stress could also have been associated with this high incidence of retained placenta. On histologic examination of fetal cotyledons and ma- ternal caruncles taken an average time of 4.75 hours after normal calving, degeneration and necrosis of the fetal villi and necrosis and degeneration of the epithelium of the maternal crypts were present, and the latter were filled with debris.35 These findings in normal cows were es- sentially similar to those in cows having a retained pla- centa. Incomplete data showed little or no histologic dif- ferences between normal cotyledons and caruncles and those in which retained placenta developed. There were morphologically three types of retained placentas; one type was associated with abortion and premature birth with immature placentomes; the second type was asso- ciated with hyperemia and were few in number; and the374 VETERINARY OBSTETRICS third and most common type was associated with small portions of necrotic epithelium between the chorionic villi and the cryptal walls.9 In retained placenta normal sep- aration and loosening of the villi from the maternal crypts is interfered with and adhesions form. In easily removed placentas the loosening process comes about by autolysis of the chorionic villi. After several days leucocytes and bacteria were in the placentomes. Therefore placentitis was a secondary phenomenon. The incidence of retained placenta is high in births occurring several days before the expected date because the placenta has not under- gone the degeneration necessary for normal detach- ment.8 Although there is as yet no definite information about the exact manner in which the fetal membranes are expelled or fall away from the caruncles, it is rather apparent that it is a complex process involving a reduc- tion of blood supply followed by shrinking of both ma- ternal and fetal placental structures, degenerative changes, and strong uterine contractions. There is evidence to show that infections of the uterus during gestation may be a cause for retained placenta. Infectious agents, such as Brucella abortus, tubercu- losis, C. fetus and various mold infections cause a pla- centitis and cotyledonitis resulting in abortion or path- ological parturition at term with retention of the placenta. Sound evidence to minimize the importance of this gen- eral cause of retained placenta has been provided.2 This author agrees that in the past too much emphasis has been placed on intrauterine infections during gestation as a cause for retained placentas. About 20 to 25 percent of 282 cases of retained placenta in one study24 were infected with Brucella abortus, but these were also as- sociated with abortions and premature births. The oc- currence of many placental retentions in herds affected with C. fetus were reported. It was stated8 that 30 per- cent of all retained placentas in cattle in Germany were due to Brucella abortus. The author has observed many mold infections, due to Aspergillus or mucor molds, causing a marked cotyledonitis and severe retention of the fetal membranes. Examination of 2027 placentas re- vealed 121 with mold.7 Of these latter 73 percent were Aspergillus. Many infected placentas were not retained. Other diseases and organisms causing abortion or pre- mature birth might also produce endometritis, placenti- tis, and retention of the fetal membranes by inflamma- tory reactions of the cotyledon and caruncle similar to lesions described in brucellosis.28 As noted in Chapter V, under uterine involution, during or following partu- rition, bacteria from the caudal portions of the genital tract or the environment invade all uteri. The degree of contamination or numbers of invading bacteria, the type and virulence of the organisms and the immunity or re- sistance of the dam determine the seriousness of the in- fection which may vary from a mild infection with a rapid recovery within a few days or weeks to a severe metritis, septicemia, toxemia and death in the same pe- riod.70 The highest incidence of retained placenta, 69 per- cent, occurred in an experimental group of cattle on low levels of carotene intake.56 The incidence could be cor- related with the various feeding levels of carotene. In hyperkeratosis, and P.B.B. toxicity, in which vitamin A levels are very low, the incidence of retained placenta, metritis, and abortion is high. Probably vitamin A is nec- essary for maintaining the health and resistance of the epithelium of the uterus and placenta. Low vitamin A levels lead to the development of infections. A defi- ciency of minerals such as iodine and selenium has been reported to be a cause of retained placenta, but this re- quires further substantiation.44 Premature calvings and calves with enlarged thyroid glands together with an in- creased incidence of retained placentas may occur in io- dine deficient herds.156 Numerous recent studies have been performed in cows to prevent retained placenta by the injection of vitamin E and selenium about a month be- fore parturition.3- 48'61'62 In Ohio and Kentucky this ther- apy proved effective in reducing the incidence of re- tained placenta but in Maryland, Virginia, New York, North Carolina, Nebraska and South Dakota it was in- effective. There were great variations in results between herds. Thus this therapy cannot be recommended with assurance of its value. Retained placenta in 1610 Holstein parturitions was 50 percent higher in both cows and heifers with dystocia than in normal births, and 50 percent higher in calvings in which milk fever occurred than in calvings where no milk fever was present.52 Heat stress during the summer months, May through September, in Georgia increased the incidence of retained placenta and metritis from 12.2 to 24.0 percent. This was apparently related to a reduc- tion in the length of gestation by 5.25 days in the cows with retained placenta compared to the cows calving dur- ing the cooler seasons.20 In the cow, many abortions occurring after the fifth month of pregnancy are accompanied by retained pla- centa. In cattle calving 1 to 2 weeks prematurely, es- pecially in twin pregnancy, retained placenta occurs in 30 to 50 percent of the animals. The ratio of retained placenta to abortions at different times of gestation was 1:7 at 121 to 150 days, 1:6 at 151 to 180 days, 1:3 at 181 to 210 days, 1:2.2 at 211 to 240 days and 1:1.7 at 241 to 250 days of gestation.46 Practically no retained placentas occurred after abortions prior to 120 days and the incidence dropped to 1.5 percent of calvings betweenINJURIES AND DISEASES OF THE PUERPERAL PERIOD 375 271 and 280 days of gestation. Progesterone deficiency may cause the retention of the fetal membranes or in- directly cause it by predisposing to early parturition.42 It may be possible that some abortions, premature calv- ings, or retained placentas are due to a progesterone de- ficiency or a cortisol excess late in gestation. Profiles of hormone levels in cows with and without retained fetal membranes 12 hours after calving were not conclusive. Further studies in the week prior to calving are indicated as low estradiol and high progesterone levels on day 6 prepartum were associated with retained placenta.15 In- ducing parturition 2 to 10 days before expected calving usually resulted in a 50 to 75 percent incidence of re- tained placenta. (See Chapter VI.) Diseases causing uterine inertia or atony result in a high incidence of retention of the fetal membranes. These are: dropsy of the fetal membranes, uterine torsion, twinning, fetal giantism, primary or secondary uterine inertia, dystocia, and other pathological conditions. Re- tained placenta was observed in about 70 percent of dys- tocia cases due to uterine torsion and failure of cervical dilation, and in about 25 percent of dystocia cases due to over-size of a living fetus.18 An incidence of 8 percent retained placenta in normal births but a 55 percent in- cidence in abnormal deliveries such as twins, cesareans, fetotomies, dystocias and abortions was reported.661’ Failure of normal uterine involution was frequently as- sociated with retained placenta. The pathological con- ditions causing these diseases or abnormal conditions re- sulting in uterine inertia—whether they be infectious, hereditary, nutritional, circulatory, or hormonal—also predispose to retention of the placenta. In a study of 7,387 calvings in one Holstein herd for a period of 25 years, the incidence of retained placenta averaged 10.5 percent and affected 38.6 percent of the 2607 cows. Retained placenta rose from 5.4 percent in primipara to nearly 25 percent at the ninth calving.23 Elimination of brucellosis from the herd did not lower the incidence of retained placentas. Twins and abortions were associated with 37.7 percent of all retained placentas. Significantly more daughters from dams having retained placentas had re- tained placentas than daughters from dams not retaining their afterbirth. Retained placentas were more common following the birth of single male calves, 56 percent vs. a 51.6 percent herd average. Twin births in which two males or one male was present also had a higher rate of retention. It was concluded23 that retained placenta is not entirely caused by previous pathological conditions, a theory strongly supported by others.696 Retained placen- tas were more common during February through April in the northern hemisphere.163'23 Retention of the fetal membranes is less common in beef breeds than in dairy breeds confined in stables for long periods. The incidence of retained placenta varies widely from herd to herd at various times. Retained pla- centas in 6.4 percent of 450 parturitions that included only brucellosis-free cows and births of living, single calves were reported.12 An incidence of 8.3 percent in 431 calvings in British herds in which brucellosis was either absent or quiescent was recorded.35 The incidence in Hannover, Germany, was 4 to 5 percent.2 In over 24,000 calves in Israel, a 5.08 percent incidence of re- tained placenta in single births and a 99 percent inci- dence in twin births, for a total over all incidence of 8.4 percent was recorded.6 In New Zealand the incidence of retained placenta was 1.96 percent in over 36,000 dairy cattle kept at pasture the year around.46 In comparison with stabled herds it may indicate that exercise, less stress, more vitamin A and a less contaminated environment is conducive to a low incidence of retained placenta. The incidence of retained placenta in herds infected with ac- tive brucellosis, in cows producing twins, or in cows aborting due to other causes is high, probably from 30 to 50 percent or more. Once retention of the afterbirth occurred in a cow, there was about a 20 percent chance of it recurring again.23 It has been repeatedly observed by the author that in a certain year a high incidence of retained placentas 30 to 80 percent, would develop in a dairy herd that for- merly had relatively few cases, 2 to 8 percent. Once re- tained placentas started nearly every cow calving there- after would be affected and/or develop postpartum metritis. These herds were free of the common enzootic infections of reproduction that cause abortion such as brucellosis, vibriosis, leptospirosis, IBR-IPV and mold infections. The affected cows were calving in the same bam and in many instances in the same calving stalls in frequent succession. When there was an hiatus of several months or more when no cows calved or when cows were calving on pasture away from the bam, the inci- dence of retained placenta and metritis dropped dramat- ically to the low levels of former years even when calv- ing was again resumed in the bam or calving stalls at a later date. This pattern of retained placentas and post- partum infection closely resembles that seen in calf scours and the metritis-mastitis-agalactia syndrome in sows. In fact the author has observed severe outbreaks of virulent scours in the newborn associated with a high incidence of retained placentas and metritis in the dams in the same herds. From these observations the author has hypoth- esized that these severe enzootic outbreaks of retained placentas and secondary metritis were due to certain highly virulent organisms of Streptococcus dysgalactiae, E coli, Staphylococcus, Pseudomonas aeruginosa, C. py-376 VETERINARY OBSTETRICS ogenes and/or other organisms which developed in these bams or calving stalls infecting the genital tract of the parturient cow at the time of calving and causing an acute metritis, uterine inertia, retained placenta and then sec- ondary placentitis and metritis. As long as cows are calv- ing in frequent succession in such an environment the infection continues from one cow to the next. When a period of several months or more elapses between cows calving in such an environment the infection dies out on the premises. Since it is difficult to thoroughly disinfect a bam or even most calving stalls a possible alternative is to remove the parturient cow from this environment to a clean noninfected one for calving. This is difficult on most farms and farmers are reluctant to go to this inconvenience even if suitable noninfected calving stalls or areas can be improvised. On affected farms where the author has secured the cooperation of the farmer to fol- low this regimen of removing the parturient cow from the infected environment for 5 to 10 days before and after calving whether by placing the cow in a nonin- fected or noncontaminated separate bam, lot, shed or stall or by putting the cow on pasture, the results have been very gratifying with a marked drop to normal in the in- cidence of retained placenta and postpartum metritis. Because of the adverse effects on reproduction and milk production the veterinarian should not hesitate to strongly recommend this often troublesome chore upon the farmer. With the increased size of many dairy herds and the trend toward “zero” pasture and the confinement of cows in barnyards and freestall housing, the author foresees the continuation of such serious problems unless manage- ment and housing designs develop so that calving stalls can be built isolated from each other and of such con- struction that lends itself to thorough disinfection as has been necessary for continuous farrowing operations to develop in the swine industry. There is evidence in En- gland, Sweden and the U.S.A. that bedding cows on sawdust is more conducive to coliform mastitis, calf scours and retained placenta and post-partum metritis than bed- ding the animals on straw. For those of my readers who are reluctant to accept the hypothesis that acute uterine infections resulting in retained placentas and metritis can develop in the few hours between the onset of parturition and the normal time of expulsion of the placenta they should note the very short period needed for the devel- opment of acute bovine mastitis, calf septicemia and acute mastitis in sows. The morbid anatomy of retained placenta may vary from slight evidence of disease to severe lesions. Ac- cording to the location of the inflammatory reactions in the uterus, placentitis may be classified as apical, cervi- cal or diffuse. The nongravid horn may or may not be involved when the placenta in the gravid horn is re- tained. The degree of placentitis in the nongravid horn is usually not as severe as in the gravid horn since the placentomes are smaller and less complex. The degree of placentitis may vary from a mild peripheral type of necrosis involving only the villi to a severe necrosis in- volving the entire cotyledon and a part or all of the ca- runcle. If the placentitis developed prior to calving or abor- tion, the allantois chorion may be edematous, necrotic or leathery, or hemorrhagic. Uterine “sand” and old or fresh clotted blood may be present. Often a reddish-brown to yellow exudate is found in the utero-chorionic space. Adventitious placentae may vary from a few small areas to nearly complete involvement of the entire endome- trium of one or both horns. In mold infections the cotyle- don is usually very large and swollen. Uterine and pla- cental disease may occasionally cause fetal disease or anoxia that results in the presence of fetal meconium in the amniotic fluid, staining the fetus. In most cases of retained placenta the calf appears quite normal. The symptoms of retained placenta are usually ob- vious, a portion of the fetal membranes hang from the vulva 12 hours or more following abortion, normal par- turition, or dystocia. Occasionally the fetal membranes do not hang from the vulva but are entirely within the vagina or uterus. In the treatment of herds severely af- fected with genital disease close observation of the cow to observe when the fetal membranes were dropped is recommended.6911 Examination of the fetal membranes can be made to be certain they are completely expelled and no portion remains in the uterus. If they are not ex- pelled normally the uterus should be examined manually per vaginam in 24 to 36 hours. After 48 hours it is usu- ally difficult or impossible to insert the hand into the uterus if no fetal membranes are within the cervix. The presence of the membranes lying in the cervix tends to retard contraction of that organ. After a dystocia the pla- centomes may be felt; if they are very swollen, hard, firm, inflamed, or congested, the placenta will be re- tained. If the placentomes are soft and pliable the cow will often drop the afterbirth within a few hours. About 75 to 80 percent of cows with retention of the fetal membranes show no marked illness. About 50 to 60 percent may exhibit slight to moderate illness by a temporary reduction in appetite or milk flow.2 About 20 to 25 percent may exhibit moderate to severe symptoms of metritis and septic metritis as shown in some cases by anorexia, depression, elevation of body temperature, increase in pulse rate, decrease in milk flow, and loss of weight. These percentages may differ in herds de- pending upon the severity of the infections causing theINJURIES AND DISEASES OF THE PUERPERAL PERIOD 377 secondary metritis. In severely affected animals retained placenta may be associated with or complicated by other diseases such as: mastitis, septic metritis with perime- tritis or peritonitis, severe straining, necrotic vaginitis, parturient paresis, and acetonemia. The bacteriological picture of the uterus in cases of retained placenta was similar to that of a uterus with delayed involution or atony without retained placenta.2 First the Streptococci dys- galactiae and the staphylococci appear, and later the diptheroids, Corynebacterium pyogenes, coliform, and anaerobic bacteria may be found. In retained placenta the white blood cell picture showed a slight to marked shift to the left. In uncomplicated cases a lymphocytosis developed. In more severe metritis cases a definite leu- copenia occurred.43 The total number of white blood cells usually do not increase markedly. After 24 hours the pla- centa begins to macerate and a fetid, putrid odor devel- ops. The afterbirth may fall away anytime within 24 hours to 14 days, depending upon the severity of the disease and possibly the type of treatment used. In most cows with retained placenta the cervix contracts after 48 to 72 hours, so that it may be difficult to insert the hand through the cervix. This contraction takes place sooner if no fetal membranes are present in the cervix. Prognosis. The mortality rate in retention of the fetal membranes should not exceed 1 to 2 percent in uncom- plicated cases.2 In retained placenta cases a mortality rate of 4 percent: emaciation, infertility, or unprofitableness in 20 percent, a short duration of the disease with tem- porary irregularities of milk production and fertility in 50 to 60 percent, and nearly undisturbed puerperium in 15 to 25 percent was reported.2 Another study24 re- viewed a substantial number of cases of retained pla- centa treated by various means in the Ambulatory Clinic of the New York State Veterinary College from 1920 to 1941. During the years 1920 to 1928, 755 cases were treated by early or late removal, and much douching, with a mortality rate of 4.2 percent. During 1928 to 1934, 1109 cases were treated by removal at 72 hours, with little or no douching, with a mortality rate of 2.8 per- cent. From 1934 to 1941, 1680 cases were treated with late removal, 72 hours or more, no douching and liberal use of sulfanilamide, with a mortality rate of 1.1 per- cent. In this same clinic, from 1943 to 1953, 3742 cases of retained placenta were treated by late removal, 72 hours or longer, no douching, and the use of sulfonamides and antibiotics, if necessary, with a mortality rate of 1.3 per- cent. This latter figure included cases in which septic metritis, mastitis, peritonitis, and other conditions were complications which undoubtedly contributed to or caused the fatalities. A very interesting study51 was conducted of 44 cases of retained placenta in 2 herds totaling 125 animals in which no manual removal of the placenta was attempted during a period of 3 years. These herds were free of brucellosis and tuberculosis. No treatment was given to any cows with the exception of 4 that became quite ill. In these 4 cows proflavine and saline solutions were introduced into the uterus but probably had no in- fluence on the course of the disease. Of the 44 cows 81.8 percent had calved at term, 18.2 percent had aborted, and 16 percent had twins. The placentas were retained from 2 to 11 days, an average of 6.8 days before drop- ping away naturally. During the first two weeks after calving the appetite was good in 31.8 percent, fair in 54.5 percent, and poor in 13.6 percent. Body weight re- mained normal in 88.6 percent. Lactation was good in 29.5 percent, fair in 63.6 percent and poor in 6.8 per- cent. When the 44 cows that had untreated retained pla- centas were compared with 44 cows in the same herds calving normally without retained placenta there was no significant difference in the numbers of cows in the two groups having to be sold because of sterility, abortion, or delayed conception. In these two herds no cows were bred back until 90 to 150 days after calving.51 The effect of retained placentas on subsequent fertility is important to consider, as delayed involution and chronic endometritis following retention of the membranes is common. Apparently after 2 to 3 months and a number of estrous periods most cattle having a retained placenta eliminate the infection and the uterus becomes normal. In 71 abnormal calvings the postpartum interval from calving to complete uterine involution averaged 52 days or only 5 days longer than in 252 cows that calved nor- mally.13 If the owner desired to breed the cow before 90 days after the abnormal calving, examination of the uterus to determine if it was completely involuted was rec- ommended. About 20 percent of cows retaining their placenta at one calving had another retention at subse- quent parturitions. Young cows having a retained pla- centa averaged one less calving than cows the same age not affected with retained placenta.23 Cows not having genital disorders such as chronic metritis following re- tained placentas were nearly as fertile as normal cows but there was a 30 to 50 percent greater probability that genital disorders would occur in affected cows. The nonreturn rate to first service before 60 days postpartum was 28.2 percent in cows with retained placenta and 50.3 percent for cows without a retained placenta; after 60 days the comparable percentages were 52.2 percent and 64.0 percent. When “nonreturn” cows after service were checked to diagnose pregnancy they found 10.6 percent of 592 cows with retained placenta at their previous calv- ing were not pregnant while only 5.4 percent of 19,173 cows with no retention were not pregnant.46 Following378 VETERINARY OBSTETRICS retained placenta in some cows, permanent sterility re- sults, due to pyometra, perimetritis, salpingitis, ovaritis, severe damage to the endometrium, or other causes re- lated to the retention. In most of the animals affected with retention of the fetal membranes the major loss is an economic one of a slight to moderate loss of milk and a slight to moderate delay in the involution of the uterus and subsequent conception. In 100 dairy cows calving within a 4-month period,1215 27 percent had retained fetal membranes of which only two-thirds were noted within 24 hours after parturition. Thirty-four percent of the cows had postpartum metritis of which 76.5 percent were secondary to other postpar- tum problems, mainly retained fetal membranes. Despite several types of local and systemic antibiotic therapy given within 24 hours of parturition to problem cows, 76 per- cent developed a secondary metritis compared to 12 per- cent of the untreated normal-calving cows. Delayed uter- ine involution at 30 days postpartum was more than twice as common in the cows with metritis than in the normal- calving cows. This recent study and review1215 confirms earlier reports on the lack of information on the inci- dence, causes and therapeutic procedures to prevent and treat herds and cows with postpartum uterine disease problems. Treatment. After reviewing the literature on bovine retained placenta and listening to many veterinarians de- scribe their methods of treatment, the author has been amazed and impressed by the infinite number and variety of techniques employed, the drugs and hormones rec- ommended, and the time lapse between parturition and the attempted removal of the placenta. With so many varied techniques and products being used, one is forced to recognize the fact that probably no treatment would be necessary in handling most cases of retention of the fetal membranes. This has been demonstrated.51 In En- gland and in Europe there is an increasing volume of opinion in favor of not making any manual attempt to detach the fetal placenta from the maternal caruncles.2 No matter how carefully the operation is performed some injury to the endometrium may result, and the risk of toxemia and septicemia is thereby increased. Presently the author conservatively recommends that all cows having a retained placenta 12 hours after calv- ing be given a parenteral antibiotic injection that may be repeated. Since the colostral milk is discarded this ther- apy causes no economic hardship and the cow is signif- icantly protected against a serious uterine or systemic infection. It is optional with the owner and veterinarian whether the placenta is removed manually. A clean, manual examination of the utems can be made. The operator should wear a surgical rubber glove and long sleeve on one arm and a surgical glove on the other to protect himself from brucellosis or an infection of the arm or hand. Disposable plastic gloves and sleeves of good quality are more sanitary and practical than rubber gloves and sleeves. He should wear rubber coveralls or an apron and boots that may be easily cleaned and dis- infected after the operation. The perineal region of the cow should be carefully cleaned and washed with soap, water, and mild antiseptic, and kept clean during the op- eration. To keep the cow, especially one with loose feces, from either defecating frequently or straining, epidural anesthesia may be used. A plentiful supply of clean water is essential. The cow’s tail should be held out of the way by an assistant or tied with a tail rope over the back to one of its fore legs. The free part of the fetal membranes should be drawn through the cervix, thereby reducing the amount of membranes in the uterus and aiding its drainage. If the fetal membranes fall away readily from the caruncles they should be removed. If much fluid is present in the uterus it should be siphoned off by a sterile soft rubber horse catheter or stomach tube held in the fist to keep the fetal membranes from plugging the end of the tube. The siphon may be started by filling the rubber tube with water and holding it pinched off as it is introduced. Douching the utems is contraindicated when membranes are present as it is difficult to remove the fluid completely. Another method of removing this ex- cess fluid is to use large swabs of absorbent cotton and gently wipe the utems free of exudate.24 Large amounts of fetid reddish watery fluid in the utems is usually ac- companied by signs of toxemia, depression, and anorex- ia. Manual removal of a retained placenta in the dairy cow is practiced by most veterinarians because the diseased, macerating fetal membranes are serving no good purpose and the farmer desires and expects the veterinarian to remove this unsightly fetid mass from the genital tract. In most cases the fetal membranes have not macerated sufficiently for easy removal before 48 hours after par- turition. Although in some cases enough autolysis has occurred so the villi separate readily from the crypts and removal may be accomplished easily as early as 12 to 24 hours after calving. The best time for removal of the placenta was reported to be 24 to 48 hours after partu- rition.6,64 These easily removed fetal membranes would probably have dropped away without aid within another 24 to 48 hours. It has been the practice of the author and many other veterinarians not to examine or treat retained placenta until 72 hours after parturition unless the cow develops anorexia, an elevated temperature or other symptoms of septicemia. At this time the uterus has con- tracted in most cases so the apex of the horn may beINJURIES AND DISEASES OF THE PUERPERAL PERIOD 379 reached. The cervix is usually still sufficiently open to allow passage of the hand and arm without resultant trauma. When removal is attempted at 72 hours after parturition the uterus has developed a protective barrier to the infection and there is less chance of a septicemia or toxemia occurring than there would be if removal is attempted earlier. At whatever time the placenta is re- moved this should be done gently and quickly within 5 to 20 minutes, in a clean manner, and with as few with- drawals and reintroductions of the arm as possible. The use of epidural anesthesia controls straining and defe- cation and makes possible a cleaner, more hygienic, and gentler operation. If the operation cannot be performed in a gentle manner, with as little interference as possible with nature’s processes, the fetal membranes should be left alone even though the cervix may contract so that on subsequent visits by the veterinarian the hand cannot be inserted into the uterus. If this happens it is best not to attempt dilation of the cervix, as it is difficult or nearly impossible to do so without severe trauma. The mem- branes should be allowed to fall away naturally, or gentle traction on the fetal membranes will remove them after the maternal caruncles and fetal cotyledons have sepa- rated from the uterine wall by autolysis. Even if the membranes or a portion of them macerate and are ab- sorbed in the uterus this is better than severely trauma- tizing the cervix in attempts to dilate it. It has been observed by the author and others that if the placenta is allowed to drop away of its own accord, or if it is gently withdrawn from the uterus even 10 to 12 days after parturition, involution of the uterus occurs sooner, and cessation of uterine discharge ceases more quickly than when the placenta is removed in a rough manner and portions are left in the uterus. In a study of 632 cows with retained placenta a conservative systemic treatment with sulfonamides orally and intravenously re- sulted in higher subsequent fertility than a more “radi- cal” treatment with manual removal and various local intrauterine treatments.29 The uterus containing a re- tained placenta may be compared with a large abscess in which the necrotic core has not separated from the surrounding tissues. The surgical procedures governing the handling of an abscess should also govern the han- dling of the infected uterus. Conservative treatment is indicated and essential. The veterinarian should have the courage of his con- victions in handling these cases, inasmuch as traumatiz- ing the uterus by attempting to remove the placenta when removal is difficult or impossible results in either im- mediate septicemia with a marked drop in milk and ap- petite, elevation of temperature, loss of weight and pos- sible death, or else a prolonged period of convalescence during which time shreds of placenta and exudate are expelled from the uterus, pyometra or chronic metritis develops, or protracted or even permanent infertility may result from a uterine abscess, perimetritis, salpingitis or severe endometritis. If in order to avoid traumatizing the uterus or leaving placental shreds and fragments in the uterus a veterinarian refuses to remove a placenta that is not ready to be separated from the maternal caruncles, and explains to the owner his reasons for the decision, this may prevent criticism by a client who formerly has been accustomed to having the placenta “taken” on the first and only call in all cases of retained placenta. Manual removal of the placenta is contraindicated in cows with an elevated body temperature, above 103° F. and in cows or heifers suffering from severe necrotic vag- initis. In the former a septicemia and toxemia are al- ready present and would be aggravated by manual ma- nipulation of the placentomes. Administration of antibiotics parenterally and locally, or sulfonamides oral- ly or intravenously in cows showing toxic symptoms is indicated for a period of several days before removal is attempted. Removal of the placenta particularly in heifers having necrotic vaginitis and vulvitis with a small, dry, swollen genital canal may make the vaginitis and vulvitis worse and may increase straining that is prob- ably already present. Since it has been proved that most cows suffering from retained placenta need no treatment, and the others only parenteral treatment with antibiotics or parenteral and oral treatment with sulfonamides to control septicemia, the removal of the placenta from a cow with an elevated temperature, vaginitis, septic me- tritis or possibly other diseases, such as acute mastitis and traumatic gastritis, is contraindicated. Removing the placenta in an incomplete, rough, insanitary manner is always inadvisable. Occasionally when the union between the cotyledons and caruncles is very firm and most of the caruncle be- comes necrotic and sloughs, it may be 10 to 15 days before the macerating placenta and cotyledons can be removed. If the fetal membranes are removed prema- turely by traction or improper manual removal, thereby leaving the fetal cotyledon on the necrotic maternal ca- runcle, these necrotic caruncles and cotyledons may be- come dry and inspissated and remain as a foreign body in the uterus for 3 to 8 weeks or longer. When found several weeks after parturition, they may be removed by injections of estrogens to relax and dilate the cervix and contract the uterus together with gentle massage of the uterus per rectum. A rubber douche tube may be used as a siphon and by suction on the caruncles by the siphon tube they may be coaxed and withdrawn through the cer- vix. If left in the uterus these may eventually macerate,380 VETERINARY OBSTETRICS but recovery is prolonged and chronic metritis, pyometra and sterility usually occur. In removing the placenta manually the third or fourth days after parturition, or earlier if the placenta can be removed easily, the hand is inserted between the endo- metrium and chorion in the intercotyledonary space and the individual fetal cotyledon and its caruncle are grasped gently, squeezed, and with the thumb and forefinger the two structures are gently separated by a rolling, pushing, squeezing motion. This may be aided by traction with the other hand on the adjacent portions of the fetal mem- branes as the separation is completed. The cotyledons in the cervical area of the uterus are removed from the ca- runcles first and then by traction with the outside hand the placenta is pulled out and tension maintained as the cotyledons in the middle portion of the horn and the non- gravid horn are removed. The ovarian pole may be dif- ficult to reach. Sometimes traction on the placenta will pull the apex of the horn nearer the cervix and thus aid removal. It is highly desirable to remove all of the fetal membranes and not leave remnants in the uterus to act as foci of infection as these must be expelled or macerate before recovery can take place.69b The blood vessels of the placenta are among the last portions of the placenta to macerate. If the entire placenta cannot be removed, it is better to insert a few capsules, tablets, or a solution of antibiotic and revisit the cow in one to three days, or let the placenta fall away naturally. The layman’s practices of tying a weight on the pla- centa or of cutting the placenta off close to the vulva are not desirable. First, the weight frequently causes the cow to strain and causes premature and incomplete breaking away of the afterbirth, leaving a part of it still in the uterus. In rare cases this weight may cause invagination of the uterine horn. Removing the placenta close to the vulva in order to prevent the cow from swinging it against the milker is likely to result in the placenta dropping back into the uterus followed by early closure of the cervix. The afterbirth may remain in the uterus long after it has separated from the caruncles, because the weight of the placenta hanging from the vulva is not present to draw it out. If the placenta is dragging on the ground it should be cut off at the level of the hocks to prevent its being stepped on and tom away from the uterus. Hormones have been widely used the treatment of re- tained placenta. The use of oxytocin has been mentioned as being of possible value in preventing retained placenta when given shortly after the expulsion of the fetus or after dystocia operations. In dystocia, besides aiding in the expulsion of the fetal membranes, oxytocin may pre- vent prolapse of the uterus. It is advisable to inject 3 to 5 ml., 30 to 50 units, immediately after calving. One to 3 further subcutaneous injections of 2 to 3 ml. of oxy- tocin at 1- to 2-hour intervals may be given. Occasion- ally injections of oxytocin precipitate milk fever in cows with subclinical hypocalcemia. The oral administration of a proprietary calcium product containing trace min- erals and vitamins within a few hours after calving re- duced the incidence of milk fever and also reduced the incidence of retained placenta by about 50 percent.19 Further studies on the administration of oxytocin and calcium to cows failing to drop their fetal membranes soon after calving is indicated as there is a close asso- ciation between milk fever and retained placenta. Oxy- tocin is of questionable value after 24 to 48 hours after calving. The estrogens have been widely used in the past in the treatment of retained placenta. Stilbestrol or estradiol has little or no effect on the rate of separation of the fetal cotyledons and maternal caruncles. Estrogens do, how- ever, exert a definite action on the uterus by increasing its tone and muscular activity, stimulating the flow of mucus, increasing the circulation, and relaxing the cer- vix. These facts, together with the reports10,57 that the uterus is better able to control or overcome infection dur- ing estrum or when treated with estrogens, show the logic of using this hormone in the treatment of retained pla- centa. Presently estrogens are rarely used to treat re- tained placenta or metritis in dairy cows because of the ban on their use in dairy cows in the U.S. to prevent their presence in milk. Some cases of uterine atony as- sociated with retained placenta may greatly benefit from the injection of calcium gluconate especially if a sub- clinical hypocalcemia is the cause of the uterine atony.24 Following the injection of calcium during the first day after calving the afterbirth is often expelled within sev- eral hours. If the uterus is severely diseased and atonic the uterine wall may be incapable of responding to the injections of hormones. In recent years many veterinar- ians have used 1 to 3 mg of ergonovine or a similar prod- uct developed from ergot that produce a more prolonged rate of uterine contraction than doses of oxytocin. The results are equivocal. A wide range of antiseptics have been used locally to control the bacterial flora in the treatment of retained placenta and the uterus following removal of the retained fetal membranes. These early drugs consisted of such products as charcoal, boric acid, acriflavine, bismuth subnitrate, bismuth formic iodide, bismuth thymol io- dide, chlorine preparations, iodine in oil, silver oxide, bismuth formic iodide in oil, chlorophyll and bismuth and iodoform in oil (Bipp). This latter product imparted an odor to the milk that prohibited its use in dairy cattle. Various products containing sodium perborate have beenINJURIES AND DISEASES OF THE PUERPERAL PERIOD 381 advocated to aid in the removal and treatment of retained placenta. On contact with tissue debris these products release much gas and cause foaming similar to that re- sulting from the use of hydrogen peroxide. These prod- ucts are slightly irritating and probably should not be used in the uterus if the cervix is contracted. Because of their effect on tissue debris a number of enzyme products containing urea, yeast, pepsin, and papain have been ad- vocated. It is doubtful if these varied preparations greatly alter the course of the disease. Sulphonamides have been used locally in the uterus and have been approved by some veterinarians. Other veterinarians indicate that these drugs are rather insol- uble, especially in a tablet form, and tend to settle in the apex of the horn and are of questionable value. Penicil- lin, streptomycin and tyrothricin have been used widely in the past in the local treatment of retained placenta. The former is usually quickly inactivated by penicilli- nase produced by the infective organisms in the uterus and the latter is rather irritating in large amounts. In re- cent years 1 to 3 gm. of the broad-range antibiotics such as oxytetracycline (Terramycin), Chlortetracycline (Au- reomycin), Tetracycline, Furacin and others have been used locally in cases of retention of the fetal membranes. For immediate response these are used as an infusion in 200 to 1,000 ml. of saline or warm water. The boluses or powder produce a slightly slower response. These ap- pear to be the first products used locally that definitely alter the course of the infection. The rate of putrefaction and lysis is greatly reduced. The usual fetid odor is largely eliminated. The retained membranes may tend to remain attached to the caruncles in the uterus for a slightly longer period. The use of these products in a case of septic me- tritis usually eliminates the local infection quite promptly and if used early, 24 to 36 hours after calving or as soon as the temperature becomes elevated or other signs of illness develop they usually bring about a prompt regres- sion of the illness. After the use of Aureomycin in the uterus in 612 cows with retained placenta, only 2 cows developed acute metritis.5 27 In 31 cows with retained placenta manual removal was not attempted and 0.5 gm of Aureomycin was placed in the uterus every 1 to 2 days until the afterbirth dropped away. This took 2 to 10 days, with an average of 5.2 days. Subsequent con- ception rates were excellent.22 It was recommended that manual removal not be attempted. After treating 508 cows with retained placenta in various ways, one study re- ported that cows receiving local tetracycline intrauterine medication had a lower conception rate than those cows not receiving medication. If medication was initiated it was better to wait until 36 hours or more postpartum. Whether the retained membranes were removed or al- lowed to drop away had no effect on subsequent fertil- ity.46 Conception rate on the first service was higher, 70 percent vs 40 to 50 percent, and days from parturition to conception were lower, 86 vs 91 to 110 days, in cows treated with intrauterine oxytetracycline within 72 hours of calving and the placenta was not removed than in cows receiving no medication. Removal of the placenta defi- nitely lowered the conception rate at first service.4 Observations and reports have shown that hormones, sulfonamides, and antibiotics are rapidly absorbed from the uterus into the bloodstream.8b'50b This systemic effect is further reason for the topical use in the uterus of these easily administered products. If large doses of antibiotics are placed locally in the uterus, the milk from treated cows should not be put in the supply for about 72 hours. If symptoms of septic metritis develop with retention of the fetal membranes, sulfonamides administered or- ally, or sulfonamides and/or antibiotics administered parenterally are of great value along with supportive treatment with saline and glucose solutions, and possibly blood transfusions intravenously as described under the treatment of septic metritis. As in horses, laminitis often accompanies septic uterine infections in cattle but is not as obvious. The local treatment of the uterus should be very gentle and manual removal of the placenta should not be attempted. In rare cases a severe anaerobe or ne- crophorus infection may invade the uterus and these in- fections are usually fatal. In Europe in areas where an- aerobe infections are common antiserum is usually administered after a dystocia. If severe straining is pres- ent with retained fetal membranes, epidural anesthesia should be given and the uterus and birth canal carefully and gently examined. In most cases the straining is due to a severe vulvitis or vaginitis, and these should be treated. Rarely it may be due to an invagination of the uterine horn. Tenesmus may also be associated with ra- bies in endemic areas. It is recommended that all cows affected with retained placenta be examined 20 to 30 days after removal of the afterbirth to determine if involution of the uterus is pro- ceeding normally and that postpartum metritis or pyome- tra is not present. If this is not done the cow may fail to show estrum and 90 days or more after parturition the disease condition will be diagnosed too late to prevent a serious delay in conception. Permanent sterility may re- sult. The owner should be advised that many older cows affected with retained placenta should not be bred until 90 days after parturition. This time interval is usually necessary for proper involution and overcoming of the infection in the diseased uterus. In valuable cows the involution and return of the uterus to normal can be checked by periodic examinations during this period. If382 VETERINARY OBSTETRICS the uterus is completely involuted, no genital discharge is present and regular estrous cycles are occurring, cows with a history of retained placenta at the last parturition may be bred at 60 days postpartum with a good con- ception rate. All cattle having a persistent mucopurulent discharge from the vulva following retained placenta should be reexamined and treated. Retained Placenta in the Mare is probably less com- mon, from 2 to 10 percent, and more variable than in the cow.67 Probably the same factors responsible for re- tention of the placenta in the cow also are present in the mare. The infection most commonly observed in asso- ciation with retained placenta in the mare is Strepto- coccus zooepidemicus but many other organisms may be involved, especially the gram-negative ones that pro- duce endotoxins and histamines. Many genital infections in the mare are related to vulvar defects leading to pneu- movagina. In some mares air and infectious organisms may be aspirated through the cervix into the uterus dur- ing the act of windsucking. Infection also gains entrance to the uterus following foaling, when the mare gets up. A rush of air often fdls the dilated genital tract and uterus and the membranes draw debris from the bedding into the uterus. Straw and shavings or sawdust are the worst offenders. It was suggested that Tartan or a similar cov- ering over a cushioning material would greatly reduce uterine infection after foaling.3 If the mare remains re- cumbent after foaling, until the placenta is about ready to drop away, the uterus is more contracted and less air is aspirated. The rush of contaminated air into the uterus after foaling might play an immediate role in the reten- tion of the afterbirth. Retained placenta more commonly accompanied the large draft foals than the light horse foals.33 A lack of breeding and foaling hygiene might possibly explain why some draft mares are more likely to have retained placenta than are Thoroughbred mares. Repeated breedings during one heat period or the breed- ing of infected mares or infected stallions may cause re- tained placenta. Placentas weighing over 14 lbs. in light mares were usually associated with infections of the uterus, and a chorion that was characterized by necrotic areas and edema.33 Retained placenta is probably less common in mares because of the simple, diffuse type of placentation and the strong uterine contractions aiding the separation of the villi from their maternal crypts and expelling the detached membranes. It is interesting that the physiologically expelled placentas of most mares, as in cows, are inverted. This apparently is due to the fact that the allantois chorion first separates from the rapidly contracting apices of the uterine horns and passes into the birth canal before it is separated from the uterine body. Retained placenta in the mare is likely to occur following abortion and prolonged gestation.69b Probably the causes for retention of the afterbirth in the mare are infection, uterine inertia and other factors similar to those affecting cattle. Symptoms. Physiologically the equine fetal mem- branes are expelled within 0.5 to 3 hours after parturition but it is fairly common to have the fetal membranes not drop away until 8 to 12 or more hours later without any observable symptoms of illness. Strong uterine contrac- tions in the mare after foaling and just before expulsion of the placenta are often accompanied by signs of ab- dominal pain, recumbency, and colic.2 The mares that retain their afterbirths exhibit no such pains and appear normal, content, eat and drink, and suckle their foals. Slow expulsion of the placenta may be due to uterine inertia or exhaustion following expulsion of the fetus. The onset of delayed expulsion is indicated by the mare developing colicy pains followed by the dropping away of the membranes in from 10 to 20 minutes. In a few nervous mares it is necessary to tie up or cut off the hanging retained placenta so that it will not frighten the mare into kicking and otherwise possibly injuring the foal. In dystocia the fetal membranes may be detached and wrapped around the fetus. The rapid separation of the fetal membranes probably accounts for the early death of the fetus in many equine dystocias. Retained fetal membranes can usually be observed hanging from the vulva. Occasionally the placenta may partially fall away and the apex or tip of the placenta will remain in the nongravid horn especially if the apex is thickened and edematous. The weight of the placenta or the mare step- ping on it may rip it away, leaving the tip of the non- gravid horn in the uterus. This piece of placenta may act as a focus of infection often resulting in a severe metritis and secondary laminitis the third to seventh day after foaling. The afterbirth of each mare should be carefully examined after it falls away, to make certain no portion of the placenta remains in the uterus. Most cases of lam- initis occurring after foaling are due to metritis often as- sociated with a portion of the placenta being retained and floating in a uterus filled with fetid fluid. Uterine in- vagination or intussusception, usually of the nongravid horn into the uterine body, may accompany retention of the fetal membranes in the mare but it is seldom of a serious nature.25 30 The prognosis of retained placenta in the mare is usually good. Treatment. It is generally recommended that removal of the placenta in the mare not be attempted for at least 12 hours after foaling.8a-30-33 No treatment until 20 to 24 hours after foaling was recommended if the mare con- tinues to eat, has a normal temperature and the pulse rate remains normal. With retained placenta it is commonINJURIES AND DISEASES OF THE PUERPERAL PERIOD 383 practice to administer 2 to 4 ml. of oxytocin, 20 to 40 units, subcutaneously or intramuscularly every 2 to 3 hours starting the fourth to twelfth hour after foaling. Vandeplassche67 recommended the administration of 40 to 60 units of oxytocin in 500 to 1000 ml of saline by slow intravenous drip over a period of 1 to 2 hours as a more physiologic way in which to give the hormone. This treatment is successful in about 75 percent of the cases.67 The placenta was often passed during this pe- riod. It may be necessary to administer a tranquilizer to control mild colic and pain associated with the uterine contractions produced. In most cases the afterbirth drops away within a few hours or before 24 hours have elapsed. Injections of Aureomycin, tetracycline or Terramycin, 1 to 3 mg. per pound of body weight daily, intrave- nously; or the intramuscular injection of 3 to 6 million units of aqueous penicillin daily and 5 gm. of strepto- mycin twice daily may be indicated to control infection for 2 to 4 days. After 12 to 24 hours postpartum the veterinarian, in a scrupulously clean manner, should administer a tran- quilizer, bandage or have the tail held out of the way and scrub the perineum of the mare with soap and water. His hand and arm enclosed in a sterile surgical glove and sleeve is inserted into the birth canal and the allantois chorion is grasped. By means of gentle traction and twisting on the fetal membranes to form a “rope,” uni- form traction may be applied to the fetal membranes as the hand is very gently forced between the endometrium and chorion in the places where it is still attached. It should be recognized that any direct manipulation of the endometrium may be damaging to it. The entire pla- centa, including the tips of the horns, should be carefully removed. If necessary, examine the placenta after re- moval to be certain that the removal is complete. A more conservative and gentle approach, which has much to recommend it, consists of inserting the hand inside the allantois chorion and gently massaging it away from the endometrium.59 If removal does not occur promptly, supportive treatment should be given and the mare reex- amined and treated 4 to 12 hours later. Another method to remove an equine retained placenta without manual intervention has recently been de- scribed.14 After preparing the mare as described above the gloved hand enters the vagina and gently draws the chorioallantois out of the vulva. The tom ends of the cervical star portion are gathered together and a stomach tube is placed through the opening into the allantoic cav- ity. Two to 3 gallons of warm dilute povidone iodine solution, 4 ounces/gallon, are slowly pumped into the cavity to distend it. The hand around the membranes and tube prevent this solution from escaping. The distended uterus stimulates the mare to attempt to expel the solu- tion. These efforts may be augmented by the injection of 40 IU of oxytocin. The exposed fetal membrane is held and the solution is squeezed back into the uterus as the chorioallantois is slowly released. This is repeated frequently. It usually takes about 15 to 20 minutes for the complete release of the placenta which comes out intact including even the microvilli of the chorioallan- tois. In one mare the author observed retained fetal mem- branes that remained firmly adherent to the endometrium for 72 hours without any adverse effect on the mare. Older local treatment consisted of inserting into the uterus a pint of oil. It is probable that the more stable but sol- uble broad-range antibiotics of the tetracycline and fur- acin groups would be of greater value in the local treat- ment of the uterus in mares, as in cows. Intrauterine therapy may be continued daily or every other day for 2 to 4 days until the uterus is well-involuted and the infection is largely overcome. It is highly desirable to administer tetanus antitoxin and probably oxytocin to a mare following removal of a retained placenta. Tem- porary skin clips or sutures may be placed in the upper two-thirds of the vulvar lips within several hours after foaling if the afterbirth has not been dropped and even after removal of a retained placenta in the mare to pre- vent aspiration of air into the genital tract.75 At present douching of the uterus after removal of a retained pla- centa is considered a questionable practice although for- mer workers advocated the general use of this technique. If the uterus is filled with fetid fluid this should be re- moved by siphoning through a sterile rubber tube. The danger of laminitis should always be considered. Ice packs should be placed on the feet and antibiotics given locally and parenterally until uterine infection subsides. Anti- histamines and phenylbutazone might also be adminis- tered. Some advocate the use of stilbestrol, 30 to 60 mg., or estradiol, 3 to 6 mg., and ergonovine, 1 to 3 mg., intramuscularly daily for several injections. Large re- peated doses of the glucocorticoids should not be given these mares. Retained Placenta in the Ewe and Doe is handled in a manner similar to that in the cow except that re- moval from inside the uterus is seldom possible. If signs of elevated temperature, anorexia, and depression indic- ative of septic metritis are exhibited, parenteral injec- tions of antibiotics, estrogens, oxytocin and antihista- mines are recommended. Manual treatment is limited to occasional gentle traction on the hanging portion of the membranes. Some veterinarians introduce a broad-range antibiotic capsule or tablet used for enteric infections in calves into the uterus after carefully cleansing the ex-384 VETERINARY OBSTETRICS temal genitalia. The placenta usually drops away within 2 to 7 days. Retained Placenta in the Sow is uncommon. It is usually impossible to determine if retention has occurred except by the symptoms of septic metritis, prostration, and a prolonged purulent vulvar discharge containing placental shreds. This condition has been reported2 as a cause of fatal metritis, however this has rarely if ever been reported in the United States. Since retained pla- centa is most likely to occur after a dystocia with pro- longed labor it would be advisable in these cases to save the expelled fetal membranes, count the umbilical cords, and to give oxytocin 1 to 3 ml., after relieving the dys- tocia. When septic metritis does occur because of a re- tained placenta, administration of stilbestrol, 10 to 20 mg. and the daily injection of intramuscular forms of antibiotics, such as 3,000,000 units of aqueous or oily preparations of penicillin, 1 to 2 gms. of streptomycin or 1 gm of intramuscular Terramycin, tetracycline, or Aureomycin are indicated. Intrauterine infusions of broad range antibiotics have been used by some veterinarians. A sterile AI catheter or a horse catheter may be used. The value of this type of therapy in the postpartum sow has not been proven. Good nursing is essential. Retained Placenta in the Bitch and Queen is un- common. It is seen most often in toy breeds in which dystocia or prolonged labor has occurred. In any such suspected case parenteral antibiotics should be admin- istered at once and continued for several weeks. If the placenta is not expelled in 12 to 24 hours an acute me- tritis may result and unless it is treated early or a hys- terectomy performed promptly, it usually is fatal in 4 to 5 days due to a necrosis of the uterine wall in the region of the placental attachments and peritonitis. Once toxic symptoms have developed in septic metritis in bitches due to retained placenta, the prognosis should be very guarded. The presence of a dark green vulvar discharge more than 12 hours after parturition is a symptom of retention of fetal membranes. If retained placenta occurs during whelping or is noticed within the first day after- wards, the retained membranes may be gently with- drawn from the birth canal and uterus with the finger. A pair of forceps padded with gauze or cotton may be rotated in the genital tract to wind up the membranes and remove them. In the small bitch the uterus might be pal- pated and massaged over the retained membrane to help to force the latter through the cervix. This might be re- peated in several hours if unsuccessful initially.2 In toy bitches after whelping and especially after dystocia a small dose of 1/2 to 1 cc., 10 to 20 units, of oxytocin may prevent retained placenta. If the bitch is valuable an at- tendant could watch her during whelping and save the placentas to make certain all are expelled. If septic me- tritis is present, with a vulvar discharge, elevated tem- perature, rapid pulse, and anorexia the prognosis is guarded and treatment with antibiotics parenterally, as well as supportive treatment similar to that in other an- imals, should be given. Careful infusion of a small amount, 30 ml., broad-range antibiotic solution into the uterus might be indicated with a small soft rubber cath- eter. Injections of oxytocin may be of value. Supportive therapy with fluids is desirable. Laparo-hysterectomy might be considered but should be performed early. Septic Metritis Following Parturition may occur with or without retention of the fetal membranes and is ob- served usually within 1 to 10 days after parturition in all species. The etiology of septic metritis is probably sim- ilar to that of retention of the fetal membranes. It usually is associated with a uterine atony or inertia. Highly pathogenic types of organisms are present in the uterus and they or their toxins are absorbed into the circulation, producing severe general symptoms associated with sep- ticemia, endotoxemia, and pyemia. The organisms most commonly present are coliform organisms, Coryn. py- ogenes, hemolytic staphylococci, Ps. aeruginosa, pro- teus, hemolytic streptococci, and in rare cases clostridia. These severe infections are characterized by a fetid, red, watery uterine fluid that is very toxic and depressing to the animal. This condition usually follows emphysema of the fetus, severe torsion of the uterus with the pres- ence of a dead and possibly emphysematous fetus, and other conditions associated with a uterine inertia such as dropsy of the fetal membranes, fetal anasarca, fetal gi- antism, twinning, peritonitis due to traumatic gastritis and retention of the fetal membranes. In many cases it may follow rough improper removal of a retained pla- centa. Probably most veterinarians in large animal prac- tice can cite several instances in which septic metritis and even death followed the injudicious removal of a retained placenta in a cow when the owner insisted upon its being removed. Septic metritis may follow a pro- longed dystocia especially if a difficult fetotomy oper- ation has been performed. It may follow a prolapsed uterus or invagination of the tip of the uterine horn associated with trauma and infection of the endometrium. Occa- sionally it may result by extension from a necrotic vagi- nitis. It may occur in all species through the introduction of infection by unsanitary practices during the relief of dystocia or removal of a retained placenta. In bitches and sows it may occur from neglect at the time of parturition or trauma to the uterus with forceps, or accidentally al- lowing one or more placentas or fetuses to remain in the uterus and macerate. The use of cortisone without an- tibiotics by farmers soon after calving for the treatmentINJURIES AND DISEASES OF THE PUERPERAL PERIOD 385 of ketosis may favor metritis.55 The symptoms of septic metritis following parturition are very similar in all species of animals. Retention of the fetal membranes is frequently observed; in the cow the placentomes are usually greatly swollen and the fetal cotyledons firmly attached to the maternal caruncles. In the mare a piece of the placenta, often a portion from the nongravid horn, is retained and found in the body or nongravid horn of the uterus. The animals exhibit an- orexia and dullness. The pulse is rapid, in the cow from 80 to 120 per minute, and usually weak. The body tem- perature in the cow may be elevated during the early phase of the disease. In advanced cases the cow’s tem- perature may be either normal or subnormal. The latter condition usually occurs shortly before death of the an- imal. The cow is less apt to show a prolonged elevation of body temperature than are the other animals. The an- imal will shiver and its extremities are cold. The respi- rations are rapid and shallow; the eyes may be sunken; the hair coat is rough; and there is a rapid loss of weight. In severe cases there is a marked atony of the digestive tract. The feces may be hard and firm or may be black, oily, fetid, and liquid in character especially in the cow. A marked drop in milk flow or agalactia occurs in all species and the newborn will exhibit signs of malnutri- tion or starvation. There is usually a reddish, watery, fetid discharge from the vulva. The genital passageways are likely to be swollen and inflamed. Straining may be present or absent before the examination but during or after the examination it is generally present. In many cases of septic metritis with secondary enteritis in the cow, a rectal examination, especially if not performed gently, results in straining or tenesmus. The tenesmus may be very persistent and is definitely undesirable and exhausting to the cow. Rectal examinations should usu- ally be confined to cows with no evidence of rectal ir- ritation or enteritis. In some cows having septic metritis without a retained placenta the cervix may be quite con- tracted. Vaginal examination may reveal a normal va- gina and clear, or only slightly cloudy, vaginal mucus, yet the uterine contents may be toxic and fetid, and oc- casionally toxic enough to cause death. The uterus in nearly all cases is atonic or flaccid. The walls are usually thin and in some cases, especially in bitches and queens, may be very friable or even necrotic, especially the pla- cental sites. Peritonitis may be present due to extension of the infection through the uterine wall with symptoms of abdominal tenderness or soreness, abdominal disten- sion, slight to moderate tympany of the rumen due to atony of the digestive tract, an arched back, stiff, slow gait, and tense abdominal muscles. The cow may exhibit a characteristic expiratory grunt due to the peritonitis. Perimetritis or peritoneal involvement with the uterine infection may occur naturally or be produced by heroic or too vigorous treatment of a severely infected and in- flamed uterus. Rectal examination on these cases in cows may reveal early fibrin deposition and adhesions present between the uterus and the adjacent abdominal viscera. If this is found, the operator should terminate the ex- amination at once, or the peritonitis and adhesions may be made worse, leading to severe peritonitis, abscess in- volvement of the adjacent structures, marked adhesions around the uterus, broad ligaments, ovaries and ovi- ducts, or even death. Arthritic symptoms, with swelling and stiffness of the joints, particularly the hock, fetlock and knee joints, may occur especially in the cow, ewe and sow. Acute laminitis in all large animals may also be present making the animal reluctant to rise and stand. The animal may be very weak, staggering, or prostrate and show symptoms of paresis and inability to rise. Since under these conditions the extremities are usually cold, this disease in the cow may easily be confused with milk fever. A mild to strong reaction to the Ross test for the presence of ketones may develop on testing the urine of cattle with septic metritis. This may be due to ketosis as a complication of the disease but more often it is caused by the severe anorexia. The blood count usually devel- ops a marked shift to the left, together with a marked drop in the total white blood cell level during the early stages of the condition. During the recovery stage the white blood cell count shifts to the right, with a leuko- cytosis developing. Occasionally secondary complica- tions of pneumonia, and laminitis in the mare, cow, sow, and ewe, and in all species pyemia with arthritis, liver, brain, or lung abscesses or endocarditis or myocarditis may develop especially if the condition is prolonged. Rough removal of the placenta, or lacerations of the en- dometrium encountered in prolapse of the uterus may allow organisms to localize in the uterine wall and cause an abscess. A careful differentiation should be made between sep- tic metritis and other conditions, such as traumatic gas- tritis, gastroenteritis, hemorrhagic septicemia pneu- monia, parturient paresis, laminitis, and mastitis which may cause paraplegia, reluctance or inability to stand and illness at parturition. The course of septic metritis usu- ally lasts from 2 to 6 days, with recovery or death oc- curring within that time. In the cow a prolonged course may extend over a period of from 1 to 2 weeks. The prognosis may be guarded to poor in many cases unless treatment is begun early before the uterus is severely damaged, peritonitis develops and the animal becomes extremely toxic. Failure to respond to treatment, per- sistent straining or complications such as mastitis and386 VETERINARY OBSTETRICS pneumonia tend to make the prognosis grave. The prog- nosis for the future breeding life of the animal may be poor in severe cases as well as in cases of perimetritis, ovaritis or abscesses of the uterine wall. If recovery oc- curs conception may be delayed due to severe chronic metritis. The treatment of septic metritis should be conserva- tive. Massage and douching of the uterus, attempts to remove the retained fetal membranes should seldom if ever be performed in cases of septic metritis, or the an- imal’s condition may become critical. Septicemia and toxemia should be overcome before these manipulative procedures are used. In early cases oxytocin, 30 to 50 I.U. in large animals or 10 to 30 I.U. in small animals may be of some value in producing tonus in the atonic uterus. Usually if the condition is severe hormones are of questionable or no value. If the uterus is filled with a large amount of fetid fluid this should be gently si- phoned off. Siphoning the uterus in large animals should be done very carefully with a sterile soft rubber hose or horse catheter since the uterine wall may be very friable and easily ruptured. In the mare and bitch, if a portion of the placenta is lying in the uterus it should be removed in as gentle a manner as possible. One to 3 gm. of the broad-range tetracycline derivatives such as Aureomy- cin, Terramycin, tetracycline or furacin placed in the bovine or equine uterus in a solution or in a readily sol- uble form may be of great value in controlling the in- fection locally and even systemically by absorption from the uterus.55 Antibiotics and possibly sulfonamide ther- apy are indicated parenterally. The antibiotics such as procaine penicillin, 3,000 to 6,000 units per pound of body weight daily and streptomycin, 5 gms. per 1,000 pounds twice daily, intramuscularly; Terramycin, or tet- racycline intravenously; or in large animals except the horse; intramuscularly, at a rate of 1 to 3 mg. or more per pound of body weight, daily, are of definite value. The older sulphonamides given orally, or intravenously, may be used alone or with other antibiotics. Other sup- portive therapy such as saline and glucose solutions, and blood may be administered daily. Calcium gluconate seems of value especially in the early cases and may increase the tone of the uterus, but large doses given too rapidly to toxic cattle may cause death. Pyribenzamine or other antihistamines may be of value. Forced feeding may be helpful. Good nursing in a suitable stall or other equally comfortable environment is essential. If possible the large animal should be on green pasture each day or provided with fresh-cut green feed and with whole oats or other coarse feeds to tempt and encourage it to eat. If straining is present epidural anesthesia should be used to control it until the cause of the condition is determined and corrected. A drop in pulse rate, an increase in ap- petite, an improvement in the tone of the uterine wall, a change in the exudate from a watery to a mucoid con- sistency are all favorable symptoms indicating that the animal is responding to therapy. Treatment should be continued until the animal has safely recovered and sep- tic symptoms have subsided. This should take place be- fore actively treating the uterus and removing the re- tained fetal membranes in the cow. It may be advisable to let the afterbirth drop away. In the mare septic metritis is more likely to cause laminitis, than in the cow, ewe or sow. The application of ice packs to the mare’s hooves, an- tihistamines and phenylbutazone, are indicated as pre- ventive therapy in septic metritis. Laminitis may also follow metritis in the cow, ewe, and sow but is usually less severe and may be unnoticed until months later when deformity of the hooves becomes evident. Postpuerperal Metritis may be observed from the time of parturition to 2 to 8 weeks or more postpartum in all species. It may persist as a chronic metritis for months or occasionally pyometra with anestrus and persistence of the corpus luteum may occur in the cow. There are no septic or general symptoms of illness accompanying this metritis. In most cases there is a reddish-brown or grey, mucopurulent, occasionally fetid discharge from the vulva. Later a creamy-yellow or grey discharge from the uterus and vulva usually mats the hair on the tail and buttocks. The condition is probably caused by many of the bacteria, especially C. pyogenes, that cause a re- tained placenta or septic metritis but either the infection is milder or the animal’s resistance and the tone of the uterus are better. It may follow the development of in- fection in the uterine lochia during involution of the uterus. It may occur following retention of the fetal membranes or a necrotic piece of membrane or caruncle that has remained in the uterus. Occasionally it may be associ- ated with a piece of the fetus, such as a hoof, left in the uterus and which has become a focus of infection. In mares it may follow a vulvar tear or laceration after foal- ing which causes persistent penumovagina and chronic metritis. Usually a cervicitis and vaginitis accompany the metritis, as by extension the infection from the uterus involves these structures. Rectal examination in cases of postpuerperal metritis reveals a larger than normal uterus undergoing a delayed involution. Uterine tone is fair but the uterine wall is thick and heavy. There may be from one-half pint to several gallons of mucopurulent material in the uterus of large animals. Vaginal examination may reveal some of this pus lying in the vagina. As late as two weeks after parturition the cervix in the cow with metritis is usually relaxed and dilated enough to admitINJURIES AND DISEASES OF THE PUERPERAL PERIOD 387 one finger. The uterine exudate is mucoid in character rather than watery as in septic metritis. Since postpuer- peral metritis usually follows a retained placenta the vet- erinarian will find it advisable to reexamine valuable cows or mares 2 to 5 weeks after a parturition associated with retention of the placenta and treat the metritis and de- layed involution of the uterus if they are present. In val- uable cows a routine genital examination is usually per- formed in 3 to 5 weeks after parturition, even though retained placenta did not occur, to make certain that in- volution of the uterus is normal and that metritis is not present. There is evidence in mares and cows that prob- ably 100 percent of parturient animals have infectious organisms invade the uterus for a short period of several days or more after expulsion of the fetus. At the time of the first estrus, at 5 to 12 days in the mare and 12 to 18 days in most cows, these infections are overcome and eliminated. In animals in which the first estrus is delayed or in animals failing to eliminate the infection, the in- fection persists as a mild to moderate metritis. With each subsequent estrous period more of these mild metritis or endometritis cases recover.59,70 The prognosis in most of these cases is good. Many animals would recover without treatment but recovery time might be prolonged and conception delayed. Ne- glected postpuerperal metritis may progress into pyome- tra, chronic endometritis or cervicitis, and delayed or permanent infertility may result. Treatment of these cases should start early, and re- peated examinations and treatment at 1- to 3-week in- tervals may be indicated. Douching of the vagina of the cow with a gallon of hot, 120 to 130° F., mild antiseptic solution of chlorine, a soapy antiseptic, dilute Lysol, or other mild antiseptic 2 to 3 times a week stimulates uter- ine contractions, and washes the purulent exudate from the vagina. Intrauterine douching should be done gently, using only a soft rubber catheter, so that the endome- trium is not traumatized. The exudate is thinned by the introduction of small amounts of a mild antiseptic so- lution, and then removed by siphoning. If the exudate is very thick, an enzyme like streptococcic domase or pan- creatic trypsin may be used to thin it and thus make it easier to siphon out. The recommendation in most of these cases is to avoid vigorous massage of the uterus or the removal of the corpora lutea in cows, since oth- erwise adhesions and perimetritis or ovaritis may de- velop. If the uterus is massaged this should be done gently. Antibiotics, and other antiseptics, such as 1 to 5 ml. of Lugols’s solution or 10 to 20 ml. of Betadine in 100 ml. of saline or water, may be introduced into the uterus for local treatment of the infection. Large or prolonged doses of estrogen should be avoided lest cystic ovaries or the transfer of infection through the oviducts with ovaritis and adhesions result. Estrogens should not be used in the dairy cow. Presently the prostaglandins such as F2a or prostaglandin analogues are used to evacuate the uterus when a corpus luteum is present. Breeding of the animal should be delayed until the uterus and cervix are normal and 2 to 3 normal estrous periods have elapsed. Most affected cows should not be bred until 90 days or more after parturition although some may be normal and be bred at 60 to 80 days (See Metritis and Endometritis, Chapter XIII). In bitches, queens, and sows parenteral treatment of postpuerperal infections with courses of an- tibiotics and oxytocic agents are indicated to assist re- covery. In rare cases laparotomy and hysterotomy with douching and infusing of the uterus with antiseptics and antibiotics might be undertaken.21 The mare may be treated similar to the cow except irritating infusions should not be used. If the mare or cow develops pneumovagina the Caslick operation should be performed. Because of the long period between lambing and breeding most ewes recover from postpuerperal metritis without treatment. Lactation Failure, Hypogalactia or Agalactia, Mas- titis-Metritis Agalactia (MMA) Syndrome of Sows is a heterogeneous disease complex with many possible causes. In this regard it resembles the postparturient paraplegic or downer syndrome in cows. Based on ex- haustive reviews of this disease syndrome,40,68b the name MMA is probably a misnomer. Much research on this syndrome over the past 20 years has shown that metritis is not a contributing factor in most cases and mastitis is not always a contributing factor. This syndrome of lac- tation failure affects 10 to 15 percent of sows farrowing in the midwest and is a contributing cause for the loss of 20 percent of the baby pigs due to starvation, hypo- glycemia, overlaying and pig scours. Lactation failure syndrome appears to be contagious but cannot be produced experimentally with regularity. The general categories of causes can be classified under infectious agents, managerial deficiencies related to nu- trition, housing and stress, endocrine imbalances and possibly heredity for lactational ability.U 40'53'58'65'66a'68b E. coli and Klebsiella are commonly associated with mastitis and lactation failure. The latter organism has been associated with wood products used as bedding as in cat- tle. As with cattle, damp contaminated farrowing crates or houses can result in “bacteria-build-up” and be a cause for mastitis.68b Endotoxins from these gram-negative or- ganisms when injected into postparturient sows produce symptoms of the syndrome. These endotoxins may come from the mammary glands or the digestive tract. In the latter they may be associated with underfeeding, over- feeding or altered feeding practices with constipation.388 VETERINARY OBSTETRICS Other bacterial agents have been associated with the aga- lactia syndrome including Streptococci, Aerobactor, Citrobacter, Actinobacillus, Clostridia, Pseudo- monas, Proteus, Mycoplasma and Staphylococcus. Endocrine studies of sows with lactation failure have revealed an elevated estrogen level 48 hours post partum in hypogalactic sows compared to normal sows. Serum prolactin levels were much lower than normal sows post- farrowing. Plasma cortisol levels were higher and thy- roxine values were lower in affected sows. Evidence was presented of altered oxytocin release, increased engorge- ment of the udder and reduced ability to maintain blood glucose levels in affected sows.40 Further correlation of these studies with management practices, infectious pro- cesses and heredity are needed to explain the pathogen- esis of this multifaceted syndrome. Overfeeding of the preparturient sow especially with finely ground feed and underfeeding causing hypogly- cemia have been associated with this syndrome. But ex- tensive studies have not revealed or demonstrated any uniform fault or deficiency in feeding practices. In fact the disease was observed with all commonly used feed- ing systems. Although selenium deficiency and hypo- calcemia have been reported as possible causes for this syndrome, the evidence is not conclusive. Exercise on pasture during gestation is highly desirable. Sows that are susceptible to this lactation failure syndrome have been reported. It is possible that selection for lowered back fat and increased growth rate may favor the de- velopment of strains hereditarily susceptible to this dis- ease. On necropsy examination of affected sows, mastitis limited to a few areas of certain glands was found in 65 percent of the sows.40 A mild metritis was present in 3 of 18 affected sows. Although all these above predis- posing factors may be categorized as stress factors, fur- ther studies are needed to elucidate the complex inter- play of the various causative etiologies.68b The clinical signs of lactation failure syndrome in- clude: depression, anorexia, elevated body temperature, increased respiratory and heart rates, infrequent defe- cation, reluctance to rise and to allow nursing. These signs occur within 1 to 3 days after farrowing. Signs of mastitis may be evident or lactation failure can occur without systemic involvement of the sow. The pigs show signs of discontent by excessive running around and vo- calizing. They become gaunt, weak and emaciated and are often crushed by the sow who is irritable and gets up and down frequently. Treatment consists of providing feed for the malnour- ished piglets until milk flow is re-established in the af- fected sow or gilt. This can be done by placing piglets with other recently farrowed piglets on another sow or feeding baby pig formula (SPF-Lac, Borden) or a for- mula of one quart cow’s milk, one ounce white syrup or honey and one ounce of cream or com oil. Piglets should be fed fresh warm formula every 1 to 3 hours for the first several weeks in amounts of about 10 percent of their body weight daily. Piglets should be left with the sow so as she returns to milk they may suckle. The affected sow or gilt should be given oxytocin 30 to 50 I.U. at 3 to 4 hour intervals along with broad- spectrum antibiotics and possibly glucocorticoids to combat the endotoxin. Some veterinarians also give the sow estradiol and promazine tranquilizers. Preventive procedures should be directed at reducing stress. Avoid sudden changes in feeding and management. Handle sows quietly. House to avoid overheating and excessive hu- midity. Place sows in the farrowing house early enough so they become accustomed to it. Feed balanced coarse- textured mildly laxative grain ration with bran or beet pulp at a rate of 2 to 3 lbs. twice a day. Keep sows lean, don’t let sows get overly fat.2'65 Feeds containing estro- genic mycotoxins should be avoided.49 A daily exercise period during the periparturient period is desirable. Far- rowing houses should be thoroughly cleaned and disin- fected and allowed to stand empty for 1 to 2 months between farrowings and farrowing periods in a house should be limited to 3 to 4 weeks to avoid “bacteria build- up.” Vigorous culling of affected sows is recommended. There is some evidence that lactation failure might be decreased by using prostaglandins to induce parturition after day 111 of gestation (See Chapter VI). Feeding high levels of antibiotics for a week before and after farrow- ing or the use of polyvalent autogenous vaccines to con- trol infections have not proven to be uniformly of value.53,68b Agalactia in sows and mares associated with the ingestion of ergot or ergot-like alkaloids or mycotoxins (fescue) has been reported.1,38 This should be considered in a differential diagnosis in dams showing no systemic clinical signs other than agalactia along with a more ex- citable temperament. The active principal of ergot from the grain may be transmitted through the milk to the pig- lets resulting in gangrene of the ears and tails. In mares on certain fescue pastures in Missouri an increased in- cidence of agalactia was reported as a serious problem. Postpartum metritis syndrome in cattle was de- scribed in 196331 and has been seen with increasing fre- quency in many dairy herds in the Northeast especially as herd numbers increase and as production rises. It is becoming a serious problem especially in the free-stall herds with over 100 cows and where the cows never are placed on pasture. There are many similarities betweenINJURIES AND DISEASES OF THE PUERPERAL PERIOD 389 this postparturient syndrome in cattle and the postpar- turient agalactia in swine. The postparturient metritis syndrome in cattle herds is characterized by a high incidence of retained placenta and subsequent metritis. Even in cows and heifers in which retained placenta does not occur, a postpartum metritis will develop. A few cases of metritis may exhibit septic symptoms but nearly 100 percent of the cows that calve during the Fall and Winter stabling season will exhibit a chronic metritis with a persistent yellowish discharge of pus that lasts for several months, a delayed involution of the uterus, a lowered conception rate and a calving interval that is increased from about 13 months to 15 to 17 months. Often an abnormally long period of anestrum follows calving. A few cases develop a persistent pyo- metra. In the early stages of the infection a wide variety of organisms are cultured but after several months C. pyogenes is the principal organism found. Economic loss is due mainly to delayed conception and culling because of infertility. From his studies the author agrees that the postpar- turient metritis syndrome is principally a problem of san- itation in the bam, the free stalls, the exercise yards, and especially the calving stalls.31 In many instances calv- ings and postpartum involution of the uterus are normal for a period of a month or more at the start of the calving season. Then after one or two cases of retained placenta and metritis occur nearly every cow that freshens in these bams and calving stalls becomes infected (See Retained Placenta in Cows). In some herds with this problem nearly every calf bom in these infected calving stalls will de- velop scours and die unless prophylactic antibiotic treat- ment is given as soon as the calf is bom. Sometimes the owners in treating the cows prophylactically by placing antibiotics into the uterus may spread the virulent infec- tion that has been established in the bam and calving stalls. Frequently this may only occur in a herd for one year. When the cows are turned to pasture or when a period of 2 to 3 months passes with no cows calving the infection will disappear. In large herds calving the year around the condition may remain a problem for years. If dry cows and pregnant heifers are removed from the herd and kept separate from the herd, calve at pasture or calve in a clean, noninfected environment and kept there for about 7 to 10 days this metritis syndrome will stop. To solve this problem some farmers have built portable 10' x 10' calving stalls that can be thoroughly disinfected between calvings and can be moved to clean ground after each calving. It is obvious that more study in the field in problem herds is needed to determine the sanitation needs and management practices to control this metritis syndrome in a practical way. Possibly by proper construction, suitable isolation, adequate disinfection and rest after each calving, stalls could be constructed as have farrowing houses, that are adequate for the needs of in- tensive dairy farming. Preventive treatment of cows in a herd where post- parturient metritis develops in nearly every cow is gen- erally not satisfactory. Autogenous bacterins or com- mercial polyvalent vaccines have been tried without success. Injections of oxytocin after calving seem to have little or no effect. Parenteral injections or local intra- uterine infusions or capsules of broad range antibiotics after calving have limited value and then only in possibly preventing some cases of septic metritis. In one exper- iment where two 500 mg. of neomycin sulfate boluses were inserted into the uterus of cows within 24 hours of calving the number of services per conception were greater in the treated than in the control cows.26 As an aid to hastening the recovery of the chronic metritis and de- layed involution of the uterus, estrogen injections or 3 to 10 mg. of estradiol and intrauterine antibiotics and/ or weak Lugol’s solution, 2 to 5 ml. of Lugol’s solution in 100 ml. of water, infused into the uterus at biweekly or monthly intervals has proven helpful. Although proper management, exercise, and clean, noninfected isolation facilities for the parturient cow are more difficult for the farmer to provide, at present it is the best way to control this economically costly metritis syndrome. Puerperal Laminitis is most likely to occur in the mare and may be commonly seen in the cow, ewe, and sow. Twenty-four percent of 170 cases of bovine lam- initis occurred within 2 to 3 days of calving.503 It usually occurs secondary to a septic metritis. In the mare the placenta may tear away, leaving the apex of the allantois chorion in the nongravid horn. This placental remnant acts as a focus of infection and the uterus fills with a fetid, watery exudate. Laminitis is apparently caused by the septic uterine contents and possibly the histamines released and results in symptoms similar to those in lam- initis of digestive origin. Usually 2 to 4 days after par- turition the animal begins to exhibit a foundered gait characterized by the hind legs being placed well forward under the body in order to remove the weight from the even more severely affected forelimbs. The hooves are hot to the touch and the digital artery has a strong, hard pulse. The animal may lie down continually, standing for only short intervals, or rarely it may refuse to lie down. Weight loss is rapid. The prognosis is fair if treat- ment is begun early. Any animal with hooves with se- vere retained placenta or septic uterine infection should be treated early to prevent the possibility of laminitis de- veloping. Treatment consists of the administration of an antihistamine in repeated doses plus the application of390 VETERINARY OBSTETRICS ice packs to the feet or having the animal stand in cold water. The author prefers alternate hot and cold packs and placing the animal on a firm supportive bedding such as sand. The placenta of any valuable mare should be examined after expulsion by the veterinarian or, if he is intelligent and informed, by the owner to make certain that none of the placenta has remained in the uterus. If laminitis develops in a mare or other animal several days post partum, the uterus should be treated as for septic metritis by gently removing the exudate and placenta if present. Antibiotics may be used in the uterus and par- enterally along with injections of oxytocin. The uterus should be examined and treated again if necessary in 24 to 48 hours and therapy continued until recovery results. Phenylbutazone or similar nonsteroid antiflammatory drugs and possibly tranquilizers make the affected mare more comfortable and speed recovery by allowing mod- erate exercise to promote circulation in the hooves. Puerperal Tetanus may occasionally occur in the mare and cow. It is possible in any species. All mares with dystocia, retained placenta and metritis and prolapsed uteri should be vaccinated promptly with tetanus antitoxin or toxoid. In the cow, even though of unusual occurrence, puerperal tetanus is the most common form of the dis- ease. It often follows retained placenta and postpartum metritis. Unsanitary handling of a retained placenta when the uterus or birth canal may be traumatized predisposes to tetanus in the cow and mare. The afterbirth drops out a short distance when the cow lies down and becomes contaminated and when the cow rises foreign material on the placenta is drawn into the genital tract. Tetanus is usually observed one to four weeks after parturition. In many cases a post-puerperal metritis is present. If possible the uterine exudate should be removed and the cow or mare treated as for an ordinary case of tetanus resulting from external wounds, that is, by the admin- istration of large doses of tetanus antitoxin, penicillin and tranquilizers. Estrogens or prostaglandins, if a cor- pus luteum is present, should be injected to evacuate the pus from the uterus. Constant, careful, quiet nursing is essential. The prognosis is guarded but recovery may oc- cur if the cow is treated early with an indwelling uterine catheter to infuse the uterus with about 50 to 100 ml of penicillin-streptomycin mixture daily and inject 5,000 units of tetanus antitoxin followed by 1500 units daily for a number of days. A tranquilizer and laxative may also administered as needed.36 Uterine Abscess, or pyometra with cervical or vaginal obstruction, may occasionally follow severe septic me- tritis, dystocia, and necrotic cervicitis or vaginitis that cause an atresia of the birth canal. It is seen in all spe- cies, but most commonly in the cow and mare. During the early stages no external symptoms may be evident but after several weeks to a month or more the uterus becomes so greatly distended with pus that it may cause a distention of the abdomen. Usually intermittent strain- ing and frequent urination are present. On rectal and va- ginal examination the enlarged fluctuating uterus can be felt protruding into the pelvic cavity and the stenotic or closed portion of the genital canal may be palpated. Adhesions between the vagina and uterus may be pres- ent, so that an incision can be safely made through the vaginal wall into the uterus to drain off the pus. In one mare so treated by the author about 15 gallons of pus were removed. Symptoms of shock developed following the removal of this large volume of pus. The uterine ab- scess may break into the rectum or vagina. The animals occasionally recover, but their breeding life is ended. This condition should be distinguished from an abscess of the uterine wall which is a small, localized lesion. Infections of the Cervix, Vagina and Vulva Postpuerperal Cervicitis due to trauma, mild lacer- ations, infectious material from the uterus passing through the cervix, infection by extension from the vagina, or infection from a retained placenta or material carried into the genital tract on the placenta, is common in animals. It is observed most commonly in the cow and in asso- ciation with a metritis or vaginitis after calving. The good blood supply, large mucus glands in the cervix, and the folded mucous membrane make severe injury, necrosis, and atresia of the cervix rare except in the mare. If cer- vicitis is present in the mare the gentle introduction of mild oily antiseptics or antibiotic infusions into the uterus and gentle dilation of the cervix with the gloved fingers may prevent stenosis occurring. This should be repeated until the cervicitis has been corrected. As long as a me- tritis is present local treatment of the cervix is usually ineffective. Once involution of the uterus takes place and the uterus rids itself of infection, the cervix also recovers unless a vaginitis, pneumovagina, or a greatly enlarged chronically infected ectropic cervix persists. Treatment for postpuerperal cervicitis is the same as treatment for metritis or vaginitis. The prognosis is usually good. Postpuerperal Vaginitis and Vulvitis may occur with or without a concurrent metritis. Following parturition either a severe necrotic vaginitis and vulvitis or a mild catarrhal inflammation of these structures may develop. Necrotic Vaginitis, Vestibulitis and Vulvitis is ob- served most often in dairy and beef heifers having a nar- row small birth canal that caused dystocia. The fetus may have been expelled without aid after a difficult, pro- longed parturition or traction may have been necessary. These factors, especially the latter, result in trauma, lac-INJURIES AND DISEASES OF THE PUERPERAL PERIOD 391 eration, excessive pressure, and abrasion of the vulvar and vaginal walls. The mucosa of the vagina and vulva may be further irritated by the presence of a retained placenta, a metritis, or a tom or ruptured perineum al- lowing infection to enter the vulva and vagina. Pressure necrosis of the vulvar and vaginal mucous membranes is often observed following the removal of an emphy- sematous fetus by traction or after a prolonged fetotomy without proper lubrication in a heifer or cow. In rare cases necrotic vaginitis may be due to douching with too irritating or strong an antiseptic. Occasionally a severe necrophorus infection of the vagina may occur. The symptoms of necrotic vaginitis and vestibulitis are usually observed 1 to 4 days after parturition and last for 1 to 2 weeks or more depending on the severity of the lesions. There is usually an arched back, elevated tail, anorexia, and rapid loss of weight. The animal may ex- hibit either no straining, straining that is intermittent and mild and only observed at the time of urination or defe- cation, or nearly continuous straining with air being sucked into the vagina and forcibly expelled. The vulva, ves- tibule and vagina may be very swollen, due to a peri vul- var and perivaginal phlegmon. A fetid, reddish, watery fluid is present. The pulse rate is usually elevated. The body temperature may be moderately elevated. Parting of the vulvar lips reveals a necrotic, diptheritic inflam- mation of the vestibule and vagina, usually most severe at the vulvo-vaginal border. The necrotic portion of the mucous membranes sloughs, and the exposed submu- cosal tissues granulate and eventually heal with a cica- trix. In an acute case, the passage of the hand through the inflamed vulva and vagina of the cow is likely to cause bleeding. This act is very painful to the animal and because of the swollen dry tissues is usually difficult to perform. Straining is probably due to the vestibular and vulvar inflammation and irritation and possibly the accompanying vaginal swelling or phlegmon, since there are many sensory nerves in the vulva and vestibule but few if any in the vagina. Straining due to vulvitis, ves- tibulitis and vaginitis should be differentiated from that caused by dystocia, an undiagnosed, retained fetus, ra- bies, or other conditions which might cause straining. In some of these cases of vulvitis, vestibulitis and va- ginitis, no matter how they are handled, marked stenosis or even atresia of the vagina may occur resulting in a distention of the cranial portion of the vagina due to pus or mucus. In advanced chronic cases, even the cervix and the uterus may be distended with 2 to 3 gallons of a mucopurulent material if infection persists, or of mu- cus alone if no infection is present. The prognosis is fair to good in mild cases treated early. In severe cases that are neglected the prognosis is guarded. If necrosis is ex- tensive, straining constant, and the animal is extremely debilitated, death may result. In cases of severe vaginal or vestibular atresia—fortunately uncommon—the fu- ture breeding life is usually terminated. The treatment of necrotic vaginitis should be gentle and conservative. Oily bland antiseptics such as 4 to 6 ounces of bismuth formic iodide or antibiotics, in oil, together with the broad range antibiotics, may be intro- duced in a gentle manner into the cranial portion of the vagina 2 to 3 times a day. As this infusion is expelled it coats the inflamed mucous membranes. If swelling, phlegmon, elevation of the temperature, and rapid pulse rate are present, parenteral administration of antibiotics and/or oral or intravenous administration of sulfon- amides are indicated daily for 4 to 6 days or until re- covery is evident. If in the cow, retained fetal mem- branes are hanging through the vulva they should be removed if this can be done easily and without injury to the vulva and vagina. In most cases the placenta is fas- tened securely and must be allowed to remain and drop away later. If the membranes are heavy and hang nearly to the floor they should be cut off at the hocks so the added weight does not aggravate the vulvitis and induce straining. If straining is present, the use of one of the longer-lasting epidural anesthetics such as lidocaine to which a small amount of adrenaline solution has been added to retard its rate of absorption. This may be given twice daily or more often if necessary. Sometimes pro- caine penicillin may be used epidurally as a fairly long- acting local anesthetic. The administration of tranquil- izers is helpful in controlling pain and tenesmus. Ele- vation of the rear parts may be helpful. In mild cases of vulvitis and vaginitis with straining, some local anes- thetic ointments containing butesin picrate or benzocaine have been used but difficulty has occurred in applying these to a moist mucous membrane and their effect is questionable. If tenesmus is severe and accompanied by marked sucking and blowing of air into and out of the vagina, the dorsal two-thirds to three-quarters of the vulva should be tightly sutured after administration of epidural anes- thesia. This prevents ballooning of the vagina with air and precludes the accompanying irritation and straining. This treatment with other supportive treatments de- scribed usually promptly controls the straining. The su- tures holding the vulvar lips together may be removed in 4 to 7 days. In rare cases it may be indicated to in- sufflate the abdominal cavity with air to prevent tenes- mus.63 Control of severe straining is essential to prevent rapid loss of weight, weakness, early exhaustion, and even death. Repeated treating and dilating of a necrotic vagina is not indicated, inasmuch as this procedure pro- longs recovery time, increases the inflammatory reaction in the vagina, and produces additional scar tissue. Fol-392 VETERINARY OBSTETRICS lowing healing, breeding may be advised if the stenosis is not severe. At the time of parturition it may be nec- essary to dilate the stenotic portion of the vagina. In many cases, however, due to the relaxation of the vaginal wall and surrounding tissues, mild stenoses disappear at the time of parturition. If the stenosis is severe and breeding is desired this might be accomplished by artificial in- semination with cesarean section at the time of parturi- tion. Most severe cases of stenosis of the vagina are slaughtered. Outbreaks of blackleg have been reported in sheep following lambing where the organism, C. fes- eri, invades the damaged vulvar tissues.11 Catarrhal Vaginitis and Vulvitis occurs following or with retained placenta, puerperal metritis, or injuries to the vulva causing pneumovagina. Following parturition this generally is characterized by a persistent mucopu- rulent discharge from the vulva. The prognosis is good. Dilute, warm vaginal douches, using 200 ppm Betadine solution, dilute Lysol or other soapy aromatic antisep- tics, or saline or sodium bicarbonate, are indicated. These may be repeated at 1- to 3-day intervals. If the vulva is tom it should be sutured, to prevent pneumovagina. If puerperal metritis is present the vaginitis may persist in a mild form until the discharge of uterine exudate ceases. In some cases when only a vaginitis is present one to three weeks after parturition, some oily antibiotics or an- tibiotics in ointment form may be placed in the vagina to aid in overcoming the infection. Puerperal and Postpartum Infections of the Genital Tract 1. Anderson, J. F. and Werdin, R. E. (1977) Ergotism Manifested as Agalactia and Gangrene in Sows, JAVMA, 170, 10, 1089- 1091. 2. Arthur, G. H. (1975) Veterinary Reproduction and Obstetrics, 4th Ed., Bailliere and Tindall, London, Williams Wilkins, Bal- timore. 3. Asbury, A. C. (1972) Management of the Foaling Mare, Proc. 18th Ann. Conv. A.A.E.P., San Francisco, Cal. 487-490. 4. Banerjee, A. K. (1965) A Study of the Action of Terramycin on the Bacterial Flora of the Uterus in Cattle Following Retained Placenta, Tijdschr, v. Diergeneesk, 90, 8, 531. 5. Beattie, J. H. and Learning, J. D. (1952) Prophylactic and Ther- apeutic Use of Aureomycin in Retained Placenta in Cows, Vet. Med., 47, 11. 6. Ben-David, B. (1962) A Survey of the Incidence and Treatment of Retained Placenta in Cattle, Refuah Vet. 19, 1, 48. 7. Bendixin, H. C. and Plum, N. (1926) Schimmel-pilze (Asper- gillus fumigatus and Absidia ramosa) Als Abortus Ursache beim Rinde, Acta Pathol et Microbiol. Scand., 6, 252. 8a. Benesch, F. and Wright, J. G. (1951) Veterinary Obstetrics, Williams and Wilkins Comp., Baltimore, Md. 8b. Bierschwal, C. J. and Uren, A. W. (1956) The Absorption of Chloretetracycline (Aureomycin) by the Bovine Uterus, JAVMA, 129, 3, 373. 9. Bjorkman, N. and Sollen, P. (1961) A Morphological Study on Retentio Secundinarum in Cattle, Acta Vet. Scand. 2, 157. 10. Black, W. G., Ulberg, L. C., Kidder, H. E., Simon, J., McNutt, S. H. and Casida, L. E. (1953) Inflammatory Response of the Bovine Endometrium, Am. J. Vet. Res., 14, 51, 179. 11. Blood, D. C., Henderson, J. A. and Radostits, O. M. (1975) Veterinary Medicine, 5th Ed., Lea and Febiger, Philadelphia. 12a. Boyd, W. L. and Sellers, A. F. (1948) Some Observations on Postparturient Cows in Four Separate Herds as Related to Ex- pulsion of their Fetal Membranes, Cor. Vet. 38, 3, 263. 12b. Bretzlaff, K. N., Whitmore, H. L., Spahr, S. L. and Ott, R. S. (1982) Incidence and Treatments of Postpartum Reproductive Problems in a Dairy Herd, Theriog. 17, 5, 527. 13. Buch, N. C., Tyler, W. J. and Casida, L. E. (1955) Postpartum Estrus and Involution of the Uterus in an Experimental Herd of Holstein Friesian Cows, J. of Dairy Sci., 38, 1, 73. 14. Bums, S. J., Judge, N. G., Martin, J. E. and Adams, L. G. (1977) Management of Retained Placenta in Mares, Proc. Ann. Conv. AAEP, Vancouver, 381-390. 15. Chew, B. P., Erb, R. E., Zamet, C. N., Colenbrander, V. F., Malven, P. V. and D’Amico, M. F. (1979) Variables Associated with Peripartum Traits in Dairy Cows. V. Hormonal Profiles Associated with Retained Fetal Membranes, Theriog. 12, 5, 245- 253. 16a. Cohen, P. (1956) A Statistical Investigation Covering Retained Afterbirth and Other Factors Associated with Bovine Repro- duction, Thesis, Royal Univ. of Utrecht. 16b. Dawson, F. L. M. (1958) Stillbirths in Cattle, Vet. Rec. 70, Aug. 16th. 17. Curtis, R. A. (1973) Oxytocin as a Preventive for Retained Fetal Membranes in Cows, Vet. Rec. 92, 292. 18. DeSutter, E. (1954) Puerperale Stoomissen na Keizersnede bij Runderen, Vlaams Diergeneesk Tijdschr., 23, 11, 273. 19. Dolge, K. (1982) Personal Communication. 20. Dubois, P. R. and Williams, D. J. (1979) Increased Incidence of Retained Placenta Associated with Heat Stress in Dairy Cows, Theriog., 13, 2, 115-121. 21. Durfee, P. T. (1968) Surgical Treatment of Postparturient Me- tritis in the Bitch, JAVMA, 153, 1, 40. 22. Easterbrooks, H. L. and Plastridge, W. N. (1955) Aureomycin for Retained Placenta in the Cow, JAVMA, 126, 934, 21. 23. Erb, R. E., Hinze, P. M., Gildow, E. M. and Morrison, R. A. (1958) Retained Fetal Membranes—The Effect on Prolificacy of Dairy Cattle, JAVMA, 133, 10, 489. 24. Fincher, M. G. (1941) Retained Placenta, JAVMA, 99, 776, 395. 25. Fincher, M. G. (1951) Foaling Mares, First Annual Stud Man- agers Course, College of Agric., Univ. of Kentucky, Lexington, Ky. 26. Fuguay, J. W., Harris, R. A., McGee, W. H., Beatty, J. F. and Arnold, B. L. (1974) Routine Postpartum Treatment of Dairy Cattle with Intrauterine Neomycin Sulfate Boluses, J. Dairy Sci. 58, 9, 1367-1369. 27. Gould, C. M., Gould, A. C. and Gray, D. F. (1961) The Treat- ment of Retention of the Placenta in the Bovine Animal, Vet. Rec., 73, 335. 28. Hallman, E. T. (1924) Further Studies in the Diseases of the Reproductive Organs of Cattle, Cor. Vet., 14, 3 , 254. 29. Hammermann, J. (1963) Treatment of Retained Placenta with Special Reference to the Fertility of the Cow, Proc. 9th Nord. Vet. Congr., Copenhagen, 1962, Vol. II, 534. 30. Heatley, T. G. (1939) A Few Notes on Retention of the After- birth in the Mare, Vet. Rec., 48, 24, 760. 31. Herrick, J. B. (1963) A Genital Infection Syndrome in Cattle, Vet. Med. 58, 4, 329.INJURIES AND DISEASES OF THE PUERPERAL PERIOD 393 32. Ishak, M. A., Larson, L. L., Owen, F. G. and Lowrey, S. R. (1981) Factors Related to Placental Retention in Dairy Cattle, J. An. Sci. 53, Suppl. 1, 108, Abstr. 33. Jennings, W. E. (1941) Some Common Problems in Horse Breeding, Cor. Vet. 31, 2, 197. 34. Jennings, W. E. (1941) Some Common Problems in Horse Breeding, Cor. Vet. 31, 2, 197. 35. Kennedy, A. J. (1947) Retention of the Placenta in the Bovine, Vet. Rec. 59, 38, 519. 36. Koning, F. (1971) Postpartum Tetanus in Cows, Proc. 4th Ann. Mtg., AABP, 12-13. 37. Lacroix, J. V. and Hoskins, H. P. (1952) Canine Surgery, 3rd Ed., Amer. Vet. Publicat. Inc., Evanston, 111. 38. Loch, W. (1981) Fesque Pasture Complications, Eq. Vet. Data, 2, 22, 304. 39. Madsen, D. E. and Nielsen, H. M. (1939) Parturient Hemo- globinemia of Dairy Cows, JAVMA, 94, N.S. 6, 577. 40. Martin, C. E. and Elmore, R. G. (1981) Mammary Glands in Diseases of Swine, 5th Edit. Edit, by A. D. Leman, Iowa State Univ. Press, Ames, Iowa. 41. Martin, C. E., Hooper, B. E., Armstrong, C. H. and Amstutz, H. E. (1967) A Clinical and Pathologic Study of the Mastitis- Metritis-Agalactia Syndrome of Sows, JAVMA, 151, 12, 1629. 42. McDonald, L. E. (1953) Placental Retention in the Cow, Proc. A.V.M.A., 90th Ann. Meeting, 418. 43. Moberg, R. (1956) The White Blood Picture During Parturition with Special Reference to Retained Fetal Membranes, Proc. Ill Intemat. Congr. on Reprod. at Cambridge, 193. 44. Moberg, R. (1959) Possible Influences on Iodine—Deficiency in Reproductive Performances in Cattle with Special Reference to Retained Placenta, Proc. HI World Congr. on Fert. and Steril., Amsterdam. 45. Moberg, R. (1959) Possible Influences of Iodine—Deficiency in Reproductive Performances in Cattle with Special Reference to Retained Placenta, Proc. HI World Congr. on Fert. and Steril., Amsterdam. 46. Moller, K., Newling, P. E., Robson, H. J., Jansen, G. J., Meursinge, J. A. and Cooper, M. G. (1967) Retained Fetal Membranes in Dairy Herds in the Huntley District, N. Z. Vet. Jour. 15, 7, 111. 47. Moore, R. W., Redmond, H. E. and Livingston, C. W. Jr. (1966) Mycoplasma as the Etiology of a Metritis—Mastitis Syndrome in Sows, Vet. Med. 61, 9, 883. 48. Morrow, D., Thomas, J. W. and Main, R. J. (1980) Effects of Vitamin E and Selenium on Periparturient Diseases and Fertility in Dairy Cattle, Bov. Pract. 16, 80-81. 49. Nelson, G. H. (1969) Mycotoxicosis, 111. State Vet. Med. As- soc. Mtg. 50a. Nilsson, S. A. (1958) About Founder in Cattle and Its Ap- pearance in the Veterinary District at Mellerud, Congr. VII Vet. Nordiscus Helsinki, 313. 50b. Paar, C. E., Cannon, R. Y. and Hawkins, G. E. (1964) Secre- tion of Sulphonamides in Milk Following Intramammary, Oral and Parenteral Administration, J. Dairy Sci., 47, 3, 251. 51. Palmer, C. C. (1932) Clinical Studies on Retained Placenta in the Cow, JAVMA, 80, 1, 59. 52. Poliak, E. J. and Pelisser, C. L. (1977) Dystocia, Milk Fever and Retained Placenta in Holsteins, J. Dairy Sci., Suppl. I, Abstr. 60, 77. 53. Ringarp, N. (1960) Clinical and Experimental Investigations Into a Postparturient Syndrome with Agalactia in Sows, Acta. Agric. Scand. Suppl. 7. 54. Roberts, S. J. (1954) Ketosis-Parturient Paresis Complex, JAVMA, 124, 926, 368. 55. Roberts, S. J. (1974) Postpartum Antibiotic Intrauterine Ther- apy in the Dairy Cow, Mod. Vet. Pract. 55, 6, 465. 56. Ronning, M., Berousek, E. R., Kuhlman, A. H. and Gallup, D. (1953) The Carotene Requirements for Reproduction in Guernsey Cattle, J. of Dairy Sci., 36, 1, 52. 57. Rowson, L. E. A., Lamming, G. E. and Fry, R. M. (1953) The Relationship Between Ovarian Hormones and Uterine Infection, Vet. Rec., 65, 335. 58. Ross, R. F., Christian, L. L. and Spear, M. L. (1968) The Role of Certain Bacteria in Mastitis-Metritis Agalactia of Sows, JAVMA, 154, 11, 1368. 59. Sager, F. C. (1949) Examination and Care of the Genital Tract of the Brood Mare, JAVMA, 115, 873, 450. 60. Shaw, R. N. (1938) Pituitary Extract in Cattle Practice, Lederle Veterinary Bulletin, 7, 1, 9. 61. Schingoethe, D. J., Kirkbride, C. A., Olsen, O. E., Owens, M. J., Ludens, F. C. and Tucker, W. L. (1981) Influence of Vitamin E and Selenium on Retained Placentas in Parturient Dairy Cows, Abstr. J. Dairy Sci., 64, Suppl. I, 120. 62. Segerson, E. C., Riviere, G. J., Dalton, H. L. and Whitacre, M. D. (1981) Retained Placenta of Holstein Cows Treated with Selenium and Vitamin E., J. Dairy Sci. 64, 1833-1836. 63. Svendsen, P. (1967) Artificial Pneumoperitoneum—The Ther- apeutic Effect in Tenesmus Rectalis and Rectovaginalis Bovis, Nord. Vet. Med. 19, 163. 64. Trainen, D. (1965) Treatment of Retained Placenta in the Cow— A Comparison of Four Methods, Refuah Vet. 22, 45. 65. Tharp, V. L. and Amstutz, H. E. (1964) Swine Diseases, 2nd Ed., Edit, by H. Dunne, Iowa State Univ. Press, Ames, Iowa, 665. 66a. Vandeplassche, M., Guerden, L., VandenWyngaert, M., Snoeck, G. and DeVos, A. (1960) Puerperal Septicemia and Toxemia in Swine, Deutsche Tierarztl. Wochenschr. 67, 14, 1375. 66b. Vandeplassche, M. and Martens, C. (1961) The Influence of Oestrogens on Length of Gestation and on Retention of the Pla- centa in Dairy Cattle, Proc. IV Intemat. Congr. on An. Re- prod., The Hague Vol. Ill, 671. 67. Vandeplassche, M., Spincemaille, J. and Bouters, R. (1971) Aetiology, Pathogenesis and Treatment of Retained Placenta in the Mare, Eq. Vet. Jour. 3, 144. 68a. Vinattieri, E., Hayward, A. H. S. and Artioli, D. (1945) Re- tention of the Placenta in Buffalo, with Associated Sequelae, Vet. Rec. 57, 46, 509. 68b. Wagner, W. C. (1982) Mastitis-Metritis-Agalactia, Vet. Clin, of N. Amer., Lg An. Pract. 4, 2, 333-341. 69a. Wetherill, C. D. (1965) Treatment of Cows with Retained Fetal Membranes—A Brief Review, Canad. Vet. J. 6, 290. 69b. Williams, W. L. (1943) Veterinary Obstetrics, 4th Ed., Ithaca, N. Y. 70. Wright, J. and Roberts, S. J. (1969) Unpublished data. Paraplegia in the Parturient Cow, The “Downer Cow” and “Fat Cow Syndrome” (“Atypical Milk Fever,” “Creeper” or “Alert Downer”) The cow that fails to rise after calving or dystocia, the cow that goes down and is unable to rise late in gestation394 VETERINARY OBSTETRICS or soon after parturition or the cow that goes down with parturient hypocalcemia and fails to respond to treatment cause a perplexing diagnostic problem for the veterinar- ian. All too often many of the following conditions are lumped together without adequate and careful attempts to make an accurate diagnosis and called a “downer cow,” a “creeper,” an “alert downer” or a cow with “atypical milk fever. ” Most of these cases reflect the disease state present in the cow entering the periparturient period and the stresses and injuries developing during this period. Each case should be studied carefully. A complete phys- ical examination of each system of the animal should be performed despite the fact the animal is recumbent. Since diseased states occurring around calving may be serious an early diagnosis, treatment, and recovery is desirable from the standpoint of the animal’s future production of milk and/or calves. Overconditioned dry cows, often fed excessive amounts of com silage high in energy, have an increased suscep- tibility to metabolic and infectious diseases including milk fever, ketosis, displaced abomasum, retained fetal mem- branes, secondary metritis, mastitis, and foot and joint diseases that are loosely described under the “fat cow syndrome.” If these animals are unable to rise for a pe- riod of a few hours pressure damage to muscles and nerves may occur. In some herds with this nutritional problem brought on by poor management the morbidity rate may reach 50 to 90 percent and the mortality rate may reach 20 percent or more.7,9 The “downer cow” syndrome can be regarded as a common complication of parturient hypocalcemia that is preventable to a significant extent by either preventing milk fever or giving early treatment when the standing cow initially shows inappetence, mild depression and cold extremities.9 In a recent study 16 normal healthy cows confined by halothane anesthesia in sternal recumbency on the right side for 6 to 12 hours developed pressure damage including ischemic necrosis of muscles and sciatic and peroneal nerve lesions. Eight of the 16 cows were able to rise within 3 hours after anesthesia but the other 8 cows remained recumbent until death or euthanasia.4a b A check-list of factors and possibilities to consider in the diagnosis of paraplegia before, at and after parturi- tion includes:1' A—Metabolic and/or Nutritional Disturbances 1. Parturient paresis, hypocalcemia, milk fever. 2. Tetany, hypocalcemia and/or hypomagnese- mia including grass and transport tetany. 3. Ketosis, usually postparturient. 4. Debility, cachexia, or weakness—due to star- vation, senility, acute or chronic wasting dis- eases including internal or external parasitisms and Johne’s Disease. 5. Zenker’s degeneration of muscle—due to a lack of selenium, vitamin E, and the presence of other factors including poor quality hay and muscle stress following a lack of exercise or following vigorous attempts to rise in cows with milk fever, nerve paralyses, or cows that are cast. B—Traumatic and/or Physical Injuries—These often occur during attempts to rise especially where the footing is slippery or in cows affected with par- turient hypocalcemia resulting in pressure dam- age to muscles and nerves.4ab 1. Paralyses—due to injuries to the obturator, Lb- sciatic, peroneal, gluteal, femoral, and bra- chial nerves or compression of spinal cord. Besides a severe injury, lymphosarcoma and abscesses may also produce spinal cord compression.12,14 2. Dislocation of the hip or sacroiliac joints,110 (See Figure 101). The latter is seen in young cows, under 5 years of age, often after a dys- tocia. 3. Fractures of the leg, pelvis, spine, and skull. 4. “Cast” often associated with myositis, Zenk- er’s degeneration, tendinitis, arthritis, muscle asthenia and ischemia, phlebitis and throm- bosis, and contusions. 5. Rupture of the gastrocnemius muscle, usually secondary to Zenker’s degeneration. 6. Exhaustion from attempts to rise or exertion from dystocia may produce a circulatory cri- sis, low blood pressure and myocarditis.13 This may be related to a lack of exercise. 7. Hemorrhage, anemia, or shock as in rupture of the uterine or pelvic blood vessels in torsion or prolapse of the uterus, laceration of the genital tract, transportation in advanced preg- nancy, violence during foaling in mares, abomasal or duodenal ulcers, coccidiosis, an- aplasmosis, leptospirosis and postparturient hemoglobinuria. C—Infectious Diseases or Inflammatory Processes 1. Septic metritis, with or without a retained pla- centa or a vulvar discharge. 2. Septic mastitis. 3. Peritonitis, or pericarditis, secondary to trau- matic gastritis, uterine rupture or abomasal ul- cers with perforation. 4. Acute laminitis.INJURIES AND DISEASES OF THE PUERPERAL PERIOD 395 Figure 101. Dislocation of the sacroiliac articulation in a cow. This is occasionally seen in young dairy cattle following a difficult parturition. 5. Septic arthritis—knee, hocks, coffin joint. 6. Miscellaneous diseases—severe pyelonephri- tis, shipping fever, blackleg, anthrax, necro- bacillosis, rabies, listeriosis, meningitis, and brain or cord abscess. D—Digestive Disturbances, Diarrheas, Toxemias and Poisonings 1. Enteritis, severe diarrhea secondary to an in- testinal stasis associated with hypocalcemia or grass tetany, winter dysentery, salmonellosis, virus diarrhea, etc. 2. Toxic indigestion due to overeating on fruit, grain, or spoiled forage. 3. Toxic indigestion of advanced pregnancy has been described5 as occurring in stabled dairy cows late in the winter confinement period and characterized by partial to complete anorexia, dullness, progressive emaciation and in- creased pulse rate. Normal activity of the gas- trointestinal tract appears impaired possibly due to large gravid uterus. The recommended treatment consists of exercise, forced if nec- essary, intravenous fluid therapy, and mild laxatives orally. In a valuable cow cesarean section or induced parturition might be indi- cated. 4. Poisonings—plant, chemical, etc. E—Miscellaneous Causes. 1. Hydrops allantois and/or amnii. 2. Lymphocytoma especially involving the spinal cord, heart, and abomasum. 3. “Malingerer.” 4. Spastic syndrome (“stretches”). 5. Severe albuminuria and uremia secondary to nephritis (rare). In making a differential diagnosis of the etiology for paraplegia, cows with infectious diseases may have an elevated body temperature and pulse rate. The latter is also elevated in digestive disturbances. Hypocalcemic states usually respond to calcium therapy intravenously or udder inflation although some response to calcium therapy may be observed in digestive disturbances. An expiratory grunt is often exhibited in cases of peritonitis. One or more of the following symptoms would be suf- ficient reason for questioning the diagnosis of parturient hypocalcemia in a cow: a pulse rate of 90 or more per minute, rapid respirations or respirations accompanied by an expiratory grunt, diarrhea, an attitude that is bright and alert, a nearly normal appetite, a body temperature of 102° F. or higher, a hot swollen udder, persistent te- nesmus, and failure of expected response to adequate calcium therapy. Although these diseases and conditions are described and listed for cows many of them are ap- plicable to mares, ewes, sows, and even bitches and queens. Because of his exposure to frequent necropsies on so-396 VETERINARY OBSTETRICS called “downer” cows the author is impressed with the frequency of physical and muscular lesions in these cases as well as the variety of the conditions found. A high incidence of muscle damage and tears together with a rising S.G.O.T. level in “downer” cows following par- turient paresis was observed.3'4 The best procedure to follow to prevent “downer” cows is to control, prevent or provide early and prompt treatment of cows with hy- pocalcemia or parturient paresis.8 In certain herds in se- lenium deficient areas, the administration of selenium late in gestation might be indicated to assist in prevent- ing Zenker’s degeneration of muscle under the stress of calving or during parturient paresis. The author is firmly convinced that obesity or exces- sive condition “the fat cow syndrome,” is highly detri- mental and dangerous to the parturient animal especially if it is coupled with a lack of exercise during the latter half of the gestation period. In cases of parturient paresis these two factors combine to greatly lower the cow’s re- sistance to stress, to favor exhaustion and a “malinger- type” of attitude and to result in difficulty in rising with the production of secondary traumatic lesions. A 20 by 20 box stall with a dirt floor for excellent footing is highly desirable for large high-producing parturient dairy cows to avoid injury. Further proof of the possible effect of lack of exercise is the list of diseases of muscular organs that are most commonly observed in cattle in northeast- ern U.S. in the late winter or early spring months after a long period of confinement namely: displaced aboma- sum or torsion of the abomasum, prolapse of the vagina, prolapse of the uterus, retained placenta possibly related to uterine inertia, torsion of the cecum, intussusception of the intestine, torsion of the uterus, indigestion of ad- vanced pregnancy and Zenker’s degeneration of skeletal muscle. The incidence of these diseases is much lower during the late spring or summer months when cows are on pasture and getting exercise. Paraplegia in the Parturient Cow 1. Adams, O. R. (1957) Preliminary Report on the Repair of Cox- ofemoral Luxation and Coxofemoral Subluxation in Cattle, JAVMA, 130, 12, 515. 2. Blood, D. C., Henderson, J. A. and Radostits, O. M. (1979) Veterinary Medicine, Lea and Febiger, Philadelphia. 3. Bjorsell, K. A., Holtineus, P. and Jacobsson, S. O. (1968) Stud- ies on Parturient Paresis with Special Reference to the Downer Cow Syndrome, Acta. Vet. Scand. 10, 36. 4a. Cox, V. S., McGrath, C. J. and Jorgensen, S. E. (1982) The Role of Pressure Damage in Pathogenesis of the Downer Cow Syndrome, Amer. J. Vet. Res. 43, 1, 26-31. 4b. Cox, V. S. (1982) Pathogenesis of the Downer Cow Syndrome, Vet. Rec. Ill, 76. 5. Fox, F. H. (1966) Personal Communication. 6. Jonsson, G. and Pehrson, B. (1969) Studies on the Downer Syn- drome in Dairy Cows, Zent. fur Vetoed. A., 16, 757. 7. Julien, W. E., Conrad, H. R. and Redman, D. R. (1977) Influ- ence of Dietary Protein on Susceptibility to Alert Downer Syn- drome, J. Dairy Sci., 60, 210. 8. Kronfeld, D. S. (1970) The “Downer” Problem in Bovine Med- icine and Surgery, Amer. Vet. Public Inc., Wheaton, 111., 394. 9. Littledike, E. T., Young, J. W. and Beitz, D. C. (1981) Com- mon Metabolic Diseases of Cattle: Ketosis, Milk Fever, Grass Tetany and Downer Cow Complex, J. Dairy Sci. 64, 1465-1482. 10. Rees, H. G. (1964) Coxofemoral Dislocation in Dairy Cattle, Vet. Res. 76, 13, 362. 11. Roberts, S. J. (1954) Ketosis-Parturient Paresis Complex, JAVMA, 124, 926, 368. 12. Robertson, J. M. and Boucher, W. B. (1963) Vertebral Body Abscess in a Heifer, JAVMA, 143, 11, 1211. 13. Sellers, A. F., Pritchard, W. R., Weber, A. F. and Sautter, J. H. (1958) Renal Function Studies on Normal Dairy Cattle and Those with Parturient Albuminurea, Amer. J. Vet. Res., 19, 580. 14. Straub, O. C., Olander, H. T. and Theilen, G. H. (1960) A Case Report of Lymphosarcoma in a Cow with Vertebral Involvement, Cor. Vet. 50, 3, 251.Part II INFERTILITY IN DOMESTIC ANIMALS Although the problem of infertility in domestic ani- mals has been studied for many years there has been a great surge of interest, activity, research, and investi- gation since 1940 when the widespread use of artificial insemination forcefully brought the problem of infertility in domestic animals, to the attention of farmers, veter- inarians, animal husbandrymen, physiologists, endocri- nologists and others. These basic studies on the problem have rapidly forwarded our knowledge of reproductive physiology in domestic animals. In the past 25 years basic and applied reproductive studies in all species of animals and man has been heavily supported by state and federal governments, as well as private foundations, because of the urgency of thoroughly understanding all areas of re- productive physiology so that effective methods may be devised to control the so-called population explosion. In that time there has also been rapid progress in the field of endocrinology. Nutritional studies have furthered our knowledge of infertility as related to the animal diet. The losses due to sterility and delayed breeding in dairy cattle were estimated in 1960 to be about twenty million dollars per year in New York State.- While it is possible that the incidence of sterility and delayed breeding is in- creasing, it is more likely that in recent years, due to more general use of artificial insemination, gradually, increased milk yield, higher value per cow, and increas- ing nutritional problems, farmers have become more conscious of their loss than they were formerly when a cow failed to conceive promptly. The average good cow should provide a farmer a net return of $500 each year over feed costs. Each monthly delay in conception re- sults in $30 to $60 loss to the farmer. Preventive med- icine is a component part of the control of infertility and as such requires an adequate record keeping system not only for informational purposes but also for evaluation of performance and indentification of deficiencies. The studies initiated in the field of artificial insemi- nation on the infertility problems in bulls and cows have done much in recent years to elucidate more clearly the importance of the bull in the overall problem of bovine infertility. These studies in cattle have in turn set the pattern and stimulated studies in the other species of an- imals. In the past 20 years reproductive studies in horses, swine, dogs and cats have grown and expanded rapidly. The increased value of the large domestic animals and the realization by the owners that knowledge is available to greatly improve reproductive rates and reduce eco- nomic losses has increased the demand for skilled vet- erinary services. 397Chapter XII PHYSIOLOGY OF FEMALE REPRODUCTION Reproductive Hormones Reproduction is a luxury function of the body not physiologically necessary for the life of the individual and usually not performed until the animal reaches nearly adult size and nutritive supplies are ample for the nutri- tion of both the dam and fetus. Any adverse influence of environment, nutrition, stress or disease on the indi- vidual will, if severe enough, exert its influence on the reproductive system. Reproduction in mammals is largely controlled by en- docrine glands and the hormones they secrete. These in- fluence all phases of reproduction. At least four tem- porary reproductive structures or organs elaborate various steroid or protein hormones; these are the ovarian fol- licle, the corpus luteum, the placenta and the endome- trial cups in the mare. The hormonal regulation of re- production is a complicated and carefully balanced system of checks and controls. The various hormones stimulate or inhibit each other and accordingly their effects on the animal’s reproductive organs. The reproductive hor- mones play a major role in the initiation and regulation of the estrous cycle, ovulation, fertilization, preparing the uterus for the fertilized ovum, protecting, insuring and maintaining pregnancy, initiating parturition, and the development of the mammary gland and lactation. With a complex hormonal system controlling these many phases of reproduction, it is remarkable how seldom reproduc- tive troubles are due to a breakdown of any portion of this mechanism. The nervous system, both central and autonomic, plays a secondary role in reproduction but one that is closely linked to the hormones produced. These nervous mechanisms in reproduction play a definite role in ovulation in those species in which ovulation is not spontaneous; with the period of sexual desire, or estrum and acceptance of the male and in such hormonal dis- turbances as nymphomania. Thus reproduction is under neuroendocrine or neurohumoral control. In many spe- cies of animals all phases of reproduction can take place even with the spinal cord severed in the lumbar region. The reproductive hormones of each mammal are not species-specific in their effect; that is, the estrogenic hormone from women or mares when injected into a cow produces the same effect as does the estrogenic hormone from the cow. All hormones are highly specific and se- lective in their action on the genetically-conditioned end, or “target,” organ. The “target” organ with its receptors reacts promptly to a specific hormone to produce the substance or changes for which it has been genetically “programmed.” Differences in the amounts of hormone required to produce specific effects occur between spe- cies, but the basic effects thus produced are often sim- ilar. A wide range of reactions to certain hormones ex- ists. Another important fact to recognize in the use of re- productive hormones is that hormones produced in a cer- tain organ or gland do not, when injected, affect that organ or gland directly. In other words, endocrine dis- turbances of the ovary do not respond directly to the ovarian hormones, but if curable usually respond to the pituitary or uterine hormones. For example ovarian hor- mones act in a direct manner on the tubular genitalia and in an inhibitory manner on the anterior pituitary gland through their indirect effect on the central nervous sys- tem and hypothalamus. The amount of hormone, the fre- quency of dosage, and the time of injection in relation to the stage of the estrous cycle have profound influences on the effects produced. Many external sensory stimuli act upon the central nervous system and hypothalamus and effect reproduc- tion. These include: light, and sight mediated by the eyes, sound, or vocalization, mediated by the ears, smell me- diated by the nose, state of nutrition, physical stimuli including cold and heat and the amount of work, stress as mediated by the release of glucocorticoids from the adrenal gland, tactile stimuli as obtained by mounting and intromission and possibly others. The olfactory stimuli have been called “pheromones.”10 Certain drugs, as well as hormones, can effect the centers in the central ner- vous system and produce changes in reproductive phys- iology. In the central nervous system, spinal cord and hypothalamus are numerous interacting reflex arcs, and centers concerned with reproductive behavior and with production of releasing factors, peptides or neurosecre- tions that result in the release of the tropic hormones from the anterior pituitary gland after they pass to the 398PHYSIOLOGY OF FEMALE REPRODUCTION 399 adenohypophysis through the hypophysial portal system. Such centers, often located in or near the hypothalamus, also control the release of prolactin from the anterior pi- tuitary gland and oxytocin and vasopressin from the neu- rohypophysis or posterior pituitary gland (see Figure 102). The blood supply to the hypophysis and hypophysial portal system used to carry releasing factors or neuroendo- crines from the hypothalamus to the adenohypophysis has been described.5 In the last 20 years much work has been done to elu- cidate the relationship of the hypothalamus and its re- leasing factors to the central nervous system and the ad- enohypophysis.--- These releasing factors (RF) are small peptides that like the other hormones are not generally species specific. The hypothalmic releasing factor or hormone in ACTH is CRH, corticotropin releasing fac- tor; for TSH is TRH, for FSH and LH is GnRH, and for STH or GH is GRH. In regard to prolactin a hypotha- lamic factor inhibiting its release from the adenohypoph- ysis, PIF or PRIF has been described. GnRH, gonado- tropin releasing hormone, is a decapeptide that has been synthesized and produced commerically as “Cystore- lin.” GnRH is sometimes referred to as LHRH or LHRH/ FSHRH because the single hormone acts on the ade- nohypophysis to release both luteinizing hormone (LH) and follicle stimulating hormone (FSH).- Both GnRH (“Cystorelin”) and human chorionic gonadotropin (HCG) are equally effective in the treatment of cystic ovaries in cows.-’-- The principal or major endocrine gland controlling the reproductive organs and functions is the adenohypophy- sis. The pituitary gland is composed of two principal parts. The anterior lobe or adenohypophysis is quite vascular. Cells in this lobe produce the gonadotropic hormones and control the activity of the gonads. The posterior lobe or neurohypophysis is divided into the pars nervosa and pars intermedia. The latter structure is small and appar- ently of limited importance. The pars nervosa, the major portion of the posterior lobe, is attached to the floor of the third ventricle or hypothalamus by a stalk or infun- dibulum. Thus the anterior and posterior lobes of the pi- tuitary gland are separate and distinct in origin, structure and functions. (See Figure 102.) Anterior Pituitary or Adenohypophsial Hormones There are 6 major adenohypophyseal hormones that have been isolated and are obtainable in a nearly pure form at the present time: ACTH—adrenocorticotropic hormone. Prolactin—this hormone promotes lactation and cer- tain other metabolic and possibly gonado- tropic functions.- STH or GH—somatotropic or growth hormone. TSH or TTH—thyroid-stimulating or thyrotropic hor- mone FSH—follicle-stimulating hormone LH—luteinizing and luteotropic hormone MSH—melanocyte—stimulating hormone—this sev- enth hormone is of little importance (FSH and LH are the gonadotropic hormones.) All of these hormones are complex proteins in nature and are water-soluble. A review of the literature on the histology and physiology of the anterior pituitary gland reported that there were three principal cell types com- posing this endocrine gland; basophilic cells, acidophilic cells and chromophobe cells. FSH, LH, TSH, and prob- ably ACTH are produced by certain basophilic cells. So- matotropic or growth hormone and prolactin are pro- duced in the acidophilic cells.--- The adrenocorticotropic hormone is essential for the maintenance and functioning of the adrenal cortex. It is sometimes called the “stress” hormone because it stim- ulates the production of glucocorticoids from the adrenal cortex. Besides its other functions, this latter hormone raises the blood sugar level and lowers milk production. This explains the value of ACTH and the glucocorticoid hormones in acetonemia or ketosis. The adrenal cortex is capable of synthesizing the gonadal steroid hormones as well as the glucocorticoids. The effects of stress on the reproductive system have been reviewed.41 The thy- rotropic hormone is essential for the functioning of the thyroid gland and the regulation of metabolism by its stimulation of thyroxine production. The somatotropic or growth hormone is concerned with body growth; moreover, it has been shown to be intimately concerned with udder development and lactation. Somatotropin causes growth of the long bones, affects protein metab- olism by increasing nitrogen retention by the body, and markedly influences carbohydrate metabolism. This hor- mone in the cow is probably more concerned with lac- tation than is prolactin. Recent studies have shown that natural or recombinantly-derived bovine growth hor- mone when injected into cows the third month of lac- tation in daily doses of 25 mg increased milk production 10 to 13 percent and improved feed efficiency 9 to 15 percent.2a,c The two anterior pituitary hormones concerned with reproduction are FSH and LH, the gonadotropic hor- mones. Probably prolactin should not be listed as a go- nadotropic hormone in domestic animals.- FSH or fol-400 VETERINARY OBSTETRICS Direct, primary effects Figure 102. Diagram of the Neuroendocrine Control of Reproduction in Female Animals. licle-stimulating hormone is necessary for the growth of the Graafian follicles and the production of estrogens in the ovary. The secretion of this hormone was formerly thought to be inhibited only by progesterone from the corpus luteum, by testosterone from the interstitial cells of the testes, or by estrogen from the follicular cells and fluid. This was considered to be a “feedback” effect of the steroids on the central nervous system and hypo- thalamus preventing the secretion of GnRH. For this rea- son in castrated animals or postmenopausal women, the plasma levels of circulating FSH and LH are high. Re- cent studies have indicated that a nonsteroidal substance in the follicular fluid has an inhibitory effect on FSH secretions and plasma levels in mares and ewes.28c Lu- teinizing hormone (LH) is released in a pulsatile or ep- isodic pattern or fluctuations.- LH, luteinizing or lu- teotropic hormone causes ovulation and growth of the corpus luteum from the granulosa cells of the ruptured Graafian follicle. The basophilic delta cells of the an- terior pituitary gland produce LH and probably FSH.- -- The continued secretion of LH is necessary to maintain the corpus luteum and the secretion of progesterone to continue pregnancy in the cow. LH is probably luteo- tropic for all domestic animals.- Prolactin is also luteo-PHYSIOLOGY OF FEMALE REPRODUCTION 401 tropic. LH and probably FSH secretion and release can be stimulated by the drug, clomiphene.13 The following drugs can inhibit or prevent LH release and ovulation: antiadrenergic agents like dibenamine; anticholinergic agents like atropine; tranquilizers like chlorpromazine; psychic energizers like iproniazid; anticonvulsants, sed- atives and anesthetics like barbiturates; and analgesics like morphine. These drugs act in a variety of ways on the cells of the C.N.S. to prevent or inhibit the release of LH. FSH and LH are synergistic in their action on the gonads. Prolactin is primarily involved in the ini- tiation and possibly the maintenance of lactation. It is believed to be intimately connected with maternal in- stincts in mammals and broodiness in hens. It may be luteotropic in ewes.-37 Because of the many essential hormones produced by the anterior pituitary gland, it has been often called the “master gland” or “motor” of the endocrine system. In the light of recent studies this designation is questionable as it is obvious that the pituitary gland is controlled by the higher reproductive “centers” in the central nervous system. Clinical abnormalities of this gland produce many and varied effects. Since the hormones produced by this gland are complex proteins, they cannot be produced synthetically and have no effect when taken orally in- asmuch as they are destroyed by the proteolytic enzymes in the digestive tract. DuVigneaud, however, won the Nobel Prize in chemistry in 1954 by synthesizing the neurohypophyseal hormones, oxytocin and vasopressin which are complex polypeptides made up of 8 amino acids. Other workers are busy studying the structure of other pituitary hormones and it is likely more may be synthesized. Repeated injections of heterologous ante- rior pituitary hormone products into animals may result in the production of antihormones, with the result that the injected hormone is neutralized or no longer effec- tive. This is probably of little importance in most ani- mals and seldom occurs unless repeated injections of these proteinaceous hormones obtained from animal sources are administered.7,32,42 The adenohypophyseal content of LH is highest in cat- tle, sheep and cats and lowest in horses and man.- Of the domestic animals, the cow and ewe secrete the great- est amount of prolactin. It has been shown that the tim- ing of the release and the amounts of FSH and LH hor- mone released is very important in the initiation of ovulation and the number of ova released. The blood serum of castrates contains an increased amount of FSH because neither testosterone, estrogen, nor progesterone is inhibiting its secretion. Large prolonged injections of these latter steroid hormones suppress pituitary gonado- tropic hormones and cause small, atrophic gonads. Smaller doses of estrogens or progesterone may cause cystic ova- ries. The urine and serum of pregnant women from about 30 to 60 days after the last menstruation and the serum of pregnant mares from about 40 to 120 days of gestation contain large amounts of gonadotropic hormone human chorionic gonadotropin (HCG) and pregnant mare serum gonadotropin (PMSG) or equine chorionic gonadotropin (ECG), respectively. In the mare this hormone is not ex- creted in the urine. In humans these gonadotropic hor- mones are produced in the chorion of the placenta and called chorionic gonadotropins; in the mare they are pro- duced by the endometrial cups of the uterus, which orig- inated from the chorionic cells, and are called equine gonadotropins. The equine gonadotropic hormones from pituitary glands and pregnant mare serum are predominately fol- licle-stimulating in character although a small amount of LH is present.343 Sheep and pig pituitary gonadotropic hormones are predominately luteinizing in character al- though some FSH is present. Chorionic gonadotropic hormone from the urine of pregnant women is almost entirely luteinizing in character. The biologic sources of the gonadotropic hormones are: human chorionic gonadotropin, HCG, from the urine of pregnant women is sold under many trade names such as “Follutein” (Squibb), and is prepared and packaged in the dry state in a sealed glass vial. This is reconsti- tuted with a saline solution before use. In liquid form it retains its potency for several weeks or months if kept at refrigerator temperature. In rare instances anaphylac- tic reactions are observed in animals into which this product is injected. These reactions are most common in animals previously treated with this form of gonado- tropic hormone. Human menopausal gonadotropin HMG, from urine is also used as a source of gonadotropin high in FSH.4b Anterior pituitary gland extracts or pituitary gonadotropic hormones, FSH and LH are prepared from the pituitary glands of sheep, horses and pigs. Some of the more common veterinary preparations are “Vetro- phin” (Diamond), a sheep pituitary product; “P.L.H.” (Armour); and equine pituitary gonadotropin products such as FSH (Armour). These are purified and prepared in sealed vials as a dry powder and reconstituted with a saline solution at the time of use. Anaphylaxis following the use of these products is unusual. Equine gonado- tropic hormone or pregnant mare serum gonadotropin, PMSG or PMS or equine chorionic gonadotropin (ECG)343 is serum that is collected approximately every 10 days, between 50 and 100 days of pregnancy in the mare. The concentration of hormone is about 50 R.U. per ml. Re- peated doses of this may cause anaphylaxis, especially in the cow. In the mare, rare cases of Theiler’s disease402 VETERINARY OBSTETRICS or infectious hepatitis have been reported to occur from 50 to 70 days to as long as 120 days after the use of this crude equine serum product. PMSG in the mare’s blood is present at 37 to 42 days of gestation and reaches a peak concentration at 70 days.4b Shetland ponies have a concentration of 335,000 I.U. per liter of serum between 55 and 76 days of gestation. This is about twice as high as larger horses that have serum concentrations of 50,000 to 100,000 I.U./liter. Mares with twin fetuses have double the serum levels, 240 I.U./ml. vs 100 I.U./ml. of mares carrying single fetuses. Mares carrying mule foals produce only one- eighth as much PMSG as mares carrying horse foals. The mucoid secretion in the endometrial cups of the mares may contain 5,000 to 210,000 I.U./gm. of PMSG. Peak concentrations of HCG in human urine occur at 50 to 70 days of gestation when 20,000 to 450,000 I.U. of HCG per 24 hours of urine is excreted. After this period about 10,000 I.U. HCG is excreted daily to near term. When the gonadotropic activity of the pituitary glands of man, horse, sheep, pig and ox were compared by as- say on rats’ ovaries highly sensitive to FSH the com- parable percentages were 100, 35, 3, 2, and 1, respec- tively. When assayed on rabbits’ ovaries highly sensitive to LH the comparable percentages were 100, 42, 62, 65, and 42, respectively. In the sheep, pig and cow FSH in the pituitary gland was low but LH was high. In the horse FSH and LH was high and in man FSH and LH were very high. The principal use of gonadotropic hormones in ani- mals is the administration of LH or luteinizing hormone in the treatment of nymphomania or cystic ovaries in cows to produce active corpora lutea and restore a normal es- trous cycle. Other uses include the injection of lutein- izing hormone at the time of estrum to hasten ovulation, or about 4 days after ovulation to increase the size of the corpus luteum and the amount of progesterone se- creted. Injection of large doses of FSH or PMSG 4 to 5 days prior to estrus causes superovulation in the cow and ewe. The use of FSH to promote estrus in anestrous an- imals may be of value under certain limited conditions. Generally the results of this therapy for the treatment of anestrus have been poor. The value of gonadotropic hor- mones to produce descent of testes in cryptorchid ani- mals is questionable. FSH and PMSG may be of value in producing estrus in sheep during the anestrous period in the spring and summer months and hastening the onset of estrus in lactating sows. Protein hormones from the pituitary gland are inef- fective if given orally because they are digested and bro- ken down in the gut. They are water-soluble and may be given intravenously where they produce a rapid ac- tion. These hormones given subcutaneously or intra- muscularly are absorbed more slowly and provide a more prolonged effect. Protein hormones must be protected from thermal decomposition as they are heat-labile. Posterior Pituitary or Neurohypophysial Hormones There are two neuroendocrine hormones secreted in the posterior lobe of the pituitary. Oxytocin produces its effect by contracting the smooth muscles such as those in the uterus, around the alveoli and lactiferous ducts of the mammary gland, and in the bladder and gut. This fraction of the posterior pituitary lobe was formerly called “obstetrical pituitrin.” Vasopressin or “surgical pitui- trin” causes contraction of the smooth muscle of the ar- terioles thus checking postpartum uterine hemorrhage and raising blood pressure. This is also an antidiuretic hor- mone, ADH. If ADH is deficient in the dog and cat,8 diabetes insipidus with symptoms of polyuria and thirst occurs. In this disease vasopressin is not present to reg- ulate the water resorption from the glomerular filtrate in the kidneys. Oxytocin and vasopressin or ADH are very similar in composition with 6 of the 8 amino acids in these two hormones being similar. Posterior pituitary hormone or extract is a stable extract of the posterior pituitary lobe containing both fractions, oxytocin and vasopressin. A combination of both fractions, rather than one alone, seems to give as good or better results than oxytocin alone for most conditions treated in the veterinary field. How- ever, since oxytocin is produced synthetically, it is the one now generally available commercially for use in an- imals. These hormones are protein in nature and water- soluble. They are stable and are usually packaged in liq- uid form with a concentration of 10 or 20 U.S.P. (I.U.) units of each fraction per ml of the solution. Evidence of anaphylaxis following injection of oxytocin or vaso- pressin is rare in animals but it was seen occasionally when the former crude hormone extract was injected in- travenously in the mare. The posterior lobe hormones are produced by neurons or cells in the hypothalmus. The posterior lobe proper composed of terminal nerve endings only stores and re- leases the oxytocin and vasopressin. The posterior pi- tuitary gland, or neurohypophysis, of the goat contains 10 to 15 units and a cow gland contains 30 to 40 units or more of oxytocin.26 The half-life of oxytocin or va- sopressin in the body is short, only 1 to 2 minutes. How- ever, there are forms of ADH that slowly release small amounts after injection to control diabetes insipidus. The posterior lobe cells filled with a fine granular material,PHYSIOLOGY OF FEMALE REPRODUCTION 403 release into the blood stream, by means of cell processes extending into the posterior lobe, the hormone repre- sented by this granular material. This is an anatomical means of passing the hormone through the blood-brain barrier. The posterior lobe is not a distinct organ or gland but is a collection of terminal cell processes which store and release the hormone produced by the cells in the hypothalamus.-- The principal use of oxytocin is to hasten the con- traction and involution of the uterus after a dystocia or prolapse of the uterus. When used immediately after par- turition, it may be of some value in the prevention of retained placenta. If oxytocin is to be used, it is essential that it be administered soon after parturition since by 48 to 72 hours the effects are slight as compared to the marked contractions produced within 12 hours or so after parturition when the uterus is still sensitized by the pres- ence of many oxytocin receptors stimulated to develop by the estrogens produced by the placenta late in preg- nancy.12 For hastening involution of the uterus, oxytocin is superior to “Lentin” or the other ecbolics with the possible exception of ergonovine which acts more slowly. Oxytocin causes contraction of the smooth muscle or myoepithelial cells in the alveoli of the udder, to produce milk ejection or “let down” in heifers or cows that be- cause of pain or for other reasons refuse to “let down” their milk even after stimulation of the udder by mas- sage. The term “let down” is probably not proper be- cause it infers the cow has voluntary control of milk ejection which she does not have. If 10 units or more are given intravenously the action is very rapid, with prompt “let down” within 30 to 60 seconds. Within this time the intra-cistern pressure increases from 30 to 40 mm to 60 to 70 mm of Hg. Under natural conditions, fright, pain or excitement apparently antagonizes, slows, or prevents the release of oxytocin by the posterior pi- tuitary gland by a central nervous system block to ox- ytocin release or possibly by the release of epinephrine which causes a vasoconstriction preventing oxytocin from reaching the myoepithelial cells. In sheep and goats ox- ytocin release and milk ejection is not necessary for sat- isfactory milking. The Ovarian Hormones The hormones produced by the ovaries are: the estro- gens, the progestogens, the androgens, and a nonsteroid hormone, relaxin. The first three are steroid hormones that are also produced by testes, adrenal cortices, and the placenta.-'30 The precursor for all steroids is preg- nenolone which is derived from cholesterol.- The further biosynthesis of the steroid hormones proceeds to pro- gesterone—testosterone—estradiol—estrone. In the cir- culation the steroids appear to be bound to binding pro- teins or globulins. The steroids are inactivated in the liver by conjugation. The estrogens are steroid substances with the ability to produce estrum when injected parenterally into female animals, even in the spayed female. Estradiol and es- trone are the natural biologic estrogens produced in an- imals by the cells of the theca interna of the Graafian follicle or the placenta.- The follicular fluid of a mature bovine Graafian follicle contains about 50 to 90 micro- grams of estradiol per 100 ml of fluid. The amount of fluid averages 2 to 3 ml. per follicle. Estradiol from the Graafian follicle produces the clinical signs of estrum in the domestic animal. These include growth and keratini- zation of the vaginal epithelium, especially in bitches and queens, increased vascularity, edema, and growth of the endometrium, uterus and cervix, and increased sensitivity and amplitude of contraction of the uterine muscles. Under its influence the cervix relaxes and gob- let cells in the cervix and anterior vagina secrete a large amount of clear viscid mucus in the cow and lesser amounts in the other species. The vulva relaxes and be- comes edematous; this is especially noticeable in the bitch and sow. Estrogens increase the rate of migration of leu- cocytes into the uterine lumen and thus increases the bactericidal activity of the uterus during estrum. Thus the genital tract sensitized by the estrogens is in a state of readiness for copulation, which in turn stimulates the release of oxytocin. The greatly increased uterine con- tractions and characteristic mucus of estrum favor the rapid transfer of spermatozoa to the pavilion of the ovi- duct, and the viability and capacitation of the sperma- tozoa in the female reproductive tract. Certain repro- ductive tissues can’t grow unless stimulated by estrogen. The uterus, vagina and mammary gland are tissues that are hormone dependent. Acting through the central ner- vous system, estradiol produces the typical clinical signs of estrum, including the female’s acceptance of the male. Gonadal hormones not only bring sexual behavior to expression at estrus they also produce a differentiation or organization of neural tissues, before or soon after birth, that establishes the basic femininity, or masculin- ity of the individual animal.43 Estradiol is responsible for the secondary sex char- acteristics of the female. It causes the growth of the duct system of the mammary gland. It has a definite effect on the deposition and distribution of body fat and it has- tens the ossification of the epiphyses of the bones. Near the time of ovulation estradiol reaches a high enough level in the body to suppress FSH production and by404 VETERINARY OBSTETRICS stimulating the release of GnRH and LH promotes ovu- lation.-- The high level of estrogens in the plasma of pregnant sows between 20 and 30 days of gestation comes from the blastocyts.-- During pregnancy the placenta produces an increasing amount of estrogen, especially the last several weeks before parturition that promotes the rapid growth of oxytocin receptors in the myome- trium and mammary gland.12 At this period estrogen ini- tiates uterine tonus by stimulating the release of pros- taglandins F2a and potentiates the effects of the latter and oxytocin on uterine contractions,- sensitizes the uterine muscle to oxytocin, relaxes the cervix, vagina and vulva, and the pelvic ligaments. Following parturition the level of estrogens drops rapidly. Estrogens are secreted in in- creasing amounts in the urine of the mare after 100 to 120 days of gestation as estrone and estriol and other forms. These are recovered as a commercial, biologic source of estrogens. The major urinary estrogen excreted in the cow is estradiol.30 During gestation the action of a low physiologic level of estrogens on the pituitary gland may be necessary to help maintain the corpus luteum by stimulating the release of LH. The presence of proges- terone during pregnancy prevents the occurrence of es- trum.- Being steroid in nature, the estrogens are soluble in oil and therefore are usually administered intramuscu- larly or subcutaneously. Estrogens may be implanted subcutaneously or intramuscularly in the form of a pel- let, from which the estrogens are absorbed slowly over a period of several months. To be successful, this pro- cedure requires a nearly sterile technique because if in- fection is introduced excessive connective tissue is built up around the pellet and absorption might be prevented. Other estrogenic preparations for injection are the aqueous suspension of fine particles of estrogen and the solution of estrogens in an alcoholic base or “Repositol” which precipitate when injected into the body tissues or come in contact with water. Following intramuscular injec- tions of the aqueous suspension and “Repositol” prod- ucts the fluid is rapidly absorbed, leaving fine particles of estrogen as a modified type of implant. These prep- arations are easier to administer but due to the fine size of the estrogenic particle it is absorbed faster than when in pellet form. Consequently injections must be repeated about every 5 to 10 days. The esterification of an estro- gen will also reduce its rate of absorption and thus pro- long its action. For example, the effects of stilbestrol in oil last 24 to 36 hours while the effects of estradiol di- propionate will last 24 to 48 hours and estradiolcyclo- pentylproprionate in oil, “E.C.P.” (Upjohn) and estra- diol valerate (Squibb) are effective over a period of 72 to possibly 96 hours or longer. In humans and animals with a simple stomach, such as the dog and cat, the es- trogens, like stilbestrol, may also be administered orally. Low levels of estrogens, such as 10 mg/day of stilbes- trol, added to the ration of feeder cattle and sheep will increase the rate of gain and growth compared to rations not containing this hormone. The naturally-occurring es- trogen, estradiol, is more rapidly destroyed than is stil- bestrol when given orally." All animals can absorb es- trogens fed in their ration. Estrogens may be applied by inunctions and absorbed through the skin or from the uterus after intrauterine infusions. There were formerly two types of estrogens available commercially; the naturally-occurring estrogens such as estradiol, estrone and estriol produced from natural sources such as the urine of pregnant mares and women, from the adrenals and testes of stallions and from the human placenta and amniotic fluid; and stilbestrol or diethyl- stilbestrol synthesized from various coal-tar derivatives and other steroids. Presently all types of estrogenic com- pounds are synthesized chemically for commericial pur- poses. In animals both compounds, estradiol and stil- bestrol, are equally effective and desirable. While in humans estradiol is preferred because there are fewer un- dersirable side reactions. Milligram for milligram estra- diol is about 10 times as potent as stilbestrol. Therefore a 50 mg. injection of stilbestrol is approximately equiv- alent to a 5 mg injection of estradiol. The U.S. Food and Drug Administration has banned the use of stilbes- trol and other estrogenic growth promotants because of public health implications. A few steroidal nonestro- genic compounds as implants have been cleared for this latter use in animals. The estrogens are probably the most widely-used hor- mones in veterinary medicine. They are used to evacuate the uterus in cases of a mummified fetus or pyometra in cattle, and to produce therapeutic abortion in all species. By increasing the uterine blood supply, increasing the contraction of the uterine muscles, and stimulating epi- thelial growth and the flow of mucus they aid in the treatment of such conditions as postpartum metritis and retained placenta. Estrogens have been shown to have a definite effect on the uterus and uterine infection by their ability to prevent, reduce, and overcome infection in the uterine cavity2'35 by their action on stimulating the pas- sage of leucocytes and bactericidal substances from the leucocytes into the uterus.- 22,23 When administered soon after an undesired service, estrogens prevent conception by their effect on the oviduct and uterus and the transport of the fertilized ova by either tubal “locking” of ova or the expulsion, death or failure of implantation of the early embryo. All of these effects on the tubular portion of the genital tract characterize the action of estrogens.PHYSIOLOGY OF FEMALE REPRODUCTION 405 The estrogens have also been used widely to produce signs of estrum in anestrous animals. This action is to be expected since proper doses of estrogens produce es- trum or acceptance of the male even in spayed females. This artificial estrum cannot be regarded as physiologi- cal since ovulation does not occur unless the estrogen is given at the time in the estrous cycle at which ovulation would normally occur. Large or moderate doses of es- trogens given at the time of estrum or ovulation often cause infertility because of their adverse effects on ova transport. Injection of estrogens in large doses over a period of time in virgin heifers or dry cows usually pro- duces varying degrees of mammary development and lactation. The peak of production following the estro- genic initiation of lactation follows a week or two after the estrogen is withdrawn and milking has begun. This phenomenon is also observed occasionally in the natural state in newborn heifers and prepubertal heifers due to excessive assimilation of estrogens from the placenta or production of estrogen by the endocrine glands. Large doses of estrogen after parturition inhibit lactation and relieve congestion of the udder. It is also used in bitches at the end of their pseudo-pregnant period to relieve udder congestion and possbily other symptoms of pseudo- cyesis. Because of its effect on the muscles and epithe- lium of the genito-urinary system it is used in low doses in dogs affected with urinary incontinence. The estro- gens are occasionally used in ointment form for their stimulating effect on epithelial tissues in obscure skin ailments or to produce comification of the vaginal epi- thelium in certain types of vaginitis. Excessive, prolonged or improper dosing with estro- gens will produce cystic ovaries or nymphomania in cat- tle, abortion, atrophy of the ovaries and cessation of the estrous cycles. In cattle and sheep estrogens will cause the regression of the corpus luteum probably by sup- pressing LH secretion, by exhausting the LH levels in the adenohypophysis or by stimulating the release of prostaglandins. In the sow and horse estrogens prolong the life of the corpus luteum. Large amounts of estrogen produce edema of the vulva, excessive relaxation of the pelvic ligaments and other supporting structures, predis- posing to prolapse of the vagina and rectum, and frac- tures of the pelvic bones. In the bitch excessive or pro- longed doses of estrogens can produce a fatal anemia due to their toxic effect on bone marrow or cause cystic en- dometrial hyperplasia with secondary metritis and pyo- metra. In animals the level of the gonadotropins in the pi- tuitary, the length of the heat period, and estrogen threshold and excretion during estrum are strikingly par- allel. The following order, from high to low is reported: man, horse, hog, sheep and cow.2 Progesterone or the corpus luteum hormone, is a ste- roid hormone produced by the granulosa cells and by the corpus luteum. In many species the secretion of proges- terone by the follicle begins before ovulation occurs- and is continued by the mature corpus luteum since the half-life of progesterone in the blood is only 3 to 5 minutes-’173,24,27 in cows and mares. Progesterone is also produced by the adrenal cortex and the placenta. Fol- lowing ovulation the corpus luteum develops from the granulosa cells of the Graafian follicle and is maintained by the luteinizing (LH), luteotrophic or gonadotropic hormone of the anterior pituitary gland.9,39 Under the stimulation of the luteotropic hormone, the lutein cells produce progesterone. Progesterone secretion by the cor- pus luteum regulates the estrous cycle by inhibiting es- trus and the ovulatory surge of LH and plays other im- portant roles in the reproduction of domestic animals.39 The corpus luteum is essential throughout pregnancy in the cow, doe, sow and bitch but for less than full term in the mare, queen and ewe. In these latter species the progesterone produced by the placenta maintains the lat- ter stages of pregnancy.18 Progesterone causes the growth of the grandular sys- tem of the endometrium of the uterus and the uterine secretions (“milk”) from the endometrial glands for the nutrition of the ovum, and the attachment of the embryo. It maintains pregnancy by producing a favorable envi- ronment for the survival of the developing embryo and inhibiting the motility of the uterus. By causing an in- hibition of the LH and FSH or gonadotropic hormones from the anterior pituitary gland, it prevents estrum, ovulation, and the occurrence of the estrous cycle and maintains pregnancy. However enough FSH is released so that follicles may form even during the luteal phase of the estrous cycle, and also during early gestation in some domestic animals especially the mare. Even ovu- lation often occurs during these two periods in the mare. Research has indicated that progesterone may act with estrogen to stimulate ovulation by promoting the release of LH.- Small amounts of progesterone injected during early estrum in the cow hasten ovulation.— Progesterone probably acts with estrogen in most species to cause signs of estms and acceptance. If progesterone from a pre- vious corpus luteum is lacking, the first ovulation is usu- ally characterized by a “silent” heat. This is seen in the early part of the breeding season in sheep, in prepubertal heifers, and in the postpartum period in the cow.- The endometrium and uterus, when under the influence of progesterone during the luteal phase of the cycle, are much more susceptible to infection and provide a fa- vorable environment for bacterial development.2 35 Pro-406 VETERINARY OBSTETRICS gesterone causes the development of the alveolar system of the udder. Following the first half of the period of pregnancy in women and in animals such as the mare and ewe, progesterone for the maintenance of pregnancy is produced by the placenta, and the corpus luteum be- comes small and inactive. In other species, such as the cow, sow and doe, the corpus luteum is essential during most if not the entire period of pregnancy in order to prevent abortion inasmuch as apparently little progester- one is secreted by the placenta.39 Because of its ability to inhibit keratinization of the vagina, to prevent sensi- tization of the uterus, and to prevent estrum, progester- one secreted by the placenta and corpus luteum prevents or possibly counteracts the action of estradiol also pro- duced in large amounts during late pregnancy. In the nonpregnant bitch and queen progesterone produces changes characteristic of pseudopregnancy. The ra- dioimmunoassay is a highly sensitive test for progester- one in milk and plasma that has been described under pregnancy tests in cows, does and mares (see Chapter II). This test is quite accurate at 21 to 23 days post ser- vice especially in nonpregnant cows. Progesterone con- centrations in dairy products are associated with the milk fat levels.17 Progesterone is produced synthetically. Progesterone is prepared in an oily base, in a “Repositol” form, or in finely-divided particles in an aqueous base. The oily preparation is effective for 24 to 48 hours when injected intramuscularly; while the latter preparations are effec- tive for about 3 to 7 days since the finely divided par- ticles precipitate in the tissues. Progesterone is used to prevent or control habitual abortion due to an actual or possible progesterone defi- ciency. It may be used to promote conception the first 20 days of gestation in the cow. In the mare, ewe, cow, sow, bitch and queen, progesterone or synthetic proges- togens can be injected or fed orally and prevent estrum from occurring by suppressing the release of the gonado- tropic hormones, for as long as the injections or feeding are continued.39 However, conception rates at the estrus following its withdrawal have been lower than in non- treated animals. Progesterone has been used experimen- tally to maintain pregnancy in animals in which the cor- pora lutea have been removed. If injections are continued beyond the normal length of gestation, prolonged ges- tation and fetal death may result. Progesterone has a “calming or tranquilizing” as well as an antiandrogenic effect and has been used for a variety of aggressive or antisocial behavior problems in dogs, cats, mares and stallions by the author and others.21 Relaxin is a water-soluble polypeptide hormone ap- parently present in the ovaries, probably the corpus lu- teum, placenta and uterus during the late stages of ges- tation and is responsible, along with estrogen, for the relaxation of the pelvic ligaments and cervix necessary for parturition in sows, ewes, cows and possibly dogs.--- In the pregnant guinea pig and gopher it is able to cause resorption of the pelvic symphysis. This relaxation effect is brought about by an enzymatic depolymerization of the ground substance or collagen. Prostaglandin (PG) was first described in 1934 after it was found in human semen. Prostaglandins are potent biologic agents found in many body tissues. Since they usually act locally, they don’t usually conform to the classic definition of a hormone. Phospholipids in cell membranes give rise to arachidonic acid, a fatty acid which is the precursor for the major prostaglandins F2a and E2. Glucocorticoids can inhibit the formation of ar- achidonic acid from phospholipids. Aspirin, phenylbu- tazone and other nonsteroidal anit-inflammatory agents can inhibit the formation of prostaglandins from arach- idonic acid. Other important and highly active metabo- lites of the arachidonic cascade23,1119 are the thrombox- anes, prostacyclins, and the leukotrienes that, together with the prostaglandins, produce a variety of effects on the reproductive, circulatory, respiratory and other sys- tems and cause inflammatory reactions in joints and other tissues. Prostaglandins are even present in the corpus lu- teum.19 Prostaglandins play a number of important roles in re- production including: gonadotropin release, ovulation in certain species, regression or luteolysis of the corpus lu- teum to control the estrous cycle, produce uterine mo- tility and contraction, oxytoxic effects, at parturition and in sperm transport.3--11'391’ Prostaglandins are also in- volved in cervical “ripening” and relaxation at the time of parturition in mares, ewes and women. In the peri- parturient sow postaglandin (PGF2a) is released from the placenta and uterus causing luteolysis of the corpus lu- teum and a decline in plasma progesterone together with a marked rise in relaxin, and a further rise in prolactin and estradiol.253 In most large domestic animals prosta- glandin is elevated for a number of hours before partu- rition but in the mare its elevation closely coincides with delivery.11 The uterine prostaglandins are produced by the en- dometrium from arachidonic acid under the influence of estrogens and oxytocin. The regulation of the estrous cycle by the luteolytic effect of the uterine formation of pros- taglandin is a complex mechanism that differs between species. Prostaglandins are short-lived and after they en- ter the general circulation they are metabolized very rap- idly by enzyme action. The prostaglandins used for lu- teolysis and estrus synchronization have no effect on thePHYSIOLOGY OF FEMALE REPRODUCTION 407 ovum, ovulation, sperm cells or the fertility of the sub- sequent breeding that occurs 2 or 3 to 10 days after the injection in the mare, cow, ewe and doe." The prosta- glandins do not cause luteolysis in sows until after the twelfth day of the estrous cycle8 and they are even more limited in value in the bitch and queen for synchronizing estrus. After ovulation in the cow, ewe, sow and mare the corpus luteum matures rapidly and produces progester- one that prevents estrus for the duration of the cycle. Prostaglandins can only cause luteolysis of the mature corpus luteum after about the fifth or sixth day after ovu- lation in the cycling cow, doe, mare and ewe. In the cow, ewe and doe, endogenous prostaglandin F2a from the endometrium travels to the corpus luteum by passing from the uterine vein to the ovarian artery which lie in close apposition. In the cow one-fifth of the required systemic dose of prostaglandin if infused into the uterus will cause luteolysis by this local pathway.28 In the mare this local venoarterial pathway is not present so prosta- glandin from the endometrium reaches the corpus luteum by the systemic circulation. In both instances the pros- taglandin constricts the blood supply to the corpus lu- teum and acts directly on the luteal cells to produce lu- teolysis.--,6’11,17b'19'28 If the animal conceives then the early embryo or blastocyst secretes hormones or substances that prevents the formation of prostaglandins in the en- dometrium and maintains pregnancy by the persistence of the corpus luteum, often called “maternal recognition of pregnancy.” Similar persistence of the corpus luteum is observed in chronic uterine infections or pyometra,39b hysterectomy performed during the luteal phase of the cycle and in rare cases of congenital hypoplasia of the endometrium and caruncular areas in heifers in which the endometrium is unable to produce prostaglandins. A number of techniques or agents have been shown to induce the secretion of prostaglandins in cycling and even pregnant animals and cause the involution or lu- teolysis of the mature corpus luteum. In the mare these include: manual dilation and manipulation of the cervix, natural breeding of a mare after administering a large dose of estrogen, douching the uterus with 500 ml. or more of physiological saline-39b and taking an endome- trial biopsy. These techniques probably stimulate the re- lease of prostaglandin by the equine endometrium and a normal estrus occurs within 3 to 10 days. In the cow these procedures include: injecting daily doses of oxy- tocin between the second and sixth day of the cycle,-19,39b injecting 5 to 10 mg. of estradiol valerate when a mature corpus luteum is present either during an estrous cycle or during early pregnancy, introducing an infectious agent, an irritating solution such as weak Lugol’s iodine or an intrauterine device (IUD) within a few days after estrus and the resulting stimulation of the endometrium causes a release of prostaglandin and the development of a short 8 to 10 day estrous cycle. It is possible that in exogenous estrogen therapy that LH release from the anterior pi- tuitary gland is also suppressed. It is also possible the introduction agents into the uterus or dilating the cervix introduces bacteria from the caudal reproductive tract into the uterus resulting in endometritis and prostaglandin re- lease. A number of stable prostaglandins (PGs) and their an- alogues have been produced commercially and are used therapeutically to cause luteolysis of the mature corpus luteum after the fifth or sixth day postovulation to pro- duce estrus or estrus synchronization or abortion in the mare, cow, ewe, doe and sow.3'4'39b,4° (See Chapter V.) Prostaglandins are not effective when the corpus luteum is immature and developing. PGs are also used to evac- uate the contents of the uterus in pyometra of the cow and bitch, and a mummified bovine fetus. Prostaglan- dins are also used, especially in sows, to induce partu- rition (See Chapter VI) and to treat “persistent” corpora lutea or “pseudopregnancy” in mares.1139b The prosta- glandins available commercially have now been offi- cially approved for use in lactating dairy cows. These products include: “Prostin,” “Lutalyse” from Upjohn Company which is prostaglandin F2a (dinoprost trome- thamine) for mares and cows, respectively, with sug- gested doses of 5 to 15 mg. (10 mg.) for mares, 15 to 35 mg. (25mg.) for cows, and 7 to 15 mg. (10 mg.) or less in ewes, does11-33 and sows. In mares this product causes mild to moderate side-effects lasting for up to one hour of sweating, increased heart and respiratory rate, defecation, urination and discomfort due to increased peristalsis.2813 Other prostaglandin analogues that do not cause these side-effects include: “Equimate” (flupros- tenol, ICI 81,008) from Haver Lockhart Lab with a dose rate for mares of 250 ug; “Synchrocept” (prostalene, RS 9390) from Diamond Lab with an equine dose rate of 2 mg., and “Estrumate” (cloprostenol, ICI, 80996) presently from Imperial Chemical Industries with a bo- vine dose rate of 500 ug. and for ewes and does 125 ug. After the injection of prostaglandins into mares, cows, and ewes or does that are cycling normally and have a mature corpus luteum, after 5 to 7 days postestrum, the corpus luteum regresses and a normal fertile estrus usu- ally occurs. In mares this is 3 to 12 days later with most mares showing estrus within 2 to 5 days and ovulation 6 to 12 days after the injection. In ewes and does estrus usually occurs 2 to 3 days post injection.33 In cows estrus usually occurs 2 to 5 days later or at about the same time as they would if the corpus luteum had been expressed408 VETERINARY OBSTETRICS manually.---1119 Estrus synchronization is generally more precise after two treatments with prostaglandins, in the mare 12 to 14 days apart, in the cow 10 to 12 days apart, in does 11 days apart and in sheep 8 to 11 days apart. In mares 2,500 IU of HCG may be injected 6 days after the prostaglandin to promote or “pinpoint” ovulation which usually occurs 24 to 48 hours later." Other Endocrine Glands Other endocrine glands that are associated with repro- duction are the thyroid, adrenal, and the pineal gland. Pheromones also exert endocrine effects on reproduc- tion. The thyroid gland secretes thyroxine and triiodothy- ronine, composed of iodinated amino acids, under the regulation of the thyrotropic or thyroid stimulating hor- mone from the basophilic beta cells in the anterior pi- tuitary gland after release by TRH from the hypothala- mus. Thyroxine and triiodothyronine have been synthe- sized. The latter is more active and potent.- The thyroid gland contains large amounts of iodine. In humans hypo- thyroidism is believed by many to be associated with sterility, infertility and abortion. Thyroid activity is nec- essary for normal reproductive functions. In the United States thyroid abnormalities such as goiter are most com- mon in the iodine-deficient areas around the Great Lakes and the northeastern part of the country. Goiter or an enlarged thyroid is produced by excessive stimulation of the thyroid gland by TSH when the gland cannot meet the body’s need for thyroxine. Hypothyroidism causes a low metabolic rate that is believed to have an adverse effect on human fertility and pregnancy and often is as- sociated with obesity. Since thyroxine and triiodothyronine are quite expen- sive when obtained from animal sources or synthesized, and because there has been little work to show the need of these in various sterility or impotency problems in animals, its use is limited. Some veterinarians have in- dicated thyroprotein may benefit males and even females that lack libido. This could be related to overcondition- ing. An iodinated casein was developed with about a 3- percent thyroxine potency. “Protamone” contained thy- roxine and triiodothyronine.- This has been marketed by the Cerophyll Laboratories in Kansas City, Missouri. In daily doses of 1 gm per 100 lbs. of weight it may be fed to livestock, in which it produces a definite increase in the basal metabolic rate, as shown by an increase of 5 to 20 percent in milk production together with a higher percentage of milk fat in lactating dairy animals (Chapter IV). Because of the cost, dangers and restrictions as- sociated with its feeding to increase milk production, the use of thyroprotein has been limited. It causes a marked loss in weight in fat animals. Preliminary clinical studies in cattle suggest thyroprotein or triiodothyronine may be of value in certain types of female infertility such as “silent” estrus,- or prolonged infertility associated with a steer-like appearance. In males, especially old, fat males, it may increase their activity and reduce their weight. In some males this may result in some improvement in sex- ual desire. However, the same purpose can usually be accomplished by restricting the rations and increasing exercise. The use of iodinated casein for reproductive diseases in livestock appears limited. Thyroid funcion tests are now available, although costly, for domestic animals.- The adrenal gland, composed of the medullary and cortical portions, secrete hormones that have profound effects on other body systems and functions and thus may indirectly affect reproduction.41 The adrenal medulla secretes adrenalin, or epineph- rine, which has been synthesized; it is protein in nature and water-soluble. This hormone stimulates the sym- pathetic nerves, whether the sympathetic nerve of the organ is excitatory or inhibitory. In cows adrenalin may prevent the normal “let down” of milk by preventing oxytocin release from the posterior pituitary lobe. It causes a relaxation of the estrogenized uterine muscle in the cow. In other species it may cause contraction of the gravid or nongravid uterus. Epinephrine has been used by some veterinarians to control hemorrhage following the man- ual removal of the corpus luteum in the cow, but there is no pharmacologic justification for its use in this con- dition. The adrenal cortex secretes steroidal hormones, such as corticosterone or cortisol that control glycogenic ac- tivity and protects the individual against various stresses, and desoxycorticosterone or mineralo-corticoids that control electrolyte and water metabolism. These hor- mones have no direct effect on the reproductive organs but glucocorticoids in moderate or large doses may cause abortion or premature birth, especially late in gestation in the cow, ewe and doe. The adrenal cortex, which originates from mesodermal cells closely related to the embryonic gonadal cells,41 secretes androgens, estrogens and progesterone in small amounts.- Progesterone is a precursor of cortisol. Stress factors on the female cause an increased secretion of cortisol mediated by CRH from the hypothalamus and ACTH from the anterior pituitary gland. Transport stress significantly increased the oc- currence of estrus in sows.41 Increased ACTH may be a factor in the cause of bovine cystic ovaries. High levels of cortisol from the fetal adrenals is closely associated with the onset of parturition in the cow and ewe. In rare instances tumors of the adrenal cortex may secrete suf- ficient androgens to cause masculinization or virilism inPHYSIOLOGY OF FEMALE REPRODUCTION 409 a female. In the cow, because of the increased demands of the body for cortical hormones during gestation and the first third of the lactation period, the adrenal cortex is usually larger than normal for that length of time. The pineal gland or body, attached in most animals by a short-stalk to the roof of the third ventricle of the brain is thought to be an endocrine gland in animals like the horse and sheep that are seasonal breeders. Current reviews-- reported that although much more research is necessary, evidence indicates that the pineal gland, stim- ulated by light by neural pathways from the eye, may secrete melatonin or a polypeptide. In mares melatonin acts as an inhibitor, or in ewes32b as a stimulator of the gonadotropic centers of the hypothalamus to regulate the breeding season in these photoperiodic species. Intra- muscular injection of 2.5 mg of melatonin daily into ewes hastened the onset of the fall breeding season or ex- tended the length of the breeding season in the spring.32b Pheromones are odoriferous substances, external “chemical messengers,” that, although they don’t meet the definition of a hormone, serve as communication media between animals.- - The sex pheromones come from modified skin glands like the preputial glands in the boar and the glands at the base of the horns in bucks. The urine apparently contains pheromones in dogs, cattle, swine and sheep, as well as saliva in boars, as do other skin glands of the external genitalia and other body re- gions in the dog and horse. The development of these pheromones occurs with puberty and the production of estrogens and testosterone. A pheromone present in the vaginal secretion of bitches in estrus that attracts dogs and stimulates them to mount the bitch is methyl p-hy- droxybenzoate.18b The flehmen stance observed in horses, and ruminants is believed to provide the vomeronasal organs, with their sensitive odor receptors in the nasal passages, concentrated pheromone laden air from the ur- ine or perineal region by closing the external nares. Tongue movements in cattle prior to the flehmen stance may force fluids, that often contain urine from estrous females being “teased,” from the oral cavity into the in- cisive pits and fissures and into vomeronasal organ.25d These olfactory stimuli along with other acoustical, vi- sual and tactile stimuli provide both the female and male animals information on the sexual state of the other that is transmitted to the brain and hypothalamus. These odors present at estrus can be recognized by other species.~5b The hormones concerned with reproduction in the male animal are described in Chapter XVIII. Puberty Puberty may be defined as the age or time at which the generative organs become functional and reproduc- tion may occur. Puberty does not signify full or normal reproductive capacity, which develops later. In the male, puberty is indicated, along with other secondary sex changes, by the ability to copulate and produce sperm. In the female animal, it is characterized by the appear- ance of estrum and ovulation. The time of onset of pu- berty in animals is greatly modified by environmental and genetic factors. A high plane of nutrition hastens the onset of estrum especially in cattle and horses. A low plane of nutrition or deficiencies of various nutrients as well as disease factors will delay puberty. Exposure to stress conditions especially during the cold months of the year delay the onset of puberty. In certain animals such as sheep which have a limited breeding season puberty does not occur until that season, at which time the an- imal may be nearly fully grown. Inbreeding tends to de- lay puberty while crossbreeding tends to hasten its oc- currence. Brahman and Zebu cattle reach puberty 6 to 12 months later than the European (Bos taurus) breeds. The larger breeds of cattle and horses tend to have a later onset of puberty than the smaller breeds.-'--4’6'15,16 The age at puberty was less variable than the weight in gilts on a high and low plane of nutrition. In 3 groups of 21 calves each, fed on the following three levels of nutri- tion, 140 percent, 100 percent, and 60 percent, as based on Morrison’s standards,1314 the heifers on the high level of nutrition reached puberty with the first estrum at an average of 37.4 weeks of age weighing 580 lbs., the heifers on the average level of nutrition reached puberty at 47 weeks of age weighing 597 lbs., and heifers on the low level reached puberty at 65 weeks weighing 502 lbs. The attainment of puberty is a slow, gradual process. Graafian follicles must attain a fairly advanced stage of development before the gonadotropins are effective. Pu- berty depends upon the release of the gonadotropic hor- mones from the anterior pituitary gland. Injection of these hormones into prepubertal animals may cause preco- cious sexual maturity. The gradual nature of the pro- cesses leading to puberty is cited in the human, in which secondary sex characteristics develop before menstrua- tion occurs, and menstruation takes place for a period of time before ovulation occurs.-'1 In 53 Holstein heifers with a mean interval from birth to the first ovulation of 296 days and a mean weight of 609 lbs, “silent” estrus was exhibited in 74 percent of the heifers at the time of their first ovulation.7 Puberty in most of our domestic animals, especially those reared and fed under the most artificial conditions occurs much earlier than does sexual maturity or full or normal reproductive capacity. Most animals that nor- mally give birth to 2 or more young at a time are less fecund immediately after puberty than they are later.-1410 VETERINARY OBSTETRICS Yearling ewes usually have only one lamb. Primiparous gilts usually have smaller litters than 2- to 4-year-old sows. Fertility denotes the ability to produce young, while fecundity denotes the number of young produced. Fer- tility is reached at puberty but fecundity increases with age to maturity and then later in life decreases. Early fertility and high initial fecundity usually indicates that an animal will have a good reproductive record in the future. Because of environmental influences, frequently es- trum occurs at such an early age that if conception oc- curred parturition would be disastrous due to the small size and lack of development of the dam. Young female animals should not be bred until their body development ensures a normal gestation and parturition. Heifers should probably be bred according to size and weight rather than by their age. Puberty is more closely related to weight than age in domestic animals, except swine. Dairy cattle usually reach puberty when their body weight is 30 to 40 percent of adult weight, beef cattle 45 to 55 percent and sheep 40 to 60 percent of adult weight.- Small breeds reach puberty earlier than large breeds.5 It has been rec- ommended that Holstein and Brown Swiss heifers not be bred until they weigh about 750 lbs., Ayrshires about 650 lbs., Guernseys about 550 lbs., and Jerseys about 500 lbs.9 Heifers may reach this size from 10 to 24 months of age depending upon feeding levels and management practices. Rapid pubertal growth in Holstein heifers started during the seventh month after birth. By the tenth month this rapid growth of the genital tract terminated and sub- sequent growth was much slower.3 By proper feeding and management it may be possible by early breeding of heifers at 10 to 15 months of age and mares at 2 years of age to produce one additional calf or foal per female. At the onset of puberty the gonadotropic hormone lev- els rise due to an increase in amplitude and frequency of periodic pulses or releases from the anterior pituitary gland. This rise is followed by gradual increases in lev- els of the gonadal steroids, estrogens and testosterone. Antral follicles must have formed to get this latter re- sponse in the female. Ovulation requires a high level of estrogen to cause an LH or gonadotropic surge.- In the cow and ewe and possibly the mare, a “silent” estrus and ovulation may precede the first observed estrus. Some workers believe a small amount of progesterone from a regressing corpus luteum is necessary along with the estrogen from a mature follicle to produce psychic estrus.- Based on rectal palpation and careful observa- tion of 37 peripuberal heifers,8 signs of behavioral and physiological estrus without standing for mounting and without ovulation were observed 38 times before the first standing estrus. The cycles were all the same approxi- mate duration, 20 days, despite the following condi- tions. Of the 245 cycles studied 7 percent had a silent estrus, 25 percent had a nonstanding estrus and 68 per- cent had a standing estrus. Anovulation occurred in 14 percent of the cycles, cystic follicles in 11 percent, cys- tic corpora lutea in 14 percent and normal corpora lutea in 61 percent of the cycles. Anovulation was associated with the signs of first estrus in nearly 50 percent of the heifers and then declined rapidly at subsequent cycles. Some anovulatory follicles progressed to cystic follicles. A normal corpus luteum was detected at the first estrus in 35 percent of the heifers and increased in subsequent cycles. Thus anovulation may be responsible for failure of conception. Control of puberty in animals is presently largely lim- ited to nutritional and environmental factors. Other lesser factors might include control of the photoperiod in sea- sonal breeders, heterosis or breed selection and social- sexual interactions between males and pubertal females. The hastening of the onset of puberty in gilts and pos- sibly heifers by the presence of males is largely condi- tioned by the male sexual odor or pheromone present in the urine and by stimulation of the hypothalamic-pitui- tary axis.5ab The use of sex steroids and gonadotropic hormones to hasten the onset of puberty have not as yet proven to be practical or successful.2'5 The onset of puberty in the domestic animals is as follows: Horses—10 to 24 months, average 18 months of age, depending on the breeding season. Cattle—6 to 18 months. Heifers in rare instances may come in estrum as early as 3-4 months of age, or if kept in a cold environment on a low level of nutrition, the first estrum may not occur until 24 months of age. In Brahman heifers puberty occurs at 19 to 27 months of age.15 Sheep—6 to 12 months, usually in the fall but de- pending on the breeding season. Swine—5 to 8 months, average 6 months. Dogs—6 to 12 months, average 7 to 10 months. Cats—6 to 16 months, average 11 to 12 months, de- pending on the breeding season.2 Since puberty occurs before conception, normal ges- tation and parturition can take place, most well-grown dairy heifers are not bred until they are 14 to 18 months of age. Beef and poorly-grown dairy heifers may be bred from 18 to 24 months of age. Fillies should not be bred until 2, or preferably 3, years of age. Gilts, unless well grown, should not be bred before they are 8 to 9 months of age. Ewe lambs under 12 months of age should not be bred. It is generally considered undesirable to breed bitches on their first estrum or bitches or queens beforePHYSIOLOGY OF FEMALE REPRODUCTION 411 they are a year old. Following breeding of the pubertal animal, the nutritive level during the first gestation should be adequate to continue normal growth and development so by the time of parturition complications such as dys- tocia do not occur. The Estrous Cycle In all species of domestic animals that have reached puberty there is a definite physiologic functional rhythm of the reproductive system, called the estrous cycle. Al- though each species has its own peculiarities regarding their estrous cycle pattern, basically all are similar. The estrous cycle lasts 16 to 17 days in the ewe, 20 to 21 days in the cow, doe and sow and 21 to 23 days in the mare.- The estrous cycle is commonly divided into 4 phases or periods that blend one into the other. Some authors prefer to divide the estrous cycle into two pe- riods the estrogenic or follicular phase comprising proestrum and estrum and the progestational or luteal phase comprising metestrum and diestrum. Proestrum is an ill-defined period during which the Graafian follicle is growing under the influence of FSH and producing increasing amounts of estradiol. There are increases in the growth of cells and cilia lining the ovi- duct, in the vascularity of the uterine mucosa, and in the thickness, edema and vascularity of the vaginal epithe- lium, with comification occurring in some species, such as the bitch and queen. In the bitch, the increased en- dometrial vascularity is characterized by bleeding. In the bitch and sow the vulva becomes definitely edematous and swollen. There is a gradual relaxation of the cervix and an increased secretion of viscid, slimy mucus from Figure 104. Normal Genital Tract of a Heifer in Estrum—Note ma- turing follicle in the right ovary and regressing C. L. in the left ovary. (Courtesy K. McEntee.) the goblet cells of the cervix and anterior vagina and from the uterine glands. In the cow and mare, the sticky, dry mucus of the preceeding period changes during proestrum to a milky, viscid mucus, and finally to a clear, transparent, stringy mucus late in the proestrous period. There is an increased excretion of estrogen in the urine and a beginning decrease of progesterone in the blood.- The corpus luteum is undergoing rapid vacuolization, degeneration, and decrease in size in the mare, cow, ewe, doe and sow. The marked increase in growth of the ep- ithelial tissues, of the activity of the musculature of the reproductive tract, of the secretion of mucus, and of the vascularity of the endometrium and vaginal mucosa is spoken of as the building-up period. It is produced by the secretion of increasing amounts of estradiol. Late in this phase of the cycle the female animal usually exhibits interest in the male. Estrum is the fairly well-defined period characterized by sexual desire, immobility in the presence of, and the acceptance of the male by the female domestic animal. (See Figures 103 and 104.) This period begins with the time of the first acceptance and ends with the last ac- ceptance of the male. During this period the female will usually seek out and accept the male. The Graafian fol- licle is large and mature. The ovum undergoes certain maturational changes. Estradiol from the maturing Graafian follicle produces changes in the tubular genital tract that reach their culmination in this period. The uter- ine tubes are tonic, the epithelium mature, and the cilia are active; contraction of the uterine tubes is occurring; and the fimbriated end of the uterine tube is assuming a close affinity to the Graafian follicle. Increased amounts412 VETERINARY OBSTETRICS of tubal fluid is being secreted. The uterus is erect, tur- gid, and some species, edematous. The blood supply to the uterus is increased; the mucosa is growing rapidly, and mucus is secreted. The vaginal and cervical mucus is greatly increased. The mucosa is pink and congested, due to the increased vascularity. The cervix is relaxed and slightly edematous. The mucosa of the vagina is greatly thickened with many comified epithelial cells being desquamated in certain species, such as the bitch and queen. The vulva is relaxed and edematous in all spe- cies, but most noticeably in the bitch and sow. Strings of mucus may hang from the vulva and tail of the cow. Toward the end of this period there may be an increase in leucocytes migrating into the uterine lumen. In do- mestic animals the elevation of estrogen to a peak in the absence of progesterone triggers the release of luteiniz- ing hormone, the LH surge, near the onset of estrus that causes ovulation a day or so later.--- In most species the rupture of the mature ovisac or ovulation occurs to- ward the end of this period of estrum. In the cow and ewe ovulation occurs about 24 to 30 hours after the onset of estrus, 35 to 45 hours in sows, 4 to 6 days in mares,- 24 to 48 hours in bitches and 24 to 30 hours after coitus in the queen. In certain species that do not ovulate spon- taneously, such as the cat, rabbit, and ferret, ovulation does not occur until coitus and/or mounting takes place; hence in the queen estrum may be prolonged 7 to 10 days in the absence of a male. The acceptance of the male during estrum is due to the influence of estradiol on the central nervous system, producing the character- istic behavior patterns of receptivity in the various fe- male animals. Female as well as male sexual behavior patterns are not sex-specific and that under certain con- ditions each exhibits the behavior patterns of the other.13 Metestrum or postestrum is a poorly defined period following estrum during which the corpus luteum grows rapidly from the granulosa cells of the ruptured follicle under the influence of the luteinizing hormone (LH) of the anterior pituitary. Metestrum is largely under the in- fluence of progesterone produced by the corpus luteum. The presence of this hormone, by inhibiting the secretion of FSH by the pituitary gland, prevents the development of more Graafian follicles and the immediate develop- ment of another estrum. During metestrum in some spe- cies the epithelium of the vagina loses most of its new growth through desquamation. In the cow, during the early part of metestrum the epithelium over the caruncles of the uterus is very hyperemic and some capillary hem- orrhage occurs. This is called postestrual or metestrual bleeding or “menstruation.” This is not similar to true menstruation in primates which occurs at the time of pro- gesterone withdrawal and is associated with a loss of the superficial layers of the endometrium. In cattle postes- trual bleeding is associated with estrogen withdrawal. The mucous secretion decreases and the glands of the en- dometrium grow rapidly. Toward the middle to the end of metestrum the uterus becomes rather soft and pliable, due to a relaxation of the uterine muscle. In bitches and queens this stage includes the pseudopregnant period. In the species having diestrual cycles, including the cow, ewe, doe, sow and mare, the length of metestrum is about equal to the time it takes for the ova to reach the uterus or about 3 to 6 days. In the bitch and queen the pseu- dopregnant period may last about 50 to 60 days and 30 to 40 days, respectively, after which the corpora lutea regress and an anestrum of varying length occurs. In the queen that is not bred ovulation and corpus luteum de- velopment doesn’t occur and the follicles become atretic. Several cycles of this sort may occur in the cat before a period of anestrum sets in. Bitches and queens do not have diestrual periods. Diestrum is the longest phase or period of the estrous cycle in domestic animals including the cow, ewe, doe, sow and mare. The corpus luteum is mature and the ef- fects of progesterone on the reproductive tract are marked. The endometrium becomes thicker and the glands hy- pertrophy. The cervix is constricted and the vaginal mu- cus is scant and sticky. The mucous membrane of the vagina is pale. The uterine muscle is relaxed. Late in this period the corpus luteum begins to show retrogres- sive changes and gradual vacuolization. The endome- trium and its glands atrophy or regress in size. Beginning development of the primary and secondary follicles and finally proestrum occurs. In certain species that are not polyestrous, anestrum may occur. Anestrum, when referred to in connection with the physiologic estrous cycle, is usually characterized by quiescent, functionless ovaries and reproductive tract. Anestrum is eventually followed by proestrum. Anes- trum is observed physiologically in most mares during the winter months and in the ewe during the late spring and summer months. In the bitch and queen a physio- logic anestrous period lasting several months may occur two or three times a year. The term anestrum is used, therefore, to differentiate it from diestrum, which lasts only a week or so and is characterized in the cow, sow, and other polyestrous animals by a mature corpus lu- teum. During anestrum in the mare the uterus is small and flaccid. The cervix is usually slight to very relaxed and the vaginal mucus is scanty and sticky. The vaginal mucosa is pale and the cervix is pale. Some follicular activity of the ovaries may develop but a mature follicle and ovulation seldom occur during the anestrous period. The relative lengths of these various periods of the estrous cycle in domestic animals are approximately as follows:--PHYSIOLOGY OF FEMALE REPRODUCTION 413 Estrum Metestrum Cow 12 to 24 hours 3 to 5 days Mare 4 to 7 days 3 to 6 days Sow 2 to 4 days 3 to 4 days Ewe 1 to 2 days 3 to 5 days Bitch 9 days (4-12) Queen 8 days without coitus2 5 days with coitus3 Diestrum Proestrum Cow 13 days 3 days Mare 6 to 10 days 3 days Sow 9 to 13 days 3 days Ewe 7 to 10 days 2 days Bitch 75 days (51-82)1 9 days (3-16) Queen 2 days(1-3) ‘Anestrum—125 days (15-265) follows pseudopreg- nancy. 2Days to next estrus—14 to 21. 3Days to next estrus—42 (30-75). (See also the Reproductive Tables at the end of this Chapter.) Animals may be divided into three classes according to their estrous cycles. Monestrous animals are those animals having one estrous cycle per year. These are usually wild animals. Polyestrous animals are the do- mestic animals such as the cow, sow, and mare that have frequent periodic estrous cycles throughout the year. During the late fall and winter months the mare, espe- cially the pony mare,- usually has an anestrous period without estrous cycles. Seasonal polyestrous animals are those, like the ewe, that have periodic estrous cycles during only certain seasons of the year. The bitch and queen are more nearly like the monestrous animals. The bitch may have 2 to 3 periods of estrus each year. Three estrous periods per year are not uncommon in small breeds of dogs. The queen may have several heat periods in succession if coitus does not occur. These recurring ep- isodes may occur two or three times a year. This arbi- trary classification of animals as monestrous, polyes- trous, and seasonally polyestrous must not be taken as entirely accurate and precise. Excellent nutrition and environment may cause bitches to show estrum at any month in the year, and more fre- quently than once or twice a year. In mares, these factors may result in successful service during any month in the year. In ewes, recent work reveals a probable subclinical abortive estrual cycle present in most ewes during anes- trum, especially the latter part of this phase. Certain breeds of sheep such as the Dorset and Merino regularly have two seasonal polyestrous periods in both the spring and fall. The fall season is more fertile than the spring and summer, and a greater percentage of ewes are cy- cling.3,21 Thus the present classification may be more a clinical than an actual classification. In swine and bitches and in most queens much of the lactation period is usu- ally characterized by a lack of estrum, termed lacta- tional anestrum.” This postpartum, “anestrous” period is prolonged in cows nursing calves.-’25 Factors Affecting the Reproductive or Estrous Cycle Factors influencing the onset of estrous cycles of do- mestic animals are many and varied and irregularities, especially in the length of the cycle, are frequently ob- served by veterinarians and farmers. These abnormal es- trous cycles may commonly be a cause of infertility. The failure of mares to have normal estrous cycles was one of the most important causes of infertility in that spe- cies.8 Some of these irregular estrous cycles are due to definite and known causes while others still remain to be completely explained. The causes of irregular estrous cycles include: Nutritive state—Any severe degree of inanition or starvation caused by a lack of TDN or energy or any nutritive deficiencies, especially those causing a loss of appetite such as phosphorus, cobalt, possibly iron, cop- per, iodine, protein and others, may impair or prevent the secretion of gonadotropic hormones by the pituitary gland and result in a failure of the estrous cycle. In cows anestrus, possibly due to the above deficiencies, may be associated with a low P.C.V. or hemoglobin below 9 mg/100 ml. of blood. In humans it is well known that starvation causes a cessation of the estrous cycle and amenorrhea before other body disturbances appear. In rats a 15 percent loss of body weight may stop the es- trous cycle. In a nutrition experiment at Cornell, in which sodium chloride was withheld from cows for long pe- riods, the animals became very thin and cachetic and estrous cycles ceased. Seasonal Influences and Light: Most animals in the natural or wild state are usually seasonal breeders and parturition generally occurs in the spring and summer when the weather is most favorable for the young and when food is most abundant for the dam. Although do- mestication has altered this pattern in some animals, the natural tendency remains. The horse and fur-bearing animals tend to come into estrum and breed during the spring months under the in- fluence of increasing daylight. Even in the cow, which is polyestrous, the best breeding months in the northern414 VETERINARY OBSTETRICS hemisphere are May, June, and July and the poorest De- cember, January, and February.18 The reverse condition is seen in ewes and does in the northern hemisphere; most breeds come into estrum under the influence of de- creasing daylight and are fall breeders. This seasonal breeding trait is regulated by the effect of light, through the medium of the eyes, possibly the pineal body, the hypothalamus and the anterior pituitary gland.--•2-5-21 The effect on the animal of the total daily amount of light is important in controlling the onset of the estrous cycle and breeding season of mammals. This is called sexual photoperiodicity. A recent report on light and its effect on the gonadotropic hormones in seasonal breeders shows that the length of the daylight period necessary for sexual stimulation does not require that light must stimulate the nervous system the whole light period. Light is most ef- ficient at only a precise period of the 24 hour daylight through dark cycle. This sensitive period varies in the different species but apparently occurs 10 to 20 hours after dawn and requires a specific period of one to sev- eral hours of light.- Further study of this phenomena is indicated for sheep, horses and possibly cats. Animals taken from one hemisphere to the other change their breeding seasons in accordance with the amount of daylight. Ewes and does confined experimentally in a darkened shed for increasing periods of time during the summer months developed estrous cycles earlier than normal. The length of estrum decreased and the length of diestrum increased in horses toward the summer months, or the end of the breeding season.8 Gradually increasing the total daily hours of light up to 16 hours per day by artificial means will hasten the onset of es- trous cycles by 40 to 60 days in mares in the spring of the year (See Chapter XIV, Infertility in the Mare). Pos- sibly this amount of continuous light may not be nec- essary. At the beginning or end of the breeding season, cycle lengths in ewes were more often longer or shorter than the average of 14 to 19 days.26 Similarly in mares abnormalities of the estrous cycle are seen most com- monly early in the spring during the transitional period and late in the breeding season with excessive estrous signs frequently observed early in the season. In the sea- sonal breeders that respond to increasing or decreasing daylight there is a refractory period that occurs at the end of the breeding season.21 Temperature—the influence of environmental tem- perature has less direct effect than has the amount of light on reproduction in animals. It has been hypothe- sized that excessive heat during the summer months, causing decreased thyroid activity, may indirectly reduce reproductive efficiency in swine, possibly cattle and sheep. This has also been shown to be caused by the effect of heat on the very early developing embryo. In the bull and ram “summer sterility” is due largely to the adverse effect of prolonged atmospheric heat on spermatogene- sis. Excessive exposure to cold, together with a reduced feed intake during the winter months, may cause failure of the estrous cycle in young growing animals or animals on a borderline of nutritive intake, since this intake must largely be used to maintain the animals’ body tempera- ture and necessary activities. By using a temperature- controlled room kept at a temperature of 45-48° F the onset of the estrous cycle in ewes was stimulated so they came into estrum 20 to 50 days earlier than control ewes subjected to the same amount of light but kept in sum- mer atmospheric temperatures.10 This was also effective in improving or maintaining the fertility of rams. Estrous periods in dairy cattle in the northern half of the U.S. A. are about 18 hours long,15 while in the Gulf States they are shorter, about 12 hours.12 It was also noted that the length of the estrous cycle in cattle under hot conditions increased to 25 days as compared to 20 to 21 day cycles in cooler weather.11 Age—In cattle and swine, the young female usually has a slightly shorter length of estrum and estrous cycle than has the adult animal. The ewe lamb will not show estrum until the fall hence the sexual cycles in this spe- cies depend more upon the season than upon the pubertal age of the young female. Senility accompanied by de- fective teeth and marked weight loss, often results in a cessation of the estrous cycle or anestrum. Old age itself is relatively seldom a cause for reproductive failure. Se- nile changes, such as the menopause in women, seldom occur in animals. Whereas cessation of reproduction in women is associated with a particular age at which the oocytes in the ovaries are largely depleted, this appar- ently is uncommon in animals. Character of work—Horses that are worked or raced hard frequently do not develop regular estrous cycles un- til the severe work schedule is stopped and they are rested, preferably on pasture for several months. Cows that are very heavy producers of milk may not have estrous cycles for 3 to 4 months or more following parturition due to a negative energy balance. Thus, heavy continuous work is a stress that can result in anestrus. Transportation stress in ewes6 and in gilts9 induced follicular growth and ovulation in a large number of an- imals within 4 to 6 days. This phenomena was not re- produced with ACTH injections but severe stress did cause cystic corpora lutea in the ewes. Estrus signs failed to occur in some ewes due to the absence of a regressing corpus luteum with the presence of some progesterone. The author has observed a similar reaction in some trans- ported mares and cows.PHYSIOLOGY OF FEMALE REPRODUCTION 415 Systemic diseases—Severe chronic wasting diseases, such as Johne’s disease, tuberculosis, mange, actino- mycosis of the jaw, severe parasitisms, and other dis- eases cause a severe negative energy balance, debility, emaciation and cessation of the estrous cycle. Pathology of the uterus or cervix is a frequent cause for irregularities of the estrous cycle. In cattle such con- ditions as pyometra, fetal maceration, mummification of the fetus, and rarely mucometra may cause failure of es- trum, and a persistence of the corpus luteum, with a ces- sation of estrual cycles. A similar effect may be pro- duced experimentally by hysterectomies in cows, swine, does and ewes.27 Early death of the embryo within 20 to 60 days after conception may cause symptoms of ap- parent failure of the estrual cycle. Endocrine disturbances often affect the estrous cycle. Cystic ovaries in cattle are frequently a cause for ces- sation of the estrous cycle. Nymphomania or cystic ova- ries in animals are also characterized by irregularities in the estrous cycle and by frequent or continuous estrum. Following calving, ovulations are often associated with a “silent” estrum. This is also observed in ewes and does at the outset of the breeding season and in heifers reach- ing puberty. It is believed that some of these “silent” estrums are due to an imbalance of estrogens and pro- gesterone with the latter often lacking.17b Short estrous cycles in the cow, long or irregular periods of estrum or lack of estrum, or long diestrous periods in the mare-'-’8 are probably of endocrine origin, but the causes for these abnormal long estrous cycles are not fully understood. A long estrous cycle of 25 days was produced in cows infused with an iodine solution on day 15 of the cycle.22,23 This was probably due to a lack of prostaglandin caused by damage to the endometrium. Short estrous cycles of 8 to 14 days in cattle have been produced experimentally by infusing the uterus with bacterial contaminants or viral agents such as IBR-IPV at the time of service, infusing the uterus with irritating iodine compounds about the third to sixth day after estrus, injecting large doses of oxytocin from day 2 to day 7 of the cycle, or surgically implanting a foreign object into the horn corresponding to the ovary containing the corpus luteum about the second or third day of the cycle. It is believed that these treatments af- fect the luteolytic mechanism especially by their stim- ulation of the production of prostaglandin by the uterine endometrium and possibly by inhibiting the release of L.H. and failure to grow and maintain the corpus lu- teum.15’19,22’23 Large doses of L.H. given during the mid- dle and last week of the estrous cycle may prolong the corpus luteum and the cycle (See Chapter XIII, Infertil- ity in Cattle). In rare cases pituitary, ovarian, and adre- nal tumors and their production or inhibition of secretion of certain hormones may cause marked changes in the estrous cycle. Miscellaneous causes for irregularities in the estrous cycle include the individual variations between animals in each species. The individual variations are usually mi- nor. However, Brahman and Zebu cattle may have very short estrous periods of only 3 to 6 hours. Copulation usually occurs at night. Pregnancy causes a prompt physiologic cessation of the estrous cycles. The presence of the ram, stallion, buck or boar hastens the onset of estrum when the male is placed with the females late in the anestrous season. This stimulating effect on the re- lease of gonadotropic hormone is probably mediated by visual, auditory and olfactory stimuli to the hypothala- mus.--4’7 Thus it can be seen that although the reproductive cycles of domestic animals are primarily under endocrine con- trol they are greatly influenced by the external environ- ment which acts through the central nervous system and the hypothalmus to initiate and regulate the release of tropic hormones from the adenohypophysis.-’- --’1’20 Coition or Copulation Coitus or the act of copulation, includes the insertion of the erect penis into the vagina, intromission, and the subsequent ejaculation of semen. This takes place only during estrum in the domestic animals. An exception to this occurs in certain barren mares early in the breeding season that exhibit a prolonged period of acceptance punctuated occasionally by true estrum and ovulation. During coitus semen is ejaculated into the vagina and onto the external os of the cervix in the cow, ewe, doe and woman. In the sow most of the semen usually is ejaculated into the uterus since the long narrow penis of the boar enters and “locks” into the cervix.6b During co- itus in the bitch, vaginal and uterine contraction waves aid the intrauterine deposition of semen.3 In the mare the penis may be forced against the relaxed dilated cervix and some semen might be ejaculated into the cervix or uterus. At the time of coitus in the mare there is a neg- ative uterine pressure capable of drawing about 80 ml. of fluid into the uterus through the relaxed cervix.5 This negative uterine pressure is observed clinically when ex- amining infected, “windsucking” mares especially at the time of estrum. The insertion of the speculum causes a sudden ballooning of the vagina and sometimes the uterus. Bubbles of mucopurulent material may be seen being drawn into the cervix. At the time of intromission the mare can be observed to take a deep inspiration and draw up her abdomen to produce this negative pressure. Usu-416 VETERINARY OBSTETRICS ally after an equine service at which time 50 to 100 ml. or more of semen is ejaculated, only 10 or 15 ml. can be recovered from the vagina. This fact is of importance in explaining the cause for infertility in “windsucking” infected mares.5 Examining the vagina with a speculum just before service is not advised as this act causes bal- looning of the genital tract and prevents the negative pressure normally produced at coitus by the penis sealing the vulva, from drawing the semen into the uterus. More work is necessary on this interesting observation. In the ram the processus urethrae does not enter the external os of the cervix of the ewe during coitus but is responsible for forcibly spraying semen over the cervix and cranial portion of the vagina.4 The duration of coitus in cattle and sheep is only a few seconds. In horses copulation is longer, lasting 10 to 30 seconds. In swine copulation takes 3 to 8 minutes with an average of about 5 to 7 minutes. In the dog co- itus takes 15 to 30 minutes; the bulbus glandis enlarges slowly, until it is large enough to dilate the caudal por- tion of the vagina. The sphincter muscles of the vestibule and vulva then contract and the male is unable to with- draw the penis until the bulbus glandis is reduced in size. The male dog usually dismounts and faces away from the bitch during the latter part of copulation.- In the cat coitus lasts 2 to 5 minutes. (See Chapter XVIII, Infer- tility in Male Animals.) It is rather interesting that the structure of the penis is somewhat related to the duration of foreplay and co- itus.-’2 In ruminants with a fibroelastic type of penis with small vascular sinuses, foreplay and coitus are very brief and the amount of semen ejaculated is small. In animals such as dogs, horses and primates the penis is charac- terized by extensive vascular sinuses and foreplay and coitus are of moderate to long duration. The exception to this observation is the boar that has a fibroelastic type of penis. The large amount of semen ejaculated in the boar may be a factor causing the prolonged period of coitus in this species. The dog and stallion also have fairly long copulatory periods and they also ejaculate rel- atively large quantities of semen. The dangers of coitus to the female animal include the possibility of young, small heifers and fillies or even older females being injured by large or overweight males. These injuries may include fracture of the pelvis, spine, or limbs; dislocation of the hips; muscle or tendon sprains; or injuries to the limbs, udder, or teats. These injuries may be avoided by using smaller males, a breeding rack, or artificial insemination. In both the mare and cow the vagina is shorter than the length of the male’s penis, but at the time of coitus the vagina stretches. In spite of this, occasional lacerations and trauma may be produced and cause swelling, hemorrhage, discharge, and straining following coitus. In rare instances the penis of a bull or stallion may actually rupture the vagina of the female and cause a perivaginal inflammation or abscess with signs resembling acute traumatic reticulitis. Fatal peritonitis may rarely be observed especially when heifers are bred on pasture by a mature bull or large vigorous stallions are bred to small mares. Vaginal and hymenal lacera- tions with bleeding after service by a stallion occur more commonly during the peak of the breeding season be- cause more mares are bred; the stallions are more ex- perienced and require greater stimulation for ejaculation because of frequent services so thrust deeper with more vigor. Occasional cases of vaginal rupture and penetration of the peritoneal cavity in the heifer and mare may not re- sult in death, especially if the damage is diagnosed promptly. Treatment consists of stopping further ser- vices for a month or more and providing stall rest and tranquilization if signs of colic or discomfort is present. The mare should be given antibiotics and tetanus anti- toxin. If signs of shock develop, cortisone and possibly intravenous fluids should be administered. If the mare has pneumovagina the vulva should be promptly su- tured.68 When large stallions are bred to small mares, or when a vigorous stallion with a large penis is bred to average- sized mares, a stallion roll, or if this is not available a double roll of cotton, may be placed against the stal- lion’s abdomen in front of the sheath to prevent too-deep penetration of the penis. In mares with a small vulva it may be necessary to lubricate the vulva to facilitate in- sertion of the penis. Vaseline or the ordinary water-sol- uble, neutral, tragacanth gum lubricating jellies are sat- isfactory. These lubricants should not contain antiseptics. Occasionally feces and other dirt particles are introduced into the vulva and vagina at the time of service and cause irritation and infection. In a mare with a tipped or horizontal vulva, occa- sionally the erect penis of the stallion may slide over the vulva and enter the rectum, causing a rupture of the rec- tal mucosa or the rectal wall. This is called “false entry” and may produce a rapidly fatal peritonitis or a pelvic diverticulum that fills with feces and causes severe straining. This is favored in mares with a vulva that has been sutured by the Caslick technique and not opened sufficiently prior to service. A rectal examination im- mediately prior to service should not be performed as it stretches the sphincter muscles of the anus of the mare permitting the penis to readily enter the rectum. False entry may also occur in the sow, ewe, doe and cow but apparently it causes little harm in these species. In thePHYSIOLOGY OF FEMALE REPRODUCTION 417 mare if the diverticulum is in the pelvic region caudal to the peritoneum, gentle, regular enemas of physiologic saline or antiseptic solution should be given to keep the diverticulum free of feces until healing takes place. An- tibiotics and tetanus antitoxin parenterally are indicated. False entry can be prevented by proper handling of the stallion at the time of service to make certain by manual direction, that the penis enters the vulva. Occasionally the withers of the mare may be lacerated by the teeth of a stallion or jack at the time of coitus. This can be prevented by muzzling the stallion or by placing a heavy pad over the withers of the mare. Many horsemen believe the stallion has given a “poor service” when he dismounts and the penis on being withdrawn brings with it an ounce or more of semen. Holding the stallion on the mare a little longer allows the size of the glans penis to be reduced and less semen withdrawn. This condition would be more likely to occur if the gen- ital tract was ballooned with air before service, so that the semen was not drawn into the uterus but remained in the vagina. There is no proof that these occasional so- called “poor services” fail to result in conception. Rarely a mare or cow may have a stenosis of the va- gina due to a previous injury or to a hereditary defect of the vulva or vagina, such as “white heifer disease” with an imperforate hymen. In these animals coitus usually results in vaginal or vulvar lacerations and straining. The author has observed two gilts and a sow that died a few days to a week after natural service with severe peritoni- tis caused by the boar’s penis entering the urethra and bladder and passing into a ureter where it caused a rup- ture about 2 to 3 inches cranial to the bladder. All of these females had cystitis with signs of straining, bloody urine, a swollen vulva, depression and anorexia shortly after an apparent normal copulation. The author has ob- served and others2b reported cystitis and pyelonephritis in a heifer and a gilt following AI when the semen had been introduced into the bladder. The heifer had a seg- mental aplasia of the vagina. Sodomy or carnal intercourse between man and the lower animals is of little importance to the veterinarian, since ordinarily this does not result in injury or disease to the larger animals. In small female animals such per- version may result in injury to the animal’s genital canal. Sadism or sexual perversion in some humans, usually male, may cause them to injure or mutilate, with sharp or solid objects such as broom handles and pointed sticks, the genital organs of animals especially the vagina or rectum of female animals such as mares, cows, goats or sows. Whenever the veterinarian is confronted with a case of injury to the genital organs or rectum of an an- imal he should attempt to determine the cause, keeping this possibility in mind, especially if several similar in- juries are diagnosed. These injuries are most often per- petrated when the animal is in estrum. Injuries of this type are rarely produced by coitus or by accident but must be caused by some person, usually of low or ab- normal mentality, who has access to the animals when no one else is present.7 Ovogenesis or Oogenesis The ovary, besides secreting the necessary gonadal hormones, produces ova. Oocytes are developed simi- larly in all domestic animals.-’--- Early in the first weeks of embryonal development the primitive large germ cells called primordial germ cells can be identified in the cau- dal extraembryonal entoblast or yolk sac.9 These pri- mordial germ cells migrate by ameboid movement from the yolk sac across the dorsal mesentery to the genital ridges.1,2 This migration occurs in porcine and bovine embryos about 24 and 35 days of gestation, respec- tively.4 In a few more days the gonadal sex can be dis- tinguished by the formation of the superficial tunica al- buginea and the central location of the germinal cells, spermatogonia, in the primitive testes and the peripheral location of the oogonia in the primitive ovary.9 These oogonia multiply by mitosis after sexual differentiation and enter the prophase of the first meiotic divisions when they are called oocytes. The number of oocytes produced may be determined by the level or amount of FSH in the embryo.9 Oogenesis is the transformation of oogonia into oocytes. Oogenesis is completed before or shortly after birth in all domestic mammals.-’10,14 Sexual differentia- tion occurs at 30 days of gestation in the feline and por- cine embryos, 35 days in the ovine embryo and 45 days in the bovine embryo.9 The period of oogonial mitoses, the end of which signifies the end of the major portion of the period of oogenesis, are 32 days of gestation to 37 days after birth in cats, 30 days of gestation to 7 days after birth in swine, 35 to 90 days of gestation in sheep and 45 to 110 days of gestation in cattle. At the end of this period of oogenesis the oocytes enter the first meiotic prophase where they pass through the leptotene and zy- gotene stage into the pachytene stage. In this stage the ova are surrounded by a single layer of follicular epi- thelium and these are called primordial follicles. Thus at birth all female calves and lambs are bom with their full complement of oocytes in primordial or older follicles and these are never replenished but only de- crease in number during the life of the animal. Bovine oocytes may rest in this pachytene phase for years if the primordial follicle does not grow.6 In most species this418 VETERINARY OBSTETRICS resting stage where the oocyte is in the primordial fol- licle is the dictyate stage.7’8’9,10 In the late dictyate stage as ovulation time approaches, follicle growth and maturation occur. The ovum itself will grow and triple in size in order to provide nutrition for early divisions of the fertilized ovum (See Table 16). Three types of follicles present at birth and throughout the life of animals are,-'4 primordial follicles in which the oocyte is surrounded by a single layer of follicle cells, growing follicles in which the oocyte is surrounded by two or more layers of follicle cells, and vesicular folli- cles having antrums or fully-formed vesicles. The num- bers of germ cells or oocytes in the ovaries of individual cattle is highly variable ranging from 0 (complete ste- rility) to 700,000. Of 69 cattle examined from birth to two years of age about 25 percent had 42,000 (0 to 73,000) germ cells, about 60 percent had 137,000 (76,000 to 218,000) germ cells, and about 15 percent of the cattle had 325,000 (223,000 to 724,000) germ cells.3'4 The numbers of primordial follicles in cattle remained fairly stable around 140,000 until about 4 to 6 years of age and then declined rapidly thereafter to 25,000 at 10 to 14 years and to near zero at 20 years of age. From 60 days after birth to 10 to 14 years of age the numbers of growing follicles per bovine animal averaged about 150 to 250 and the number of vesicular follicles 25 to 30. In cows over 15 years of age these numbers declined to 70 and 12, respectively. Normal vesicular follicles predom- inated up to 10 years of age in cows but after that time atretic vesicular follicles were in greater numbers. Two Table 16. Developmental States in the Maturation of the Ovum* Chromosome Number Time Period 2N Primordial germ cells Migrate to gonodal area in bovine embryo from 25-35 days of gestation Mitosis Oogonia Multiplication occurs in bovine embryo from 45-110+ days of gestation Oogonia A Oogonia A (resting) Oogonia B Oocytes, primary Meiosis Prophase I (1st maturation division) Leptotene stage Zygotene stage 4N Pachytene stage—bovine species Diplotene stage—porcine species Resting stage Birth to Old age Dictyate stage—other species Primordial follicle Growing follicle (Diakinesis) Vesicular follicle Metaphase I Anaphase I Graafian follicle Estrum Telaphase I (mature) 2N Oocytes, secondary—Ova 1st polar body extruded** Prophase II (2nd maturation division) Ovulation Metaphase II Ova into Anaphase II Telaphasell 2nd polar body extruded oviducts IN Union of male and female pronuclei within ovum*** Ova transport to uterus 2N Zygote Atresia of nonovulating follicles *After Rajakoski, Henricson and Rajakoski, Kennelly and Foote, Erickson (1965) and Mauleon. **In bitches and probably mares the 1st polar body is released after ovulation and the 2nd polar body is usually not released unless fertilization occurs. This is probably why the canine ova remain in the oviduct 5 or more days. ***The male and female pronuclei in the rabbit duplicate chromosomes before syngamy thus the fertilized ovum is tetraploid for a very short period until the two-cell stage occurs.13PHYSIOLOGY OF FEMALE REPRODUCTION 419 20-year-old cows that had produced 16 and 17 calves, respectively, were considered to be sterile at slaughter with one cow being anestrous and the other showing ir- regular cycles. The numbers of primordial follicles in these two cows were 100 and 2000, growing follicles 80 and 50 and vesicular follicles 10 and 7. Thus these old cows were approaching the menopausal state that occurs in women. Women had an ovarian oocyte population of 200,000 to 400,000. During the postmenopausal years a complete disappearance of oocytes occur.5 Since during the lifetime of a 10-year-old cow pro- ducing a calf each year about 30 to 50 ova might be ovulated it is obvious that most oocytes degenerate and die in a process called follicular atresia. Although de- generation of oocytes and follicular atresia may occur in the prenatal period in cattle, germ cell quality in pri- mordial follicles remains high until 6 to 8 months of age and then it declines rapidly thereafter until at 4 years of age and older most oocytes or primordial follicles are in an obvious degenerative state. The process of bovine fol- licular atresia and oocyte degeneration is a very pro- tracted process extending over a period of years.4 Oogo- nia and oocytes in the first stages of meiotic prophase disappear or degenerate during prenatal and early post- natal periods.-9 Only those oocytes in the pachytene through dictyate stages remain into later life. Further evidence was presented that following puberty the average bovine female has only approximately 240 oocytes in growing or vesicular follicles upon which she is dependent for the production of fertile ova throughout the rest of her life.4 Since the numbers of these growing or vesicular follicles was closely correlated with the total number of primordial follicles there may be a relation- ship between germ cell numbers and fertility in females. When the ovaries of fertile and infertile 5-year-old cows were compared, the average numbers of primordial, growing, and vesicular follicles present were 119,000 and 18,000; 78 and 35; and 211 and 54, respectively.4 In a study on genetic hypoplasia of the ovaries in Swed- ish Highland cattle normal yearling cattle had an average total of about 50,000 primordial follicles in both ovaries (range 6,000 to 100,000). Heifers with a unilateral par- tial hypoplasia and unilateral total hypoplasia had 23,000 and 19,000 primordial follicles, respectively, in both ovaries.11'12 Of 7 heifers with one ovary completely hy- poplastic and the other ovary partially hypoplastic, two heifers had no primordial follicles and five had 100 to 400. In heifers with bilateral total hypoplasia, no pri- mordial follicles were present. Animals with less than 500 primordial follicles did not ovulate. Animals with one hypoplastic ovary had definitely fewer Graafian fol- licles than normal heifers and were more infertile. In freemartin cattle the gonads have no germ cells. - Folliculogenesis and Ovulation Under the influence of the gonadotropic hormones FSH and LH, especially the former, vesicular or Graafian fol- licles grow and develop. This development occurs in fe- tal animals, young animals prior to puberty, and even during the pregnancy period. Follicular growth and de- velopment culminating in the mature Graafian or vesic- ular follicle and ovulation occurs only in nonpregnant animals after puberty during a reproductive cycle under the influence of the gonadotropic (FSH-LH) hormone. However horses frequently ovulate during early gesta- tion and diestrus and cows may very rarely do so. The exact mechanisms governing the follicles that mature and ovulate and those that fail to mature and ovulate but re- gress and become atretic are not understood. Without the Graafian follicle and the secretion of es- trogens and progesterone including some androgens from the granulosa and theca cells under the influence of FSH and LH, signs of estrum would be lacking, ova could not be released and corpora lutea could not form. Growth of the primordial follicles, those where the oocyte is sur- rounded by a single layer of epithelial cells gives rise to growing or secondary follicles and vesicular follicles or those with antrums called Graafian follicles. In Graafian follicles the oocyte has reached the dictyate stage of de- velopment in the cow.-’25 By this time the connective tissues around the growing follicle have organized into the theca which consists of an outer zone of stroma cells called the theca externa, and an inner zone of epithelial- like cells called the theca interna which later secretes steroid hormones including estrogens. As growth con- tinues, the antrum forms and enlarges in the epithelial cells around the ovum. The epithelial cells lining this antrum form the membrana granulosa. The fluid in the follicle is called the liquor folliculi. This fluid is believed to be secreted by the granulosa cells. The actively grow- ing Graafian follicle is responsible for its own ovulation by secreting estradiol that causes the LH surge that re- sults in ovulation and the development of the corpus lu- teum.-- In the early stages of the maturation of the ovisac, or follicle, the oocyte is in a mass of epithelial cells, called the discus proligerus, attached to the granulosa layer of cells. The egg and its adjoining granulosa cells are called the cumulus oophorus. Between the cumulus cells and the oocyte proper is the corona radiata, a compact layer420 VETERINARY OBSTETRICS of cells surrounding the zona pellucida, which extends cytoplasmic projections through the zona pellucida to the vitelline membrane to provide nutrients to the oocyte for its maintenance and growth.-'27 The cumulus may be lo- cated projecting into the follicular fluid anywhere on the circumference of the membrana granulosa.-25 As the fol- licle approaches maturation and ovulation, the cumulus oophorus either separates from the membrana granulosa and floats free in the follicular fluid or more often it is only tenuously attached. The ascent of the follicles to the surface of the ovary coincides with the appearance of the thecal layers. The theca interna develops a wedge- like cone that precedes the follicle through the ovarian stroma to the surface. In all species of domestic animal, except the mare, ovulation can occur over the entire ovarian surface. In the mare ovulation occurs only in the ovulation fossa or concave ventral medial portion of the ovary that is not covered by a dense tunica albuginea and mesovarium.-'14'21’24'29 Ovulation takes place by a thinning process, usually avascularization and rupture, with slight bleeding, of the outer portion of the follicle wall and peritoneum. The ovum with the enclosing cumulus cells are washed out in the gradually-released gelatinous follicular fluid and are caught by or pass into the fimbriated end and am- pulla of the uterine tube, where fertilization takes place.- In the cow, mare and other species the outer thin follic- ular wall that usually feels tense and firm during proes- trum and early estrum becomes more flaccid and soft just prior to ovulation.-- In rare instances the ovum and its cumulus cells may be caught and retained in the col- lapsing walls of the Graafian follicle at the time of rup- ture. This may be a rare cause for failure of fertilization. In domestic animals a circumscribed avascular area appears on the apex of the follicle that projects above the surface of the ovary.-'3'4 This thins out until a fine transparent membrane bulges above the surface. This is the basement membrane separating the granulosa and thecal layers of the follicle. This breaks and the follicular contents ooze from the follicle. Collapse of the follicle walls doesn’t occur until after the cumulus has passed through the small stigma in the surface of the follicle. Ovulation may require a few seconds to several minutes or longer depending on the size of the stigma and the location of the cumulus in the follicle. Intrafollicular pressure is not the cause for ovula- tion.-'4 The stigma is small and nearly round or oval. There is no sign of tearing of the follicle wall. As noted above just prior to ovulation the follicle becomes more flaccid and less tonic. Observed ovulations are not vi- olent eruptions. Where the intrafollicular pressures have been measured there has been no increase in pressure prior to ovulation. Recent work presented evidence to indicate that ovulation was probably brought about by the release of LH that releases histamine and possibly prostaglandin- causing ovarian hyperemia. This hyper- emia may stimulate the release of proteolytic enzymes, such as collagenase into the follicular fluid which may be responsible for the separation of the cumulus from the side of the follicle. Thus the proteolyte enzymes weaken the wall of the follicle and the stigma or avas- cular area develops and ovulation occurs at the super- ficial projecting area where the wall is not supported by the ovarian stroma.15,23 After the follicle ruptures and the ovum is released a slight amount of bleeding may occur into the follicle. This is then called the corpus hemorraghicum in the cow, ewe and sow and other species. In the mare a large blood clot, which can be palpated per rectum, and may feel like a follicle, fills the large lumen of the follicle. This bleeding occurs through the follicle walls and not at the site of rupture of the follicle. In the cow fibrin “tags” may develop on the ovary or fine adhesions between the ovary and the fimbria may occur following ovulation. This has no effect on fertility. It is possible that the en- zyme reaction that weakens the follicle wall to produce ovulation acts for a longer period of time in the mare and therefore a greater amount of bleeding occurs through the follicle wall after ovulation. Ovulation is largely under endocrine control. Under the stimulus of FSH from the anterior pituitary a number of vesicular follicles begin developing. As these follicles develop, an increasing amount of estradiol is produced by the theca interna and is absorbed into the circulation of the body as well as being present in the follicular fluid. In the body estradiol produces the typical changes in the tubular portion of the reproductive tract seen in proes- trum and estrum. It also produces the characteristic symptoms and manifestations of estrum or heat by its action on the central nervous system. Except for the fol- licles that are to mature, usually only one in uniparous animals and a moderate number in the multiparous an- imals, there is a sudden wave of atresia that strikes many different size follicles a short time, about 12 to 24 hours or possibly more, before ovulation of the mature follicle. Atresia of the small Graafian follicles begins in the oo- cyte while in medium and large Graafian follicles atresia begins with degenerative changes in the granulosa and theca interna with the changes in the oocyte developing slightly later.-25 Obliterative atresia occurs in small and medium-sized follicles but in large follicles cystic atresia occurs in which the antrum and follicle fluid are reduced only after complete degeneration of the follicle wall with fibrotic changes in the theca. Follicular atresia can occurPHYSIOLOGY OF FEMALE REPRODUCTION 421 at any stage of growth, and degeneration of the oocyte may start at any stage of atresia.16 Cystic atresia may occasionally be associated with a degree of luteinization of the cystic follicle. The cause for the atresia of the “second rank” follicles and the mechanism controlling the number of follicles allowed to mature and ovulate are not known. Progesterone produced in the Graafian follicle before ovulation may play an important role in cattle in the re- lease of LH and ovulation.6'9,11 More work is required in order to elucidate the nature of the exact mechanism of ovulation in animals. Release of LH by the anterior pituitary is necessary for and causes ovulation of the ma- ture Graafian follicle. A large amount of LH is released from the bovine anterior pituitary gland usually within 1 to 5 hours after the onset of estrum by the stimulus of a rising estradiol blood level produced by the maturing follicle.-'11'13,26 The corpus luteum which was already developing from the granulosa cells lining the Graafian follicle at the time of ovulation grows very rapidly following ovulation. The production of progesterone by the corpus luteum then suppresses LH and FSH production. If fertilization and pregnancy take place, the corpus luteum is maintained by the secretion of luteotropic hormone or LH from the anterior pituitary gland and the lack of release of pros- taglandin from the endometrium caused by the influence of the conceptus. If pregnancy does not occur, then the corpus luteum degenerates and, with the decline in the production of progesterone late in the estrous cycle FSH and LH are again produced and a new wave of follicles begins to grow followed by the onset of proestrum. The approximate minimum time required for the develop- ment of the follicles and ovulation in domestic animals is 3 to 4 days, as revealed by work on sheep, and the manual removal of the corpus luteum in the cow. In the cow a wave of follicular growth with an ac- cumulation of small Graafian follicles, less than 5 mm in diameter occurred during the third and fourth days of the cycle resulting in a large follicle 9 to 18 mm in di- ameter at the 13th day. A second-wave of follicular growth occurred between the 12th to 14th day with the produc- tion of small follicles 5 to 8 mm in size resulting in a single large follicle, 12 to 16 mm, at 16 days that usually ovulates 4 or 5 days later.25 A wave of atresia follows each growth wave leaving in most cows only one large follicle. Thus it apparently took 7 to 9 days from early follicle growth to ovulation in the cow. This diphasic growth wave of follicles has not been reported in other domestic animals. Recent studies have shown a continuous growth and atresia of large follicles during the estrous cycle in the cow with an increased rate of atresia, growth and re- placement from day 13 to ovulation, especially after day jg 6,12,19,28,30 smap follicles decreased from day 3 to 18 and medium sized follicles were most numerous day 13 just after blood estrogen levels rose at mid cycle. These studies did not support the previous two-wave theory of Rajakoski.25 The corpus luteum has an inhibitory action on large follicles on days 8 to 13 even though medium- sized follicles increased. Apparently the largest active follicle in unipara exerts an inhibiting intraovarian affect on smaller follicles.19 The ovulatory follicle in the cow varies from 10 to 20 mm. in diameter and secretes large amounts of estradiol at the time of onset of behavioral estrus that promotes the LH surge.28 The latter hormone acting on the LH receptors in the granulosa cells induces ovulation of the follicle. Even though nearly all the reproductive function can occur without nervous innervation of the lower portion of the body, there is definite evidence that ovulation, as well as other phases of the reproductive cycle, are in- fluenced by the nervous system in the intact animal. Heifers, when bred by a vasectomized bull, ovulated an average of 7.7 hours after the end of estrum as compared to 9.9 hours when not bred.18 The ovulation of heifers was delayed 24 to 66 hours by the administration of mas- sive doses of atropine at the onset of estrum; but when chorionic gonadotropin, or LH was administered shortly after the atropine, ovulation occurred about 10 hours ear- lier than normal.7 This indicated that atropine prevented the normal release of LH from the pituitary. The admin- istration of gonadotropic hormone during early estrum shortened to 1.25 hours the normal time of 10.5 to 12.25 hours from the end of estrum to ovulation.17 Progester- one given in 5 to 15 mg doses intramuscularly at the onset of estrum reduced the average length of estrum 3.6 hours, the average time from the end of estrum to ovu- lation 5.4 hours, and the average time from the onset of estrum to ovulation by 9 hours.8 Atropine blocked the effect of progesterone and this blocking action took place in the hypothalamus.11 The LH release mechanism is stimulated by the action of estrogen, and in certain spe- cies other external factors such as coitus in the queen, affecting the hypothalamus. Ovulation is spontaneous in all animals except the rab- bit, cat, and ferret. In these latter species one or repeated mountings or intromissions may be required to release LH from the pituitary and cause ovulation. Ovulation in these species may be caused by stimuli, such as gently manipulating a glass rod in the vagina simulating coitus or by the injection of luteinizing hormone. Ovulation usually occurs at a fairly constant time following the stimulus of coitus or the injection of LH at estrus. In the422 VETERINARY OBSTETRICS rabbit it occurs about 10.5 hours later, and in the cat about 27 hours later. This stimulus in the rabbit is ap- parently emotional and can be produced by the excite- ment of being mounted by another doe. It can also be produced by coitus when the vagina and vulva are anes- thetized.- When 25 I.U. of LH was injected intravenously into isolated mature female rabbits, 50 percent of them ovu- lated between 10-1/2 and 10-3/4 hours later. This ther- apy can be given to queens to terminate estrum. These are other examples of the way in which peripheral and central nervous stimuli affect ovulation. With the exception of the cow, ovulation usually oc- curs before the end of estrum in all domestic animals that ovulate spontaneously. The cow, due to its low threshold for estrogen, remains in estrum only a short period and then an “estrous block” of central nervous origin develops and the cow goes out of estrum even though additional amounts of estradiol are being pro- duced.1 The approximate time of ovulation for the var- ious domestic animals is as follows.----- — Cow and ewe—about 24 to 30 hours after the onset of estrum. In the cow this is 10 to 14 hours after the end of estrus. Sow—about 35 to 45 hours after the onset of estrus. Mare—about 4 to 6 days after the onset of estrus. Bitch—24 to 48 hours after the onset of estrus. Queen—24 to 30 hours after onset of estrus and co- itus. The ovum of the bitch and probably the mare don’t extrude the first polar body for several days after ovu- lation at which time fertilization can occur.--- Superovulation—Discovery of the gonadotropic hor- mones, and interest and research in embryo transfer have resulted in experiments on various means of inducing superovulation, or the release of numerous ova from the ovaries of uniparous animals. (See Chapter 20.) This can be produced during late metestrum, diestrum, and early proestrum by daily subcutaneous injections of FSH for 3 to 6 days, followed by an intravenous injection of LH, or, if timed properly so that the last FSH injection comes just before estrum, the cow may ovulate the numerous artificially produced follicles by means of its own se- cretion of LH.6 2 5a'5b (See Chapter XX.) Superovulation can be produced in cattle by injecting 2,500 to 3,000 I.U. of PMSG intramuscularly on the 16th day of the cycle or when the corpus luteum is manually removed. Five days later 2,000 I.U. HCG may be given intrave- nously to promote ovulation although it is not necessary as the female’s own LH causes ovulation. In sheep and goats 1,000 to 1,500 I.U. PMSG injected on the 12th day and 16th day of the cycle, respectively, will induce superovulation in these species. In sows and mares FSH injections to cause superovulation is not yet satisfactory or practical. PMSG is of no value for superovulation in mares and presently is not available in the U.S. In cattle about 15 percent of the superovulated ova were mor- phologically abnormal. By using prostaglandin preparations superovulation to obtain embryos for transfer is facilitated. Presently PMSG or more commonly a purified FSH gonadotropic product is injected into the donor cow on day 8 to 12 of the estrous cycle. The gonadotropic hormone (FSH) is given twice daily at gradually reducing doses for 5 days.2 On the third day after the initial injection of either PMSG or FSH, a luteolysing dose of prostaglandin is admin- istered with estrus occurring several days later. In cows the desired number of embryos produced is about 8 to 10. There are great sources of variation in the response of cows to gonadotropins and the number of ova or em- bryos produced. These variations have been related to the variable potencies of the gonadotropic hormones em- ployed and the different breeds and ages of cattle used as donors. Further study is indicated.1,2 Because numerous corpora lutea form following su- perovulation the bovine ovary may be five to ten times normal size. Thus it is recommended not to inject FSH into animals 4 to 5 days prior to estrum if superovulation is to be avoided. A cow given PMSG, “Gonadin” was bred and conceived 6 days later but aborted sextuplets at 6 months of gestation.20 After repeated injections of gonadotropic hormones cows may become refractory to them unless a proper “rest” period is provided. Since antihormones are produced when impure products are used, repeated injections of the proteinaceous gonado- tropic hormones may result in fewer ova being ovulated. Ova (Embryo) and Sperm Transport and Fertilization Ova transport—As ovulation approaches there is a marked increase in the tonicity, edema and motility of the fimbriae of the uterine tubes in domestic animals; the fimbriae nearly clasp the ovary in order to receive the egg. These effects are under the endocrine control of es- trogen during the estrous period. Following ovulation, the cumulus oophorus which was liberated from the ma- ture Graafian follicle is transported from the surface of the ovary into the uterine tube. This transfer is effected by the direct action of the cilia of the fimbria and in- fundibulum on the cumulus as well as the currents of fluid created by the beating cilia flowing toward the os- tium of the uterine tube. Essential to these immediate transport mechanisms are the contractions of the smoothPHYSIOLOGY OF FEMALE REPRODUCTION 423 muscle of the mesovarium and regular contractions that change the position of the ovary with respect to the in- fundibulum and fimbria.--’9,22'25 The rate of transport of the ova through the ampullar portion of the oviduct to the area of the ampullary-isthmic junction is quite rapid and is probably accomplished in a relative few minutes, 8 to 30.--- This transport is ef- fected by peristaltic and antiperistaltic muscular con- tractions of the smooth muscle in the ampulla together with ciliary activity under the hormonal control of es- trogens. The cilia in the rabbit uterine tube beat at a rate of 1500 per minute. The beat of the cilia towards the uterus creates currents in the tubal fluid and the con- tractions of the uterine tube keeps the ovum in constant motion which aids in egg and sperm contact and fertil- ization.-’22,25 Sperm penetration of the ovum and fertil- ization which requires several hours, occurs in the am- pulla of the uterine tube. The physiological significance of the oviduct fluid which is secreted in greatest amounts during estrum is not well understood.25 Most of this fluid passes into the peritoneal cavity. Adhesions and obstruc- tion or ligation of the distal or fimbriated portions of the bovine uterine tube causes hydrosalpinx. Some fluid may pass through the isthmus into the uterus. The ova or eggs of domestic animals at the time of ovulation are one of the largest cells in the body and vary from 120 to 185 microns or 0.12 to 0.185 mm in di- ameter not including the zona pellucida.-1'23 In ungulates the ovum contains very little glycogen but large amounts of lipid material; whereas in rodents the reverse is true. These materials are necessary for energy production to produce protein biosynthesis in the ovum. Certain ova may be defective and have obvious structural abnor- malities including: small or giant ova, oval or flattened ova, ova with a ruptured zona pellucida, ova with large polar bodies or vacuoles within the vitellus, ova with an abnormal cytoplasm, abnormal-shaped ova, atypical 2- blastomere ova and etc.23 These abnormal or degener- ated eggs may be due to improper maturation of the oo- cyte, genetic or environmental factors or failure of polar body extrusion. The incidence of abnormal ova varies between the breeds and strains and is greatest in older females.-23 The cumulus and corona cells around the zona pel- lucida of the ovum in most domestic animals only persist for a few hours or less after ovulation and fall away in the oviduct. In the bitch and queen the corona cells may persist for several days. The protoplasmic projections from these cells into the zona pellucida are withdrawn soon after ovulation due to contact with fibrinolytic enzymes in the oviduct fluid. The cumulus and corona cells die and separate from the ovum aided by the ciliary and muscular activity of the oviduct. Inside the zona pellu- cida is the vitelline membrane or vitellus which is similar to the plasma membrane of somatic cells. The zona pel- lucida is a homogeneous semipermeable structure sur- rounding the ovum composed of conjugated protein ca- pable of being dissolved by proteolytic enzymes such as trypsin and chymotrypsin. After fertilization the vitellus shrinks and a perivitelline space is formed between the zona pellucida and the vitelline membrane into which the polar bodies are extruded. Most ova of domestic animals have ovulated when the second maturation division has reached metaphase and the first polar body has been extruded. In the bitch and probably the horse, ova are ovulated as a primary oocyte and mature in the oviduct. The fertile life of ovulated ova in domestic animals is relatively short, 6 to 24 hours or less except in the bitch where they may remain fertile in the uterine tube for 4 or more days due to their de- layed maturity.--- In cattle inseminated 2 to 4 hours after ovulation both the conception rate and the percentage of normal embryos at 35 days were 75 percent.11 When in- semination took place 6 to 12 hours after ovulation the conception rate was 60 to 75 percent but only 30 percent of the embryos were normal at 35 days. Insemination after 12 hours following ovulation resulted in conception rates that were very low, and normal embryos were un- usual. A high rate of fertilization in cows inseminated at 13 hours post-ovulation in cattle but no fertilization at 16 to 22 hours postovulation was reported.33 The loss of fertility or viability is not rapid or sudden and aging eggs may be fertilized normally but produce embryos that die early in gestation. With further loss of viability of the ovum, fertilization may be abnormal or fail to occur. Under usual conditions of estrus and natural ser- vice in situations where a male is present with the fe- males, spermatozoa will reach the site of fertilization in the oviduct before ovulation and the arrival of the ova. Under conditions of artificial insemination this orderly sequence of events may be altered and infertility result. Fertilization of “old” eggs in swine is associated with polyspermy and abnormal development.29 In domestic animals the eggs or ova remain in the ovi- duct in the ampullary-isthmic area for 3 to 4 days before passing rapidly through the isthmus and the uterotubal junction into the uterus. In the sow the ova may pass into the uterus in 1-1/2 to 3 days possibly associated with multiple ovulation.- After rapid transfer to the am- pullary-isthmic junction, swine eggs remain there for about 30 to 45 hours and enter the uterus 30 to 60 hours after ovulation.40 Ovine ova remain in the ampullary-isthmic junction for 50 to 60 hours following ovulation due to the strong antiperistaltic contractions in the isthmus.- In424 VETERINARY OBSTETRICS most domestic animals fertilized ova require 3 to 5 days to pass through the uterine tube into the uterus; but may require 6 to 8 days in the dog, 5 to 9 days in the cat, possibly 6 days in the mare- and 2 to 3 days in the sow.- --- An accelerated rate of uterine tubal transport of ova has been reported in superovulation in the cow possibly due to elevated steroid levels.16 The normal transport of ova through the uterine tube can be severely disturbed by injections of estrogen, progesterone or other drugs and anesthetics. The stage of the estrous cycle, the species of animal and the dose levels of the above agents all produce varying effects on the isthmus and the rate of ova transfer to the uterus.25 Depending upon the dose of estrogen and the species injected some ova may be trapped or blocked in the ampullary-isthmic portion of the uterine tube, “tubal locking”; while in others the ova are rapidly passed into the uterus and are expelled through the cervix into the vagina.21 The failure to demonstrate “tubal locking” in a recent experiment may have been due to the very low dose of estradiol injected.16 These effects appear to be due to the reaction of the isthmic portion of the uterine tube to the injected hormone or drug. It has been suggested that edema in the isthmic area might play a role in tubal regulation of the time of transport, but muscular effects by the gonadal hormones seem more logical from the evidence.8 Under ordinary conditions the fertilized ovum or developing zygote re- mains in the uterine tube until the corpus luteum is formed and the endometrium is under the influence of proges- terone so a proper environment and nutrition is available upon entering the uterus. If the egg is not fertilized it fragments into many irregular cytoplasmic segments and disintegrates in the uterus under the influence of phago- cytosis. In the mare unfertilized ova may be retained in the uterine tube for weeks or possibly months. This trap- ping phenomenon has been reviewed- but no satisfactory explanation has been proposed other than the possibility that the fertilized ova by its “hormonal” secretions con- trols its passage through the uterine tubes. Sperm transport in the female—In the cow, ewe, bitch and queen the ejaculate at coitus is forcibly sprayed over the cervix and anterior vagina forming a “seminal pool” in the cranial portion of the vagina. In the bitch the large ejaculate, 7 to 20 ml., is carried into the uterus through the relaxed cervix by the muscular activity of the genital tract. In the mare and sow, as described ear- lier, the semen at coitus is largely placed into the uterus. There is no evidence that seminal fluid passes from the vagina into the uterus in the cow, sheep, queen, doe or 39 man. After ejaculation the spermatozoa in the seminal plasma migrate or diffuse from the plasma into the mucus of the female genital tract where they may be protected, nour- ished and transported. In the cow as much as 150 ml. or more of cervical mucus may be obtained at estrum. Bovine cervical mucus contains mucoids (amino acids, sugar and sialic acid), glycogen, protein, enzymes, glob- ulins, salt, urea and very small amounts of glucose. Va- ginal and cervical mucus in the other domestic animals under the influence of estrogens also changes from a tough tenacious consistency in diestrus or anestrus to a more liquid, viscid, stringy mucus during proestrum and es- trum. This permits and favors sperm cell migration. The velocity of sperm cells in bovine cervical mucus at es- trum is 56 microns per second, (3 mm./minute) versus 132 microns per second in saline.42 The “fern test” of cervical mucus is positive when mucus from the cow or other animals in estrum is smeared on a slide and al- lowed to dry producing a fern-like aborization due to the high NaCl and water content of the mucus at this stage of the cycle. No specific substance harmful to sperma- tozoa has been recovered from normal cervical mucus. Leucocytic phagocytosis, bacterial endotoxins, and ab- normal pH may play a role in preventing the penetration of sperm cells through cervical mucus. “Hostile” cervi- cal mucus is a catchy term loosely used to describe cer- tain conditions affecting the cervical mucus in women. The passage or transport of spermatozoa from the va- gina through the cervix and uterus and into the uterine tube is very rapid, less than 15 minutes, in all domestic animals and man. Sperm cells in the bitch are at the uter- ine entrance of the uterine tubes 25 seconds after ejacu- lation.- Spermatozoa have been found throughout the bitch’s genital tract within 20 minutes after the onset of copulation. This transport time was 8 minutes in the ewe.36 It was demonstrated that in the cow spermatozoa were transported from the cervix to the ovarian ends of the uterine tubes in less than 2 to 4 minutes.45,46 This oc- curred whether the spermatozoa were living or dead and followed either natural or artificial insemination. The in- terval from ejaculation to the presence of spermatozoa in the uterine tubes was reported to be somewhat longer in species other than the cow, one-half to several hours.- Spermatozoa could also gain entrance to the uterine tubes in cows and sows during the luteal phase of the cycle.20 Movement of the spermatozoa in the uterine lumen is due to strong contractions of the uterine wall augmented by the release of oxytocin at coitus or artificial insemi- nation.46 Fright and/or excitement might release epi- nephrine and interfere or inhibit temporarily the uterine contractions. There is no evidence that epinephrine re- lease at coitus or soon after affects fertility. Prostaglan- din, a substance from the seminal vesicles present in sheep, goats, possibly other animals, and human semenPHYSIOLOGY OF FEMALE REPRODUCTION 425 is an oxytoxic agent that can also stimulate the smooth muscle of the genital tract. Since the vaginal mucous membrane is permeable to prostaglandin it may also play a role in spermatozoan transport.42 The spermatozoa are thus transported largely in a fluid medium or mucus by capillary action in the cervix and by ciliary activity and contractions of the walls of the genital tract. The sperm cell’s contribution to this transport up the female tract is a small one because of the relatively slow rate of move- ment for the long distance to be traversed. However, this motility of the spermatozoa is probably important at the natural barriers of the cervix, the utero-tubal junction, the isthmus of the oviduct and in the initial penetration of the sperm cell into the cumulus. Motility of the sperm cell is essential to fertility. Since dead sperm cells and inert particles will pass through the uterus and into the uterine tube, the motility may be most essential to tra- verse the cervix and penetrate the cumulus cells or zona.36 Millions to billions of spermatozoa are usually ejacu- lated into the female genital tract of domestic animals at coitus. In the mare, bitch and sow most of these promptly enter the uterus. In the other species only about 10 or 100 million spermatozoa pass through the cervix into the uterus with more sperm cells being in the base of the horns than in the apex of the horns. Several hundred to less than a thousand spermatozoa gain access to the am- pulla of the uterine tube, and only 10 to less than 100 would be in vicinity of the unfertilized ovum. Appar- ently the uterotubal junction and the isthmus have some controlling role in the numbers of spermatozoa that gain access to the uterine tube. In the rabbit after mating, and just before ovulation, the distribution of spermatozoa in the doe’s genital tract were as follows: 20 x 106 sperm cells in the vagina, 12 x 106 in the caudal portions of the uterus, 50 x 104 in the apical portions of the uterus, 4 x 103 in the uterine tubes but only 500 spermatozoa in the ampulla of the uterine tube where the ova were fertilized.10 In sows the number of spermatozoa in the uterine tube is affected by the volume of semen entering the uterus as well as the concentration or numbers of spermatozoa.5 When 1 ml. of fresh or frozen semen con- taining millions of live spermatozoa was placed in mid- cervix in heifers, 4 hours later 469 and 191 spermatozoa were in the uterine tubes, and 1559 and 733 spermatozoa were in the uterus, respectively.30 Four hours after in- semination only 3 percent of the inseminated sperma- tozoa could be recovered. A review of the literature, indicates that in mammals only a small proportion of spermatozoa ejaculated at co- itus reach the distal end of the uterine tube.32 Some sperm cells may actually enter the peritoneal cavity.25 Appar- ently natural barriers at the cervix and uterotubal junc- tion limit the number of spermatozoa going to the site of fertilization. Rabbits inseminated with less than 20,000 to 100,000 spermatozoa per insemination failed to con- ceive.15 This number of spermatozoa varied with the ex- tender and the degree of dilution. A 0.6 percent decline in conception rate in cattle with each million decline from 12,000,000 to 4,000,000 spermatozoa inseminated was reported.47 Below the latter figure the decline in con- ception rate was very rapid, about 3.6 percent for each million decline in sperm cell numbers to about 1,500,000. Conception rates, when 12 to 14 million, 6 to 8 million, and 1 to 3 million actively motile bovine spermatozoa were inseminated were 67, 64 and 49 to 53 percent, re- spectively when based on 60 to 90 day nonreturns. Thus a minimum number of motile spermatozoa is necessary for fertilization and conception. In sows and probably mares and bitches a minimum volume of ejacu- late or artificially inseminated semen is also necessary for optimum conception rates. In most domestic animals sperm cells can only retain their viability and fertility at a high level for about 24 to 48 hours in the female genital tract. The longest fertile period for spermatozoa in the female tract of most do- mestic animals is 48 to 72 hours.3 - - In the mare and the bitch spermatozoa may survive and be fertile for 5 to 6 days. Like aging ova, aging spermatozoa may be ca- pable of fertilizing the ovum but this may result in em- bryonic deaths.29 The most common result of aging sper- matozoa whether they age in liquid semen at 5° C or in the female genital tract is failure of fertilization. The loss of fertilizing capacity of frozen semen, especially in liq- uid nitrogen, is very slow and gradual and extends over a number of years. The vagina of the sow and ewe is not a favorable site for sperm cell survival and they lose their motility and die in 6 to 12 hours or less. The cervix with its viscid mucus of estrum is the most favorable site for the sur- vival of spermatozoa in the cow and ewe. Sperm cells live in the cervix for 36 to 48 hours or possibly slightly longer and this site appeared to act as a sperm cell res- ervoir for spermatozoa in the cow, ewe and doe.35,36 Sperm cells retain their motility in the uterus and oviducts for about 24 hours. The uterus is not a highly favorable site for sperm cell survival because the presence of sper- matozoa stimulate the invasion of leucocytes and the phagocytosis of spermatozoa. In swine it was shown that by 30 minutes after service the volume of seminal fluid in the uterus was greatly reduced and leucocytes were entering the lumen.31 Sperm cell survival in sows ap- peared to be longest in the mucous folds of the utero- tubal junction. Ciliated cells in the apex of the uterine horns of sows were observed. By 8 hours postcoitus the426 VETERINARY OBSTETRICS numbers of leucocytes were greater than the spermato- zoa and by 27 hours after service only rarely were sper- matozoa found in the sow’s uterus. The uterotubal junc- tion was a “sperm reservoir” in the sow.25 The elimination of spermatozoa following their death in the female gen- ital in the other domestic animals is by phagocytosis as in the sow.34 35 Possibly a few dead spermatozoa may be expelled through the dilated cervix. Fertilization of the ovum occurs in the ampulla of the oviduct within one to two hours after ovulation if the spermatozoa are present in the oviduct. By this time the second reduction division of the ovum is in progress ex- cept in the bitch and probably the mare in which this division is delayed.- Fertilization involves the penetra- tion of the ovum by the spermatozoon, the activation of the ovum, the formation of the male and female pronu- clei and the mingling of the maternal and paternal chro- mosomes to constitute the genome of the new zygote with a diploid number of chromosomes. A recent study reported evidence for species-specific sperm plasma membrane receptors for the zona pellucida. This sperm- egg interaction further assures their mutual attraction and the process of fertilization.-41 Capacitation of spermatozoa is the process that sper- matozoa of all animals must undergo in the uterus or oviducts before achieving the capacity to fertilize ova. Capacitation time in sheep is 1-1/2 hours. Capacitation time in the other domestic animals is also about 1 to 6 hours.-33 There is evidence that ejaculated bull, stallion and boar semen has a decapacitation factor that is lost in the female genital tract.- - In rabbits spermatozoa placed in the oviducts 2 hours before or after ovulation failed to result in conception. If they were placed in the oviduct 4 hours before, 6 percent of the ova were fertilized, and 6 hours before ovulation, 78 percent of the ova were fertilized.13,14 Spermatozoa can penetrate porcine ova within 3 hours of insemination.27 Capacitation produces a change in the acrosome called the “acrosome reaction” with a release of lytic enzymes such as hyaluronidase. No changes occur in the sperm head proper in the uterus but a functional change in the sperm head may take place when the sperm cell contacts the granulosa cells of the cumulus. Thus capacitation may allow the “acrosomal or vesiculation reaction” to occur to permit the sperm cell to penetrate the granulosa cells and zona pellucida. This enzyme permits the sperm cell to penetrate the cu- mulus cell mass around the ovum by depolymerizing the hyaluronic acid-protein matrix of the cumulus. The cu- mulus cells including the corona radiata in most domes- tic animals break down and separate from the zona pel- lucida early. In the bitch and queen the corona cells may remain for some period of time. This early breakdown of the cumulus cells is caused by autolytic changes, ac- tion of the bicarbonate ions in the oviduct, ciliary and muscular activity of the oviduct and hyaluronidase or possibly other enzymes if spermatozoa are present. Before the sperm cell can penetrate the zona pellucida it loses the acrosome cap and plasma membrane expos- ing the perforatorium and inner acrosomal membrane which are responsible for the penetration through the zona pellucida.3 4 6 7 It is reported that a lytic enzyme such as trypsin together with hyaluronidase may permit the sperm cell to dissolve in oblique “tunnel” through the protein- aceous zona into the peri vitelline space.43 When the plasma membrane of sperm head and vitelline membrane are in contact, the two structures unite and the entire sperm cell passes into the cytoplasm of the egg. In certain sterile bulls, boars and dogs, the spermatozoa have defective or knobbed acrosomes. These animals are sterile because their spermatozoa cannot penetrate the ovum. Usually when the sperm cell contacts the vitelline membrane in most domestic species, maturation of the ovum by meiosis is resumed with the expulsion of the second polar body. The cause of this “activation” of the ovum is not known but it proceeds to pronucleus formation. Two factors are apparently responsible for preventing, except on rare occasions, the penetration of more than one sperm cell into the ovum. The first is the relatively few spermatozoa in the oviduct at the time of fertiliza- tion. The second is when the first sperm cell contacts the vitelline membrane a rapid reaction takes place both in the zona pellucida and the vitelline membrane that blocks the further entrance of sperm cells.1,2 It is be- lieved that this reaction is brought about by the release of a substance from the vitelline membrane or the cor- tical granules just beneath this membrane. It is not un- common when examining fertilized eggs to see many sperm cells on or in the zona pellucida and in certain species in the perivitelline space. After the male and female pronuclei form, the chro- mosomes in each pronuclei unite to form the zygote. This union of the two chromosome groups is called syngamy, at the conclusion of which fertilization is complete. The diploid or tetraploid zygote usually immediately divides into two blastomeres and the cleavage of the ovum pro- gresses rapidly in the next few days to the blastula stage.4411 The approximate number of days from ovulation to the blastocyst stage of development is 6 in the horse, 7 to 8 in the cow, 6 to 7 in the ewe, 5 to 6 in the sow and 4 to 5 in the queen. The time of entry of the cleaving fertilized ova into the uterus in domestic animals is about 2 to 6 days after ovulation. This is usually shorter in swine and in superovulated cattle,1,2 longer in bitches, queens and mares. The passage of the ova through the isthmus of the uterine tube is rapid. The passage of the fertilized cleaving ovum into the uterus and the controlPHYSIOLOGY OF FEMALE REPRODUCTION 427 of this passage by the gonadal steroidal hormones acting on the muscular isthmus of the uterine tube has been (described previously. Some interesting time relations in regard to fertilization in domestic animals have been re- viewed.2 Sperm cell penetration of the ovum begins about 3 hours after ovulation in ewes, pronuclei are formed 11 to 39 hours after ovulation in the cow and 3 to 9 hours after ovulation in the ewe. The fertilized egg divides into the two-cell stage about 24 hours after ovulation in the mare and 19 to 24 hours after ovulation in the ewe. The most common abnormalities of fertilization are polygyny and polyspermy. Polygyny is incomplete mat- uration of the egg with a failure to expel the second polar body resulting in a triploid zygote. Polyspermy where more than one, usually two, sperm cells enter the egg is also characterized by triploidy or a 3N instead of a normal 2N chromosome complement in the zygote. Aging of the egg increases the incidence of these an- omalies. Twenty percent or more of swine zygotes were polyspermic or digynic when the sow was bred more than Table 17. The Reproductive Cycle of Domestic Animals* Animal Onset of Puberty Average Recom- mended Age for First Service Length of Estrous Cycle Follicle Diameter (mm) Length of Estrum Time of Ovulation Optimum Time for Service Ovum Transport Time Advisable Time to Breed After Parturition Mare 10-24 m. (18 m.) 2-3 yr. 19-23 d. (21 d.) 35-55 + 2.0-13 d (7.2±2.9 d) (5.7 d) 1-2 d. before the end of estrum 2-4 d. before end of estrum or the 2nd-3rd d. of estrum 4-6 d. About 25-35 d. or 2nd estrum; about 9 d. or 1st estrum only if normal in every way Cow 4-24 m. (6-18 m.) 14-22 m. 18-24 d. (21 d.) 10-20 12-28 h. (18 h.) (Temperate Zone) 10-15 h. after the end of estrum Just before the middle of estrum to the end of estrum 3-4 d. 60-90 d. Ewe 4-12 m. (first fall) 12-18 m. 14-20 d. (16.5 d.) 15-19 24-48 h. (30-36 h.) 12-24 h. before the end of estrum 18-24 h. after the onset of estrum 3-4 d. Usually the following fall Goat 4-12 m. (first fall) 12-18 m. 15-24 d. (20 d.) 30-60 h. (36-48 h.) About the last day of estrum 24-36 h. after the onset of estrum 3-4 d. Usually the following fall Sow 5-8 m. 8-9 m. 18-24 d. (21 d.) 7-10 1-4 d. (2-3 d.) 30-40 h. after the onset of estrum 12-30 h. after the onset of estrum 2-3 d. First estrum 4-9 d. after weaning Pigs Dog 6-12 m. (7-10 m.) 12-18 m. 1-3 cycles per year (1.6 cycles per year) aver, every 7 months 6-8 4-12 d. (9 d.) 1-2 d. after the onset of true estrum 2-3 d. after onset of true estrum or 10-14 d. after onset of estrous bleeding 6-8 d. Usually the first estrum or 3-4 weeks after weaning pups Cat 6-15 m. (8-10 m.) 12-18 m. 15-21 d.‘ 9-10 d.1 4 d.2 24-30 h. after coitus (27 h.)2 2 4-8 d. Usually the 1st estrum or 3-4 weeks after weaning kittens ♦Numbers in parentheses are average figures. 1, 2, 3, 4, 5, 6, 1L ‘The cat has several cycles each breeding period. The latter occur usually 2 or 3 times a year if it is not bred. 2The cat does not ovulate spontaneously. If coitus occurs the cat goes out of estrum in about 4 days.428 VETERINARY OBSTETRICS 36 hours after the onset of estrus.37,38 Migration of the early zygote from one uterine horn to the other horn is fairly common in ewes, mares, bitches, sows and queens but rare in cows. Migration of the ova across the peri- toneal cavity of domestic animals has not been reported. The formation and development of the corpus luteum under the influence of LH results in the production of progesterone necessary for the preparation of the uterus and probably the rapid passage of the zygote through the isthmus into the uterus. Progesterone is also essential to the maintenance of pregnancy. Because of the effect of the blastocyst on the endometrium, the release of pros- taglandin is inhibited and LH secretion maintains the corpus luteum. Otherwise in nonpregnant animals start- ing about 16 days in the cow and sow and about 10 to 12 days in the ewe and mare the corpus luteum would begin to involute resulting in another estrous period 4 to 5 days later. Placement of or spacing embryos in the uterus in multiparous animals occurs during this early embryonic period. The blastocyst elongates rapidly in the cow, ewe, and sow but remains spherical in the mare, bitch and queen. The uterine luminal fluid or “uterine milk’’ is rich in mucopolysaccharides, protein, free amino acids, salts like an ultrafiltrate of blood plasma supple- mented by secretions of the uterine glands. The shedding of the zona pellucida is probably caused by intrinsic fac- tors in the developing blastocyst.-24'25 Normal gestation and zygote passage into the uterus is carefully synchro- nized. The early loss of fertilized eggs or embryos is usually not recognizable and is called infertility or ste- rility. A thorough knowledge of the various physiologic re- productive phenomena of each domestic species is es- sential in order for the veterinarian to understand and intelligently treat the various causes of infertility and su- pervise artificial insemination, embryo transfer and re- productive health programs. The knowledge in this basic field is being rapidly advanced and as more information is obtained clinical application of this knowledge and treatment will be based increasingly on facts instead of empiricism. The basic physiologic reproductive knowledge nec- essary for all veterinarians on the domestic species is given in Table 17. These are average or mean figures. Individual animal variations and differences are common but as a general guide this information is useful. A more complete discussion of the reproductive cycle, endocrine effects on the cycle and the reproductive physiology of the postpartum period and pubertal period will preface each of the following Chapters on female infertility in the various domestic species. References General on Physiology of Reproduction L Altman, P. H. and Dittmer, D. S. (1962) Growth Including Re- production and Morphological Development, Biological Hand- book, Federation of Amer. Soc. Exper. Biol., Washington, D.C. 2. Asdell, S. A. (1964) Patterns of Mammalian Reproduction, 2nd Ed., Cornell Univ. Press, Ithaca, N.Y. 3. Cole, H. H. and Cupps, P. T. (1977) Reproduction in Domestic Animals, 3rd Ed., Academic Press, N.Y.C. 4. Fraser, A. F. (1968) Tables of Data on Livestock Reproduction, Edinburgh Univ. Press, Edinburgh. 5. Ginther, O. J. (1979) Reproductive Biology of the Mare, Cross Plaines, Wise. 6. Hafez, E. S. E. (1980) Reproduction in Farm Animals, 4th Ed., Lea and Febiger, Philadelphia. 7. Hartman, C. G. (1963) Mechanisms Concerned with Conception, McMillan Comp., N.Y.C. 8. McDonald, L. E. (1975) Veterinary Endocrinology and Repro- duction, 2nd Ed., Lea and Febiger, Philadelphia. 9. Nalbandov, A. V. (1964) Reproductive Physiology, 2nd Ed., W. H. Freeman and Comp., San Francisco. 10. Parkes, A. S. (1966) Marshall’s Physiology of Reproduction, Vol. 3, Little, Brown and Co., Boston. LI. Swenson, M. J. (1977) Duke’s Physiology of Domestic Animals, 9th Ed., Cornell University Press, Ithaca, N.Y. 12. Teppermen, J. (1962) Metabolic and Endocrine Physiology, Year- Book Medical Publisher, Chicago. 13. Turner, C. D. (1961) General Endocrinology, 3rd Ed., W. B. Saunders Co., Philadelphia. 14. Velle, W. (1963) Gonadal Hormones in Domestic Animals, in Advances in Vet. Sci., Vol. 8, Edit, by C. A. Brandley and E. L. Jungherr, Academic Press Inc., N.Y.C. 15. Von Euler, U. S. and Heller, H. (1963) Comparative Endocri- nology, Vol. 1, Academic Press, N.Y.C. 16. Zuckerman, S. (1962) The Ovary, Vol. I and II, Academic Press, N.Y.C. Reproductive Hormones 1. Amoroso, E. C. (1955) Hormone Control of the Oestrus Cycle, Vet. Rec., 67, 1072. 2a. Bauman, D. E., DeGeeter, M. J., Peel, J. C., Lanza, G. M., Gorewit, R. C. and Hammond, R. W. (1982) Effect of Recom- binantly Derived Bovine Growth Hormone on Lactational Per- formance of High Yielding Dairy Cows., J. Dairy Sci., 65, Suppl. I, 121, Abst. 86 and An. Sci. Mimeo Series #56, 1982 Dairy Days, N.Y.S. Col. of Agric., Ithaca. 2b. Bell, T. G., Smith, W. L., Oxender, W. D. and Maciejko, J. J. (1980) Biologic Interaction of Prostaglandins, Thromboxane and Prostacyclin: Potential Nonreproductive Veterinary Clinical Applications, JAVMA, 176, 10, 1195-1120. 2c. Bines, J. A. and Hart, I. C. (1982) Metabolic Limits to Milk Production Especially Roles of Growth Hormone and Insulin, J. Dairy Sci., 65, 1375. 2d. Black, W. G., Ulberg, L. 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P., Kindahl, H., Edqvist, L. E. and Gustafsson, B. (1980) Physiologic and Path- ophysiologic Aspects of Prostaglandin F2a During the Repro- ductive Cycle, JAVMA, 176, 10, 1187-1194. 40. Schultz, R. H. and Copeland, D. D. (1981) Induction of Abor- tion Using Prostaglandins, Acta Vet. Scand. Suppl., 77, 353- 361. 41. Wagner, W. C. (1979) The Adrenal Gland in Reproductive Suc- cess and Failure, Proc. of Soc. for Theriog., Mobile, Ala. ,119- 130. 42. Willett, E. L., Buckner, P. J. and McShan, W. H. (1954) Re- fractoriness of Cows Repeatedly Superovulated with Gonado- tropins, J. of Dairy Sci., 36, 10, 1083. 43. Young, W. C., Goy, R. W. and Phoenix, C. H. (1964) Hor- mones and Sexual Behavior, Science, 143, 212. Puberty 1. Asdell, S. A. (1955) Cattle Fertility and Sterility: Little, Brown and Co., Boston, Mass. 2. Britt, J. H. (1979) Prospects for Controlling Reproductive Pro- cesses in Cattle, Sheep and Swine from Recent Findings in Re- production, J. Dairy Sci., 62, 651-665. 3. Desjardins, C. and Hafs, H. D. (1969) Maturation of Bovine Fe- male Genitalia from Birth Through Puberty, J. An. Sci., 28, 4, 502. 4. Foote, W. C., Waldorf, D. P., Chapman, A. B., Self, H. L., Grummer, R. H. and Casida, L. E. (1956) Age at Puberty of Gilts Produced by Different Systems of Mating, J. An. Sci., 15, 4, 959. 5a. Izard, M. K. and Vandenbergh, J. G. (1982) The Effects of Bull Urine on Puberty and Calving Date in Crossbred Beef Heifers, J. An. Sci., 55, 5, 1160. 5b. Jochle, W. (1979, 1981) Review: Puberty and Reproductive Ag- ing I, II, An. Reprod., An. Health News, 2, 10 and 4, 22, Den- ville, N.J., 07834. 6. Menge, A. C., Mares, S. E., Tyler, W. J. and Casida, L. E. (1960) Some Factors Affecting Age at Puberty and the First 90 Days of Lactation in Holstein Heifers, J. Dairy Sci., 43, 8, 1099. 7. Morrow, D. A. (1968) Estrous Intensity and Ovarian Conditions in Postpuberal Dairy Heifers, J. Dairy Sci., 51, 6, 949. 8. Morrow, D. A., Swanson, L. V. and Hafs, H. D. 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(1945) The Levels of Ovarian Hormones Required to Induce Heat and Other Re- actions in the Ovariectomized Cow, J. of An. Sci., 4, 3, 277. 2. Betteridge, K. J. (1980) Embryo Transfer in Farm Animals, in Current Therapy in Theriogenology, edited by D. A. Morrow, W. B. Saunders Co., Philadelphia, 74-76. 3. Blandau, R. J. (1967) Oogenesis-Ovulation and Egg Transport, in Comparative Aspects of Reproductive Failure, edit, by K. Benirschke, Springer-Verlag, N.Y.C. 4. Blandau, R. J. and Rumery, R. E. (1963) Measurements of In- trafollicular Pressure in Ovulatory and Preovulatory Follicles of the Rat, Fert. and Steril., 14, 3, 330. 5a. Hafez, E. S. E. and Sugie, T. (1961) Superovulatory Responses in Beef Cattle and an Experimental Approach for Non Surgical Ova Transfer, 4th Intemat. Congr. on An. Reprod., Netherlands. 5b. Hafez, E. S. E., Sugie, T. and Gordon, I. (1963) Superovulation and Related Phenomena in the Beef Cow, J. Reprod. and Fertil., 5, 359. 6. Hansel, W. (1953) Neurogenic Factors in Ovulation, Iowa State Col. J. of Sci., 28, 1, 1. 7. Hansel, W. (1958) Neurogenic Factors Affecting Ovulation in Animals, Intemat. J. of Fertil., 3, 1, 42. 8. Hansel, W. and Trimberger, G. W. (1952) Effect of Progesterone on Ovulation Time in Dairy Heifers, J. Dairy Sci., 35, 1, 65. 9. Hansel, W., Trimberger, W. W. and Bearden, H. J. (1952) The Effect of Estradiol on Ovulation Time in Dairy Heifers, J. An. Sci., 11, 4, 793. 10. Harper, M. J. K. (1961) The Time of Ovulation in the Rabbit Following Injection of Luteinizing Hormone, J. of Endocrinol., 22, 147.432 VETERINARY OBSTETRICS 11. Hough, W. H., Bearden, H. J. and Hansel, W. (1955) Further Studies on Factors Affecting Ovulation in the Cow, J. of An. Sci., 14, 3, 739. 12. Ireland, J. J., Coulson, P. B. and Murphee, R. L. (1979) Fol- licular Development During Four Stages of the Estrous Cycle of Beef Cattle, J. An. Sci., 49, 5, 1261-1269. 13. Jubb, K. and McEntee, K. (1955) Observations on the Bovine Pituitary Gland, Cor. Vet., 45, 4, 570. 13. Jubb, K. and McEntee, K. (1954) Personal Communication. 14. Kupfer, M. (1928) The Sexual Cycle of Female Domesticated Mammals, 13th and 14th Reports of the Director of Veterinary Education and Research, Part 2, 1211, Union of South Africa, Pretoria. 15. Lipner, H. (1968) Personal Communication, Cornell University. 16. Marion, G. B., Gier, H. T. and Chondary, J. B. (1968) Micro- morphology of the Bovine Ovarian Follicular System, J. An. Sci., 27, 2, 451 and 466. 17. Marion, G. B. and Smith, V. R. (1951) The Effect of Admin- istering an Unfractionated Gonadotropic Pituitary Extract During Estrus on the Time of Ovulation and the Length of the Estrual Period of Dairy Heifers, J. of Dairy Sci., 34, 6, 496. 18. Marion, G. B., Smith, V. R., Wiley, T. E. and Barrett, G. R. (1950) The Effect of Sterile Copulation on Time of Ovulation in Dairy Heifers, J. Dairy Sci., 33, 885. 19. Matton, P., Adelakoun, V., Couture, Y. and Dufour, J. J. (1981) Growth and Replacement of the Bovine Follicles During the Es- trous Cycle, J. An. Sci., 52, 813-820. 20. Montfort, E. L. (1955) Personal Communication. 21. Osborne, V. (1966) Univ. of Sidney, Personal Communication. 22. Nalbandov, A. V. (1953) Gonadotrophic Activity of Pituitary Glands and the Induction of Ovulation, Iowa State Col. J. of Sci., 28, 1, 45. 23. Pool, W. R. and Lipner, H. (1966) Inhibition of Ovulation by Antibiotics, Endocrinol., 79, 858. 24. Prickett, M. E. (1968) Personal Communication. 25. Rajakoski, E. (1960) The Ovarian Follicular System in Sexually Mature Heifers, Acta Endocrinolgica, 34, Suppl. 52. 26. Rakha, A. M. and Robertson, H. A. (1965) Changes in Levels of Follicle Stimulating Hormone and Luteinizing Hormone in the Bovine Pituitary Gland at Ovulation, J. Endocrinol., 31, 245. 27. Shettles, L. B. (1958) The Living Human Ovum, Amer. J. Obst. and Gynec., 76, 398. 28. Staigmiller, R. B. and England, B. G. (1982) Folliculogenesis in the Bovine, Theriog., 17, 1, 43-51. 29. Strassman, E. O. (1961) The Theca Cone. The Pathmaker of Growing Human and Mammalian Follicles, Intemat. J. of Fert., 4„ 2, 135. 30. Villa-Godoy, A., Ireland, J. J., Wortman, J. A., Ames, N. K. and Fogwell, R. L. (1980) Luteal Function in Heifers Following Destruction of Ovarian Follicles at Three Stages of Diestrus, J. An. Sci., 53, Suppl. 1, 372, Abstr. 31. Willett, E. L. (1953) Egg Transfer and Superovulation in Farm Animals, Iowa State Col. J. of Sci., 28, 1, 83. Ova and Sperm Transport and Fertilization 1. Austin, C. R. (1962) The Mammalian Egg, C. C. Thomas Publ. Co., Springfield, 111. 2. Austin, C. R. (1963) Fertilization and Transport of the Ovum, in “Mechanisms Concerned with Conception,” Ed. by C. G. Hartman, McMillan Co., N.Y.C. 3. Austin, C. R. (1967) Capacitation of Spermatozoa, Intemat. J. of Fert., 12, 1, 25. 4. Austin, C. R. (1969) Fertilization and Development of the Egg, in Reproduction in Domestic Animals, 2nd Ed., Cole and Cupps, Academic Press, N.Y.C. 5. Baker, R. D., Dzuik, P. J. and Norton, H. W. (1968) Effect of Volume of Semen and Number of Sperm and Drugs on Trans- port of Sperm in Artificially Inseminated Gilts, J. An. Aci., 27, 1, 88. 6. Bedford, J. M. (1967) Experimental Requirement for Capaci- tation and Observations on Ultra-Structural Changes in Rabbit Spermatozoa during Fertilization, J. Reprod. and Fert., Suppl. 2, 35. 7. Bedford, J. M. (1968) Ultrastructural Changes in the Sperm Head During Fertilization in the Rabbit, Amer. J. Anat., 123, 329. 8. Black, D. L. and Davis, J. (1962) A Blocking Mechanism in the Cow Oviduct, J. Reprod. and Fert., 4, 21. 9. Blandau, R. J. (1967) Oogenesis—Ovulation and Egg Trans- port, in Comparative Aspects of Reproductive Failure, edit, by K. Benirschke, Springer-Verlag, N.Y.C. 10. Braden, A. W. H. (1953) Distribution of Sperm in the Genital Tract of the Female Rabbit after Coitus, Austral. J. Biol. Sci., 6, 693. 11. Casida, L. E. (1950) The Repeat-Breeder Cow, Vlaams Dier- geneesk. Tijdschr., 19, 12, 273. 12. Casida, L. E., Warwick, E. J. and Meyer, R. K. (1944) Sur- vival of Multiple Pregnancies Induced in the Ewe Following Treatment with Pituitary Gonadotropins, J. of An. Sci., 3, 22. 13. Chang, M. C. (1951) Fertilizing Capacity of Spermatozoa De- posited into the Fallopian Tubes, Nature 168, 697. 14. Chang, M. C. (1951) Fertility and Sterility as Revealed in the Study of Fertilization and Development of Rabbit Eggs, Fert. and Steril., 2, 3, 205. 15. Cheng, P. and Casida, L. E. (1948) Fertility in the Rabbit as Affected by the Dilution of Semen and the Number of Sper- matozoa, Proc. Soc. Exptl. Biol, and Med., 69, 36. 16. Crisman, R. O., McDonald, L. E. and Thompson, F. N. (1980) Effects of Progesterone or Estradiol on Uterine Tubal Transport of Ova in the Cow, Theriog., 13, 2, 141-154. 17. Crisman, R. O., McDonald, L. E. and Wallace, C. E. (1980) Oviduct (Uterine Tube) Transport of Ova in the Cow, Amer. J. Vet. Res., 41, 4, 645-647. 18. Doak, R. L., Hall, A. and Dale, H. E. (1967) Longevity of Spermatozoa in the Reproductive Tract of the Bitch, J. Reprod. and Fert., 13, 1, 51. 19. Dukelow, W. R., Williams, W. L. and Chemoff, H. N. (1965) Biochemical Nature of the Decapacitation Factor in Seminal Plasma, J. Dairy Sci., 48, 6, 807. 20. First, N. L., Short, R. E., Peters, J. B. and Stratman, F. W. (1965) Transport of Spermatozoa in Estrual and Luteal Sows, J. An. Sci., 24, 3, 917 (Abstr.). 21. Greenwald, G. S. (1967) Species Differences in Egg Transport in Response to Exogenous Estrogen, Anat. Rec., 157, 163. 22. Hafez, E. S. E. (1959) Tuboovarian Mechanisms and Ova Re- ception in Mammals. A Comparative Study, Cor. Vet., 49, 4, 459. 23. Hafez, E. S. E. (1961) Structural and Developmental Anomalies of Rabbit Ova, Intemat. J. of Fertil., 6, 4, 393. 24. Hafez, E. S. E. (1963) Physiologic Mechanisms of Implanta- tion, Cor. Vet., 53, 3, 348. 25. Hafez, E. S. E. and Blandau, R. J. (1969) The Mammalian Oviduct, Sympos. at Wash. State Univ., Univ. of Chicago Press, Chicago, 111.PHYSIOLOGY OF FEMALE REPRODUCTION 433 26. Hartman, C. G. (1963) Mechanisms Concerned with Concep- tion, McMillan Co., N.Y.C. 27. Hunter, R. H. F. and Dzuik, P. J. (1966) Fertilization of Pig Eggs Three Hours Postinsemination, J. An. Sci., 25, 4, 1265. 28. Kirton, K. T. and Hafs, H. D. (1965) Sperm Capacitation by Uterine Fluid or Beta-Amylase in vitro., Science, 150, 618. 29. Lanman, J. T. (1968) Delays During Reproduction and Their Effects on the Embryo and Fetus, New Engl. J. of Med., 278, 993, 1047, 1092. 30. Lineweaver, J. A., Hafez, E. S. E., Ehlers, M. H., Dickson, W. M. and King, J. R. (1970) Sperm Transport in Cattle, Cor. Vet., 60, 3, 372. 31. Lovell, J. E. and Getty, R. (1968) Fate of Semen in the Uterus of the Sow, Amer. J. Vet. Res., 29, 3, 609. 32. MacLeod, J., Gold, R. Z. and McLane, C. M. (1955) Corre- lation of the Male and Female Factors in Human Infertility, Fert. and Steril., 6, 2, 112. 33. Mahajan, S. C. and Menge, A. C. (1966) Influence of the Uter- ine Environment on the Fertilizing Capacity of Sperm in Cattle, J. An. Sci., 24, 4, 1083. 34. Mahajan, S. C. and Menge, A. C. (1967) Influence of Repro- ductive Phase on the Inflammatory Response and Rate of Sperm Removal in the Uterus and Oviduct of the Cow, Amer. J. Vet. Res., 28, 125, 1037. 35. Mattner, P. E. (1968) The Distribution of Spermatozoa and Leu- cocytes in the Female Genital Tract in Goats and Cattle, J. Re- prod. and Fert., 17, 253. 36. Mattner, P. E. and Braden, A. W. H. (1963) Spermatozoa in the Genital Tract of the Ewe, Austral. J. Biol. Sci., 16, 2, 473. 37. McLaren, A. (1967) Advances in Reproductive Physiology, Ac- ademic Press Inc., N.Y.C. 38. McLaren, A. (1980) Fertilization, Cleavage and Implantation, in Reproduction in Farm Animals, edit, by E. S. E. Hafez, Lea and Febiger, Philadelphia, Pa., 4th Edit. 39. Noyes, R. W., Adams, C. E. and Walton, A. (1958) Transport of Spermatozoa into the Uterus of the Rabbit, Fert. and Steril., 9, 4, 288. 40. Oxenreider, S. L. and Day, B. N. (1965) Transport and Cleav- age of Ova in Swine, J. An. Sci., 24, 413. 41. Peterson, R. N., Russell, L., Bundman, D. and Freund, M. (1980) Sperm-egg Interaction. Evidence for Boar Sperm Plasma Membrane Receptors for Porcine Zona Pellucida, Science, 207, 4, 73-74. 42. Sobrero, A. J. (1963) Sperm Migration in the Female Repro- ductive Tract, in Mechanisms Concerned with Conception, C. G. Hartman, edit., McMillan Co., N.Y.C. 43. Stambaugh, R. and Buckley, J. (1968) Zona Pellucida Disso- lution Enzymes of the Rabbit Sperm Head, Science, 161, 585. 44a. Starke, N. C. (1949) The Sperm Picture in Rams of Different Breeds as an Indication of their Fertility. II—The Rate of Sperm Travel in the Genital Tract of the Ewe, Onderstep, J. Vet. Sci. and An. Ind., 22, 2, 415. 44b. Szollosi, D. (1966) Time and Duration of DNA Synthesis in Rabbit Eggs After Sperm Penetration, Anat. Rec., 154, 2. 45. Van Demark, N. L. (1958) Spermatozoa in the Female Genital Tract, Intemat. J. of Fertil., 3, 1, 220. 46. Van Demark, N. L. and Hays, R. L. (1954) Rapid Sperm Trans- port in the Cow, Fert. and Steril., 5, 2, 131. 47. Willett, E. L. and Larson, G. L. (1952) Fertility of Bull Semen as Influenced by Dilution Level, Antibiotics, Spermatozoan Numbers and the Interaction of these Factors, J. Dairy Sci., 35, 11, 899. 48. Williams, W. L., Abney, T. O., Chemoff, H. N., Dukelow, W. R. and Pinsker, M. C. (1967) Biochemistry and Physiology of the Decapacitation Factor, J. Reprod. and Fert., Suppl. 2, 11.Chapter XIII INFERTILITY IN THE COW It has been estimated by Asdell that sterility and re- productive troubles in dairy cattle in the United States cost $250,000,000 annually. In New York State these losses annually amount to $20,000,000 when figured on the basis of data collected on the causes of culling from Dairy Herd Improvement Association herds. Culling of cows on the basis of sterility has increased from 1.1 per- cent to 2.5 percent in the last 15 years.3 Much of this rise may be accounted for by better recording. In North- eastern United States 12 to 19 percent of dairy cows culled from herds each year were culled because of infertility or sterility.104 140,160 The great economic importance of cattle infertility on a world wide basis has been consid- ered.45 Artificial insemination, increased productivity of cows, higher costs of raising and feeding cows, and bet- ter education of the farmer and veterinarian all have served to emphasize the importance of maintaining the fertility in dairy and beef herds and individual cows. The control of brucellosis by vaccination and testing, and trichomoniasis by AI, and vibriosis with antibiotic- treated semen and vaccination of cows has greatly re- duced the severe problem of contagious genital infec- tions but has focused attention on other causes of abor- tion and infertility. The increased movement of purebred cattle between states and herds has occasionally resulted in the introduction of an infectious venereal disease that seriously affected the herd’s fertility. The widespread use of hormones as aids or cures in treating certain ste- rility problems has been recognized. With larger herds and greater mechanization of farms, management prob- lems of handling cattle, detecting estrus for artificial in- semination, maintenance of records, and nutritional problems are becoming increasingly important. With more veterinarians taking an active interest in this field many farmers are coming to realize the value of the routine preventive health practices of pregnancy and routine genital examinations in maintaining good productive and reproductive levels in a herd. A well-managed dairy herd should have 60 to 70 per- cent of the cows conceive on first service with an av- erage of 1.3 to 1.7 services per conception. There should be less than 10 percent of the cows with reproductive “problems.” The calving interval from one calving to the next should be between 12 and 13 months. It has been reported that for every day a cow has failed to conceive beyond 90 to 100 days postpartum it is costing the farmer 1 to 2 dollars. Thus in a poorly-managed herd of 100 cows with a calving interval of over 13 months for every 30 days reduction in the calving interval the farmer would realize an increase in income of $3,000 to $6,000 in 1982 dollars.87 132 Even in high-producing cows it is necessary to maintain this 12 to 13 month calving interval because in the cow’s lifetime there would be more peaks of high production and a greater total production of milk. Fur- thermore with longer calving intervals the cow is more likely to freshen at the time of year when prices for milk are the lowest and there is a greater chance for culling the cow for economic reasons. In beef herds the cow that fails to conceive during the breeding season is usually culled for economic reasons. Since 95 percent of the variation in calving intervals or breeding efficiency is due to nongenetic reasons, the importance of manage- ment and veterinary supervision of the reproductive ac- tivities in the herd is obvious.40,152 There is no such thing as a normal infertile cow. Either there is a clinical or nonclinical pathologic cause or the animal has not been properly exposed to fertile semen during an estrous period. In the next section will be a discussion of the reproductive physiology of the bovine animal. This is essential to the understanding of the pathologic causes of infertility and for the devising of management practices that will promote a high level of fecundity. Bovine Reproductive Physiology The Bovine Estrous Cycle—The cow is polyestrous and comes in estrum throughout the year. The estrous cycle length in heifers is an average of 20 days with 85 percent of the heifers having cycles of 18 to 22 days. In cows the average length of the estrous cycle is 21 days and 84 percent of the cows have cycles of 18 to 24 days.2 The individuality of the animal may affect the cycle length, but the season has no effect on cycle length. In beef cattle the average length of the estrous cycle is 20 days; 434INFERTILITY IN THE COW 435 79 percent of the cattle have cycles of 17 to 23 days. It was reported that 83 percent of the heifers had estrous periods within the range of 10 to 21 hours in length while 93 percent of the cows fell within the range of 13 to 27 hours.2 The average duration of estrum was about 18 hours."138 Ovulation is spontaneous in the cow and oc- curs an average of 10.5 to 15.5 hours, average 12 hours, after the end of estrum. This range of time may vary from 2 to 26 hours. Heifers tend to ovulate about 9 hours after the end of estrum. About 80 percent of the ovu- lations occur from 4 P.M. to 4 A.M.2,4 In Zebu and crossbred Zebu cattle the average length of estrum is short, 4.7 to 7.4 hours, range 2 to 14 hours, respectively.I 32'109'"3 Zebu cows tend to associate with the bull for a longer period with many of the cattle ex- hibiting estrum during the night and early morning hours.118 The average duration of estrum in European dairy or beef cattle in tropical countries and in southern states is shorter, 12 to 13 hours, than in the temperate zone.32'47'60 Bos indicus, Zebu or Indian cattle, or their crosses are more heat tolerant, and have a higher fertility in spring, summer and fall months in the countries near the equator.17 They tend to be less fertile in the winter months. They seldom come into estrum while nursing their young, possibly for nutritional reasons.32 Brahman cattle have calving intervals of 414 to 554 days.113 They seldom show heterosexual activity of mounting other cows. Brahman cattle had a lower LH peak at estrus, a smaller corpus luteum and lower progesterone values in diestrus than European cattle.113 Their gestation periods vary from 271 to 310 days, average 293 days.109 Euro- pean cattle, Bos taurus or cattle of the temperate zone are less adapted to hot climates. Three to 6 percent of pregnant cows, especially the first trimester of pregnancy, exhibit signs of estrus and up to 85 percent of these cows were rebred during pregnancy493 (see Chap. II, Pregnancy Diagnosis). In 5970 pregnancy examinations in cows, 59.2 percent were pregnant in the right horn and 40.8 percent in the left. Of 4290 heifers, 54.4 percent were pregnant in the right horn and 45.6 percent in the left horn.103 Thus 55 to 60 percent of the ovulations and pregnancies occur in the right ovary and horn. Transuterine migration of the bo- vine embryo is very rare. Manual removal of the corpus luteum, which is only possible in cattle, produced estrum in 3 to 5 days, the average time being 4.2 days.4 In over 300 Herefords in which the corpus luteum was expressed manually about equal numbers came into estrum on each day from 2 to 7 days.14 In the author’s experience, most cattle show estrum the third day after removal of the corpus luteum and if external symptoms of estrum are not observed, the animal should be inseminated or bred late on the third day or on the fourth day. Because of the occasional hem- orrhages and secondary adhesions or rare deaths, this practice is presently seldom followed as equally satis- factory results can be obtained with a luteolysing dose of a prostaglandin with the onset of estrus occurring in the same time period as manual removal of the corpus luteum. The symptoms of estrum in the cow are characterized by a great amount of homosexual behavior. Normal and abnormal estrous behavior patterns in cattle have been described.44'46'59 The amount of sexual activity is generally related to the amount of estrogen present but in a few ovariecto- mized animals estrogen failed to produce symptoms of estrum possibly due to a lack of progesterone since the latter is synergistic with estrogens in producing signs of estrum.4,93 There are great differences in individuals in the intensity of estrous symptoms exhibited. Heifers usu- ally exhibit more marked symptoms of estrum than do cows. When artifical insemination is practiced and a bull does not run with the herd, careful observation of cows by the owner or herdsman twice a day or more often at non-feeding periods is essential for the maintenance of a satisfactory breeding program. The onset of estrum was gradual over a period of several to 24 hours in 66 percent of the cows and heifers, and abrupt in 34 percent.115 An- imals in the “coming in” stage of estrum were often rest- less, raised and twitched their tails, discharged some milky-colored mucus from the vulva and often associ- ated with a larger or more aggressive cow. This “coming in” stage was more noticeable in heifers. The cow in estrum is usually restless and often re- mains standing rather than lying down. The appetite, ruminations, and milk yield may be slightly decreased. Bellowing is frequent especially if the cow is separated from the herd. The cow in estrum will attempt to mount other cows and will stand to be mounted by others cows. This latter sign of standing to be mounted is the most significant and important sign to observe in the detection of estrus. This characteristic immobility or willingness to stand without moving for the male to mount and com- plete the copulatory act is the cardinal sign of estrus in all domestic animals, cow, mare, ewe, doe, sow, bitch and queen. Although the vulva of the cow in estrum was sniffed by other cows, the cow in estrum was never observed to sniff the external genitals of the other cattle.115 The heterosexual and homosexual behavior of the cow in es- trum was always more intense than that of its partners. The tail may be raised and there is often a long string of clear mucus hanging from the vulva or present on the436 VETERINARY OBSTETRICS tail or buttocks. The vulva is usually somewhat con- gested, flaccid, edematous, and relaxed. The cow in a stanchion tends to hold her head high and has an alert, interested, even inquisitive, attitude. The cow may uri- nate frequently. Three to 6 percent of cows, with oc- casional reports as high as 14 to 18 percent of cows showed signs of estrum after conception.39,60'112 This oc- curred most often the first trimester of the gestation pe- riod over a range of 11 to 213 days with a mean of 63 days. On vaginal examination the vaginal mucosa, espe- cially the cranial portion, is congested and slight edema- tous. The large amounts of stringy mucus, 50 to 100 ml., present in the vagina at estrum comes from the va- ginal and cervical mucous cells under the influence of estradiol.88 At the time of estrum the viscosity of the mucus is lowest, and its flow elasticity greatest. When estrous mucus is smeared thinly on a slide and dryed the high salt or NaCl content crystallizes into a fern or ar- borization pattern. The external os of the cervical canal is usually pink, congested, edematous, and slightly re- laxed and open at the time of estrum. The cow in estrum seldom objects to and usually stands well for a vaginal examination. The vaginal speculum slips in easily due to the viscid mucus present in the vagina. Vaginal smears during proestrum and estrum show increased numbers of comified cells, but variations between cows are so great that the vaginal smear in the cow cannot be regarded as a reliable indication of estrum. During diestrum the va- gina is pale and dry and the mucus is scant and rather sticky. The speculum therefore passes with greater dif- ficulty than during estrum. On rectal examination during estrum and for 1 to 2 days before and afterwards, the uterus is usually erect, turgid, and somewhat edematous due to the estrogenic stimulation of the uterine muscle and tissues. This is most noticeable in heifers. Usually 1 to 5 smaller follicles start development but undergo atresia during estrum and after ovulation. On rectal palpation early in estrum the ovar- ian follicle is about 1 cm. in diameter or less, and smooth, convex, tense and slightly fluctuating due to the follic- ular fluid present. This fluid is amber in color. The ma- turing Graafian follicle before rupture is 10 to 20 mm, or 1 to 2 cm, in diameter. At the time of ovulation in the cow only a very slight amount of bleeding occurs at the rupture site. The corpus luteum develops rapidly from the granu- losa and theca cells of the collapsed follicle under the tropic influence of LH from the pituitary gland. By 48 hours after ovulation the corpus luteum is about 1.5 cm in diameter and slightly crepitant on palpation per rec- tum. By 7 to 8 days after ovulation the corpus luteum has reached its maximum size of 2 to 2.5 cm. in di- ameter. The corpus luteum in the cow is irregular in shape, usually oval, and with a cone-like projection about 1/2 to 1 cm. above the surface of the ovary. The corpus lu- teum of estrum weighs from 4.1 to 7.4 grams and is nearly similar in size and weight to the corpus luteum of pregnancy.12 The size of the corpus luteum based on manual palpation and observation on laparotomy at 7 to 8 days postestrus has no correlation with progesterone production or plasma progesterone levels.113c The corpus luteum of pregnancy decreases in size just before par- turition but may be palpable for many months after par- turition as the corpus albicans, a small fibrous structure, on the ovary. The mature corpus luteum is brownish yel- low to yellow orange in color, giving it the common name of “yellow body.” In about 25 percent of the corpora lutea there is a small cavity about 0.4 cm. in diameter. In a few cases large cavities 1 cm or more in diameter, filled with an amber fluid may be present.4,12 These cor- pora lutea containing large cavities are spoken of a cystic corpora lutea. Cystic corpora lutea have not been ob- served in a cow in the last third or half of the gestation period.79 Graafian follicles that failed to ovulate but be- came partially luteinized are called luteal cysts. These pathologic luteal cysts have a smooth convex surface due to the thick-walled fluid-filled follicle that failed to ovu- late. While the cystic corpus luteum follows a normal ovulation and although it contains a variable amount of fluid in its center, lutein tissue protruding through the site of ovulation produces an irregular, raised area on the surface of the ovary.12 Normal corpora lutea are ir- regular in outline and have a liver-like consistency. Cys- tic corpora lutea are similar to normal corpora lutea on palpation except they are usually larger, more spherical and fluctuate on pressure. The cystic corpora luteum is not considered to be pathological but the luteal cyst is pathological. The corpus luteum maintains its size until about 48 hours before estrum, after which time its size diminishes rapidly. Its color at this time of rapid invo- lution is light orange to yellow. By 48 hours after estrum its size is about 1 cm. and by about 10 days after estrum 0.5 cm.12 As it becomes older its color turns to dark orange and then brick red. This eventually becomes a small white fibrous area the size of a large pin head, the corpus albicans. On rectal palpation, when one ovary is definitely larger than the other the difference is usually due to the presence of a corpus luteum in that ovary. Cysts may also cause this discrepancy in size. In cows, body temperatures taken deep in the vagina were lowest just before estrus, high on the day of estrus due to the cow’s activity, low at the time of ovulation and high during the luteal phase of the cycle as inINFERTILITY IN THE COW 437 women.170 Determining body temperature changes, the glucose content, or the arborization or fern pattern of cervical mucus were not practical tests for indicating es- trus or heat and the time to breed cattle.9,75’170 Direct vi- sualization of the ovaries of cattle during the estrous cycle by endoscopic methods has been reported.8 92 About 15 to 36 hours after ovulation, about 24 to 48 hours after estrum, or about 40 to 60 hours after the on- set of estrum a discharge of blood and mucus from the vulva may be observed in many cows. This metrorrhagia from the edematous endometrium in the caruncular areas occurs due to a breakdown of congested capillaries. Al- though clinical evidence of bleeding occurs in only 80 percent of heifers all show the presence of red blood cells on examination of vaginal swabbings at this time.159 Metrorrhagia in cattle was observed in about 75 percent of heifers, and 48 percent of cows.4 In any particular animal clinical bleeding may not be observed following every estrum. It is a common belief amongst a few farmers that post- estrual bleeding following service is an indication that conception did not occur. In 100 heifers that were bred, 81 showed clinical prostestrual bleeding. Eighty-five percent of those that conceived bled, and of those that did not conceive, 74 percent bled. In another group of 100 cows, 61 bled and 69 percent of those that con- ceived bled, and of those failing to conceive, 39 percent showed metrorrhagia.141 The metrorrhagia that occurs in cattle is not similar to menstruation in primates, as it occurs at the end of the estrogenic phase of the cycle or early metestrum, following estrogen withdrawal. While in primates bleeding occurs at the end of the luteal phase of the cycle or the end of diestrum, following proges- terone withdrawal.65 Small perimetrial hemorrhages in the subserosa of heifers’ uteri were commonly seen from estrum to the fourth day postestrum. Hemorrhages of this nature were not observed in pluriparous cows.159 Optimal service time—Insemination of cattle be- tween 8 to 24 hours, or especially 7 to 18 hours, before ovulation results in the highest rates of conception.146 Ovulation should occur in heifers in the temperate zone about 22 to 36 hours after the onset of estrum. Concep- tion rates were still better than 50 percent from service more than 24 hours before ovulation, if the cow was in estrum, to within 6 hours of ovulation. Conception rates drop rapidly in cows bred after ovulation or after 10 to 18 hours after the end of estrum.20 138 146 In other studies11,146 conception rates of cows inseminated about 10 hours after the onset of estrum was about 82 percent; at 20 hours after the onset of estrum or soon after going out of estrum 62 percent; by 30 hours after the onset of estrum or near the expected ovulation time, the concep- tion rate was 28 percent. This rate dropped rapidly so that by 50 to 60 hours after the onset of estrum very few cows conceived. However, a conception rate of 20 to 30 percent was reported if cattle were inseminated while they were showing metrorrhagia and a bloody mucous dis- charge.7,85 Based on the above data, the best time for insemination is from just before the middle of estrum to 6 hours after estrum or from 6 to 24 hours after the onset of standing estrus.1036 (See repeat-breeding cows.) In 7,346 dairy herds in which 455,196 cows were artificially in- seminated in one year the nonreturn rate of ()6 percent was similar for cows serviced once a day at about the same hour, once a day either in the A.M. or P.M. or twice a day with cows observed in estrus in the A.M. serviced that P.M. or cows in estrus in the P.M. being serviced the next A.M. When the herd size was 20 to 50 cows, 51 to 100 cows, 101 to 150 cows and over 151 cows the nonreturn rates were 68, 66, 64 and 62 percent respectively. Cows in loose housing had a 64 percent nonreturn rate compared to 67 percent in tie or stanchion housing.1036 Although the possibility of conception may be some- what less in cows with shorter- or longer-than-normal cycles of 17 to 25 days, many of those cows do conceive when they are bred.149 Intravaginal deposition of semen in artificial insemi- nation gives poor conception rates because of the small numbers of spermatozoa deposited. The rectovaginal technique for introducing semen into the cervix was su- perior to the speculum technique with about 16 percent better conception rate.149 Deposition of semen in the cra- nial cervical canal gave equally as good results as semen deposited in the uterine body or horns and the technique was simpler. Because the endometrium is easily injured, and infection and occasional abortion may result from intrauterine deposition of semen in pregnant cows, and since about 3.5 to 6 percent of pregnant cows show es- trum, it has been recommended that cervical deposition be used instead of the uterine deposition of semen.149 Hormones of the Estrous Cycle—The level of hor- mones in cattle, with the possible exception of LH, are low in comparison to other domestic animals. In recent years highly sophisticated assay techniques have been devised that have further delineated the hormonal control of the estrous cycle in cattle. The subject of hormone levels in the reproductive endocrine glands and the blood plasma at different stages of the estrous cycle and during pregnancy was reviewed.25,116,156 Follicle stimulating hormone (F.S.H.) plasma levels range from 300 to 550 ng/ml., with low values for 3 or 4 days after estrus and higher values at estrus coinciding with peak values of luteinizing hormone (LH). Luteinizing hormone (L.H.)438 VETERINARY OBSTETRICS plasma levels range from 1-1/2 to 3 ng/ml. produced by frequent daily episodic fluctuations or pulses with a gradual rise to 4 or 5 ng/ml. just before the next estrus with a very high peak, the LH surge, of 11 to 15 ng/ ml. early in estrus that lasts for only a few hours. Progesterone levels in plasma average 5 to 7 ng/ml. (range 4 to 9 ng/ml.) during the midcycle from 6 to 19 or 20 days when two to three days before the next estrus regression or involution of the corpus luteum occurs rap- idly under the influence of prostaglandins from the en- dometrium and possibly the corpus luteum and proges- terone levels fall below 1 ng/ml. during estrus and then slowly rise to normal diestrual levels by day 6. Follow- ing superovulation in the cow progesterone levels in the last milk rose from 8.2 ng/ml. at midcycle to 52.6 ng/ ml. and correlated with the number of ovulations and embryos recovered.433 Estradiol levels in plasma average 2 to 7 pg/ml. from the day after estrus with a slight peak at midcycle to 2 or 3 days before the next estrus when the estradiol level rises and reaches a peak early in the next estrus of 10 to 20 pg/ml., after which it falls rapidly. An excellent recent review of the physiology and en- docrine control of the estrous cycle of domestic food- producing animals has been published.66b The role of oxytocin in luteolysis is discussed in light of the recent observation that oxytocin is present in considerable con- centration in the bovine corpus luteum where it is prob- ably synthesized. Large quanities of arachidonic acid, a prostaglandin precursor, is also found in the corpus lu- teum as well as the uterine endometrium. Recent studies have shown that PGI2 is luteotropic and PGF2a is luteo- lytic. Thus a balance of these two prostaglandins may determine the functional state of the bovine corpus lu- teum. The presence and release of oxytocin from the bo- vine ovary during the estrogenic phase of the estrous cycle may be responsible for the greatly increased tone of the uterine musculature characteristic of estrus in the bovine species. The blood plasma levels of certain reproductive hor- mones during the bovine estrous cycles are generally quite different from those during the gestation period when F.S.H. and L.H. are low, the latter about 1.0 ug/ml. Progesterone levels are about the same as during diestrus and decline to very low levels at parturition. Estrogen levels rise during late gestation to a peak at parturition of 3000 to 5000 pg/ml. total estrogen. The half-life of the progesterone in the blood in cattle was short, about 10 to 20 minutes, indicating the need during the estrous cycle and pregnancy for a continuous large supply.76 Normal corpora lutea in pregnant heifers at 15 days after insemination contained an average of 270 mg. total pro- gesterone and no pregnant heifers had less then 100 mg. which was the minimum necessary for embryo sur- vival.136 In ovariectomized cows conditioned with 0.2 to 0.4 mg of estradiol/1000 lbs, 1 to 4 mg of progesterone would produce maximal synergistic action with the production of typical estrum lasting 6 to 12 hours.93 Both of these hormones necessary for typical expression of estrus are produced in the ovary during the preovulatory devel- opment of the follice. The CL from the previous cycle contains measurable progesterone for several days after estrus.54 Large doses of progesterone 30 to 60 mg. an- tagonized or prevented estrous behavior in estrogen-treated ovariectomized cattle. Puberty and the onset of estrous cycles (See Chapter 12)—As discussed previously placing young heifers on a nutritious diet high in TDN from birth can hasten pu- berty and the onset of estrous cycles. This can also per- mit heifers to be bred successfully at a younger age if they are continued to be fed well during the first ges- tation period. Breeding heifers on the basis of body weight is therefore indicated, so that heifers can calve at about 2 years of age without serious calving problems. Crossbred heifers tend to show estrus a month or so earlier in life than the parent breeds. Depending on the level of nutri- tional intake, heifers first show estrus from 7 to 18 months or 28 to 72 weeks of age. In 53 Holstein heifers the time after birth at which first estrus occurred was more vari- able than the weight which averaged 42 weeks and 610 lbs., respectively.96 During the prepuberal period most heifers had one or more follicles with a diameter of 0.5 to 2 cm. and showed evidence of increased follicular ac- tivity about 20 to 40 days before the first ovulation. Variable signs of estrus were observed at these times. At the first estrus 74 percent of the heifers exhibited “silent” estrus, or failed to show signs of estrus. This percentage dropped to 43 percent the second estrus and 21 percent the third estrus. Thereafter the estrous periods and signs were normal. Ovulation failed to occur in 13 percent of 53 heifers after the first estrus but thereafter failure of ovulation was rare. Nearly similar results were reported in 37 Holstein heifers in a later study.101 Heifers should be of sufficient age and weight to reach puberty prior to any hormonal treatment to induce or control es- trous cycles if acceptable pregnancy rates are desired.1326 The postpartum period and the onset of estrous cycles—A review of the literature on postpartum ovar- ian activity and uterine involution indicated the interval from parturition to first observed estrum varied from 30 to 76 days in dairy cattle and 40 to 48 days in beef cattle.98 "100 The time required for uterine involution based on rectal palpations and clinical observations and mea-INFERTILITY IN THE COW 439 surements varied from 26 to 52 days in dairy cattle and 38 to 56 days in beef cattle. In general the interval from calving to first estrus was greater in cows with higher production, in cows nursing calves or being milked 4 times a day, in cows on a poor or low level of nutritive intake, and in older pluriparous cows with 4 or more parturitions.121157 A longer postpartum interval to first estrum occurred in nursed dairy cows, anemic cows and in those being fed thyroprotein. When Brahma-Hereford heifers were allowed to suc- kle their calves only once a day, starting at postpartum day 30, the postpartum interval to first estrus was 69 days average vs 168 days for control heifers that suckled their calves normally. These times were shortened to 32 and 124 days when the experiment was started at 21 days postpartum and the level of nutrition was increased.113b This relationship of nursing and the delayed onset of es- trous cycles after calving was further reported upon.165 Involution of the uterus was prolonged in pluriparous cows when compared to primiparous cattle and also in abnormal parturitions characterized by dystocia, retained placenta, twinning, metritis, milk fever, displaced aboma- sum and other disease or stress factors. Ovariectomy and physiologic doses of estradiol had no effect on uterine involution but progesterone delayed uterine regression.90 However others43 reported that progesterone and estra- diol somewhat shortened the intervals to ovulation and conception. Thus uterine involution proceeds normally even if reproductive cycles and estrus do not occur. Ex- ogenous estrogens or progesterone, ovariectomy, or nursing calves have little or no effect on the rate of uter- ine involution.133 Sloughing of caruncular tissue oc- curred between 7 and 14 days postpartum and by 30 days the surface epithelium over the caruncular areas were re- generated.157 Normal cows usually develop a mature fol- licle that ovulates and is followed by the formation of a corpus luteum at 13 to 15 days after calving.89,98'100157 The duration of the estrous cycle from the first ovulation to the second ovulation was 3 to 4 days shorter than the normal length cycles, 20 to 21 days, that followed there- after. “Silent” estrus occurred in 77 percent of the first postpartum ovulations, 54 percent of the second and 36 percent of the third ovulations, and was more common in high-producing cows.98-100 Cystic corpora lutea and cystic follicles were fairly common and a failure of ovu- lation occurred occasionally in up to 10 percent of the cycles.'1 Ninety percent of the first corpora lutea devel- oping within 15 days after calving formed on the ovary opposite to the previously gravid horn; this percentage dropped to 60 percent in cows ovulating 15 to 20 days after parturition.89 The corpus luteum of pregnancy had regressed at 4 days postpartum to 1 X 1.5 cm in size and was usually not palpable after 14 days postpartum. Uterine involution in normal cows is largely com- pleted as indicated by the size of the uterus and the con- dition of the endometrium at about 30 days postpartum and since normal estrous cycles are usually occurring by 30 days after calving98"100,157 it is logical to ask whether it might not be feasible and practical to commence breeding a month before the generally previously rec- ommended minimal time of 60 days postpartum. In the early 1950’s a number of studies conducted on early postpartum breeding of dairy cows indicated that breeding cows prior to 60 days resulted in conception rates below 50 percent, an increased number of services per conception and even prolonged the postpartum in- terval to conception with adverse effects on the subse- quent pregnancy and parturition.74,125,142"146 Subsequent studies on large numbers of cows showed that conception rates per service in cows bred 20 days or less postpartum average 18 percent, those bred 20 to 40 days averaged about 35 to 45 percent, from 40 to 60 days postpartum about 50 to 60 percent. A definite in- crease in number of services per conception occurred in cows bred prior to 50 days postpartum. These early bred cows had a shorter calving interval, often averaging 11 to 12 months, due to a reduction in days from calving to con- ception. There was no evidence that early postpartum breedings were associated with an increased incidence of delayed returns to estrus, infertility or subsequent abortions or retained placentas. 15,42'57,106,131b,137a-161,162 Since the optimum calving interval for maximum daily milk production in high-producing dairy herds is contro- versial and since for high milk production a dry period of 42 days or more is essential,42 a somewhat flexible management program is indicated based on the age and productivity of the individual cow, the ease of calving and the presence or absence of periparturient disease and the evaluation of the recovery or involution of the genital tract based on routine postpartum rectal examinations. Two and three-year-old cows had a 61 percent postpar- tum first service conception rate. Cows 4 years-old and older had only a 35 percent conception rate on first ser- vice postpartum. The occurrence of one or more post- partum diseases reduced the first service conception rate and milk production was negatively correlated with con- ception.I37a A desirable goal of a calving interval of 12 to 13 months in a high-producing herd translates into a postpartum “open” interval of 85 to 115 days, respec- tively, for all of the cows in a herd. Having many cows over or under these figures in order to arrive at a desir- able average figure should be regarded as poor manage- ment. Further information on this important postpartum period will be discussed later in this chapter.440 VETERINARY OBSTETRICS Conception rates for estrous cycles of less than 18 days in length were poor, about 34 percent, in cows not bred at the previous estrus.38,145 Increased calving intervals in dairy and beef cows often occur after they reached 5 years of age or after their fourth lactation period. Physiologic utero-pituitary-ovarian relationships and the luteolytic mechanism controlling the estrous cycle—The corpus luteum, follicle, and the placenta are the only three transitory endocrine glands. The under- standing of the mechanisms controlling the formation and involution of the corpus luteum is essential. The corpus luteum is present and active in the fertile cow for about 320 days a year. It only involutes long enough in the normal cow to permit a follicle to mature and ovulate in order to perpetuate the species. The presence of a func- tioning corpus luteum on the ovary is of much more sig- nificance than various stages of follicular development or atresia. Although more work is required to explain certain as- pects of the utero-pituitary-ovarian relationships, the major aspects of this relationship have been re- viewed.50,51,133 It is generally accepted that LH which is the principal luteotropic hormone in the cow128 is re- leased from the anterior pituitary gland to produce ovu- lation; corpus luteum formation from the granulosa and thecal cells; corpus luteum persistence; and secretion of progesterone necessary for suppression of follicle growth, early embryonic growth, development and attachment, and for the maintenance of normal pregnancy. The pres- ence of the embryo with its elongated trophoblast is nec- essary by about the 14th day of the cycle to prevent the involution of the corpus luteum which starts, in the ab- sence of the embryo, about the 15th or 16th day of the cycle. The process causing the regression or involution of the corpus luteum of the estrous cycle to permit Graafian follicle development is called the luteolytic mechanism. This releases prostaglandin F2a from the en- dometrium in the absence of the substance or hormone from a developing blastocyst.10 This mechanism of es- trous cycle regulation is more complex than realized ten years ago and possibly involves a balance or interaction between ovarian steroids, gonadotropic hormones and the luteotropic action of prostacyclin early in the cycle94 as well as other unknown influences. If conception has occurred the conceptus prevents the release of prosta- glandin and the resulting involution of the corpus luteum and causes pregnancy to be maintained. In the cow the prostaglandin from the endometrium is carried to the ovary by the local utero-ovarian pathway.52 Many studies in- fluencing and elucidating but not completely explaining, the luteolytic mechanism have been performed.52,116 Thyroidectomized or parathyroidectomized cows were fertile and could carry fetuses to term and rebreed. Low fertility associated with high environmental temperatures was not associated with depressed thyroxine secretion rates.162 There was no evidence that feeding iodinated casein caused infertility, even after 2 years of continuous feeding. The thyroxine secretion rate in dairy cattle was 67 percent higher than in beef cattle.108 Adrenal function in relation to reproduction was reviewed in relation to ovarian inactivity, cystic ovaries and prolonged or short- ened gestations.151,155 Other endocrine effects—Typical signs of estrus can be produced both clinically and on vaginal and rectal examination in an ovariectomized heifer by the daily in- jection for 3 days of 0.10 mg. of estradiol or 0.25 mg. of stilbestrol.5 Thus it makes more understandable the reason why massive therapeutic doses of 4 mg of estra- diol and 40 mg of stilbestrol, greatly exceeding the phys- iologic dose, can cause cystic ovaries. Other associated endocrine phenomena related to the uterine luteolytic mechanism and uterine-pituitary-ovar- ian physiology include the following.49-51 Exogenous es- trogens, such as 5 mg estradiol valerate or injections of estradiol having a prolonged effect, given to cattle at midcycle caused early CL regression.18166 This is prob- ably due to an interference with LH release since con- current injections of gonadotropins prevent the regres- sion of the CL. Exogenous estrogen is luteolytic and levels of FSH and LH that promote increased estrogen secre- tion might also promote luteolysis.68 Daily exogenous injections of 100 IU of oxytocin days 2 to 6 after estrus caused the failure of the corpus luteum to develop with an early return to estrus and a short cycle of 10 to 14 days.18,35,37 The author has observed this as a cause for repeated short cycles and infertility when the owner of a high-producing cow gave repeated daily injections of oxytocin to cause milk “let down.” These short cycles are due to the release of prostaglandins from the uterine endometrium by the exogenous oxytocin and the sub- sequent luteolysis is produced by the released prosta- glandins.946 Adrenocorticotropin (ACTH) 100 units daily on days 2 though 8 of the cycle significantly reduced CL weight. The effect of ACTH on the adrenal gland to pro- duce corticosteroids that can cause abortion as well as uterine involution is noteworthy.18 An injection of LH in an adjuvant at midcycle or daily injections of HCG starting at day 15 prolonged the life of the CL and in- creased estrous cycle length in cattle.164,167 Although these injections of HCG caused accessory corpora lutea to de- velop, it had no effect on embryo survival. Thus, as ex- pressed by Short127 the CL can be “murdered” by the local effect of the uterine luteolysin prostaglandin on the CL; it can be “starved to death” by the removal of theINFERTILITY IN THE COW 441 tropic stimulus, LH, due to the systemic effect of prosta- glandins and estrogens on the hypothalmus and pituitary gland; or the CL can die of “old age” since the CL in each species has a finite life span. Synchronization of Estrous Cycles or Ovulation Control—Estrus synchronization or control of the es- trous cycle and ovulation whereby one to many heifers or cows in a beef or dairy herd could be brought into estrum at a specific time is highly desirable from a prac- tical, economic standpoint to breed cows artificially to proven sires, to shorten the breeding season and cluster calvings, and to improve estrus detection. Manual re- moval of the corpus luteum per rectum was a common practice for producing estrus until recently. (See Section on Anestrus.) This practice frequently produced bleed- ing, adhesions and ovarian damage with occasional hemorrhage and deaths. The first endocrine products available and used for this purpose were stilbestrol and other estrogenic products. These products could produce signs of estrus within 24 hours after injection but since a physiologic estrus and ovulation did not occur con- ception rates were extremely low and occasionally cystic ovaries were produced. The gonadotropic hormones be- came available and results in inducing estrus were poor, the costs of the drug high, and occasionally superovu- lation or anaphylaxis was produced. About 25 to 30 years ago progesterone and progestins became available that by injection or feeding would sup- press the gonadotropic hormones and the estrous cycle for long periods of 20 to 25 days during which the cor- pus luteum would involute. When the progesterone or progestins were withdrawn estrous cycles with ovula- tions would occur within the next 2 to 6 days. However conception rates at this controlled estrus were too low, 15 percent below controls, to be of practical or economic value.66 Many hundreds of experiments with many hor- mones, such as estradiol and gonadotropic or GnRH hor- mones in combination with progesterone have been per- formed to improve synchronization and fertility with equivocal or little success. The two most promising of these current experimental procedures for synchronizing estrus involve a short term exposure to progesterone of 7 to 9 days. One treatment consists of an estradiol in- jection at the time of implantation of a progestogen, (Syncromate-B) or norgestomet (Searle) under the skin of the ear of heifers or lactating cows that is removed 9 days later.66'80131 This procedure has been combined with the administration of prostaglandins on day 7 or with removal of nursing calves for 48 to 60 hours. (Shang treatment.)26'78131 The second treatment is to insert a progesterone releasing intravaginal device (PRID) fol- lowed by the injection of a luteolytic dose of prostaglan- din the day before removal of the PRID on the seventh day.66 This experimental treatment resulted in 76 percent of the heifers being in estrus within a 24 hour period. This degree of synchrony is important for AI. Concep- tion rates were about 80 percent for both treated and con- trol heifers in which estrus detection practices were ex- cellent and heifers were bred 12 hours after estrus was observed. In another report 44 cyclic Holstein heifers were synchronized with a PRID and 10 mg estradiol benzoate. The PRID was removed 12 days later and 2 days thereafter 84 percent of the heifers were in estrus and bred by fixed AI 56 and 74 hours after PRID re- moval with a 63 percent conception rate.826 Further stud- ies are indicated. Currently only the former of these lat- ter three treatments with steroid or progesterone com- ponents have been approved for use in the U.S. Within the last 5 to 10 years many experimental trials have been conducted to control the estrous cycle with prostaglandins F2a and its analogues.66 When a luteolytic dose of prostaglandins is injected between days 5 and 16 of the estrous cycle, estrus and ovulation follows within 3 to 6 days. They are ineffective when given the first five days of the cycle.66 Currently these products are ap- proved for use in beef cattle, dairy heifers and dairy cows. Increased concentrations of PGF2a or its metabolites can only be detected in the first milking after treatment.66129 Many varied treatments or procedures have been used in synchronizing heifers and cows with the prostaglandins (Lutalyse, (PGF2a) 20 to 35 mg. IM or 5 mg. intrauter- ine) or an analogue (Estrumate or closprostenol, 0.5 mg or 500 ug IM). Some protocols of these treatment pro- cedures include: (1) Heifers are observed carefully for 5 days and bred about 12 hours after estrus. On the fifth day the re- mainder of the heifers are given a single dose of pros- taglandin and these are observed and bred similarly dur- ing the next 4 or more days. Conception rate for control heifers was 74 percent and for treated heifers was about 60 percent.66 Other experiments have utilized breeding by bulls or timed inseminations, either once at 60 to 80 hours, or twice at 72 and 96 hours. If estrus occurs late on the second or early on the third day after the injection of prostaglandin earlier breeding than 72 hours is indi- cated. If a cow shows estrus the day after breeding at 72 hours she should be rebred to get the best conception rates. The best results were obtained when the heifers or cows were bred 12 hours after estrus was first ob- served.1619'28,66'80 A recent report using 12.5 mg PGF2a by this system was superior to (2) as more cows showed estrus, 65 vs 43 percent, respectively and the cost was lower. Breeding based on observed estrus was superior to timed insemination.326442 VETERINARY OBSTETRICS (2) All heifers were injected with prostaglandin twice 11 days (10 to 12 days) apart to attempt to synchronize all heifers and then bred to bulls or with AI on observed estrus or at timed inseminations either single services at 60 to 80 hours, or double services at 60 to 72 and 80 to 96 hours.16'28'80 (3) A variation of the treatments used in (1) or (2), especially for herds with many unobserved estrus pe- riods, would be to rectally examine all heifers and cows every week and treat those that are nonpregnant with a mature corpus luteum and breed on both observed estrus and at a timed insemination unless they coincided within a few hours.123124 (4) Inject all heifers and breed on observed estrus. Those not in estrus after the first injection would be given a second injection in 10 to 12 days and bred at observed estrus or on a timed insemination.16,19 28,80 (5) Many other variations and procedures can be used to assist or improve results including careful observation for estrus at frequent intervals, every 4 hours, from 2 to 5 days after injection, and the use Kamar or other heat detection devices. The use of GnRH or a small dose of estradiol to promote the LH surge after giving prosta- glandins has not proven to be of value.66 Recent studies on estrus synchronization have shown that 10 to 25 percent of beef cows and heifers were not detected in estrus within 5 days after PGF2a administra- tion due to failure of regression of the CL, or the CL regressed but estrus was not observed or estrus occurred 7 to 10 days after PGF2a injection. PGF2a was less ef- fective in regressing the CL between days 4 and 9 of the cycle than later in the cycle.816 It was also noted that the interval to estrus after PGF2a treatment was affected by season, age of the female (shorter in heifers), breed and plasma progesterone level at treatment.816 Estrus re- sponse following the first PGF2a injections was low, 45 to 50 percent, in 6 beef breeds and the pregnancy rate after PGF2a injections was poor, 20 to 35 percent, in the Brahman and Brahman-crossbreed cattle, compared to Angus, Hereford and Simental cattle, 60 to 65 per- cent.1482 In two groups of dairy heifers injected with PGF2a between 6 to 10 days and 11 to 16 days of the cycle response rate was 59.3 vs 95.6 percent respectively and the conception rate was 50 vs 74 percent respectively.1582 Prostaglandin injection had no adverse effect on fertility. In 2000 cows bred within 24 hours after the onset of induced and observed estrus, conception rate was 69 per- cent compared to 60 percent in untreated herdmates.916 The interval from PGF injection to the onset of estrus is often too variable to result in high pregnancy rates with set-time inseminations. Prostaglandin injections can be highly beneficial in cycling dairy cows with unobserved estrus to achieve conception in a minimum time pe- riod.966 It is important to realistically assess an owners man- agerial ability. The use of prostaglandins will not “cure” or alleviate infertility due to underfeeding, infectious ve- nereal diseases, defective or poor semen, improper in- semination practices, poor records, a lack of observation of estrus, a lack of, or improper identification of ani- mals, and a lack of cattle handling facilities. If prosta- glandins are given to pregnant cows or heifers especially under 150 days after gestation, they usually will abort. Thus the status of the cows and heifers in the herd, the degree of managerial ability and organization are vital to successful estrous synchronization. It is unfortunate that usually the herds deficient in this organization are the ones that request or expect a “one-shot” cure. If 70 percent of the properly synchronized estrus periods and ovulations are observed and the conception rate at that service is 60 percent there will only be 42 percent con- ceptions in the treated animals. A conception percentage above this level requires healthy cattle and excellent management as rates below this figure are commonly ex- perienced in herds attempting estrus synchronization. References Bovine Reproduction Physiology 1. Anderson, J. (1944) The Periodicity and Duration of Estrus in Zebu and Grade Cattle, J. Agric. Sci. 34, 57. 2. Asdell, S. A. (1964) Patterns of Mammalian Reproduction, 2nd Ed., Comstock Publishing Co., Inc., Ithaca, N.Y. 3. Asdell, S. A. 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(1982) The Incidence of Reproductive Disorders and Their Effects on Reproductive Performance in Commercial Dairy Herds, J. Dairy Sci. 65, Suppl. 1, 205, Abstr. 132a. Speicher, J. A. and Meadows, C. E. (1967) Milk Production and Costs Associated with Length of Calving Interval in Hol- stein Cows, Paper at 62nd Ann. Meeting Amer. Dairy Sci. Assoc. Cornell Univ., Ithaca, N.Y. 132b. Spitzer, J. C. (1982) Pregnancy Rate in Peripuberal Beef Heif- ers Following Treatment with Syncromate B and GnRh, Ther- iog. 17, 4, 373. 133. Stabenfeldt, G. H. (1970) Recent Advances in Bovine Repro- ductive Physiology, Bov. Pract. 5, 2. 134. Stabenfeldt, G. H., Edqvist, L. E., Kindahl, H., Gustafsson, B. and Bane, A. (1978) Practical Implications of Recent Phys- iologic Findings for Reproductive Efficiency in Cows, Mares, Sows, and Ewes, JAVMA 172, 6, 667-676. 135. Staples, R. E. and Hansel, W. (1961) Luteal Function and Em- bryo Survival in the Bovine, J. Dairy Sci. 44, 11, 2040. 136. Staples, R. E., McEntee, K. and Hansel, W. (1961) Luteal Function as Related to Pituitary and Ovarian Cytology and Em- bryo Development in the Bovine, J. Dairy Sci. 44, 11, 2049. 137a. Studer, E. and Morrow, D. A. (1978) Postpartum Evaluation of Bovine Reproductive Potential: Comparison of Findings from Genital Tract Examination per Rectum, Uterine Culture and Endometrial Biopsy, JAVMA, 172 4, 489. 137b. Swanson, L. V. and Hafs, H. D. (1970) Luteinizing Hormone and Prolactin in Blood Serum Through Estrus in Heifers, J. Dairy Sci. 53, 5, 652 (Abstr.). 138. Swanson, L. V. (1977) Duke’s Physiology of Domestic Ani- mals, 9th Ed., Cornell Univ. Press, Ithaca, N.Y. 139. Tanabe, T. Y. and Almquist, J. O. (1960) I Estrus and Estrual Cycles, The Nature of Subfertility in Dairy Heifers, Bull. #672, Penn. State Univ., Univ. Park, Pa. 140. Thompson, N. R. and Patterson, W. N. (1967) Cow Turnover in Virginia Dairy Herds, J. Dairy Sci. 50, 4, 610 (Abstr.). 141. Trimberger, G. W. (1941) Menstruation Frequency and Its Re- lation to Conception in Dairy Cattle, J. of Dairy Sci., 24, 9, 819. 142. Trimberger, G. W. (1948) Breeding Efficiency in Dairy Cattle From Artificial Insemination at Various Intervals Before and After Ovulation, Univ. of Neb. Agric. Exp. Stat. Res. Bull. 153. 143. Trimberger, G. W. (1954) Conception Rates in Dairy Cattle from Services at Various Intervals After Parturition, J. Dairy Sci., 37, 9, 1042. 144. Trimberger, G. W. (1955) Unpublished data. 145. Trimberger, G. W. (1956) Ovarian Functions, Intervals Be- tween Estrus, and Conception Rates in Dairy Cattle, J. Dairy Sci. 39, 4, 448. 146. Trimberger, G. W. and Davis, G. K. (1943) The Relationship Between Time of Insemination and Breeding Efficiency in Dairy Cattle, Nebr. Agr. Exp. Stat. Res. Bull. 129. 147. Trimberger, G. W. and Hansel, W. (1955) Conception Rate and Ovarian Function Following Estrus Control by Progester- one Injections in Dairy Cattle, J. of An. Sci., 14, 1, 224. 148a. Tucker, N.P., Jameson, G. J., Johnston, L. F. and North, W. A. (1982) Conception Differences Among Beef Breeds Treated with PGF2a, J. Dairy Sci., 65, Suppl. 1, 230, Abstr. 148b. Ulberg, L. C., Christian, R. E. and Casida, L. E. (1951) Ovar- ian Response in Heifers to Progesterone Injections, J. An. Sci 10, 3, 752. 149. VanDemark, N. L. (1952) Time and Site of Insemination in Cattle, Cor. Vet. 42, 2, 215. 150. VanDemark, N. L. and Salisbury, G. W. (1950) The Relation of the Postpartum Breeding Interval to Reproductive Efficiency in the Dairy Cow, J. An. Sci. 9, 3, 307. 151. Van Rensburg, S. J. (1965) Adrenal Function and Fertility, Jour. S. Afr. Vet. Med. Assoc. 36, 4, 491. 152. Van Vleck, L. D. (1968) Can you Manage the Calving Interval to Get More Milk, Dairy Herd Management, 5, 11, 28. 153. Varman, P. W., Smith, E. P. and Hull, M. W. (1964) Estro- gen Secretion and Excretion During Estrus in Dairy Cows, J. Dairy Sci. 47, 6, 687. 154. Wagner, J. F., Veenhuizen, E. L., Gregory, R. P. and Ton- kinson, L. V. (1968) Fertility in the Beef Heifer Following Treatment with CAP, J. An. Sci. 27, 6, 1627. 155. Wagner, W. C. (1979) The Adrenal Gland in Reproductive Success and Failure, Proc. of Soc. for Theriog., Mobile, Ala 119-130. 156. Wagner, W. C. (1980) Principals of Hormone Therapy, in Current Therapy in Theriogenology, Edit, by D. A. Morrow, W. B. Saunders, Co., Philadelphia. 157. Wagner, W. C. and Hansel, W. (1969) Reproductive Physi- ology of the Postpartum Cow, J. Reprod. and Fert. 18, 493. 158a. Watts, T. L. and Fuquay, J. W. (1982) Age of Corpus Luteum as a Possible Limiting Factor in PGF2a-Induced Cycle Syn- chronization, J. Dairy Sci. 65, Suppl. 1, 230. 158b. Weber, A. F., Morgan, B. B. and McNutt, S. H. (1948) Clin- ical and Post Mortem Observations on Metrorrhagia in the Vir- gin Heifer, N. A. Vet., 29, 11, 705. 159. Weber, A. F., Morgan, B. B. and McNutt, S. H. (1949) Peri- metrial Hemorrhage in Virgin Heifers, Cor. Vet. 39, 3, 261. 160. White, J. M. and Nichols, J. R. (1965) Reasons for Disposal of Pennsylvania Holstein Cattle, J. Dairy Sci. 48, 5, 512. 161. Whitmore, H. L., Tyler, W. J. and Casida, L. E. (1972) Early Postpartum Breeding in Dairy Cattle, Proc. 5th Ann. Conf., A.A.B.P., Milwaukee. 162. Williamson, N. B., Quinton, F. W. and Anderson, G. A. (1980) The Effect of Variations in the Interval Between Calving and First Service on the Reproductive Performance of Normal Dairy Cows, Austral. Vet. J. 56, 477-480. 163. Williamson, N. B., Quinton, F. W. and Anderson, G. A. (1980) The Effect of Variations in the Interval Between Calving and First Service on the Reproductive Performance of Normal Dairy Cows, Austral. Vet. J. 56, 477-480. 164. Wiltbank, J. N. (1965) Discussion, Proc. of Conf. on Estrous Cycle Control in Domestic Animals, Miscel. Pub. 1005, Univ. of Nebr., Lincoln, Nebr., 58, 60 and 62. 165. Wiltbank, J. N. and Cook, A. C. (1958) The Comparative Re- productive Performance of Nursed Cows and Milked Cows, J. An. Sci. 17, 3, 640. 166. Wiltbank, J. N. and Kasson, C. W. (1968) Synchronization of Estrus in Cattle With an Oral Progestational Agent and an In-INFERTILITY IN THE COW 447 jection of an Estrogen, J. An. Sci. 27, 1, 113. 167. Wiltbank, J. N., Rothlisberger, J. A. and Zimmerman, D. R. (1961) The Effect of Human Chronic Gonadotropin on the Maintenance of the Corpus Luteum and Embryonic Survival in the Cow, J. An. Sci. 20, 4, 827. 168. Wiltbank, J. N., Shumway, R. P., Parker, W. R. and Zim- merman, D. R. (1967) Duration of Estrus, Time of Ovulation and Fertilization Rate in Beef Heifers Synchronized with D.H.P.A., J. An. Sci. 26, 4, 764. 169. Woody, C. O., First, N. L. and Pope, A. L. (1965) Effect of Exogenous Progesterone on Estrous Cycle Length, J. An. Sci. 26, 1, 139. 170. Wrenn, T. R., Bitman, J. and Sykes, J. F. (1958) Body Tem- perature Variations in Dairy Cattle During the Estrous Cycle and Pregnancy, J. Dairy Sci. 41, 1071. INFECTIOUS DISEASES CAUSING INFERTILITY IN COWS The infectious reproductive diseases of cattle may be divided into the systemic diseases such as tuberculosis, which occasionally or rarely may affect the reproductive organs, and the more important venereal diseases which infect the genital tract such as: trichomoniasis, vibriosis, brucellosis, and possibly mycoplasmosis and ureaplas- mosis. Granular venereal disease, infectious pustular vulvovaginitis due to the IBR-IPV virus and other mis- cellaneous infections may also affect the reproductive tract and fertility. It is significant that in trichomoniasis, vib- riosis and brucellosis a local immunity develops in the genital tract and antibodies may be found in the vaginal mucus for variable, but not prolonged, periods. Any combination of these infectious diseases may occur si- multaneously in an animal or herd. A recent review de- tailed our present knowledge of the reproductive tract, including the reproductive hormones, as a component of the secretory immune system.68b Trichomoniasis Definition—Trichomoniasis is an insidious venereal disease of cattle characterized by infertility , early abor- tion, and pyometra and is caused by the protozoan, Tri- trichomonas fetus, transmitted to cows by the chroni- cally-infected bull. Etiology—According to Morgan this disease was first described by Kunstler in France, in 1888, but Mazzanti of Italy in 1900 is generally credited with the discovery. Because of the widespread interest in the discovery in 1897 of Bang’s disease, or contagious abortion, appar- ently little or no work was done on trichomoniasis until the 1920s and 1930s.5 In 1932 trichomoniasis was found in Pennsylvania by Emmerson and since that time the disease has been found in nearly every state in the United States and has been worked on intensively by many in- vestigators. Trichomoniasis has been reported in many countries throughout the world. In Wisconsin, where trichomoniasis was a problem 1,577 bovine uteri from a local packing plant for trichomonads were examined.57 Of 997 pregnant uteri only 2 were positive. Of 580 non- pregnant uteri there were 100 cases of pyometra and 13 percent were positive for Tritrichomonas fetus. In 9 infected herds involving 800 cattle, it was conservatively estimated that the losses totalled $200,000 due to loss of potential milk and calves and loss of value of the in- fected sires.7 In recent years trichomoniasis has been di- agnosed in the U.S. more frequently in beef herds and less frequently in dairy herds probably due to the exten- sive use of artificial insemination in dairy cattle. Tricho- moniasis is a major contributor to poor calf crops (50 percent) and prolonged calving seasons in beef herds.24d The results of a survey of 828 western range bulls in 34 herd associations for trichomoniasis showed 7.5 per- cent of the bulls and 26 percent of the associations were infected.42 In two other recent studies 7.8 and 7.3 per- cent of range beef bulls were infected with T. fetus in Oklahoma and Florida.6,68 The disease has also been de- scribed in range cattle in Australia.25 Since 1940 over 10 A.I. Studs in the U.S.A. have experienced outbreaks of trichomoniasis in their bulls.12'32 Beef herds, dealers’ herds, valuable purebred herds, and institution herds that frequently change or purchase bulls and cows, are those in which trichomoniasis is most likely to appear. The causative agent of this disease, Tritrichomonas fetus, is a flagellated protozoa with a pyriform or pear- like body. Three small flagella are located at the cranial end of the trichomonad. An undulating membrane ex- tends the length of the body and terminates in a single caudal flagellum. The organism varies from 10 to 25 mi- crons in length and 5 to 10 microns in width. A red blood cell is 5 to 7 microns in diameter. It is about one-third larger than the head of a bovine sperm cell. In fresh preparations the organism is actively motile, exhibiting a jerky, twisting, irregular, spiral continuous rolling and erratic type of movement.152 Progressive rapid forward movement is seldom observed. T. fetus is rapidly killed by drying, by the presence of antiseptics, excessive heat and by other adverse conditions or environment. Once dead it quickly loses its shape, so that it is difficult to distinguish from cellular debris. A common type of vag- initis in women is caused by T. vaginalis, an organism distinctly different from T. fetus. Recent studies have shown that it is highly probable that Trichomonas suis frequently found in the digestive448 VETERINARY OBSTETRICS tract and nasal cavity of swine is similar to T. fetus based on morphology, clinical signs produced by injections of T. suis into the genital tract of heifers and on serologic tests.30,39,41,49"51 The fact that these two protozoa from different body sites in swine and cattle are apparently identical may well account for the spread of the disease from swine to cattle, especially beef cattle where the two species are often housed together. In cattle, T. fetus is found only in the female genital tract, vagina, cervix, uterus, and uterine tubes, and on the penis and prepuce of the bull. In rare and unusual instances retrograde trichomonad infections of the sem- inal vesicles or epididymides may occur.1216 The great- est concentration of organisms in the bull was found in the fomix, on the glans penis and adjacent prepuce.12,37 Trichomoniasis is a venereal disease spread from an- imal to animal at the time of coitus or artificial insem- ination. Trichomoniasis may be spread from bull to bull in an AI stud at the time of semen collection or if bulls are allowed to run together and mount each other. Only rarely is it spread by other means such as by grooming animals that have a discharge from the vulva, or by the use of contaminated instruments, speculums or preputial or vaginal douching nozzles.12 Placing many T. fetus organisms on the vulva of heifers failed to cause infec- tion.25 The transmission of trichomoniasis by artificial insemination was first reported in 1939.33 By means of 7 inseminations, the disease was produced in 6 out of 9 uninfected females, and thus demonstrated that tricho- moniasis could be spread by artificial insemination with fresh undiluted semen from an infected bull.7,12 Semen from an infected bull was diluted 1 to 25 to 1 to 80 times in an egg-yolk-citrate buffer with sulfanilamide.66 Of 600 cows inseminated by semen from the infected bull 5 showed early abortion and 1 developed pyometra. Trichomonads were present in 7 out of 28 ejaculates col- lected from infected bulls. Storage of the liquid infected semen in the usual manner, and the addition of anti- biotics and extenders apparently had little or no inhibi- tory effects on the organisms.44 In 1953 examination of 168 bulls in 5 artificial insemination associations found 23 infected.13 The rate of transmission of infection by artificial insemination was estimated at less than 1 per- cent. This would not be serious in artificially insemi- nated cows and the percentage of conceptions on first service of infected bulls would not be noticeably af- fected.46"48 On the other hand in some herds bred arti- ficially, the incidence of infection was as high as 20 per- cent.63 The transmission rate might be serious, however, if the infected cows were bred to the herd sire and the disease thereby transmitted. The low incidence of infec- tion from artificial insemination is due to the methods of collection, storing, and dilution of the liquid semen. Only by the recovery of the organism in occasional isolated abortions or pyometra cases can trichomoniasis be traced to infected bulls used in artificial insemination. A high infection rate in nonimmune heifers when bred artifi- cially with infected semen was reported even though the semen was extended 1 to 40.66 A great difference be- tween infected bulls in the ability of their semen to trans- mit infection when used for artificial insemination was noted. This may be due to the great difference in the number of organisms present in the sheaths of different bulls.12 The previous evidence was reviewed and con- firmed the fact that T. fetus could survive in frozen and thawed extended bull semen even though glycerol was toxic to T. fetus. In glycerol-egg yolk-citrate extender T. fetus did not survive freezing and thawing; while in glycerol-egg-yolk phosphate or glycerol-milk extenders some organisms did survive. Thus bulls used in AI ser- vice should be free of trichomoniasis or spread of the disease might rarely occur.45 In natural service the transmission rate of the disease is about 80 percent. In 24 susceptible females bred to an infected bull, only 28 natural breedings were necessary to produce infection in all the females.7,9'12 After natural service to an infected bull 23 of 26 heifers became in- fected but the conception rate was 45 percent.65 Of twenty heifers bred to an infected bull, 19 became infected after one service. From 15 to 50 days postservice organisms were found in all 8 slaughtered heifers in the vagina and cervix, in the uterus in three-quarters of the heifers and in the uterine tubes in one half of the heifers.59 No gross or microscopic lesions were present in these heifers. In 12 heifers slaughtered between 60 and 100 days post- service, 7 had acute or chronic lesions in many areas of the genital tract, 2 of these had impending abortions and 1 had pyometra. The other 5 heifers of the 12 had no microscopic lesions and in only one of these was T. fe- tus recovered from the cervix and vagina.59 In another transmission trial a noninfected bull bred an infected cow and then bred nonexposed cows within 20 minutes; 25 percent of the latter became infected. If the time between services was extended to 3 to 24 hours none became in- fected and all conceived. Thus noninfected bulls may passively transmit infection during mating but the rate of transmission is low.25 Bulls were also quite suscep- tible to infection with 4 of 9 bulls becoming infected after the first service to an infected cow. However, 2 of 9 bulls proved highly resistant and could not be infected after 6 services to infected females. Young bulls with less well-developed mucosal crypts and folds in the pre- puce are much more resistant to experimental infections than are older bulls. Bulls under four years of age areINFERTILITY IN THE COW 449 seldom found naturally infected and are difficult to infect experimentally.2 Exceptions to this observation may be due to breed or individual differences in susceptibility as a few 2 year-old infected bulls have been reported.152 Bulls, unlike cows, do not seem to be able to develop immunity, even after 2 or 3 infections. If given sexual rest for a period of time cows will usually develop an immunity and rid themselves of the infection; whereas once a bull becomes infected the infection is permanent and only occasionally does spontaneous recovery occur. Cows may readily be infected experimentally by the in- troduction of T. fetus into the vagina or uterus. Al- though bulls are less susceptible to artificial infection of the prepuce, they more readily contract trichomoniasis after natural service to an infected cow. Except in spo- radic cases due to artificial insemination the disease usu- ally appears in a herd as an insidious venereal enzootic infection. Signs—Being insidious in nature, trichomoniasis is often well-established in a herd before the symptoms reach proportions sufficiently alarming so that a veterinarian is called. The breeding records of any herd affected with sterility should be carefully studied. The possibility of the presence of this disease can often be surmised on the basis of good breeding records. Often the original source of the infection can be traced to a certain bull or non- pregnant cow added to the herd. Purebred herds that sell breeding stock should be extremely cautious in accepting “returned” infertile animals back into their herd after they have been exposed to cattle in other herds.“4d Infertility frequently starts after such additions. Once the disease has been diagnosed, herd records are also of value in planning a control program. After the cows have been exposed by coitus to a trichomonad-infected bull the fol- lowing signs may be observed; (1) Trichomoniasis will fail to become established in a small number of cows or heifers either because of the small numbers of trichomonads introduced or because of the natural resistance of the female. Conception and a normal gestation period will follow. Approximately 5 to 20 percent of the cows or heifers may fall in this cate- gory. Normal gestation and parturition may result in spite of the infection.57,65 Trichomonads have been isolated on rare occasions throughout a gestation period terminating in a normal parturition. (2) When T. fetus becomes established after coitus there is no reaction nor any clinical lesions or discharge for the first 3 or 4 days. However, by 4 to 9 days the presence of a moderate vulvovaginitis and cervicitis may be observed on clinical examination. Discharges from the genitals are absent or very scanty during most infec- tions unless pyometra occurs and then a mucopurulent exudate is usually discharged irregularly. Under field conditions these symptoms in most cattle would usually pass unnoticed.12 The above symptoms are so slight as to be of little significance and other infections of a non- specific type may produce similar symptoms. In rare in- stances a more severe and chronic type of vaginitis may develop in the cranial portion of the vagina in cows with trichomoniasis. This is characterized by a rough, rasp- like corrugated vaginal mucosa. Some clinicians indicate that this lesion when observed is nearly pathognomic for the disease. Trichomonads may be found in the vaginal exudate, which is usually watery, clear, or cloudy, often containing whitish-yellow flakes of pus. The presence of trichomonads in a cyst of Gartner’s duct 11 weeks after the apparent recovery of the cow from trichomoniasis was reported.15 In general, clinical symptoms are absent or mild and usually pass unnoticed by the herdsman. The acutely or chronically-infected bull shows no gross lesions. (3) The most common symptom of trichomoniasis is infertility, characterized by the necessity for many ser- vices per conception and by the frequent occurrence of a prolonged period between estrual periods after breeding. One herd of 50 cows during the height of the infection had an average of 5.15 services per conception over a 2-year period. Prior to the development of the disease the conception rate had been a normal 1.82 services per conception.7'9 '012 Some cows must be bred 6 to 8 times before conception occurs. T. fetus produces a mild in- flammation of the uterine tubal epithelium, endome- trium, cervical and vaginal mucous membranes, and af- fects the developing embryo and fetus. There is no evidence to show that it may interfere with fertilization of the ova. Nearly 40 percent of infected cows after breeding showed shorter- or longer-than-normal inter- estrual periods during the time they were infected.12 The longer interval between estrums were most commonly noted. Most of the trichomonad abortions or resorptions are caused by the early death of the embryo and fetus from 15 to 80 days of gestation rather than the less com- mon and often observable abortions occurring after three months of gestation. In early embryonic deaths the em- bryos usually macerate and are absorbed in the uterus or are expelled unnoticed. Occasionally pyometra may re- sult from a macerating embryo and the accompanying endometritis. If cows are infected at one service to an infected bull and fail to conceive, a subsequent service to a clean bull, either naturally or artificially, will not result in a safe conception until the cow develops an im- munity and eliminates the organism. Thus infertility pro- duced by the original infected bull persists even though subsequent breedings are to a noninfected bull. Tricho-450 VETERINARY OBSTETRICS moniasis is actually characterized mainly by infertility and only occasionally by observable abortions and pyometra. (4) Abortions due to T. fetus usually occur between 1 and 16 weeks of pregnancy.57 Abortions occurring after 5 months of pregnancy are very rare. If an exposed cow has conceived and carried a normal fetus for 6 months, abortion due to trichomoniasis will probably not occur. Most fetuses aborted before 90 days are not observed. Those aborted the third to fifth month of gestation are usually slightly macerated and autolyzed and are ex- pelled with the fetal membranes around the fetus along with a variable amount of dark, reddish-brown exudate. Occasionally on routine rectal examinations in infected herds these dead fetuses may be diagnosed. Retained placenta is very seldom observed following a tricho- monad abortion. The number of observed abortions will vary in an outbreak, depending upon the severity of the infection, the closeness with which the cows are ob- served, and whether the outbreak is during the summer pasture season or during the winter months when the cows are stabled. Occasionally a mucopurulent reddish-brown discharge may precede an abortion. In a careful study of 50 infected cows, only 2 abortions were recognized and 5 cows developed pyometra.7 9'10 '2 In 5 herds studied in Maryland involving 300 beef and dairy cattle, only 1 abortion and 1 pyometra were observed. In an outbreak involving about 20 cattle which the author was able to study and follow closely, 1 cow aborted a recognizable fetus and 1 had pyometra. An outbreak in a herd of 75 animals was cited2122 in which 9 observed abortions and 7 unobserved abortions occurred in cows previously di- agnosed pregnant. No cases of pyometra were noted. More often the history in an outbreak of trichomoniasis is that the herdsman believed a cow safely pregnant and then 60 to 90 days or more after service, estrum is again ex- hibited. (5) Pyometra may be present in 0 to 10 percent of the cows in an outbreak of trichomoniasis. Trichomonad pyometra is postcoital or postservice and not postpar- tum. When death of the developing embryo or early fe- tus occurs and abortion or maceration and absorbtion do not occur, pyometra develops. The corpus luteum in the ovary persists and the cervix may remain tightly closed and sealed with no discharge of pus. More often, how- ever, the cervical seal breaks down and a slight amount of pus escapes into the vagina and is discharged occa- sionally from the vulva. Since estrum does not occur with pyometra this condition may pass unnoticed for up to 8 or 9 months unless a vaginal discharge is observed or a diagnosis is made on rectal examination. The amount of pus in the uterus varies from about 60 to 8000 ml. with an average of 1500 ml.58 The pus in trichomonad pyo- metra has a characteristic thin, yellow-grey, watery, flocculent consistency, often containing yellow flakes of pus and shreds of fetal membranes and tissues; in rare cases small fetal bones may be present. The pus has been described as having a “potato soup” color and consist- ency. Odor may be absent or rather sweetish, but is not fetid. No evidence of perimetritis or other uterine lesions are present. If on rectal examination a diagnosis of pyometra cannot be made positively, another examina- tion 1 or 2 months later is indicated. Usually tricho- monads may be recovered in pure culture from this pus. In examining 20 cases of trichomonad pyometra tricho- monads were found in every case in numbers from 320 to 3,520 million per ml. with an average of 1552 million per ml.58 Diagnosis—The history of the introduction of a new infected animal into a herd followed by a gradually in- creasing problem of infertility characterized by failure of conception after frequent services, prolonged periods after service before the next estrual period including cows ap- parently conceiving but coming into estrum several months later, and the occurrence of occasional early abortions and pyometra are characteristic symptoms of this dis- ease. In recently infected herds all cows and heifers are susceptible. In more chronically infected herds most cows have an acquired immunity, while virgin heifers are sus- ceptible. These symptoms are also quite characteristic of vibriosis due to Campylobacter fetus venerealis. Some bulls are infected with both vibriosis and trichomoniasis. The positive diagnosis of trichomoniasis, as in vibriosis, requires the finding of the organism in one or more in- fected animals or a diagnosis based on immunologic re- actions due to the local immunity developed in the gen- ital tract. Diagnosis in the bull consists of checking the natural breeding records and finding which older bulls are prob- ably chronically infected and checking the preputial smegma of these particular animals carefully, and if nec- essary repeatedly, by the swab, the pipette, or the douche method. These older bulls are of great diagnostic value for detecting the presence of T. fetus infection in a herd.2 After natural service the numbers of organisms on the penis and sheath are reduced. Following a period of sex- ual rest for 5 to 10 days to allow the numbers of organ- isms to increase, the bull is confined in a stall, chute or stanchion. A sideline on the bull is often helpful in re- straining the animal in a stall. To avoid fecal or other contamination from the preputial hairs, they are clipped and the preputial orifice is thoroughly washed with soap and water, rinsed, and wiped dry. After its head is fas- tened and its tail pushed up and forward as restraint, theINFERTILITY IN THE COW 451 abdomen is stroked and then the sample is taken from the prepuce. This sampling procedure can be hazardous to the operator because all range bulls and most dairy bulls resent this sampling and will kick violently unless they are accustomed to being handled and groomed. The use of a bull electroejaculator may be helpful in diverting the bull’s attention and getting him to stand quietly.5hb For direct examination of the preputial smegma for the presence of T. fetus, the swab, the pipette or the douche method may be used. In the swab technique, a sterile cotton swab or one made with one-half of a 4 x 4 gauze pad soaked in a physiological saline or lactated Ringer’s solution is introduced into the sheath on a 36 to 40 inch wire or long narrow forceps, or wrapped around the bris- tles of a small brush on the end of a long wire. The sheath is swabbed in a back-and-forth circular motion in the region of the fornix and glans penis where most of the trichomonads are located. The swab is then removed and placed in a small amount of physiological saline so- lution. This may be examined at once on the farm or later in the laboratory. The pipette technique12'10 12 con- sists of introducing a 24-inch sterile, Bartlett, plastic preputial or plastic A1 pipette with attached bulb or sy- ringe from which the air has been expelled. In the av- erage adult bull which has not been used for service in several days, 1 to 10 ml. or more of smegma and fluid may be removed by aspiration from the sheath by a back- and-forth gentle scraping motion of the end of the pipette in the region of the glans penis. This is flushed into a vial containing 5 ml. of physiological saline, lactated Ringer’s solution or Kupferberg broth48 refrigerated and examined later in the laboratory. The douche technique consists of introducing 200 to 250 ml. of sterile physi- ological saline into the sheath and closing the external orifice with the fingers to prevent the loss of the saline solution.17,29’37 The solution is vigorously massaged back and forth in the sheath for several minutes and allowed to run back out of the sheath into a broad-mouthed beaker and poured back into a bottle for laboratory examination. Occasionally this procedure will stimulate the bull to uri- nate and require the douching to be repeated. Since the T. fetus organisms often occur in the in- fected bull in small numbers they must be located in fresh samples in which the organism is alive and motile or cultured to increase the number of organisms. The com- bination of the pipette technique with culturing is about 95 percent accurate.1 Samples must therefore be handled properly after collection, by avoiding extremes of tem- perature, contact with harmful chemicals, and evapora- tion. It is highly desirable to examine samples or culture them within a few hours of collection. If an immediate examination is not possible the samples may be kept in a cool place such as a refrigerator or shipped to a lab- oratory under refrigeration to control bacterial growth, and examined within 24 to 48 hours. Ordinary freezing at 32° F. will destroy trichomonads. Pipette samples should be allowed to settle for several hours or centrifuged for 10 minutes at 2000 R.P.M. After most of the supernatant fluid is poured off, the superficial layer and the sediment where the organisms are concentrated are mixed. This material is dropped on a glass slide to make a thin pool that is examined under low power with a reduced amount of light. A cover glass should not be used; 3 slides must be carefully examined before the sample is considered negative. A similar technique is used in examining swabs. In the douche technique, the 250 ml. of saline solution and preputial washings are centrifuged for 10 minutes at 2000 R.P.M. at the laboratory. [If a large centrifuge is not available allow the preputial washings to settle for one-half hour and draw off 15 ml. of the sediment and centrifuge the latter. Take a small amount from the bot- tom of the tube and examine on a warm slide under sub- dued light for the presence of trichomoniasis.243] After the supernatant fluid is decanted, the remaining material is centrifuged in a like manner in a 15 ml. centrifuge tube. The supernatant fluid is poured off and the sedi- ment is mixed with 0.5 to 1 ml. of the remaining fluid and examined. The pipette method was superior to the swab technique, and the douche technique superior to both.29 In the field where a laboratory was not available the swab and pipette methods were most practical. Using the pipette technique a positive test was recorded on 42 to 85 percent of the samples from known infected bulls.13 Two infected bulls were considered atypical inasmuch as only 8.5 to 19.5 percent of the preputial samples from them were positive. Of 23 infected bulls of 168 bulls examined, 15 were diagnosed on the first sampling, 6 on the second and 2 on the third sampling. In rare in- stances positive bulls may not be found until the fifth sampling with the pipette; for this reason these workers recommended that at least 6 negative samples at weekly intervals be considered as a minimal diagnostic routine under practical conditions. The use of the more cum- bersome douche technique might reduce the numbers of preputial samples required. The direct swabbing or scrubbing of the exposed glans penis with gauge sponges in saline solution appeared promising in detecting in- fected bulls when the numbers of trichomonads present were low. The penis was exposed manually after tran- quilization of the bull. Semen examinations for tricho- monads are not feasible since sperm motility interferes with the examination. By the use of modified Plastridge or Diamond’s or other media containing nutrients and antibiotics, prepu-452 VETERINARY OBSTETRICS tial smegma material can be layered on culture media and incubated for 3 to 5 days and examined.1,3,35,43,483 This method utilizes the collection techniques outlined above and the modified douche technique for obtaining a sample of smegma. The smegma or mucus for culture when placed on top of the media allows the motile an- aerobic Trichomonads to migrate to the bottom of the culture tube while the contaminating bacteria remain at the top of the tube. The inoculated tube is incubated at 38° C and the fluid at the bottom of the tube is pipetted out and examined in 24 and 48 hours for trichomonads. Culture techniques save a great deal of time when com- pared to the direct microscopic examination by a skilled person. It is also a more accurate technique. Diagnosis in the cow may be accomplished by ex- amination of the aborted fetal membranes, the mouth cavity of the fetus, the fetal fluids, the stomach contents of the fetus, or the exudate in the uterus for T. fetus. Following abortion the organisms usually disappear within 48 hours. In cows with postcoital pyometra the exudate should always be examined for trichomonads. T. fetus are often found in such great numbers that dilution is necessary in order to observe them clearly. In cows bred artificially, early abortion and pyometra are about the only conditions in which trichomonads might be found or suspected. The early occurrence of vaginal immunity to the organism is responsible for the disappearance of trichomonads from the vagina. The organism which is motile traverses the cervix into the uterus where it re- mains and produces an endometritis that lasts for one to several months. During this time organisms may be found periodically in the vagina. Vaginal samples from sus- pected females should be examined during the early vag- inal phase of the infection, which lasts for about 5 weeks after the coitus that produced the initial infection. There- after the presence of vaginal infection may occasionally be observed about 3 to 7 days before estrum.38 This pat- tern occurs only in previously uninfected animals. Con- sequently in selecting females to culture it is best to se- lect if possible virgin heifers bred the first time to a supposedly infected or suspect bull. Sample the vaginal mucus with a 14- to 16-inch-long, plastic pipette in a manner similar to the examination of the bull. These samplings should be made 12 to 19 days after the in- fecting service and then 3 to 7 days prior to each sub- sequent estrum. In one trial only 7 of 36 cows bred to infected bulls had positive cervical-vaginal mucus cul- tures about 90 to 100 days after service. Seven of the 36 cows, 2 percent, aborted but only 3 of these, or 8 percent of the 36 cows had positive cultures.3 Finding the trichomonad organisms in cows cannot be done as regularly nor as easily as in bulls so the cow is less fre- quently employed for routine diagnostic purposes.2,3 It may be desirable to check certain bulls further and for this purpose 2 or more virgin heifers may be bred naturally and vaginal samples taken regularly from 12 to 19 days later. If no positive recoveries of the organism are made, the bull may tentatively be considered free of the infection. Vaginal exudate, if present, should be taken from any suspected cow and especially from cows ex- hibiting a rough, rasplike corrugated vagina and exam- ined for T. fetus. The living Tritrichomonas fetus can be readily iden- tified under the microscope by its characteristic size, shape, undulating membrane, and jerky, erratic motion and continuous rolling.52 T. fetus in live culture seldom if ever ceases to move, whereas other protozoa occa- sionally stop moving. Other protozoa, such as: T. ru- minatum, Entrichomastix ruminatum, Bodo fetus and others, may also be observed, especially in contaminated samples containing feces.57 Their size and motion how- ever, differs from that of T. fetus and they have no un- dulating membrane. These other forms of protozoa are more likely to be observed if samples are held for 18 to 48 hours at room temperature before examination or if samples are taken from the cranial portion of the pre- puce. In pregnancies that terminate in abortions at 90 to 150 days or in pyometra, T. fetus may survive for 4 to 5 months in the genital tract of a cow. In most cows how- ever the infection may persist for only a few weeks, 4 to 5, in the vagina and for up to about 60 to 90 days, 2 to 3 months, in the uterus before local immunity results in spontaneous recovery. Infected bulls may remain as carriers of T. fetus but no lesions or inflammation of the sheath or penis is produced in either acutely or chroni- cally infected males. A vaginal mucus agglutination test has been de- scribed.49-51 Since agglutinating antibodies are devel- oped locally in both the vagina and uterus this has been used as a herd test for T. fetus infection. It is not sat- isfactory for testing individual animals. The antibodies appear as early as 18 to 21 days after infection but reach a high level by 40 days. No systemic antibodies with blood titers were ever observed. In northern Ireland this test was used as a herd screening test to locate those herds that were infected. Prognosis—The prognosis is usually good if the owner follows a carefully planned control program. In the in- dividual cow the prognosis is good because the non- pregnant cow tends to develop an immunity which al- though temporary, eliminates the infection in about 3 to 6 months. However the immunity produced is relatively short-lived and reinfection may occur.1,2 In certain casesINFERTILITY IN THE COW 453 of uterine infection in pregnant cows, or of pyometra, the infection may survive in the uterus for much longer periods or until abortion or parturition occurs or the pyometra is cured. Occasionally secondary invading or- ganisms such as C. pyogenes may produce a more se- vere pyometra and sterility. Cows very rarely, if ever, carry T. fetus infection in their uterus through an entire gestation period. In some longstanding cases of infertil- ity due to pyometra or chronic endometritis, conception may fail to occur and the cow is sold for economic rea- sons. The prognosis for bulls is more guarded. Since older bulls are usually permanently infected and only very rarely recover spontaneously they usually are sold for slaughter unless they are valuable and treatment is decided upon. Any bull not worth more than 3 times his salvage value should be slaughtered. If the bull is valuable then treat- ment and posttreatment testing involving a period of about 3 to 4 months is indicated. Treatment and the many post- treatment test samples required are expensive. Fortu- nately treatment is highly effective.63 Herd treatment—The various possible programs that can be used to eliminate the infection should be carefully explained to the herdsman and the owner. The veteri- narian can usually outline a practical plan or procedure for the control of trichomoniasis in the herd. There is no satisfactory or successful method to immunize cows ar- tificially against trichomoniasis. The most practical and easy method to control and eliminate trichomoniasis in a dairy herd is stop all nat- ural service and breed all cows having normal genital tracts by artificial insemination to disease-free bulls for a period of about one to two years before resorting again to natural service by bulls proven free of T. fetus, or by virgin bulls. Cows with pyometra should be treated and cows that abort or have an embryonic resorption should not be rebred for 1 or 2 months after the uterus involutes to its normal state. If artificial insemination is utilized for all cows, this author sees no benefit from requiring that all cows have 3 normal length cycles prior to re- breeding to ensure that most cows will have freed them- selves of the infection. This may promote a higher rate of conception on first service but the loss of production would be excessive by such a delay in service on many cows in the herd that may be nearly recovered or have recovered from T. fetus infection. However the owner should be warned that an increased number of services will be necessary, especially on cows that had been re- cently infected and have not developed an immunity. In- fected bulls should be sold or, if valuable enough, should be treated. Breeding infected bulls to supposedly im- mune cows may result in fairly satisfactory conception rates but the infection will continue in the herd. Im- munity to trichomoniasis lasts only a short period of months. Even cows that have conceived and had a nor- mal gestation period and parturition should not be bred back by natural service within 90 days of calving, since cows may rarely carry the infection through the gestation period. Infected and noninfected cows may be housed or pastured together with practically no danger of spread of the disease since trichomoniasis is rarely spread ex- cept by venereal contact. This above practical artificial insemination procedure will work well for most dairy and a few beef herds, if no bulls are kept and if close veterinary supervision and good management are avail- able. Another control method that is rather difficult to carry out is to divide the herd of female cattle into two groups (1) the clean nonexposed cows and heifers including virgin unbred heifers, pregnant or open heifers or cows that have never been bred by a known trichomonad-in- fected bull or a bull suspected of being infected and non- pregnant cows that have recently calved after a normal gestation period and have not had a service by an in- fected or suspect bull. Any cow or heifer where the breeding history is not definitely known should be placed in the second “infected” group. (2) the infected or possibly infected cows or heifers include those pregnant or nonpregnant animals that have had coitus with an infected or suspect bull and have not had a normal gestation period following that service. In Group 1 the noninfected cows and heifers may be bred by a noninfected or virgin bull or by artificial in- semination. In Group 2 the “infected” or “suspect” non- pregnant females should be given 60 to 90 days, or 3 normal estrous cycles, sexual rest before being rebred to cheap noninfected “sacrifice” bulls which can be slaugh- tered at the end of the breeding season. All pregnant and nonpregnant cows should be examined at monthly or bi- monthly intervals until they are pregnant 6 months or more, or are sold as infertile. Females with pyometra, abortions or metritis should be treated before breeding or sold for slaughter. After calving these cows should not be rebred for a period of 60 to 90 days and then they may be bred naturally to a noninfected bull. This latter method has been employed successfully in a number of beef herds where the “infected” and “noninfected” herds can be kept some distance apart with no danger of con- tact or mixing of animals between the two herds. In a few beef herds the disease was eradicated by breeding virgin bulls to virgin heifers and keeping these animals together and separate from the infected herd for a num- ber of years until the infected herd could be eliminated or replaced. Accurate breeding records, carefully iden- tified cows and bulls, good fences and intelligent man-454 VETERINARY OBSTETRICS agement is necessary to eliminate this disease by meth- ods other than by selling all bulls and going into an artificial breeding program for all the females in the herd. Individual treatment—The treatment of most infected cows is not necessary, inasmuch as these animals if given sexual rest will overcome the infection. Cases of pyo- metra and abortion and secondary metritis must be treated and handled as described later in this chapter. Many vet- erinarians feel that with treatment, recovery may be more rapid and complete. To satisfy the owner that something is being done for these heifers or cows, many of which have been bred repeatedly, treatment is often under- taken. These treatments which are of questionable value may include douching of the vagina and possibly the uterus with 2 to 3 ml. of Lugol’s solution in 100 ml. of water, 4 to 5 percent sodium perborate solution, 1 to 3 percent chlorine solution, or 1 percent acriflavine solution, once or at several intervals a week or 10 days apart. Various antiseptic treatments of the genital tract of the infected cow were useless in elimination of the organisms, which can be done only by the development of immunity.65 Some veterinarians will sample and culture the cervical and va- ginal mucus or uterine exudate in pyometra. If infection is present they will treat the cows orally or parenterally with drugs recommended for the treatment of bulls. Treatment for bulls has received much attention in the last 30 years. For the first 20 years a number of dif- ferent techniques and drugs were used to affect a cure mainly by local treatment of the prepuce and penis, often at repeated intervals that was very time-consuming and expensive. These treatments of “Bovoflavin Ointment,” acriflavine ointment and hydrogen peroxide and others used locally and sodium iodide intravenously or their combination has been described.60 These treatments are presently seldom used because of the difficulty or dan- gers in their application and the not uncommon failures in the cure of the T. fetus infection. Presently the treatment of choice is the oral adminis- tration of 50 mg/kg or 25 mg/lb of body weight of di- metridazole (l,2-dimethyl-5 nitroimidazole) (Rhodia Inc. N.Y.C. or Emtryl, Salisbury Laboratories, Charles City, Iowa). This drug is used for the treatment of blackhead in turkeys and like the following drug is not approved in cattle.1'24'52 54'56 Another similar drug metronidazole (1 -B-hydroxyethyl-2-methyl-5-nitroimidazole (Searle, Chicago, 111.) is used for treating T. vaginalis in hu- mans.134 The dose of this latter drug was 10 to 75 mg/ kg of body weight intravenously every 12 hours for 3 injections or once daily for 2 days. Dimetridazole can also be given intravenously in a 10 to 20 percent sulfuric acid solution at a dose level of 10 mg/kg of body weight daily for 5 days or 50 to 100 mg/kg of body weight at a single injection. Because of severe side-effects of dyspnea, ataxia, recumbency and weakness from intra- venous therapy the oral therapy is preferred. Dimetri- dazole is usually administered by boluses, drench or by stomach tube. When mixed with feed it may be unpal- atable so it may not be completely consumed. Since bulls on a high concentrate ration may develop rumen stasis, a ration high in roughage should be fed before and dur- ing treatment. Following therapy a designation of a cure should be based on 3 consecutive negative cultures over a period of six weeks starting 45 to 60 days after treat- ment.52 The possibility of strains of T. fetus developing resistance to dimetridazole has been reported.55 Dime- tridazole has been used at the dose level of 25 mg/lb daily for 5 days orally to treat over 100 bulls with tricho- moniasis with 90 to 95 percent success in eliminating the infection.“4a It is doubtful that any commercial com- pany will for economic reasons go to the expense of ob- taining official approval of dimetridazole for the treat- ment of trichomoniasis in bulls and cows. Preliminary evidence indicates the drug may be present in milk from treated cows for a period of 4 to 6 days.24a'b Treatment of bulls without eradication of Tricho- monas fetus in the herd is useless, since bulls which have recovered are susceptible to reinfection. Careful observation and repeated checking of the bulls after treatment is necessary. This is the most important aspect of the treatment of bulls for trichomoniasis. For 3 months after treatment with Bovoflavin Ointment negative pre- putial samples even if collected twice a week have little significance. Furthermore, test matings with susceptible females were not reliable during this period. Coitus with 2 or more virgin heifers might be allowed at intervals during this posttreatment period and vaginal mucus sam- ples should be examined and cultured frequently be- tween 12 and 19 days after coitus. If still negative the bull can be restored to service but careful observations should be made on females bred to him. Further studies on cure rates and the required testing protocol to be followed in assessing the posttreatment status of bulls after the use of the nitroimadazole drugs is indicated. Prevention—Preventing the introduction of tricho- moniasis into a herd is of vital interest to an owner and his veterinarian. The precautions should include: knowl- edge of the reproductive efficiency in the herd of origin of any stock purchases; thorough examination of newly- purchased suspect bulls with a pipette to obtain preputial samples for culture, at least 3 to 6 times at weekly in- tervals; repeated examinations 12 to 19 days after coitus of the vaginal mucus of the first 3 or 4 cows and heifers bred to these bulls; and prohibition of coitus for newly-INFERTILITY IN THE COW 455 purchased non virgin, nonpregnant heifers and nonpreg- nant cows that have had coitus since their last calving, to prevent the introduction of trichomoniasis by females. These animals should be bred by artificial insemination. All recently acquired cows that are pregnant should be withheld from coitus for 90 days after calving and al- lowed to pass at least 2 heat periods before being bred naturally.12 In artificial breeding centers the need for a careful ex- amination and history on the bulls before purchase, and proper and frequent examination, 3 to 6 negative pre- putial examinations at weekly intervals, of all service- age bulls as they enter the stud and periodically there- after is essential to prevent the possible introduction and spread of this infection into many herds. Owners should be careful of their source of semen for artificial insem- ination in their herds especially if a herd sire is also maintained. References 1. Abbitt, B. (1980) Trichomoniasis in Cattle, in Current Therapy in Theriogenology, edit, by D. A. Morrow, W. B. Saunders Co. Philadelphia, 482-488. 2. Abbitt, B. (1981) Trichomoniasis, Proc. Ann. Meet. Soc. for Theriog., Spokane, Wash., 31-37. 3. Abbitt, B. and Ball, L. (1978) Diagnosis of Trichomoniasis in Pregnant Cows by Culture of Cervical Vaginal Mucus, Ther- iog., 9, 523-528. 4. Abbitt, B. and Meyerholz, G. W. (1979) Trichomonas fetus Infection of Range Bulls in South Florida, Vet. Med. Sm. An. Clin. 74, 9, 1331-1342. 5. Abelein, R. (1938) Behandlung von Bullen mit Trichomonaden, Dtsch. Tierartzl. Wschr., 46, 46, 721. 6. Bartlett, D. E. (1946) Experimental Treatment of Trichomonas Fetus Infection in Bulls, Am. J. Vet. Res., 7, 25, 417. 7. Bartlett, D. E. (1947) Trichomonas Fetus Infection and Bovine Reproduction, Am. J. Vet. Res. 8, 29, 343. 8. Bartlett, D. E. (1948) Further Observations on Experimental Treatment of Trichomonas Fetus Infection in Bulls, Am. J. Vet. Res., 9, 33, 351. 9. Bartlett, D. E. (1949) Infectious Disease as a Cause of Infer- tility: A Review, J. of Dairy, Sci., 32, 1, 36. 10. Bartlett, D. E. (1949) Procedures for Diagnosing Bovine Ve- nereal Trichomoniasis and Handling Affected Herds, JAVMA, 114, 866, 293. 11. Bartlett, D. E. (1954) (1966) Personal Communication. 12. Bartlett, D. E. (1968) Bovine Venereal Trichomoniasis and Bo- vine Abortion in “Abortion Diseases of Livestock” Edit, by L. C. Faulkner, C. C. Thomas Co., Springfield, 111. 13. Bartlett, D. E., Moist, K. and Spurrell, F. A. (1953) The Trichomoniasis Fetus—Infected Bull in Artificial Insemination, JAVMA, 122, 192, 366. 14. Bartlett, D. E., Teeter, K. G. and Underwood, P. C. (1947) Artificial Insemination as a Means of Transmission of Bovine Venereal Trichomoniasis, JAVMA, 111, 845, 114. 15. Beattie, H. E. R. (1955) A Bovine “Trichomonad Cyst”, Aus- tral. Vet. J. 31, 6, 146. 16. Bielanski, W. (1958) Personal Communication. 17. Binns, W. (1954) Personal Communication. 18. Binns, W. and Thome, J. L. (1955) Personal Communication. 19. Brodie, B. O. (1970) Trichomoniasis, in Bovine Medicine and Surgery, Amer. Vet. Public. Inc., Wheaton, 111., 219. 20. Bruner, D. W. and Gillespie, J. H. (1973) Hagan’s Infectious Diseases of Domestic Animals, 6th ed, Cornell Univ. Press, Ith- aca, N.Y., 631-636. 21. Cameron, H. S. (1935) Bovine Trichomoniasis, Cor. Vet. 25, 2, 99. 22. Cameron, H. S. (1938) Bovine Trichomoniasis, Univ. of Ca., Agr. Exp. Stat., Bulletin 624, Berkeley, Cal. 23. Cardwell, W. H. (1956) Personal Communication. 24. Cardwell, W. H. (1982) Personal Communication. 24a. Cardwell, W. H. (1980) A Practical Approach to the Diagnosis and Treatment of Trichomoniasis, Proc. 12th Ann. Conv. A.A.B.P. 135-136. 25. Clark, B. L., Dufty, J. H. and Parsonson, I. M. (1977) Studies on The Transmission of Tritichomonas fetus., Austral. Vet. J. 53, 170-172. 26. Dunton, R. K. (1966) Personal Communication. 27. Fincher, M. G. (1953) Current Problems in Cattle Practice In- cluding Mastitis, Canad. J. Comp. Med. and Vet., and Vet. Sci. 17, 193. 28. Fincher, M. G. (1954) Personal Communication. 29. Fitzgerald, P. R., Hammond, D. M., Miner, M. L. and Binns, W. (1952) Relative Efficiency of Various Methods of Obtaining Preputial Samples for Diagnosis of Trichomoniasis in Bulls, Am. J. Vet. Res. 13, 49, 452. 30. Fitzgerald, P. R., Johnson, A. E. and Hammond, D. M. (1963) Treatment of Genital Trichomoniasis in Bulls, JAVMA, 143, 3, 727. 31. Fitzgerald, P. R., Johnson, A. E., Thome, J. L. and Hammond, D. M. (1958) Experimental Infections of the Bovine Genital System with Trichomonads from the Digestive Tract of Swine, Amer. J. Vet. Res. 19, 73, 775. 32. Gabel, A. A., Tharp, V. L., Thorne, J. L., Graves, H. F., Koutz, F. R. and Amstutz, H. E. (1958) Trichomoniasis in an Artificial Insemination Stud, JAVMA, 132, 11, 476. 33. Garlick, G. (1939) Transmission of Bovine Venereal Tricho- moniasis through Artificial Insemination, Vet. Med., 34, 43. 34. Gasparini, G., Gaghi, M. and Tardini, A. (1963) Treatment of Bovine Trichomoniasis with Metronidazole, Vet. Rec. 75, 940. 35. Gilman, H. (1965) Personal Communication. 36. Habel, R. E. (1956) A Source of Error in the Pudendal Nerve Block, JAVMA, 128, 1, 16. 37. Hammond, D. M. and Bartlett, D. E. (1943) Establishment of Infection with Trichomonas Fetus in Bulls by Experimental Exposure, Am. J. Vet. Res., 4, 10, 61. 38. Hammond, D. M. and Bartlett, D. E. (1945) Pattern of Fluc- tuations in Numbers of Trichomonas Foetus Occuring in the Bo- vine Vagina During Initial Infections, Am. J. Vet. Res., 6, 19, 84. 39. Hammond, D. M. and Leidl, W. (1957) Experimental Infec- tions of the Genital Tract of Swine and Goats with Tricho- monas fetus and Trichomonas Species from the Cecum or Feces of Swine, J. Vet. Res. 18, 68, 461. 40. Hess, E. (1951) Diagnose and Therapie der Trichomonaden- seuche beim Zuchstier, Tierartzl Umschau, 7, 11 and 12, 191. 41. Hibler, C. P., Hammond, D. M., Caskey, F. H., Johnson, E. A. and Fitzgerald, P. R. (1960) The Morphology and Incidence of the Trichomonads of Swine, Tritrichomonas suis (Greeby456 VETERINARY OBSTETRICS and Delafond. Trichomonas rotunda, n. sp. and Tritricho- monas buttrey, n. sp., Jour, of Protozool. 1, 2, 159. 42. Johnson, A. E. (1964) Incidence and Diagnosis of Trichomon- iasis in Western Beef Bulls, JAVMA, 145, 10, 1007. 43. Johnson, A. E. (1975) The Diagnosis of Trichomoniasis in the Bull, Proc. 69th Ann. Meeting U.S.L.S.A., 183. 44. Joyner, L. P. (1954) The Elimination of Trichomonas Fetus from Infected Semen by Storage in the Presence of Glycerol, Vet. Res., 66, 47, 727. 45. Joyner, L. P. and Bennett, G. H. (1956) Observations on the Viability of Trichomonas fetus during the Process of Freezing to —79° C. and Thawing in the Presence of Glycerol, Jour, of Hyg. 54, 335. 46. Kendrick, J. W. (1953) An Outbreak of Bovine Trichomoniasis in a Group of Bulls Used for Artificial Insemination, Cor. Vet. 43, 2, 231. 47. Kendrick, J. W. (1963) Infectious Causes of Infertility in Bulls, Personal Communication—Seminar. 48a. Kendrick, J. W. (1979) Bovine Trichomoniasis, Classroom notes, Univ. of Calif., Davis, Calif., 1-9. 48b. Kerr, W. R. (1957) Personal Communication. 49. Kerr, W. R. (1955) Vaginal and Uterine Antibodies in Cattle with Particular Reference to Br. abortus, Brit. Vet. Jour. Ill, 4, 169. 50. Kerr, W. R. (1958) Experiments in Cattle with Trichomonas suis, Vet. Rec. 70, 613. 51. Kerr, W. R. and Robertson, M. (1953) Active and Passive Sen- sitization of the Uterus of the Cow in vivo against Trichomonas fetus Antigen and the Evidence for the Local Production of An- tibody in that Site, Jour, of Hyg. 51, 3, 405. 52. Kimsey, P. B., Darien, B. J., Kendrick, J. W. and Franti, C. E. (1980) Bovine Trichomoniasis: Diagnosis and Treatment, JAVMA, 177, 7, 616-619. 53. Larson, L. L. (1953) The Internal Pudendal (Pudic) Nerve Block for Anesthesia of the Penis and Relaxation of the Retractor Penis Muscle, JAVMA, 123, 916, 18. 54. McLoughlin, D. K. (1965) Dimetridazole, a Systemic Treat- ment for Bovine Venereal Trichomoniasis, Oral Administration, J. Parasitol. 51, 835-836. 55. McLoughlin, D. K. (1967) Drug Tolerance by Tritrichomonas fetus, J. Parasitol. 53, 646. 56a. McLoughlin, D. K. (1968) Dimetridazole Treatment of Bovine Trichomoniasis, J. Parasitol. 54, 1038. 56b. Mongini, F. (1977) Practice Methods, Proc. 10th Ann. Conv. A.A.B.P., St. Louis, Mo., 195. 57. Morgan, B. B. (1944) Bovine Trichomoniasis, Burgess Pub- lishing Co., Minneapolis, Minn. 58. Morgan, B. B. and Whitehair, C. K. (1943) The pH of Bovine Trichomonad Pyometra Fluid, N.A. Vet. 24, 12, 729. 59. Parsonson, I. M., Clark, B. L. and Dufty, J. H. (1976) Early Pathogenesis and Pathology of Tritrichomonas fetus Infection in Virgin Heifers, J. Comp. Path. 86, 59-66. 60. Roberts, S. J. (1971) Veterinary Obstetrics and Genital Dis- eases, 2nd Ed., Woodstock, Vt. 61. Robertson, M. (1960) The Antigens of Trichomonas foetus Isolated from Cows and Pigs, J. Hyg. Camb. 58, 207. 62. Swangard, W. M. (1939) Trichomoniasis in Cattle; Biological Studies and a System of Control, JAVMA, 95, 749, 146. 63. Thome, J. L., Shupe, J. L. and Miner, M. L. (1955) Diagnosis and Treatment of Trichomoniasis in Bulls, Proc. 92 Ann. Meet- ing, AVMA, 374. 64. Todorovic, R. and McNutt, S. H. (1967) Diagnosing of Tricho- monas fetus Infection in Bulls, Amer. J. Vet. Res. 28, 126, 1581. 65. Vandeplassche, M., Florent, A., Paredis, F. and Brone, E. (1954) Pathogenese, Diagnose en Behandeling van de Trichomonas-in- fectie bij Runderen, Competes Rendus De. Recherches, No. 13, Dec. 1954. 66. Vandeplassche, M., Paredis, F. and Doorme, H. (1948) L’ln- semination Artificielle Et La Trichomoniase Chez Les Bovine, Zootecnica e Veterinaria-La Fecondazione Artificiale, Numen Speciale in Occasione del 1 Congress di Fisiopatoligia della ri- produzione animale e di Fecondazione Artificiale 23-30, Guigno, 3. 67. Vereerbrugghen, W., Vandeplassche, M. and Paredis, F. (1952) The Treatment of Trichomoniasis in Bulls, The II Intemat. Congr. of Physiol, and Path, of An. Reprod. and of Art. Insem., 132. 68a. Wilson, S. K., Kocan, A. A., Gaudy, E. T. and Goodwin, D. (1979) The Prevalence of Trichomoniasis in Oklahoma Beef Bulls, Bov. Practit. 14, 109-110. 68b. Winter, A. J. (1982) Microbial Immunity in the Reproductive Tract, JAVMA, 181, 10, 1069. 69. Witherspoon, D. M. and Walker, D. F. (1966) New Way to Diagnose Trichomoniasis in Bulls, Mod. Vet. Pract., 47, 14, 50. VIBRIOSIS Definition—Vibriosis or venereal campylobacteriosis is a venereal disease of cattle caused by Campylobacter fetus venerealis spread at the time of coitus or at the time of artificial insemination with improperly handled and treated semen, and characterized by infertility with an increased number of services per conception. Early embryonic deaths are common and abortions from 4 to 7 months of gestation are occasionally observed. The cow develops an immunity to the infection and will have a subsequent normal gestation period but may remain a carrier for many months. The older bull remains a chronic carrier of infection. Although the name of the organism has been changed from Vibrio to Campylobacter the disease will continue to be called Vibriosis.24 Etiology—Vibriosis was first described in 1910 and 1913 in sheep and cattle. During the period of 1918 to 1923 a number of reports were made on the causative agent, pathogenesis, and other factors associated with this disease68 69,70 and the organism called Vibrio fetus now called C. fetus. This organism may appear as mo- tile, or nonmotile, gram-negative, short, comma-shaped rods, or as double spiral-shaped filaments. It grows slowly, scantily, and with difficulty on most laboratory media. All laboratory animals except guinea pigs appear refractory to infection but the organism may be patho- genic for chick embryos. C. fetus, is pathogenic for man in which it causes an undulating fever, placental infec- tion and abortion.25 26 There is a close genetic relation- ship between certain ovine, bovine and human vibriosINFERTILITY IN THE COW 457 so human vibriosis might be acquired by contact with animals. Within the past 25 years the various pathogenic vibrio have been isolated and studied.8'18'19'24 50'80 (See Table 18.) C. fetus venerealis is a serologically homogenous strain and both Type I and Subtype I (or Type II)27-29'50 are similar in antigenicity and pathogenicity. C. fetus in- testinalis is also pathogenic in that it is a common cause of abortion in sheep and causes sporadic abortions in cat- tle. C. fetus intestinalis only rarely produces infertil- ity.19 It can survive for a period of time in the gut of animals but does not persist in the genital tract of cows. There are 3 serotypes of C. fetus intestinalis; A and B are found in the intestine of sheep and cattle while C, including C. fetus jejuni, are found in the intestines of mammals and birds. This latter serotype C causes abor- tion in sheep and enteritis in dogs and man.24 C. bub- ulus also found in the genital tract does not produce dis- ease and24 does not persist in the genital tract of cows. C. bubulus is a nonpathogenic vibrio that is commonly found in fecal material and in the cranial portion of the prepuce of bulls. C. fetus venerealis is an obligate parasite found only in the female genital tract and its contents, fetus and pla- centa, and in the prepuce of the bull. C. fetus venerealis localizes in the anterior vagina and cervix and usually invades the uterus about 7 days after natural service to an infected bull. The infection remains in the uterus and oviducts for a number of weeks to 3 months producing a moderate endometritis and salpingitis.24,64 This results in infertility and early embryonic or fetal deaths. When an immunity develops the infection is eliminated. How- ever, the infection may remain in the cervix and vagina for 8 to 18 months or more. Rarely a cow may carry the infection through a normal gestation period.19 22 53 58 59 Vulvar exposure of susceptible heifers with C. fetus failed to produce infection so spread of the disease by contact is unlikely.47 Young bulls under 4 or 5 years of age are difficult to infect. They may carry the organism from cow to cow during the breeding season but rapidly be- come free of infection when isolated from infected cows. In bulls over 5 years of age vibriosis may become a chronic infection in the prepuce and persist for years. The numbers of vibrio organisms in the sheaths of in- fected bulls varies greatly. Most of the organisms are present in the deeper portions of the sheath around the glans penis and fornix but no lesions are pro- duced.21,28,63’77 Thus the carrier female as well as the car- rier bull are responsible for maintaining the infection in the herd from year to year. Under certain circumstances bulls may develop immunity. The immunity or resis- tance in cows is not a strong one but is sufficient in most cases to permit conception and a normal gestation even if the organisms survive in the tract for several days or weeks.31'32'34'35 C. fetus venerealis from the prepuce contaminates the semen as the organism has never been found in the deeper portions of the male reproductive tract. Special media, techniques and experience are required for the laboratory recovery of C. fetus venerealis from mucus from the vagina, cervix and uterus of cows and especially the con- taminated mucus of the bull’s prepuce. The Campylo- bacter organism is highly susceptible to light, drying and other adverse influences. It cannot live in the alimentary tract of the cow.8 Vibriosis is a venereal disease of cattle spread by the chronically-infected bull to susceptible cows by either natural or artificial service. The initial studies on this disease were done in the early 1950s.4145,46 7175 C. fetus venerealis was probably the most important cause of infertility in beef cattle in the western range states until preventive vaccines were commercially avail- able.28'2936,79 It may still produce significant infertility and losses in range beef herds. Until the advent of the widespread use of artificial insemination with antibiotic treated semen it was also a very common cause of in- fertility in dairy herds in the U.S.A. Vibriosis has been reported widespread in nearly every state in the United States, in Australia, South Africa, Sweden, England, Holland, Canada, and other countries in the world. The presence of C. fetus in the semen can be explained in the same manner as the presence of Table 18. Cultural Characteristics of the Common Campylobacter Organisms Vibrios Catalase H2S Production Tolerance to 3.5% NaCl Tolerance to 1% glycine Fluorescent Antibody Reaction* C. fetus venerealis (Type I & Subtype I) + - — — + + + C. fetus intestinalis + + - + (+) C. bubulus - + + + + + - *Congugate prepared from C. fetus venerealis (Obtainable from Armour-Baldwin Lab.).4J8 VETERINARY OBSTETRICS trichomonads in the semen, namely by contamination of the artificial vagina at the time of service. C. fetus in- fections were found in 25 of 45 herds investigated in the region of Beltsville, Maryland.2021 A 38 percent inci- dence of vibriosis infection in beef herds in California was reported based on the mucus agglutination test.39 These herds had histories that were suspicious of vib- riosis. Sixty percent of the 105 herds in Sweden studied by means of the mucus agglutination test were, or showed evidence of having been, infected with vibriosis.6 Thus vibriosis is probably much more widespread and com- mon than is trichomoniasis and for this reason is of greater economic importance. Although abortion has been pro- duced in a few animals by the intravenous injection of the organism, introduction of organisms into the ani- mal’s body by any means other than the genital tract of the female or the prepuce of the male has not resulted in infection. It is probable that natural infection of the cow except by coitus or artificial insemination is rare. Occasionally the infection might be spread from cow to cow by improperly cleaned instruments or insanitary procedures used in the treatment of the genital tract of cows. Infection except by coitus or insemination rarely if ever occurs even when infected and noninfected ani- mals run together.2141'46 In artificial insemination studs there is definite evidence of the intrastud spread of in- fection. Of 143 bulls in an artificial breeding stud 56 percent were infected; the percentage of infected animals was the same for 39 bulls that had never had a natural service as it was for 104 bulls that had previously been in natural service.38 It was felt that contact and spread of infection between clean and infected bulls occurred on teaser bulls or steers at the time of semen collection or in pens where a number of bulls ran together and mounted each other. Over 20 percent of all bulls used artificially in Denmark were infected with C. fetus.60,61 The incidence of infection in susceptible cows is high following coitus with infected bulls. For example, of 30 virgin heifers bred with infected fresh semen at a dilution rate of 1 to 4 with extender without antibiotics, 26 heif- ers developed vibriosis.38 Prior to the addition, of anti- biotics to semen, artificial insemination was probably a major factor in the spread of this disease.60 It is signif- icant that in one large AI organization that conception rates based on 60 to 90 day nonreturns rose from 52 percent in May of 1948 to 74 percent in September of 1949 after the addition of antibiotics to the semen. No other changes or treatments were made in the semen col- lection, processing, or insemination. Since the advent of the regular and proper addition of antibiotics to semen the incidence of the disease is practically limited to herds using natural service. As with trichomoniasis the disease is more prevalent in dealer’s herds, valuable purebred herds, and institution herds, where there is a higher in- cidence of purchase and sale of cows and bulls. Virgin heifers and virgin bulls are free of the infection. Signs—Vibriosis like trichomoniasis, is insidious in the manner in which it enters a herd. The condition may not be recognized for several months or more, until signs of infertility with failure of conception occur in a large number of cows. Herd infections have been described in the following manner.6,106-21-41 The acute type of infer- tility problem is seen when the infection is first intro- duced by an infected bull into a susceptible herd. The drop in conception rate is marked, occasionally to less than 10 percent and the infertility may last for 2 to 6 months or more. Within this time the cows usually de- velop immunity with the production of antibodies of the IgA class that persist for months in the vagina. While the IgG antibodies are found in the uterus and rid that organ of infection in the convalescent phase of the dis- ease,1324 a cell mediated immunity may also be in- volved.13 Conception will follow breeding to either an infected or noninfected bull. Prior to the development of this immunity, breeding to a noninfected bull or with noninfected semen does not correct the infertility as the C. fetus organisms are present in the female from the original infecting service. The chronic or subacute type of infertility in a herd may be characterized by a history of an acute fertility problem in the past. Only a vague or intermittent infertility is present in the cows or in newly- purchased cows but a considerable amount of infertility may be present in the heifers after being bred to older infected bulls. This may not occur until the second breeding period if it is a practice to breed the virgin heif- ers in a herd to a virgin noninfected bull. In some herds the infertility may be limited to the portion of a herd served by a single bull, or it may involve all cows bred naturally, while cows being bred artificially with anti- biotic-treated semen conceive normally. Examination of the bull and its semen usually reveals no abnormalities or lesions or explanation for the infertility. Abortions may occur in both the acutely or chronically affected herds but are more frequent in the acute outbreaks. Some vir- gin heifers have a natural immunity or develop it promptly and conceive within 2 months. Others conceive promptly but remain carriers of the organism for months. While others remain infected for months, have many services, or abort.58'59 The specific signs of vibriosis in cattle may be listed as follows: (1) Vibriosis may fail to become established in a sus- ceptible animal after coitus with an infected bull, either due to natural resistance or because the numbers of or-INFERTILITY IN THE COW 459 ganisms were too small to cause infection. Conception and normal gestation may occur. Occasionally the in- fection fails to establish itself rapidly in the uterus and cause the early death of the young embryo. Gestation therefore may continue for a number of months and then terminate in 3 to 7 months in abortion. The number of susceptible animals bred to an infected bull that fail to become infected are small, probably less than 5 to 25 percent. Thirty heifers that were artificially infected at the time of insemination; 7 conceived on first service and in 24 the infection became established.38 (2) Endometritis and occasionally salpingitis has been described in C. fetus infection of the genital tract of cows and heifers.41,46'75 No vaginitis or cervicitis or other le- sions were noted.28,53 A slight mucopurulent exudate may be present in the vagina. This may occasionally be noted as a discharge from the vulva and probably comes from the uterus or is due to other secondary infections. The infection or inflammation produced by C. fetus is mild in its effect on the mucosa. The estrual mucus may be cloudy and increased in amount in recently-infected heif- ers. The cervix may be reddened and postmortem gross and histologic examination of the uterus and endometrial biopsy may reveal an exudate and a slight to moderate degree of endometritis. By 30 days after inoculation of the cervix a subacute diffuse muco-purulent endometritis with a periglandular lymphocytic infiltration was pres- ent. The pathogenesis of C. fetus infection in cattle has been described.14 As the cow develops immunity and overcomes the infection, the estrual mucus becomes clear before pregnancy is established. In most recently in- fected animals the symptoms of endometritis pass un- noticed by the average owner or herdsman or are not detectable clinically. If cows are examined for failure of conception or infertility no specific signs of vibriosis can be observed. Rectal examination of the uterus is of no value in the diagnosis of an endometritis since the in- flammation is so mild no obvious uterine changes are produced. No physical symptoms or lesions have been observed in the recently-infected bull. Most infertile C. fetus-infected cattle conceive before the endometritis and the organisms have completely disappeared.13,28 30 (3) Infertility or failure of conception lasting for a pe- riod of 2 to 6 months, and in some herds 12 months, in susceptible cows or heifers bred naturally to an infected bull or bred artificially with fresh or frozen semen to which no antibiotic has been added is the most common symptom of vibriosis. Before 1950, it was thought that C. fetus was characterized principally by abortion; since 1950, however, infertility due apparently to the early death of the embryo caused by the C. fetus organism has been shown to result in the greatest economic loss. This symptom of infertility and failure of conception, as in trichomoniasis, is the most constant and severe condition encountered with vibriosis. This has been demonstrated by field observations.21,41 In experimentally infected an- imals 19 artificially infected heifers required from 1 to 16 services, with an average of 5, per recognizable preg- nancy.45 In a similar experiment 20 heifers were in- fected.41 They required an average of 5.1 services per conception compared with an average of 1.3 to 1.6 ser- vices per conception for control heifers bred to unin- fected bulls. A herd using 5 bulls, 1 of which was in- fected with C. fetus was described.20 21 The cows bred to the 4 noninfected bulls conceived with an average of 1.1 to 1.8 services per conception with 2.5 to 32 as the average number of days lost from first service to preg- nancy. Of 18 cows bred to the infected bull, 5 failed to develop any infection and all 5 conceived on first service while the other 13 became infected and were bred an average of 3 services per conception with an average loss of 89 days from first service to pregnancy. Vibriosis in a range beef herd may be suspected when many cows continue to come into estrum in the latter part of the breeding season. The calving season is prolonged with a significant number of calves produced early followed by a period when relatively few calves are dropped and then late in the calving season more calves are bom.28 36 79 Pregnancy rates as low as 20 to 70 percent may be seen in some beef herds at the end of the breeding sea- son. In other chronically-infected herds the pregnancy rates may be 60 to 85 percent with a poor conception rate in the virgin heifers. If routine vaccination of all breeding stock is practiced the pregnancy rate is usually from 80 to 95 percent.28,36,79 In an extensive field ex- periment it was reported that cows inseminated with se- men from C. fetus-infected bulls had a much greater embryonic mortality rate and much lower nonreturn rate than with noninfected semen or with semen containing streptomycin.28,36,78 Cows bred with semen from infected bulls to which no antibiotic was added had a 42.7 per- cent conception rate compared to a 62.3 percent con- ception rate from similarly diluted semen from appar- ently noninfected bulls. (4) Long estrous cycles ranging from 27 to 53 days with an average of 32 days are experienced by many recently infected cows and heifers.46 Prolonged irregular estrous cycles of 25 to 60 days and even to 100 days are common following the first service of a susceptible fe- male to an infected bull.6,21’41,75 This delayed or long in- terval may occur following any service in infected cows. Long cycles may be explained on the basis that fertil- ization takes place, the fertilized embryo may survive for 12 to 14 days or longer and is then killed or destroyed460 VETERINARY OBSTETRICS by the C. fetus organisms, early embryonic death. If the fertilized ovum is destroyed prior to 14 days after fertilization then estrum will probably occur at the reg- ular cycle length. Fertilization is apparently not affected by C. fetus infection.20-22 (5) Abortion was formerly considered the principal symptom of the disease. A 4 to 20 percent abortion rate of recognizable fetuses with an average of 12 percent in a herd was reported.59 After reviewing the literature it was found that 3.4 to 29 percent of aborted fetuses from brucella-free cows were found positive on culture for C. fetus.62 An incidence of 8.6 percent of 1302 aborted fe- tuses were reported as positive for the presence of C. fetus in England.41 In both of these series a fairly large group of fetuses were so contaminated that recovery of pathogenic bacteria such as C. fetus was impossible. Of the 112 fetuses found positive in the latter study, 1 aborted embryo was recovered at 38 days, 1 at two months, 1 at two and one-half months, 5 at three months, 8 at four months, 30 at five months, 39 at six months, 15 at seven months, 3 at eight months, and 9 unknown. In a report on 198 aborted fetuses, the number of fetuses and the time of abortion was: 9 from one to two months of ges- tation, 14 from two to three months, 17 from three to four months, 29 from four to five months, 52 from five to six months, 36 from six to seven months, 26 from seven to eight months, 12 from eight to nine months, and 3 expelled dead at term. This was based on bacte- riologic evidence in about 50 percent of the cases and on uncertain serologic evidence in the rest. Thus the greatest incidence of observed abortion is from 4 to 7 months of gestation. It is highly probable, according to our present knowledge, that abortions prior to 4 months are more common but are not observed and are consid- ered as infertility or failure to conceive. Usually there is some indication of impending abortion after the fourth or fifth month of gestation by the presence of a vulvar discharge and slight edema of the vulva. Some enlarge- ment of the udder may occur. In early abortions the pla- centa is usually expelled with the fetus. In late abortions retention of the fetal membranes may occur. Pyometra is rarely observed in C. fetus infection in cattle. The lesions in abortions at middle or late gestation are mainly in the fetal membranes, the fetus suffering secondarily because of interference with its circulation. The lesions resemble those of Brucella abortion. The intercotyle- donary spaces are filled with a thick, purulent, viscid material. The cotyledons may be greyish white in color with much cheesy exudate between the maternal carun- cle and the fetal cotyledon. The membranes may be thickened and edematous and the amniotic fluid turbid due to fetal diarrhea. C. fetus organisms may be found in the placenta. The aborted fetus usually shows auto- lytic changes of subcutanous edema; thin, bloody fluid in the body cavities; and a thick, yellow, flocculent, tur- bid material in the stomach that usually contains many C. fetus organisms. The stomach content of normal fe- tuses is clear, semi-liquid, and mucoid in nature. Lack of libido in bulls—Infected bulls pasture-bred on susceptible cows copulate frequently. Because of the excessive sexual load occasioned by many of the cows returning to estrus, the bull may lose weight and libido. Diagnosis—On the basis of the herd history or symp- toms, a careful review of the breeding records, and a careful physical examination of the individual animals in the herd, including the bull, to be certain that no sem- inal pathology is present, a tentative diagnosis of vib- riosis or trichomoniasis might be made. Since in most areas vibriosis is more common than is trichomoniasis as a cause for herd infertility and failure of conception, vibriosis is usually the diagnosis; but trichomoniasis should be suspected until sufficient tests have been made to make certain of the diagnosis. Pyometra is rare in vibriosis but is occasionally ob- served in trichomoniasis. Abortions in trichomoniasis usually occur within the first four months and seldom after the fifth month of gestation while in vibriosis abor- tions in the fifth through eighth months are common. It is possible to find both vibriosis and trichomoniasis in a bull, a cow, or a herd. Herds with infertility due to ster- ile or infertile bulls with defective semen or infertility due to a lack of energy intake, especially in beef herds, may simulate the signs of vibriosis and a careful differ- ential diagnosis is imperative. Since vibriosis, similar to trichomoniasis, is not a sys- temic disease, antibodies are rarely found in the blood serum. Thus blood or serologic tests for diagnosing vib- riosis are seldom used as reliable results cannot be ob- tained. Since the infection in the female genital tract produces a local immunity, the agglutination test on vaginal mu- cus is useful for diagnosing the presence of vibriosis in a herd. Tests on vaginal mucus for the presence of an- tibodies to C. fetus was first described in 1949.7175 This test was improved and made highly reliable for diag- nostic purposes.6'39'46 The vaginal mucus from a cow or heifer infected with C. fetus gives a positive agglutin- ation reaction approximately 30 to 80 days following the infecting service. This reaction persists in most cows for about 7 months or a range of 4 to 23 months. The mucus should not be taken from cows that have recently calved or for 3 to 4 days after estrum, as these cows may have metestrual blood in the mucus. Samples taken at these times may give false positive reactions. The excessiveINFERTILITY IN THE COW 461 amounts of mucus from cows in estrum should not be used for this agglutination test as false negative results may be obtained because the antibody level is diluted. In infected heifers only 21 percent of the vaginal mucus samples taken during estrum gave an agglutination re- action while 91 percent of samples taken agglutinated from about 4 to 5 days after estrum to 1 to 2 days before estrum.41 The agglutination test at the proper time on samples obtained from about 10 heifers which had been bred for the first time at least 2 months, but not over 9 months previously, should establish or disprove a di- agnosis of vibriosis in a herd. The vaginal mucus ag- glutination test is most useful in dairy herds where the stage of the estrous cycle of open cows is usually known and confinement of cows in stanchions is often possible. The tampon method of collecting vaginal mucus sam- ples was perfected.73 The technique of collecting vaginal mucus samples consists of holding the cow’s tail to one side and washing the vulva and adjacent parts with soap and water. The vulvar lips are held open, and the vulva rinsed with clean water; a plastic 12 inch speculum con- taining both a tampon made of a gauze pad with a 16 inch string attached and the placement rod is inserted into the vagina. The speculum should be pushed as far forward as possible, and then the rod pushed forward, moving the tampon out of the speculum and into the cra- nial part of the vagina. To prevent air from entering the vagina and ballooning it, the thumb should be held over the end of the speculum while it is being withdrawn. The free end of the string is tucked between the vulvar lips to prevent its being soiled by feces. The tampon is left in the vagina at least 20 minutes to absorb an adequate sample of mucus. To remove the tampon wash the cow’s vulva again, grasp the string and pull out the tampon and place it and the string in a plastic sample bottle. Samples should be kept in a refrigerator until mailed or taken to the laboratory. Inasmuch as no preservatives are added to the samples, they should not be sent through the mail over weekends or holidays to avoid spoilage. The nec- essary equipment may be supplied by the laboratory or made by the veterinarian. The use of a human vaginal tampon introduced into the cow’s vagina with a plastic insemination pipette and transported in 4 ounce plastic bottles available in supermarkets has been described.39 The laboratory should be sent an unused tampon and bot- tle for weighing. This is necessary to ascertain the amount of mucus present in each sample for dilution purposes. Care should be taken that infection is not spread from cow to cow. Separate equipment is necessary for each animal. Only certain vibrio antigens were suitable for the vaginal mucus agglutination test. Those that give too many false positive reactions when tested on virgin heifers should be discarded.6 Any titer is significant but 1:25 is • • • 38 39 considered suspicious and 1:50 or more is positive. The number of positives in a representative sampling would vary, but one positive animal is probably suffi- cient to establish the presence of the infection in a herd. Cultures of vaginal, cervical or uterine mucus taken at estrum from heifers and cows by pipette have been described.75 Culturing of cervical mucus was the pre- ferred method of diagnosing vibriosis in range beef herds as the animals only needed to be handled once and sam- ples could be taken at any stage of the estrous cycle or even during pregnancy.28,23 Artificial insemination pi- pettes attached to 2-1/2 ml plastic syringes to produce a vacuum were adapted to collect cervical mucus sam- ples. IOb,28,3°'33 The pipettes were passed through a sterile plastic or glass speculum to avoid contamination in the vestibular area. The pipettes were sealed with polybulbs and shipped to the laboratory in dry ice; freezing the pi- pettes in liquid nitrogen was not satisfactory because of breakage. The efficiency of recovering C. fetus from frozen vaginal or cervical mucus samples in the labo- ratory drops about 20 percent after 2 days in dry ice.10 This technique must be performed carefully and samples taken promptly to a laboratory for culture. In 88 samples of mucus from artificially- or naturally-infected heifers, vibrios were recovered in about 26 percent of the sam- ples.47 In another study 83.1 percent of the samples of mucus recovered from infected heifers at the time of es- trum were positive on culture while only 26.5 percent of samples collected at other phases of the cycle were pos- itive.41 Positive cultures were obtained from vaginal mu- cus samples taken by a specially-designed instrument, from animals recently bred, repeatedly bred, after calv- ing, and after conception. A total of 429 vaginal mucus samples were collected and 26 percent were positive for C. fetus.21 Positive isolations from vaginal mucus were made as early as 11 days and as late as 224 days after conception. Positive cultures were obtained from 8 cows 21 to 196 days after calving. In a total of 114 vaginal mucus samples from 71 known virgin heifers none was positive for C. fetus. On routine examination of C. fe- tus-infected cows or heifers C. fetus was recovered from vaginal mucus in 76 percent of the cattle for only 40 days; in 12 percent the organism was found for 2 to 6 months; and in the remaining 12 percent for 7 to 12 months.21 About 50 percent of heifers were positive on culture one week after exposure to C. fetus.33 From 3 to 9 weeks after breeding large numbers of vibrio were present in the samples. During the first 3 months after exposure nearly all open heifers, 80 to 90 percent, were positive so at this time random samples from 6 to 10 open heifers in a herd would be adequate for a diagnosis.462 VETERINARY OBSTETRICS In cattle exposed 6 months previously only 20 percent were positive so 20 samples of mucus should be taken from open heifers or cows at this stage of the infection. Samples taken at the time of calving gave poor results. A biopsy instrument to recover the organism from the uterus of infected cows or heifers was described.75 Culture of C. fetus from semen and preputial smegma—Although the other diagnostic tests are very useful, the isolation of C. fetus is the only unequivocal test. When cervicovaginal mucus can’t be cultured promptly after collection the F.A. test is the best.3 Cul- tures of C. fetus can usually be recovered by a well- equipped laboratory with trained personnel. In culturing 306 ejaculates taken in as sanitary a manner as possible from 81 infected bulls vibrio were recovered in 20 per- cent of the samples.38 In 307 samples on another trial C. fetus was recovered 20 percent of the time, or once in 5 ejaculates.21 The culturing of preputial smegma samples taken in the same manner as for recovering trichomonads was described.67,82 This procedure was more accurate than the culturing of semen samples. Special techniques were necessary because of bacterial contam- inants in the prepuce. A fluorescent antibody screening test was developed to use on preputial and vaginal mucus samples; a positive test required confirmatory vibrio cul- tures, since certain C. fetus intestinalis strains and oc- casional C. fecalis strains fluoresced.80,82 Another rather cumbersome technique used to detect C. fetus in bulls is to breed them to 2 or more virgin heifers and obtain vaginal mucus for culture from the fifteenth to the thirtieth day.21 After inseminating 1 ml. of undiluted semen into the cervical canal of 2 or more virgin heifers during estrum, samples were taken from the uterus 4 days after service and once a week there- after, regardless of the phase of the cycle. In 8 heifers bred in this manner to known infected bulls 32 of 35 uterine biopsy samples were positive for C. fetus, while only 15 of 35 vaginal mucus samples taken at various times in the estrous cycle were positive on culture.1,2 This technique resulted in a positive diagnosis 14 days after breeding the heifer. Later, as a means of diagnosing vib- riosis in a bull it was recommended to take 3 ejaculates from a bull in the same vagina, and douche the prepuce with saline solution. The semen and saline douche fluid were mixed and centrifuged. One ml. of sediment was inseminated into the cervix of a heifer in estrum and the heifer was cultured as described previously.60,61 Procedures have been developed so veterinary prac- titioners can collect vaginal mucus, semen or preputial samples in the field in a proper manner and have them reach the laboratory in satisfactory condition for culture. More laboratories are being equipped with facilities and personnel for performing this culturing technique. The fluorescent antibody technique aids greatly in the diag- nosis of vibriosis by detecting C. fetus in cervical mucus cultures.43 Aborted fetuses should always be cultured as this is one of the easier methods of diagnosing the presence of C. fetus in a herd. Immediately following abortion the fetus and possibly the fetal membranes if clean and not heavily contaminated should be taken to the laboratory for culture. The stomach contents and lungs are the or- gans in the large fetus from which C. fetus may most commonly be cultured. In small fetuses the amniotic fluid may be cultured. Some workers have reported finding the organism on direct smear or by fluorescent antibody techniques or culture of the stomach contents or exudate on the fresh cotyledons of the placenta.24 If the fetus is small and cannot be taken immediately to the laboratory in the fresh state, it may be frozen, packed in dry ice, and sent by special delivery. If the fetus is large, the esophagus, duodenum and trachea may be carefully li- gated and the stomach and lungs removed and handled as above. Ten to 39 ml. of stomach fluid from the aborted fetus may be removed in an aseptic manner and placed in a sterile vial. This may be frozen and shipped. If the fetus lives for even a short time, usually the stomach contents are contaminated by many bacteria. It is often possible in abortions caused by C. fetus to obtain pure cultures of this organism from the stomach contents of the fetus. The finding of the organism is a certain di- agnosis that C. fetus is present in the herd. A differential diagnosis should be made between C. fetus venerealis and C. fetus intestinalis in cases of bovine abortion. Prognosis—In vibriosis the prognosis in the cow is usually favorable as the infertility ordinarily is tempo- rary in nature and after a period of 3 to 6 months most infected cows develop immunity to the infection and conceive. The greatest loss is economic and is due to the delay in conception. Most cows if they abort conceive after a suitable period of sexual rest unless a secondary infection produces permanent damage. Old bulls remain chronically or permanently infected unless isolated and treated. In many young bulls the infection is transient and disappears when they are removed from service. Treatment—Our present knowledge is adequate to largely control vibriosis in beef herds and to eradicate the disease in dairy herds. Basically, the control methods are the same as in trichomoniasis. Genital contact be- tween infected and noninfected animals should be pre- vented. Presently systemic vaccination with bacterins is highly effective in controlling infertility due to vibriosis in cattle.5,,0a,b 28,40 In a dairy herd the best and easiest way to controlINFERTILITY IN THE COW 463 vibriosis is to breed only artificially with semen from noninfected bulls; or with semen from infected bulls, that has been diluted or extended at least 1 to 25 with ex- tender to which 500 to 1000 units of penicillin and 50 to 1000 micrograms of streptomycin or other effective antibiotics for each ml. of extender have been added. This extended semen should be held at refrigerator tem- perature for at least 6 hours before use. The semen should be collected, diluted, cooled, and held according to methods outlined in the chapter on artificial insemina- tion, to assure maximum sperm survival. The handling of infected semen in this manner will, by the time of insemination, destroy any vibrio organisms present.54 Vibrio-infected semen diluted 1 to 4 with extender with- out antibiotics resulted in 26, or 86.6 percent of 30 heif- ers becoming infected with vibriosis after insemina- tion.38-45 When the infected semen was similarly diluted 1 to 25 with an extender without antibiotics and used to inseminate 29 heifers only 4, or 13.8 percent, became infected. This indicated the value of dilution in reducing the incidence of infection. In 94 heifers inseminated with infected semen diluted 1 to 25 with extender to which 500 units of penicillin, 500 micrograms of streptomycin and 3 mg of sulfanilamide per ml. had been added, then stored for 6 hours, none developed vibriosis. C. fetus was not isolated from 99 “repeat breeding” cows and heifers and cows from 7 herds that had been artificially inseminated with antibiotic treated semen from known infected bulls.21-22 Streptomycin alone was as effective as combinations of streptomycin and penicillin and sul- fanilamide in controlling the spread of C. fetus in the semen.78 The author has never recovered a fetus positive for C. fetus from an aborting cow that had been bred only artificially with antibiotic-treated semen. However the use of antibiotics in semen was considered an un- certain method of controlling vibriosis. The author knows that on the basis of the above data and his experience this method is highly effective but agrees that it is a thin line of defense against the disease. Bulls used for arti- ficial insemination should be free of vibriosis to be cer- tain that they cannot accidentally spread C. fetus in the semen. The control of C. fetus in frozen semen is more dif- ficult than in the extended liquid semen because the glycerol interferes with the effect of the antibiotics on the organism. Evidence was presented to show that fro- zen semen from vibrio-infected bulls extended with egg- yolk-citrate buffer with penicillin and streptomycin added in the proportions of 500 to 1000 units and 500 to 1000 ug respectively, did not produce vibriosis or infertility when used for the insemination of virgin heifers.44 Al- though ampules of recently frozen semen may contain viable vibrios holding frozen semen for several weeks resulted in their destruction. This has been confirmed over the past 20 years as very few cases of vibriosis have been reported in cattle bred with properly treated frozen semen. Two heifers were reported to have been infected with frozen semen stored for a year in an antibiotic and glycerol extender.51 Such occurrences are probably rare. The addition of 500 units of polymyxin B sulphate, 500 units of penicillin and 1000 ug of dihydrostreptomycin per ml. of extended frozen semen also was an effective means for the control of vibriosis.72 Recent studies have shown the importance of the antibiotic treatment of raw semen before it is extended and frozen and to evaluate the efficacy of antibiotic treatment procedures with each extender and processing technique used by the AI in- dustry to prevent the spread of C. fetus in semen. An- tibiotic treatment of C. fetus-infected semen extended in 3 common extenders did not eliminate the organism in one of them.36b In controlling vibriosis in a herd, artificial breeding to a noninfected bull, or to an infected or suspect bull after proper dilution and treatment of the semen with anti- biotic and storage before use, should probably be con- tinued for at least 2 to 3 years, in light of work indicating that vibrio will survive in the cow for only a short time in 75 percent of the animals, for longer periods of 2 to 12 months or more in another 24 percent of the infected females, and in a few cows for as long as 196 days after the termination of a normal pregnancy initiated by in- fected semen. Further work is necessary on this aspect of the disease. A total insemination program for most beef herds is impossible to accomplish so other control methods, particularly vaccination are necessary. Some veterinarians advocate a period of 3 month’s sexual rest for the acutely infected herd, after which breeding can be resumed with the infected bull or by artificial insemination inasmuch as within this time the cows have probably developed a satisfactory degree of immunity or resistance to the infection. The value of a 3-month rest period is questionable except to conserve the bull, as some females recover more promptly than others and if these were withheld from service the eco- nomic loss would be unnecessarily increased. Following natural infection a good immunity to vibriosis is pro- duced that lasts from one to three years.2-8'31 The virgin heifers may be bred to young virgin bulls, which should continue to be used on them for the second pregnancy and thereafter. The infected bulls may be mated to the infected, immune cows and this program continued until the infected herd is eliminated. This procedure is diffi- cult to follow over a period of years without an accident that would allow the infection to spread by venereal con-464 VETERINARY OBSTETRICS tact from the infected cows or bulls to the vibrio-free herd. In beef herds where artificial insemination is impract- ical and the maintenance of two herds, a clean one and an infected one, is not possible, vaccination each year with a commercially-available adjuvant bacterin of all animals of breeding age a few months before the breed- ing season is indicated. Vaccination with a proven highly antigenic bacterin at either one or two intervals provides a good level of immunity even in virgin heifers bred to infected bulls.511,12'23’35-36-40-43'52'57 Although C. fetus or- ganisms may occasionally be found in the genital tract of vaccinated heifers soon after service to infected bulls, conception occurs promptly and the organisms disappear rapidly in most animals due to the presence of antibodies of the IgG variety.13 But a vaccinated animal may be a short-time carrier of the infection and infect a susceptible bull that serves her. This resistance produced by vacci- nation is usually sufficient to overcome the carrier state in cows13 and possibly bulls.511'40 Conception rates of 90 percent are common in vibrio-positive beef herds fol- lowing vaccination. Commercial adjuvanted vaccines (Vibrin, Norden Lab, Bo-Vibrio, Armour-Baldwin Lab. and Tri-vib, Fort Dodge Lab.) with either one to three strains of V. fetus venerealis and others, some com- bined with leptosphal vaccines appear equally effective in cattle herds in producing immunity and controlling the disease in the U.S. when given once a year. Vaccination of heifers 6 months or more before the breeding season may result in some loss of immunity by the time of ser- vice to an infected bull. Even though a good degree of immunity is present a year or more after vaccination, yearly vaccination 10 to 14 days before the breeding sea- son is recommended.4 It is advised in order to maintain a high level of immunity and better conception rates. Vaccinal immunity and convalescent immunity de- creased from 1 to 4 years after vaccination or expo- sure. 10a'b'31 So an annual single vaccination of all cows in infected herds 30 to 120 days before breeding is usu- ally recommended. Systemic vaccination with an adjuvant bacterin pro- duces sufficient IgG to protect the cow or heifer against uterine infection even though antibodies in the blood are low. 13 24 Thus by means of either artificial insemination with properly controlled vibrio-free semen, separation of the herd into vibrio-free and vibrio-infected groups with proper isolation and control, by yearly vaccination with a bacterin of all breeding females or by a combination of these methods vibriosis as a cause of infertility in a herd can be controlled. Treatment of individual cows by the intrauterine in- fusion of about one gram of streptomycin together with penicillin in an aqueous or oily base has proven quite effective in controlled studies in eliminating the vibrio organism from the female genital tract. Elimination is most efficient if given within 24 hours after service to an infected bull.1 15 49 74 Practitioners evaluating such treatments should realize that within a few weeks after the initial infection and endometritis most cows are de- veloping immunity and recovering from the disease. Treatment of infected cows, unless it closely follows the infective service, is in reality being given to convales- cent animals. Thus antibiotic infusions of infected cows are of limited or uncertain value. The treatment of bulls for vibriosis—Most young infected bulls have only a transient short-term infection and then spontaneously recover in a few weeks or months if the organism is not reintroduced into the prepuce. Twenty-two young bulls were repeatedly exposed pre- putially to C. fetus. They became long-term carriers be- tween 40 and 70 months, 3 and 5-1/2 years, of age. Four of these bulls developed a temporary carrier state of 4 to 29 days prior to the long-term carrier state. The use of young bulls to limit spread of C. fetus is of dubious value. Vaccination of bulls is a better preventive mea- sure.10bl5b Bulls over 5 years of age may remain per- manently infected although occasionally even old bulls will spontaneously recover from the disease.10 Bulls do not develop a long-lasting or permanent immunity to the infection. However effective vaccines incorporating large amounts of antigens and adjuvants have been developed in Belgium and Australia that will apparently produce sufficient immunity to terminate natural and prevent new infection in bulls.5'11'12 With immunized bulls temporary or passive contamination of the penis and sheath after breeding an infected heifer is not an important or sig- nificant factor in the spread of genital infection of C. fetus.123 Only 1 of 47 susceptible heifers bred by a vac- cinated bull shortly after service with an infected heifer developed an infection with C. fetus. Although bulls are usually vaccinated with bacterins in the U.S., it should be noted the C. fetus lives com- mensally in the crypts and on the surface of the epithe- lium of the prepuce without producing any inflamma- tion. Therefore it is difficult to envision circulating IgG diffusing into the prepuce and eliminating the organism unless there is enough “inflammation or trauma” pro- duced at repeated copulations. Large repeated doses of vaccine might prevent or cure infection in bulls. 10b,4° Further studies in the U.S. with available vaccines are needed.40 If bulls are cured with antibiotics or vaccines they may readily be reinfected. There is little value to eliminating infection in a bull if he is to remain in natural service in infected herds. In an AI stud it is highly de-INFERTILITY IN THE COW 465 sirable to eliminate vibriosis from all bulls even though the addition of antibiotics to the semen has proven quite effective in controlling vibriosis. Swedish and Danish AI studs have eliminated vibriosis and this was accom- plished in a large AI stud in the U.S.A.42 Prior to treat- ment of bulls rigid control measures on the movement of bulls and hygienic measures in the collection of semen were instituted. All bulls in the stud were tested semi- annually by culturing and immunofluorescence of pre- putial smegma samples. Each new bull entering the stud was tested similarly during the isolation period of several months. All bulls infected with C. fetus venerealis were treated with 5 gm. of dihydrostreptomycin sulfate in 10 ml. of a 50% aqueous solution infused in the preputial cavity and massaged thoroughly through the skin of the sheath for 5 minutes while the preputial orifice was closed. This was repeated daily for 5 treatments. At the time of the first and third treatments two subcutaneous injections of 22 mg/kg of body weight of dihydrostreptomycin were given.42 Repeated tests of preputial mucus were con- ducted at biweekly intervals after treatment. Test breed- ing of virgin heifers to treated bulls followed by repeated cultures of the cervical mucus of the heifers could be done to determine if the treated bulls had eliminated the infection. This technique is more costly than the direct sampling of the preputial smegma. Treatment produced mild focal reddening and ulcerations of the penile mu- cosa that healed promptly. Other antibiotics in the treat- ment of vibriosis in the bull have been tried because of fear of producing streptomycin-resistant vibrio organ- isms, since streptomycin is also used to control the or- ganism in semen. These antibiotics, tylosin and furacin have not proven as effective as streptomycin in the treat- ment of infected bulls. References Vibriosis 1. Adler, H. C. (1957) Genital Vibriosis in Bovine Experimental Investigations with a Special View to Diagnosis, Prophylaxis and Therapy, Nord. Vet. Med., 9, 474. 2. Adler, H. C. and Lindegaarde, L. E. (1965) Bovine Genital Vibriosis: Eradication from Danish AI Centers, Nord. Vet. Med. 17, 237. 3. Andrews, P. J. and Frank, F. W. (1974) Comparison of Four Diagnostic Tests for Detection of Bovine Genital Vibriosis, JAVMA, 165, 8, 695-697. 4. Berg, R. L. and Firehammer, B. D. (1978) Effect of Interval Between Booster Vaccination and Time of Breeding on Protec- tion Against Campylobacteriosis (Vibriosis) in Cattle, JAVMA, 173, 5(1), 467-474. 5. Bouters, R., DeKeyser, J., Vandeplassche, M., Van Aert, A., Brone, E. and Bonte, P. (1973) Vibrio Fetus Infection in Bulls, Curative and Preventive Vaccination, Brit. Vet. J. 129, 52. 6. Boyd, H. (1955) Bovine Genital Vibriosis, Dept, of Obst. and Gynecol. Royal Veterinary College, Stockholm Sweden. (The- sis) 7. Bruner, D. W. and Gillespie, J. H. (1966) Hagan’s Infectious Diseases of Domestic Animals, 5th Ed., Cornell Univ. Press, Ithaca, N.Y., 241. 8. Bryner, J. H., Frank, A. H. and O’Berry, P. A. (1962) Dis- sociation Studies of Vibrios from the Bovine Genital Tract, Amer. J. Vet. Res. 23, 92, 32. 9. Bryner, J. H., O’Berry, P. A. and Frank, A. H. (1964) Vibrio Infections of the Digestive Organs of Cattle, Amer. J. Vet. Res. 25, 107, 1048. 10a. Carroll, E. J. (1967) Personal Communication. 10b. Carroll, E. J. and Hoerlein, A. B. (1972) Diagnosis and Control of Bovine Genital Vibriosis, JAVMA, 161, 11, 1359 (Review). 11. Clark, B. L., Dufty, J. H., Monsbourgh, M. S. (1975) Studies on Venereal Transmission of Campylobacter fetus by Immu- nized Bulls, Austral. Vet. J. 51, 531-532. 12. Clark, B. L., Dufty, J. H., Monsbourgh, M. J. and Parsonson, I. M. (1976) Immunization Against Vibriosis due to Campy- lobacter fetus subsp. fetus biotype intermedius. Austral. Vet. J. 52, 362-365. 13. Corbeil, L. B., Corbeil, R. R. and Winter, A. J. (1975) Bovine Venereal Vibriosis: Activity of Inflammatory Cells in Protective Immunity, Amer. J. Vet. Res. 36, 4, 403-406. 14. Dennis, S. M. (1961) Studies on the Pathogenesis of Vibrio fetus, Ph.D. Thesis, Univ. of Sydney, Sydney, Australia. 15a. Dozsa, L. and Olson, N. O. (1964) The Effect of Various An- tibiotics on the Uterine Mucosa of Vibrio fetus—Infected Cows, Amer. J. Vet. Res. 25, 104, 108. 15b. Dufty, J. H., Clark, B. L. and Monsbourgh, J. J. (1975) The Influence of Age on the Susceptibility of Bulls to Campylo- bacter fetus Subsp. venerealis. Austral. Vet. J. 51, 294-297. 16. Elliott, F. I., Murphy, D. M. and Bartlett, D. E. (1961) The Use of Polymyxin B. Sulphate with Dihydiostreptomycin and Penicillin for the Control of Vibrio Fetus in a Frozen Semen Process, 4th Intemat. Congr. on An. Reprod., Ill, 539. 17. Estes, P. C., Bryner, J. H. and O’Berry, P. A. (1966) Histo- pathology of Bovine Vibriosis and the Effects of Vibrio Fetus Extracts on the Female Genital Tract, Cor. Vet. 56, 4, 610. 18. Florent, A. (1959) Les Deux Vibrioses Genitalles la vibriose due a V. fetus venerealis et la vibriose d’origine intestinale due a V. fetus intestinalis, Mededel d. Veertsenyschool v. Gent, 3, 60. 19. Florent, A. and DeKeyser, P. (1964) Problems of Infertility in Livestock in Belgium, Brit. Vet. J. 120, 407. 20. Frank, A. H. (1950) Impaired Breeding in Cattle—Field Ob- servations and Results of Treatment, Proc. AVMA 87th Ann. Meeting, 190. 21. Frank, A. H. and Bryner, J. H. (1953) Observations on Vib- riosis of Cattle in Relation to Impaired Fertility, Proc. U.S. Livestock Sanit. Assoc., 57th Meeting, 165. 22. Frank, A. H., Bryner, J. H. and O'Berry, P. A. (1964) Repro- ductive Patterns of Female Cattle Bred for Successive Gesta- tions to Vibrio fetus-infected Bulls, Amer. J. Vet. Res. 25, 988. 23. Frank, A. H., Bryner, J. H. and O’Berry, P. A. (1967) The Effect of Vibrio fetus Vaccination on the Breeding Efficiency of Cows Bred to Vibrio fetus-infected Bulls, Amer. J. Vet. Res. 28, 126, 1237. 24. Gillespie, J. H. and Timoney, J. F. (1981) Hagan and Bruner’s466 VETERINARY OBSTETRICS Infectious Diseases of Domestic Animals, 7th Ed., Cornell Univ. Press, Ithaca. 25. Gilman, H. L. (1960) Vibrio fetus Infection in Man and Ani- mals, Intemat. J. of Fert. 5, 4, 411. 26. Gilman, H. L. (1962) Personal Communication. 27. Hoerlein, A. B. (1967) Personal Communication. 28. Hoerlein, A. B. (1968) Bovine Genital Vibriosis, In “Abortion Diseases of Livestock,” Edit, by L. C. Faulkner, C. C. Thomas & Co., Springfield, 111., 18. 29. Hoerlein, A. B. (1970) Vibriosis, in Bovine Medicine and Sur- gery, Amer. Vet. Public. Inc., Wheaton, 111., 91. 30. Hoerlein, A. B. (1980) Bovine Genital Vibriosis, in Current Therapy in Theriogenology, Edit, by D. A. Morrow, W. B. Saunders, Co., Philadelphia, 479-482. 31. Hoerlein, A. B. and Carroll, E. J. (1970) Duration of Immunity to Bovine Genital Vibriosis, JAVMA 156, 6, 775. 32. Hoerlein, A. B., Carroll, E. J., Kramer, T. and Beckenhauer, M. H. (1965) Bovine Vibriosis Immunization, JAVMA 146, 8, 828. 33. Hoerlein, A. B. and Kramer, T. (1963) Cervical Mucus for the Diagnosis of Vibriosis in Cattle, JAVMA, 143, 8, 868. 34. Hoerlein, A. B. and Kramer, T. (1963) Artificial Stimulation of Resistance to Bovine Vibriosis, Amer. J. Vet. Res. 24, 102, 951. 35. Hoerlein, A. B. and Kramer, T. (1964) Artificial Stimulation of Resistance to Bovine Vibriosis; Use of Bacterins, Amer. J. Vet. Res. 25, 105, 371. 36a. Hoerlein, A. B., Kramer, T., Carroll, E. J., Brown, W. W., Jr., Scott, J. A. and Ball, L. (1964) Vibriosis in Range Cattle, JAVMA, 144, 2, 146. 36b. Howard, T. H., Vasquez, L. A. and Amann, R. P. (1982) An- tibiotic Control of Campylobacter fetus By Three Extenders of Bovine Semen, J. Dairy Sci. 65, 1596. 37. Hughes, D. E. (1953) A Study of the Diagnosis of Bovine Vib- riosis with Special Reference to the Detection of Agglutinins in the Vaginal Secretions, Cor. Vet. 43, 3, 431. 38. Hughes, D. E., McEntee, K. and Gilman, H. L. (1954) Recent Developments in the Diagnosis and Control of Bovine Vibriosis, Vet. News, 17, Nov.-Dee., 17. 39. Kendrick, J. W. (1967) The Vaginal Mucus Agglutination Test for Bovine Vibriosis, JAVMA, 150, 5, 495. 40. Kendrick, J. W. (1976) Bovine Vibriosis, Classroom Notes, Univ. of Cal. Davis, Cal. 41. Lawson, J. R. and MacKinnon, D. J. (1952) Vibrio foetus In- fection in Cattle, Vet. Rec., 64, 763. 42. Lein, D., Erickson, I., Winter, A. J. and McEntee, K. (1968) Diagnosis, Treatment, and Control of Vibriosis in an Artificial Insemination Center, JAVMA, 153, 12, 1574. 43. Lincoln, G. J. and Trout, K. J. (1967) Evaluation of a New Trivalent Bovine Vibriosis Bacterin Using Fluorescent Antibody Technique, Vet. Med. 62, 6, 561. 44. McEntee, K., Gilman, H. L., Hughes, D. E., Wagner, W. C. and Dunn, H. O. (1959) Insemination of Heifers with Penicillin and Dihydrostreptomycin-Treated Frozen Semen from Vibrio fetus Carrier Bulls, Cor. Vet. 49, 2, 175. 45. McEntee, K., Hughes, D. E. and Gilman, H. L. (1954) Pre- vention of Vibriosis in Inseminated Heifers by Treating the Se- men from Vibrio-infected Bulls with Penicillin, Streptomycin and Sulfanilamide, Cor. Vet. 44, 3, 395. 46. McEntee, K., Hughes, D. E. and Gilman, H. L. (1954) Ex- perimentally Produced Vibriosis in Dairy Heifers, Cor. Vet. 44, 3, 376. 47. McEntee, K., Hughes, D. E. and Wagner, W. C. (1959) Failure to Produce Vibriosis in Cattle by Vulvar Exposure, Cor. Vet. 49, 1, 34. 48. Mellick, P. W., Winter, A. J. and McEntee, K. (1965) Diag- nosis of Vibriosis in the Bull by Use of the Fluorescent Anti- body Technic, Cor. Vet. 55, 280. 49. Melrose, D. R., Morgan, W. J. B. and Stewart, D. L. (1959) The Treatment and Subsequent Reinfection of Heifers Infected with V. fetus, Vet. Rec. 71, 411. 50. Mohanty, S. B., Plumer, G. J. and Faber, J. E. (1962) Bio- chemical and Colonial Characteristics of Some Bovine Vibrios, Amer. J. Vet. Res. 94, 23, 554. 51. Morgan, W. J. B., Melrose, D. R. and Stewart, D. L. (1959) The Effect of Streptomycin on the Survival of Vibrio fetus in Semen and Other Diluents Stored at 5° and -79° C., J. Comp. Path, and Therap., 69, 257. 52. Newhall, J. H. (1966) Results of Field Trials and Controlled Laboratory Studies on Bovine Vibriosis Bacterins, JAVMA, 149, 12, 1643. 53. Newsom, I. D. B. and Peterson, J. E. (1964) Persistence of Vibrio fetus in the Genital Tract of Experimentally Infected Heifers, Brit. Vet. Jour. 120, 223. 54. Orthey, A. E. and Gilman, H. L. (1954) The Antibacterial Ac- tion of Penicillin, Streptomycin and Sulfanilamide Against Heavy Suspensions of Vibrio fetus Added to Semen Extender, J. of Dairy Sci. 37, 4, 407. 55. Orthey, A. E. and Gilman, H. L. (1954) The Antibacterial Ac- tion of Penicillin and Streptomycin Against Vibrio Fetus In- cluding Concentrations Found in Naturally Infected Semen, J. of Dairy Sci. 37, 4, 416. 56. Plastridge, W. N., Easterbrooks, H. L. and Williams, L. F. (1953) The Tampon Method of Collection and the Examinations of Cervico-vaginal Mucus for Vibrio Fetus Agglutinins, JAVMA, 122, 921, 516. 57. Plastridge, W. N., Kersting, E. J. and Williams, L. F. (1966) Resistance of Vaccinated Heifers to Vibriosis, Amer. J. Vet. Res. 27, 116, 186. 58. Plastridge, W. N., Stula, E. F. and Williams, L. F. (1964) Vi- brio fetus Infection and Reinfection in Heifers as Determined by Cultural Tests Using Blood Agar Plus Antibiotics, Amer. J. Vet. Res. 25, 106, 710. 59. Plastridge, W. N., Williams, L. F., Easterbrooks, H. L., Walker, E. C. and Beccia, R. N. (1952) Vibriosis in Cattle, Univ. of Conn., Storrs Agr. Exp. Stat. Bulletin 281, Storrs, Conn. 60. Rasbech, N. O. (1951) Study of the Spreading of V. Fetus by Bulls Used in Artificial Insemination (Abstr.), Vet. Rec. 63, 657. 61. Rasbech, N. O. (1954) La Vibriose Bovine au Danemark, Re- port of the 22 Session Office International Des Equizooties, R. No. 341. 62. Roberts, S. J., Gilman, H. L. and Larsen, P. H. (1950) Vibrio Fetus Infection in Cattle, Cor. Vet. 40, 2, 111. 63. Samuelson, J. D. and Winter, A. J. (1966) Bovine Vibriosis: The Nature of the Carrier State in the Bull, Jour, of Infect, Dis. 116, 573. 64. Schurig, G. D., Hall, C. E., Burda, K., Corbeil, L. B., Dun- can, J. R. and Winter, A. J. (1974) Infection Patterns in Heifers Following Cervicovaginal or Intrauterine Instillation of Cam- pylobacter (Vibrio) Fetus Venerealis. Cor. Vet. 64, 4, 533- 548. 65. Seger, C. L., Lank, R. B. and Levy, H. E. (1966) Dihydro- streptomycin for Treatment of Genital Vibriosis in the Bull, JAVMA, 149, 1634. 66. Seger, C. L. and Levy, H. E. (1962) Collection of Bovine Cerv-INFERTILITY IN THE COW 467 ical Mucus with Insemination Pipettes for the Isolation of Vib- rio fetus, IAVMA, 141, 9, 1064. 67. Shepler, V. M., Plumer, G. J. and Faber, J. E. (1963) Isolation of Vibrio fetus from Bovine Preputial Fluid, Using Millipore Filters and An Antibiotic Medium, Amer. J. Vet. Res. 24, 101, 749. 68. Smith, T. (1918) Spirilla Associated with Disease of the Fetal Membranes in Cattle (Infectious Abortion), Jour. Expt. Med. 28, 701. 69. Smith, T. (1919) The Bacteriology of Bovine Abortion with Special Reference to Acquired Immunity, Jour. Expt. Med. 30, 325. 70. Smith, T., Little, R. B. and Taylor, M. S. (1920) Further Stud- ies on The Etiological Role of Vibrio Fetus (Agglutination Tests), Jour. Expt. Med., 32, 683. 71. Stegenga, Th. and Terpstra, J. I. (1949) Over Vibrio fetus- Infecties bij het Rund en “Enzootische Sterileit,” Tijdschr. vor Diergeneesk., 74, 293. 72. Sullivan, J. J., Elliott, F. I., Bartlett, D. E., Murphy, D. M. and Kuzdas, C. D. (1966) Further Studies on the Use of Poly- myxin B. Sulphate with Dihydrostreptomycin and Penicillin to Control Vibrio fetus in a Frozen Semen Process, J. Dairy Sci. 49, 12, 1569. 73. Szabo, L. (1951) Infektionspathologiske Problemer i Forbin- delsa med Afrugbarhed hos Kveget, Nord. Vet. Med., 3, 597. 74. Te Punga, W. A. and Boyes, B. W. (1959) Vibriosis in Cattle, New Zeal. Vet. Jour., 6, 147. 75. Terpstra, J. I. and Eisma, W. A. (1951) Vibrio Fetus Infection in Cattle and Enzootic Infertility, Tijdschr. vor Diergeneesk., 76, 12, 433. 76. Vandeplassche, M. (1979) Personal Communication. 77. Wagner, W. C., Dunn, H. O. and VanVleck, L. D. (1965) In- cidence of Vibriosis in an AI Stud, Cor. Vet. 55, 209. 78. Willett, E. L., Ohms, J. I., Frank, A. H., Bryner, J. H. and Bartlett, D. E. (1955) Nonreturn Rate and Embryonic Mortality From Inseminations by Bulls with Vibrio Fetus, J. of Dairy Sci., 38, 12, 1370. 79. Wiltbank, J. N., Warwick, E. J., Vernon, E. H. and Priode, B. M. (1961) Factors Affecting Net Calf Crop in Beef Cattle, J. An. Sci. 20, 3, 409. 80. Winter, A. J. (1968) Personal Communication. 81. Winter, A. J. and Caveney, N. T. (1978) Evaluation of a Trans- port Medium for Campylobacter (Vibrio) fetus, JAVMA, 173, 5(1) 472-474. 82. Winter, A. J., Samuelson, J. D. and Elkana, M. (1967) A Com- parison of Immunofluorescence and Cultural Techniques for Demonstration of Vibrio fetus, JAVMA, 150, 5, 499. BRUCELLOSIS Brucella abortus infection has been discussed pre- viously under the section on abortion, (See Chapter V) as that is the principal characteristic of the disease. How- ever, evidence indicates that Brucella infection of the uterus plays a definite role in infertility even though in- fertility and endometritis did not occur in the recently infected nonpregnant animal.17 The role of the bull in the transmission of brucellosis is minor but interesting. According to early field observations, the bull was gen- erally supposed, to be one of the more important factors in the spread of the disease. But the transmission of bru- cellosis from infected bulls to susceptible cows by nat- ural service has not been demonstrated in controlled ex- periments. Infected bulls when bred naturally to heifers in estrum rarely spread the disease even when the pre- puce had been artificially contaminated with Brucella or- ganisms prior to service.54'55'75 However, it has been demonstrated that susceptible cows artificially insemi- nated into the uterus with infected semen from a positive Brucella-infected bull would develop brucellosis.16'54'55 Most infected bulls harboring foci of infection in the genital tract discharge Brucella organisms intermittently in the semen, but one bull had viable organisms in 80 consecutive ejaculations over a period of 18 months.55 The uterine infection produced in heifers by intrauterine insemination of infected semen resulted in impaired fer- tility; only 1 susceptible heifer conceived on the first ser- vice out of 12 inseminated; 8 of the 12 susceptible an- imals became infected; only 2 infected animals conceived, and 1 of these aborted at 104 days of gestation. Each animal was inseminated an average of 3.5 times. The infertility was temporary, lasting 3 to 12 months. These results were interesting when compared with 12 other susceptible heifers bred artificially to the same bull but with the semen being inseminated into the external os of the cervix; 9 of 12 animals conceived on the first ser- vice.318 From these experiments Brucella abortus should be included with C. fetus and T. fetus as an agent that can and will produce infertility or temporary sterility when introduced into the bovine uterus. Under natural condi- tions B. abortus, not being motile, cannot invade the uterus from its vaginal deposition as can C. fetus and T. fetus. This is a further reason for inseminating cows by placing semen into the cervical canal rather than into the uterus. Intrauterine insemination may introduce other patho- genic bacteria that may cause failure of conception, en- dometritis, and temporary sterility especially if insemi- nation is done late in the estrous period or in metestrus when the genital tract is under the influence of proges- terone. Following abortion due to Br. abortus, a sexual rest period of 90 days or more and possibly several uter- ine treatments may be necessary to aid involution and recovery of the endometrium necessary for conception. Aborting animals should be isolated, as ingestion of in- fective material and discharges from the genital tract is the most common means of spreading brucellosis. Further evidence of the adverse effect of brucella in- fection of the uterus was a report20 that sterility was 4 times more frequent in suspects and 8 times more fre- quent in Brucella reactors than in negative animals. Bru- cella-positive cows averaged 2.8 services per conception468 VETERINARY OBSTETRICS following normal calvings and 3.6 services per concep- tion following abortions.61 Other evidence of this type was cited.65 A more severe endometritis was present in infertile Brucella positive cows than in infertile Brucella- negative cows.18 These many reports serve to emphasize strongly the role of Brucella abortus in causing infer- tility in a herd, and the necessity of controlling this dis- ease to prevent severe economic losses due to reproduc- tive failure and abortion. GRANULAR (NODULAR) VENEREAL DISEASE (GRANULAR VULVITIS) AND MYCOPLASMA, UREAPLASMA AND HEMOPHILUS INFECTIONS According to Williams this disease was first described in Switzerland by Isepponi in 1887 as a cause for infer- tility and abortion.82 Since that time there has been much debate on whether or not the disease is an important cause of infertility. Most workers agree at present that there is no evidence linking this disease with abortion. Williams stated: “It may be said to be a lesion without a known cause and regarding the effect of which there is scant knowledge.” No disease of the reproductive system of cattle has been so unproductive of conclusive results on research as has granular venereal disease. Only in the area of histopathology is there any agreement on the na- ture of this disease. The lesions and the mucopurulent vulvar discharge often following service, are readily noted by both farmers and veterinarians. Therefore granular venereal disease or granular vulvitis has frequently been incriminated as a cause for infertility in cattle. The term granular vaginitis used to designate this disease is a mis- nomer as the papules or granules are largely limited to the vulvar mucosa and are only sporadically found in the vagina.45 The disease is seen most commonly in heifers during the breeding period for their first and second pregnan- cies. The condition has been noted occasionally in calves as young as 11 days of age and in heifers prior to pu- berty. It is less acute and severe in middle-aged and older cows. It is observed most commonly in postpartum heif- ers and cows especially following natural service and less commonly as pregnancy progresses toward term. It is rarely observed at the time of parturition. Granular ve- nereal disease is seen in practically any herd at any time of year with an incidence varying from 10 to 90 percent of the cows or heifers. Occasional acute herd outbreaks are observed that spread rapidly through the herd and even affect prepubertal heifers. This may be due to the vulvar sniffing which is common in cattle. This may carry the organism from the nose of one animal to the vulva of the other.13-;u;:6-51 Since the mycoplasma and He- mophilus organisms are commonly found in the respi- ratory as well as the lower genital tract spread of infec- tion is favored by this behavior. The lesions differ greatly in severity between heifers and cows in a herd. In gen- eral the disease occurs more commonly and more se- verely in young cows or heifers being bred naturally by the bull than in those being artificially inseminated. The lesions of this condition may be observed on the penis and prepuce. The lesions are present more commonly in bulls serving cows naturally than in bulls in an artificial insemination stud that ejaculate into an artificial vagina. The disease in bulls should be called granular venereal disease or granular balanoposthitis. The mode of spread of the disease is not known, but apparently if it is due to an infectious agent, it is spread rapidly and easily. This is difficult to prove, inasmuch as isolated control heifers may develop the condition. This condition in cows more properly should be called a granular vulvitis. In the acute stage in cows these nod- ules are reddened and highly inflamed, causing a mu- copurulent type of discharge that may mat and hang from the vulvar tuft of hairs. If these cattle are bred by a bull, or if a speculum is passed, the granules or nodules are likely to bleed. The cow or heifer in this acute stage exhibits some pain when the vulvar lips are handled and may exhibit irritation and pain when urinating, as well as by not standing quietly to be bred. In these acute se- vere cases there are many nodules, usually appearing confluent and tending to be in ridges or rows on the top of the folds of mucous membrane. The vulva may be slightly swollen. Occasionally discrete, 2 to 5 mm, white inclusion cysts containing an exudate may be observed in the dorsal commissure or lateral walls of the vulva.23,25,45 Bulls with acute severe lesions may occasionally refuse to copulate or will be slow to breed. Coitus tends to ag- gravate the lesions especially in heifers with a small vulva that are bred to a large bull. In mild and chronic cases of granular venereal disease the lesions are few in num- ber and are usually found around the lower half of the vulva and around the clitoris. The chronic nodules are pale yellow in color and no exudate or inflammation of the mucosa is apparent. Following breeding the granules that were pale before breeding ordinarily become con- gested and reddened. Thus chronic lesions may become acute. But chronic lesions are much more common es- pecially in cows the last half of the gestation period. These nodules or granules histologically are lymph follicles, lymphoid accumulations, or hyperplasic lym- phoid elements beneath the mucosa and therefore the disease may be a normal response to various insults. It is interesting to note that similar lesions have been de-INFERTILITY IN THE COW 469 scribed in the dog.1 In the male dog a follicular bala- noposthitis with hypertrophied lymph follicles may oc- cur. In the bitch similar lymph follicles in the vulva were described. These lesions are common in the genital tract of sheep, goats and swine, but in a mild form.1,45,82 These granular or papular hypertrophied lymphoid le- sions in the mucous membrane are similar to those ob- served beneath the third eyelid in follicular conjunctivitis in dogs and in follicular pharyngitis in horses. These lat- ter two conditions are usually ascribed to and associated with bacterial or possibly viral infections. The cause of granular venereal disease has been as- cribed in many reports over many years as due to Strep- tococcus vaginitidis, a hemophilus-like pleomorphic rod, a vims and other organisms, mycoplasma, C, pyogenes, Staphylococci, and E. coli, and most recently ureaplas- mas or T.-mycoplasmas and Hemophilus som- nus l'2'22'23a’b'26b'43'51’69 Mycoplasmas or ureaplasmas are very small bacteria that lack a cell wall. They are commonly found in the upper respiratory tract and lungs and the vagina and vulva of cattle and also humans. lney are generally susceptible to the tetracycline antibiotics.23 Mycoplasmas and ureaplasmas vary greatly from non- pathogenic to pathogenic strains. Some authors, indicate they may be part of the normal flora of the vagina and vulva and prepuce and penis. They are seldom found in the uterus and oviducts. 13,21,62,73 Pathogenic ureaplasmas were inoculated into the uterus or cervix of 23 virgin heifers, 16 of 19 heifers developed granular venereal dis- ease lesions in about 4 days from which the organism could be isolated for 13 to 41 days. Clinical cases of the disease persisted for several months. However the urea- plasma could only be isolated from the uterus or uterine tubes for 1 to 7 days. Only a short-lived endometritis and salpingitis were produced.25,26 When heifers were bred naturally to a bull infected with Mycoplasma agalactiae var bovis the IgA levels in the vagina rose to high levels while the IgG levels in the noninfected uteri remained low. Thus this reaction resembles that seen in vibriosis. The evidence indicates that IgA provides protection for the animal in the superficial areas such as the vagina and the nasal cavity and the IgG provides protection for the deeper organs of the body such as the uterus and lungs.21 One study showed that pathogenic ureaplasma (T. my- coplasma) could cause cessation of ciliary activity, cil- iary collapse and sloughing and finally disorganization of epithelial tissues with necrosis and desquamation73 which might explain the underlying cause of infertility when these organisms affect the ciliary activity of cells in the cervix, uterus and oviducts of upper genital tract of cows. These studies, though quite convincing,23-26,71 require further confirmation as others have doubted whether a specific agent is the cause of bovine granular venereal disease.45,70 The incubation period for the development of the acute stage of granular venereal disease is short, 2 to 5 days, after exposure or breeding with the formation of nodules or papules in the vulva and around the clitoris that are red and inflamed and result in a mucopurulent discharge. The acute phase gradually recedes over the next 2 to 3 months unless reinfection occurs. But this latter response is much less severe than the initial reaction.25 26 Others have reported a 2 to 3 week incubation period with an increase in severity and number of granules developing, through the eighth week.22 The lesions of granular ve- nereal disease consist of small elevated papules or gran- ules found mainly on the vulvar mucosa just inside the vulvar lips most commonly in the region around the cli- toris. (See Figure 105.) In more severe cases the gran- ules may extend up the lateral walls of the vulva to the dorsal commissure. Diagnosis is based on the clinical signs and lesions of granular venereal disease. In the 1950’s about 10 percent of 2530 cows were found affected with granular venereal disease.76 The fer- tility of affected animals was 6 percent lower than that of the other 90 percent. Of 4616 cows being bred by artificial insemination; 49 percent had no evidence of granular venereal disease; 44 percent, or 2,065 had mild symptoms; and 7 percent, or 289 cows, had severe le- sions.76 The conception rates on first service in each group were 68.9 percent, 65.7 percent, and 58.1 percent, re- spectively. Therefore the difference in rates was signif- icant. Whether C. fetus was present and influencing these results was not reported. A temporary infertility was as- Figure 105. Granular Venereal Disease in a Heifer—Note the con- centration of lymphoid follicles around the clitoris.470 VETERINARY OBSTETRICS sociated with granular venereal disease.22 Canadian researchers23'26'50'51,62 have isolated urea- plasma (T. strains of mycoplasma). Mycoplasma bovi- genitalium and Hemophilus somnus from clinical cases of granular venereal disease. Ureaplasmas were isolated from 100 percent of acute granular vulvitis cases, from 74 percent of chronic cases and from 23.5 percent of normal herdmates.23 Recent advances in laboratory cul- ture methods, special transport media,51 refrigeration and rapid transport to the laboratory are necessary to isolate these organisms. These organisms are commonly found in the external genital organs, vulva and prepuce, and respiratory tract of cattle. Mycoplasma which encompass many species of acholeplasma, including A. laidlawii, and M. bovi- genitalium and M. (agalactiae) bo vis and the ureaplas- mas of which there are many species, are found on ser- osal or mucosal surfaces of the urogenital and respiratory tracts, mammary gland, joints and eyes. Hemophilus somnus is a Gram negative coccobacillus that causes septicemia, pneumonia, thromboembolic meningo-en- cephalitis, probably the calf diphtheria syndrome in feedlot or young cattle, and arthritis.51 These organisms may be found in both normal and diseased animals. Further stud- ies are indicated to differentiate the pathogenic and non- pathogenic species of these organisms by serologic or other methods and to better understand their role in abor- tions, granular venereal disease (vulvitis and balanopos- thitis), endometritis, toxic metritis, salpingitis and sem- inovesiculitis in cattle and other animals. It should be further noted that mycoplasmas and ureaplasmas also cause infertility, abortion and urethritis in humans.316'40 The prognosis is usually fair to good in granular ve- nereal disease but in acute cases it may be 2 to 4 weeks or more before the acute signs subside. As far as com- pletely curing the condition in cows and bulls the prog- nosis is guarded, as sometimes several months or more are required. Granular venereal disease may remain chronic, or acute lesions may recur. In longstanding cases in bulls, the lymphoid enlargments may become fibrotic. If a high incidence of early embryonic deaths occur with this disease one should suspect a combined infection with C. fetus and/or T. fetus. Mycoplasma bovigenitalium, ureaplasmas and He- mophilus somnus were isolated from acute cases of granular vulvitis or granular venereal disease in cattle associated with a purulent discharge, endometritis and infertility. This acute form of the disease was seen most commonly with intensive management, over-crowded, unsanitary free-stall bams, and heavily fed, stressed dairy cows and heifers in the winter.23-26'51 First service con- ception rates dropped from over 50 percent to 30 percent during the acute phase of the disease and returned to 50 percent after intensive therapy with postbreeding infu- sions of 1 gm of tetracycline or oxytetracycline into the uterus, cervix and vagina and using a sheathed or pro- tected insemination pipette for AI or intrauterine infu- sions to reduce the numbers of pathogenic organisms carried from the vulva into the cervix and uterus. Since bulls carry these organisms in their prepuce and occa- sionally in their seminal vesicles, semen used for AI should contain levels of antibiotics to eliminate these or- ganisms and prevent their spread. Minocycline HCL is effective in the control of mycoplasma and ureaplasma in the extended semen and lincomycin and spectino- mycin controls mycoplasma. H. somnus is readily elim- inated by a variety of antibiotics. Tetracyclines cannot be used in extended semen because of their harmful ef- fect on spermatozoa. Granular vulvitis, endometritis and salpingitis have been produced experimentally by the in- troduction of certain of these three organisms, especially the ureaplasma, into the vulva, cervix and uterus. Based on early studies recovery from uterine infections and en- dometritis may be quite prompt. The treatments for granular venereal disease are so many and varied that the author believes this condition fits into the category with other conditions treated with a similar wide variety of therapy in which probably any treatment within reason or no treatment at all would be equally successful. The older more commonly used treatments in affected cows and bulls are locally applied antibiotics and antiseptics but their value is questionable. When conception rates were greatly reduced, due to ureaplas- mal infections 1 gm of tetracycline in solution infused into the uterus cervix and vagina 24 hours after service gave encouraging results.23'266 Treating the granular le- sions in the vulva with irritating or cauterizing drugs ap- pears to clinically result in the most rapid improvement in acute cases of granular vulvitis. They should not be used in bulls. These include 1 to 2 percent acriflavine ointment, straight Lugol’s solution, or 4 to 5 percent sil- ver nitrate solution repeated as needed every 7 to 10 days. Since this condition tends to improve with time and since copulation aggravates the condition, breeding is stopped in the severe cases, especially in bulls, for sev- eral weeks or longer. The owners are advised to breed their affected cows and heifers by AI possibly using a small plastic speculum or tube to guide and protect the AI pipette so that it does not contact the vulvar mu- cosa.23'266 51 This seems to cause no exacerbation of symptoms. If they cannot be bred artificially, a period of sexual rest for 2 to 4 weeks is advised in the severe cases. A killed vaccine is currently available for im- munizing against H. somnus but its value in genital in- fections needs study. In recent years investigations have resulted in ad-INFERTILITY IN THE COW 471 vancing our knowledge of the my coplasmas, ureaplas- mas and Hemophilus organisms. The pleuropneumonia like organism (PPLO) now called Mycoplasma bovi- genitalium is only mildly pathogenic in the female gen- ital tract and is frequently isolated from the tract. My- coplasma bovigenitalium was isolated from cattle in several herds suffering from infertility and occasional abortions.23a’28,51 In some cases ovarian adhesions and cervicitis were present; in others a mucopurulent dis- charge was noted several days after coitus. The organism was found in semen. Varying degrees of endometritis, salpingitis and adhesions between the fimbria and peri- toneum was produced in 7 of 8 heifers receiving an in- trauterine inoculation of a suspension of mycoplasma (M. agal. bovis) recovered from a case of bovine mastitis.36 The doses used were considered to be excessive. This condition, produced experimentally, has not yet been de- scribed as a clinical entity. The M. bovis organism which is quite pathogenic for the female genital tract is seldom found there. The common occurrence of mycoplasma and ureaplasma in the prepuce of bulls and in the semen has been described under infertility in the male.1'2 It is ques- tionable if many of the isolated mycoplasma spp. are pathogenic as heifers inseminated with infected semen samples did not become infertile. Only one group of iso- lates produced inflammatory changes in the endome- trium. A study of many strains of mycoplasma by mor- phological, cultural and serologic means as an aid to separating pathogenic and saprophytic organisms has been conducted.1'2’5’6 Similar studies are needed with the urea- plasmas and H. somnus. Many mycoplasma cultures are a mixture of several strains, 166 pure strains were re- covered by cloning, characterization and serologic tech- niques and 13 serotypes were found not including the bovine T. strains or ureaplasmas. Serotype B or My- coplasma bovigenitalium caused vulvovaginitis, epi- didymitis, seminovesiculitis, arthritis and rarely masti- tis.I'2'5’6’25'26 Serotype F or Mycoplasma agalactiae var bovis caused mastitis, endometritis, salpingitis, salpin- goperitonitis and abortion.40 This type of organism was cultured from semen from a bull that when bred to heif- ers apparently produced conception but the animals came back into estrum in about 4 weeks and thereafter were infertile.63 Acholeplasma (M.) laidlawii was recovered from the oviducts in 52 or 71 percent of 73 repeat breeders,41 while only 42 or 24 percent of 179 cows slaughtered for other reasons were infected. Lesions were found in 117 in- fected uterine tubes. Many workers'5,23 consider this Mycoplasma nonpathogenic. It is possible that the early workers in studying this PPLO or mycoplasmal organ- ism were actually dealing with vibriosis and recovered these rather ubiquitous mycoplasmas. This PPLO organ- ism was found in semen in 94 percent of the bulls.3 Freezing of mycoplasma in semen had no adverse effect on the organisms,39 and they were quite resistant to an- tibiotics commonly used in semen extenders.23 Hemophilus spp. was reported to cause an outbreak of vaginitis and cervicitis in a herd of dairy cattle,12 It was characterized by a copious, purulent, yellowish-white discharge from the vulva and a hyperemia of the vagina and cervix lasting for 2 to 3 months. The disease could be spread by coitus and resembled viral vaginitis de- scribed previously. The vulva was not affected. A he- mophilus-like organism was described as a cause of granular vulvitis.22 Hemophilus somnus has been iso- lated from cases of granular venereal disease.25,26 In a review of the role of the Mycoplasmas in diseases of bovine reproduction it was reported that mycoplasmas have been isolated from the genital tracts of cattle, hu- mans, horses, dogs, pigs, goats and cattle.1,2 Those or- ganisms associated with lower genital tract infections of granular vulvitis were M. bovigenitalium, ureaplasmas (T. mycoplasmas) and A. laidlawii. Those organisms associated with the upper genital tract infections of en- dometritis and salpingitis are M. bovigenitalium and M. agalactiae bovis, ureaplasmas and H. somnus. In bulls M. bovigenitalium and ureaplasmas and occa- sionally M. agal. bovis can cause seminovesiculitis and possibly orchitis and epididymitis and be present in se- 1,23-26,51 men. Many more studies will be needed on mycoplasmas, ureaplasmas and Hemophilus organisms commonly found in the lower reproductive tract, vulva and prepuce and upper respiratory tract to determine the pathogenic and nonpathogenic serotypes and the mechanisms whereby they gain access to the upper reproductive tract, uterus, uterine tube, seminal vesicles and testes. These further studies are necessary to clarify the presently very con- fusing literature and clinical disease picture. With the rapid advances in microbiology and immunology in re- cent years the isolation of these organisms and the de- lineation of their importance, pathogenesis, epidemiol- ogy and therapeutic control measures should be forthcoming. Other Bacterial Infections Leptospirosis due to L. pomona has not been shown to be the cause of infertility or early death of fertilized embryos; although abortions, especially the latter half of the gestation period, are common. Statements that L. hardjo and L. mini-szwajizak have been associated with infertility in enzootically infected herds have appeared recently in the literature, a careful perusal of the articles472 VETERINARY OBSTETRICS cited34b'36a do not support this observation. Infertility as- sociated with abortions, secondary retained placentas, and metritis and delayed conception are characteristic se- quelae of any abortifacient disease including leptospi- rosis. Leptospiral organisms have not been shown to be a cause of early embryonic deaths or conception failure. Streptoccic infection characterized by cervicitis was described in 1932 as a common cause for infertility in cows. This organism was frequently recovered from in- flamed genital tracts of cows failing to conceive but it is unlikely that it was responsible for enzootic outbreaks of infertility. The author observed one herd of dairy cat- tle with much infertility characterized by a mucopurulent discharge from the vulva in some animals and early em- bryonic deaths with long intervals between services. On culture of the vagina of the cows at necropsy a pure in- fection of Streptococcus dysgalactiae was isolated. En- dometritis was present. Sanitary conditions in the herd were marginal; all cows calved in the same calving stall. The bull may have spread the infection at the time of coitus. Corynebacterium pyogenes has been described as a cause for failure of conception, for a persistent muco- purulent discharge from the vulva and even occasionally for permanent sterility.37'38 Apparently it gains entrance to the genital tract at the time of parturition or when a retained placenta is present. This organism causes a chronic postpuerperal metritis, endometritis, salpingitis, or pyometra with delayed involution of the uterus. This invasive organism may be difficult to cure and the prog- nosis should be guarded35b (See Endometritis). C. pyogenes infection of the postpartum genital tract is occurring with increasing frequency as the herds of cattle get larger and close confinement, “zero pasture,” and overuse of a few calving stalls that are not properly “sterilized” between cows. In affected herds nearly 90 percent or more of cows calving in the infected envi- ronment or in those calving stalls become infected and develop a copious, yellow, mucopurulent discharge that lasts for 2 to 6 months resulting in great delays in con- ception even though eventually the infection is overcome and the cows conceive. Retained placenta and calf scours are also commonly observed in these same herds due to the unsanitary conditions. Since the infection obviously occurs at or soon after calving, having the cows calve in a different clean environment away from the contam- inated facilities or at pasture often results in a prompt and dramatic reduction in clinical cases of vaginitis, cer- vitis and metritis. Enough properly designed calving stalls that can be thoroughly disinfected or sterilized between calvings and/or moved, if portable, to a clean location are necessary for large free stall dairy herds. A vulvovaginitis due to C. pyogenes occurring one to four days following coitus has been described.14 These infections persisted for 7 to 14 days but often recurred at a subsequent breeding to the same bull. Similar C. pyogenes organisms were cultured from the vagina of affected cows and the prepuce of the bull. An acute vul- vovaginitis was reported due to E. coli toxins introduced by coitus with an infected bull.14 Signs developed within 4 to 6 hours of service and lasted for only several days. Other low grade infections found in the genital tract of sterile or infertile cows or cows exhibiting a muco- purulent exudate include: * Micrococci * Diphtheroids * Pseudomonas aeruginosa *E. coli Bacilli Staphylococci, albus and aureus * Enterococci and others Actinomyces Yeast Neisseria Mycobacteria Flavobacterium Salmonella Sarcina Alkaligenes Proteus Gaffkya Molds Chromobacteria The organisms most commonly found. These infections have been described as being found in the genital tract and uterus of cows that fail to con- ceive.4,2735a,c'38'52 These ubiquitous organisms recovered from the bovine genital tract were mainly saprophytic strains in normal cows but in infertile cows the strains were primarily pathogenic.35a,c Undoubtedly they may gain access to the tract at the time of parturition or breeding and if the conditions are favorable they establish them- selves at least temporarily and possibly cause varying degrees of inflammation of the uterus, cervix, vagina, vulva, and oviduct possibly resulting in infertility. Twelve heifers artificially inseminated with semen from bulls with semino-vesiculitis due to Ps. aeruginosa developed varying degrees of metritis, cervicitis and vaginitis and the organism could be recovered in 4 of 8 heifers 44 days postservice.32 The discussion of the diagnosis and treat- ment of these nonspecific infections will be made later in this Chapter. (See Endometritis.) Cases of infertility due to these various wound-infection type of organisms are usually sporadic and not associated with an enzootic type of infertility. The organisms mentioned above, in- cluding streptococci, C. pyogenes and PPLO or myco- plasmas are ubiquitious and will occur in some cows de- spite proper management. Their treatment is largelyINFERTILITY IN THE COW 473 symptomatic. The same organisms are frequently pres- ent in bull semen but apparently seldom pass beyond the vagina and cervix to establish themselves in the uterus. Pseudomonas, coliforms, and staphylococci are more common in bulls’ semen than in the genital tract of cows, probably due to contamination of the semen with organ- isms common in the sheath. A condition similar to an enzootic venereal disease in naturally-bred cattle occurred in some artificially insem- inated herds, with 15 percent or more of the cattle show- ing varying degrees of infertility even when neighboring herds of the same breed served by the same technician have less than 5 percent “repeat breeders.”31 This con- dition may occur after 2 to 3 years of artificial insemi- nation and no C. fetus or T. fetus are isolated from the cows. These workers were unable to isolate the causative organism or determine its mode of spread. Other re- searchers have found similar perplexing problems.17 In the future, therefore, possibly other organisms including viruses may be found as causes of “enzootic” infertility. Necrotic vulvitis of feedlot heifers has been well-de- scribed. The cause is unknown. It has been observed in lots where hogs are present and injuries and vulvitis have been blamed on them. It may occur following rectal ex- amination. Anovulvitis may be observed secondary to a diarrhea where an irritant is apparently present in the fe- cal material. Body temperatures may be slightly elevated for a few days but healing occurs in two weeks. Infer- tility in affected heifers has not been reported. It has been suggested that an allergic factor may be involved. Actinomycosis—Two cases of actinomycosis of the bovine genital tract, characterized by large swellings that proved to be multiple sclerotic abscesses with extensive pelvic adhesions were described.112 One of these cases developed following a retained placenta. Actinomycosis is difficult to differentiate from tuberculosis but the swellings in the latter are more nodular. Due to the ex- tensive lesions the prognosis was poor and both cases were cultured and diagnosed after slaughter. Tuberculosis—Tuberculosis of the genital tract of the cow has not been observed the last 50 years in the Am- bulatory Clinic of the New York State Veterinary Col- lege. With the almost complete eradication of this dis- ease in the United States the opportunities for observing it in this country are very rare. However, in other coun- tries where tuberculosis is still prevalent the infection may involve the female genital tract and produce ste- rility and abortion. Tubercular lesions of the vulva, vagina, cervix, uterus, oviducts, and ovary have been re- ported.11,82 (See Figure 106.) The disease usually affects the uterus and oviducts producing characteristic nodular swellings, enlargments and adhesions between the uterus, Figure 106. Genital Bovine Tuberculosis—involving the ovaries and mesometrium. (Courtesy of F. Megale.) oviduct, ovary, surrounding broad ligaments, rectum, and other organs and tissues. The genital discharge from these lesions is usually non-fetid. In most cases the uterine involvement is bilateral, a fact which may differentiate the condition from other infectious or pathologic lesions of the uterus. Bovine tuberculosis due to Mycobacte- rium bovis is by far the most common type affecting the uterus and causing sterility and abortion. Occasion- ally the avian type may be found.29,68 This type is char- acterized by small abscesses about 0.25 inch in diame- ter, involving the endometrium. The avian type of tuberculosis is not readily diagnosed per rectum because of the lack of enlargement of the uterus or oviducts and the fact that adhesions do not develop. The tuberculin test may fail to detect animals severely affected with bo- vine tuberculosis. Avian tuberculin may be of assis- tance in diagnosing the avian form, although it is usually diagnosed on postmortem examination. Culture of the genital discharges together with the presence of char- acteristic nodular swellings and adhesions aids in the di- agnosis of this disease. Severely affected animals are usually hopelessly sterile and should be slaughtered. In milder infections conception may occur, but abortion or retained placenta may result. Infection of the genital tract of the cow may result in the spread of tubercular infec- tion to the penis and prepuce of the bull at coitus.474 VETERINARY OBSTETRICS INFECTIOUS VIRAL DISEASES CAUSING BOVINE INFERTILITY Infectious Pustular Vulvovaginitis (IBR-IPV) (Vesicular Venereal Disease, Coital Vesicular Exanthema, Infectious Balanoposthitis, Genital Cowpox, or Blaschenausschlag) This viral disease has been described previously with IBR-IPV abortion (See Chapter V) since the two dis- eases are caused by the same herpes viral agent. Infec- tious pustular vulvovaginitis (IPV) is described as a non- vesicular viral disease characterized by papules, pustules, but no vesicles, that rapidly coalesce to form a diphthe- ritic membrane that detaches leaving ulcers in the mu- cosa of the vulva, vestibule and vagina especially over the areas of the lymphoid follicles.33,46 Intranuclear in- clusion bodies can be found in affected cells in the mu- cosa of the genital tract. The cows exhibit an elevated temperature for several days early in the course of the disease. Edema, pain on urination, and a yellowish se- rous to purulent discharge from the vulva is character- istic of the disease. The ulcers, diphtheritic membranes and severity of the infection differentiates I.P.V. from granular venereal disease. The disease may spread rap- idly through the herd and even affect unbred heifers. The respiratory and abortion forms of the disease rarely ac- company the genital form. However rare outbreaks have been reported where simultaneous infections with the upper respiratory, genital and conjunctival forms of IBR- IPV, but no abortions, occurred.49 Abortions in pregnant cows commonly occur after the respiratory disease but are only rarely observed following the genital form of the disease. The cause for this is not completely understood. (See IBR-IPV Abortion, Chapter V.) Natural service by the bull may spread the disease as this virus may produce a balanoposthitis, but other means of spread such as by switching tails of cows confined in stanchions or groom- ing may also spread the disease from one cow’s rear parts to the next. The farm dog licking the genital discharges on the vulvas of affected cows and then normal cows may transmit the disease. The IBR-IPV virus may be transmitted by artificial insemination in liquid or frozen semen and cause an endometritis and a temporary short- lived infertility.47,66,72 Although this disease is rather common in Europe and Australia it is observed only occasionally in the United States. Even though IBR, the respiratory form of the dis- ease, is common in New York State only 1 to 3 out- breaks of IPV are reported each year. A similar obser- vation was made in California.74 Two outbreaks occurred in the same herd 4 years apart.69 Similar reoccurrences of the disease in the same herds have been reported in Europe. In one study66 when bulls harboring preputial infections of IBR-IPV were bred naturally to susceptible heifers lesions of infectious pustular vulvitis resulted but conception rates were normal. However if IBR virus was infused into the uterus after breeding infectious pustular vulvovaginitis developed and the conception rate was low, 40 percent. An increased number of services per con- ception was required due to the endometritis and salpin- gitis produced. About 30 percent of the estrous cycles were shortened due to the endometritis.66 The onset of the disease is rapid and within 3 to 6 days involves 60 to 90 percent of a herd; the incu- bation period is short, usually 48 to 72 hours. Similar lesions occur on the penis and prepuce of affected bulls. Affected bulls may refuse coitus. Although infectious pustular vulvovaginitis interferes with breeding until the lesions heal, this form of the disease is not known to result in sterility, infertility, or abortion. The prognosis is generally favorable, as healing oc- curs in about 2 to 4 weeks. Occasionally severely af- fected bulls may develop adhesions between the penis and prepuce, or a stenosis of the prepuce may occur, possibly due to secondary infections. Scarring or adhe- sions of the vulva or vagina have not been reported. Treatment is usually unnecessary and oftentimes is difficult to administer because of the problem of re- straining the affected cattle due to the painful vulvar le- sions. However, some authors recommend douching with mild antiseptics. Regular douching of the sheath of the affected bull with oily preparations might be indicated to distend the sheath and prevent adhesions. Breeding should cease for 3 to 4 weeks or until the affected ani- mals recover. Because of its highly transmissible nature, this disease should be reported to the State Veterinarian. Veterinarians, inseminators, and others working in these herds should be careful not to carry and spread the in- fection. Vaccination with IBR vaccine is not indicated once the disease has appeared. When IBR-IPV virus was present in semen used for intrauterine insemination of heifers it produced a nec- rotizing endometritis, short estrous cycles of 11 to 15 days in length, many cystic corpora lutea and only 1 of 12 heifers conceived.47,66 A number of practitioners have reported that low rates of conception occurred in heifers bred within one month of subcutaneous or intramuscular vaccination with an attenuated IBR vaccine. This has not been observed with the intranasal vaccines. Specific Bovine Venereal Epididymitis and Vagi- nitis or “Epivag” is a chronic disease of cattle, trans- mitted by coitus and found only in East, South and Cen-INFERTILITY IN THE COW 475 tral Africa. The cause is apparently a virus.58 Vaginitis in cattle in South Africa may also be due to a viral agent similar to the IBR-IPV virus.30'56 The disease is char- acterized by a severe mucopurulent vaginal discharge in females, permanent adhesions of the Fallopian tubes, and by a hardening and swelling of the epididymis in the bull. This disease has been well-described.42'71,77 Etiology—European cattle are very susceptible to the infection whereas Zebu cattle are resistant to the disease, at least, clinical symptoms are not exhibited. The disease has been transmitted experimentally by genital swabs from cow to cow or by placing minced infected epididymal tissue in the vagina. The material was bacteriologically sterile and no protozoa were found. The disease in the natural state is transmitted only by coitus. Preliminary attempts to produce the disease by filtrates of the ma- terial have failed. The disease is the most important cause of bovine sterility and infertility in Kenya. In herds having breeding trouble 42 percent had this disease and in these herds 34 percent of the bulls became permanently sterile. The disease may remain latent in a herd for some time.7 Symptoms—The incubation period is 2 to 8 days. During the active stage of the infection there is an odor- less, mucoid vaginal exudate, egg-white in consistency but opaque and yellow in color. The discharge from the vulva mats the hair on the tail and buttocks, forming dull, grey, yellow flakes as it dries. Speculum exami- nation reveals diffusely reddened areas in the cranial portion of the vagina but there are no ulcers, vesicles, or granular lesions. A diagnosis of this disease in a herd is easy but in individual animals may be difficult. The acute infective stage may last for 2 weeks to 9 months. Estrous cycles are normal, but service is rarely followed by conception. In grade herds most cows and heifers re- cover eventually but 15 to 25 percent are permanently sterile due to unilateral or usually bilateral involvement of the uterine tubes with adhesions, hydrosalpinx, or ovarian and bursal adhesions. In the bull a balano-posthitis may occur but it is mild and frequently not observed. The characteristic lesion in the bull is an enlargement and hardening of the epidid- ymis that is usually bilateral. Although the entire epi- didymis is involved, the tail is involved most severely and may resemble a billiard ball in size and hardness. Occasionally an orchitis of a temporary nature may pre- cede this epididymal enlargement and testicular degen- eration and atrophy may occur. Bulls can be infected by intraurethral injection. The lesions in bulls take 3 to 6 months to develop and sexual desire remains normal. In advanced cases there are adhesions between the scrotum and the epididymis. On postmortem examination dry ad- hesive areas of peritonitis or pleuritis may be found. The vesicular glands of bulls usually become enlarged and firm and changes may take place in the vas deferens.7 Treatment—The disease can easily be controlled by artificial insemination using noninfected bulls. In time it will spontaneously disappear from the females. More work is required on the determination of the etiologic agent, the length of time cows remain infected, and the prac- tical methods of control when artificial insemination is not possible. Miscellaneous Viral Infections of the Bovine Female Genital Tract Contagious Anterior Vagino-Cervicitis in cattle has been described in South Africa as resembling the disease just described. However no permanent lesions are pro- duced in the cow and no lesions are observed in the bull. The cause is not known. An involvement of the uterus causing sterility as a se- quela to lumpy skin disease of cattle in South Africa has also been described.77,79 A catarrhal vaginitis and cervicitis clinically similar to “epivag” in cows was described in 4 herds in Califor- nia.48,59 Affected cattle had a profuse nonodorous yellow mucoid discharge from the vulva. The cervix and vagina of the diseased cows was hyperemic and edematous but no pustules were present as in IPV. No other portions of the genital tract were involved. Although the disease appeared to spread following coitus, the bulls showed no clinical signs of the infection. The course of the dis- ease lasted from 7 days to 3 months. Fertility was low- ered and conception often was delayed several months. A few cows conceived during the clinical stages of the disease. The cause of this vagino-cervicitis was an en- tero-virus culturally different from the virus of “epivag. ” Sterility did not occur in this disease. Antibiotic treat- ments were of no value and immunity was short-lived. Viral infertility in cattle has been characterized by a vaginitis, edematous endometritis, a mucopurulent gen- ital discharge, abortions at 2 to 8 months of gestation with edematous fetal membranes, and by a temporary infertility in bulls.60 The incubation period was 3 to 10 days. The disease could be spread to susceptible cattle by coitus and intravaginal, but not the intravenous in- jection of filtered genital mucus from infected cattle. It was reported that the virus, and possibly more than one was present, could be passed through eggs.476 VETERINARY OBSTETRICS Transmissable viral fibropapillomas may occasion- ally be observed on the vulva and perineal region of heif- ers and the prepuce and penis of young bulls. The growths may be single or multiple. These tumors might be trans- mitted by coitus. The tumors in heifers are similar to the common skin wart and usually regress spontaneously in 2 to 6 months. This process may possibly be hastened by the use of wart vaccine. This condition does not cause infertility in heifers. The fibropapillomas may be re- moved surgically.34 Bovine Virus Diarrhea (BVD)-Mucosal Disease (MD) virus is widespread in cattle. It has been incriminated in early embryonic deaths8 in cattle as well as in abortion, maceration, fetal mummification, congenital cerebellar disease and cataracts and other ocular defects. Serone- gative cows for BVD-MD when bred naturally to a bull with semen containing the BVD-MD virus or given an interuterine injection of the virus after a natural service, all seroconverted within a few weeks but had a mark edly reduced conception rate until this conversion oc- curred.57-81 No effect was observed in seropositive cows. Thus because most cows in the population are seropo- sitive and BVD-MD virus is only rarely excreted in the semen, this virus is probably not a major cause of con- ception failure or repeat breeding.81 It has been demonstrated that BVD-MD virus may re- main for weeks in the uterus and oviducts of cows. It has also been shown that BVD-MD virus causes no consistent lesions in the genital tract and no abnormal- ities of the estrous cycle occur as in IBR-IPV. But evi- dence has been presented that the BVD-MD virus may inhibit the normal development of preimplantation bo- vine embryos8-10 Further studies on the effect of BVD virus on developing embryos as a possible cause of re- peat breeding is indicated. Parainfluenza-3 virus infection given either intramus- cularly or infused into the uterus after breeding had no effect on the breeding efficiency of infected susceptible heifers compared to control heifers not infected.19 References 1. Afshar, A. (1975) Diseases of the Bovine Reproduction Asso- ciated with Mycoplasma Infections, Vet. Bull., 45, 211-216, A Review. 2. Afshar, A., Stuart, P. and Huck, R. A. (1966) Granular Vul- vovaginitis of Cattle Associated with Mycoplasma bovigeni- talium, Vet. Rec., 75, 15, 512. 3. Albertsen, B. E. (1955) Pleuropneumonia-Like Organisms in the Semen of Danish Artificial Insemination Bulls, Nord. Vet. Med., 7, 3, 169. 4. Alford, J. A., Gunther, J. J. and Edwards, C. D. (1955) Re- productive Tract Infection in a Herd Caused by Group A. Strep- tococci, Cor. Vet., 45, 3, 357. 5. Al-Aubaidi, J. M. (1969) Bovine Mycoplasma: Purification, Characterization, Classification and Pathogenicity, Ph.D. The- sis, Cornell Univ., Ithaca, N.Y. 6. Al-Aubaidi, J. M. (1970) Personal Communication. 7. Anderson, J., Plowright, W. and Purchase, H. S. (1951) Patho- logical and Seminal Changes in Bulls Affected with a Specific Venereal Infection, Jour, of Comp. Path, and Therap., 61, 3, 219. 8. Archbald, L. F. (1981) Role of the Virus of Bovine Viral Diar- rhea (BVD) in Infertility in the Cow. Proc. Ann. Meet., Soc. for Theriog., Spokane, Wash., 38-54, (A Review). 9. Archbald, L. F., Fulton, R. W., Seger, C. L., Al-Bagdadi, F. and Godke, R. A. (1979) Effect of the Bovine Viral Diarrhea (BVD) Virus on Preimplantation Bovine Embryos: A Prelimi- nary Study., Theriog., 11, 1, 81-89. 10. Archbald, L. F., Gibson, C. D., Schultz, R. H., Fahning, M. L. and Zemyanis, R. L. (1973) Effects of Intrauterine Inocu- lation of Bovine Viral Diarrhea-Mucosal Disease Virus on Uter- ine Tubes and Utems of Nonpregnant Cows, Amer. J. Vet. Res., 34, 1134-1137. 11. Arthur, G. H. (1964) Wright’s Veterinary Obstetrics, 3rd Ed., Williams and Wilkins, Baltimore, Md. 12. Ayalon, N., Numan, L., Harrari, H. and Szidon, A. (1960) A Newly Identified Hemophilus spp Associated with Bovine Vaginitis and Cervicitis., Clinical Observations and Experimen- tal Transmission, Refuah Vet., 17, 41, 153. 13. Ball, H. J., McCaughey, W. 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(1974) Serotype Szwajizak, Isolated from Bovines in Ore- gon, Proc. U.S.A.H.A., 78, 119. 35a. Gunter, J., Collins, W. J., Owen, J., Sorenson, A. M., Scales, J. W. and Alford, J. A. (1955) A Survey of the Bacteria in the Reproductive Tract of Dairy Animals and Their Relationship to Infertility, Am. J. Vet. Res., 16, 59, 282. 35b. Hartigan, P. J., Griffen, J. F. T. and Nunn, W. R. (1974) Some Observations on Corynebacterium Pyogenes Infection of the Bovine Uterus, Theriog., 1, 5, 153-167. 35c. Heist, C. E. and Tanabe, T. Y. (1974) The Nature of Subfer- tility in Dairy Heifers VII, Prevalence and Types of Uterine Mi- croflora. Bull. 794, 1-56, Penn. State Univ., Agr. Exper. Stat. Univ. Park, Pa. (A Review). 36a. Hanson, L. E. (1976) Bovine Leptospirosis, J. Dairy Sci., 59, 1166-1170. 36b. Hartman, H. A., Tourtellotte, M. E., Nielsen, S. W. and Plast- ridge, W. N. (1964) Experimental Bovine Uterine Mycoplas- mosis, Res. in Vet. Sci., 5, 3, 303. 37. Hignett, S. L. (1940) Bovine Sterility, Vet. Rec., 52, 19. 38. Hignett, S. L. (1949) The Complex Nature of Herd Infertility, Proc. 14th Intemat. Vet. Congr. Section 4 (c), 128. 39. Hirth, R. S., Plastridge, W. N. and Tourtellotte, M. E. (1967) Survival of a Mycoplasma in Frozen Bovine Semen, Amer. J. Vet. Res., 28, 122, 95. 40. Hirth, R. S., Plastridge, W. N., Tourtellotte, M. E. and Neil- sen, S. W. (1966) Genital Mycoplasmosis in Cattle and Man, JAVMA, 148, 3, 277. 41. Hoare, M. (1969) A Survey of the Incidence of Mycoplasma Infection in the Oviducts of Dairy Cows, Vet. Rec., 85, 351. 42. Hudson, J. R. (1949) A Specific Venereal Disease of Cattle Characterized by Epididymitis in Bulls and Vaginitis in Cows and Heifers, Proc. 14th Intemat. Vet. Congr., II, Section 3 (j), 487. 43. Hunter, A. G., Henderson, B. W. and Dardiri, A. H. (1958) Infectious Pustular Vulvovaginitis of Cattle, Cor. Vet., 48, 4, 458. 44. Hunter, A. G. Henderson, B. W. and Dardiri, A. H. (1958) Granular Vulvovaginitis: A Review, J. Dairy Sci., 41, 8, 1024. 45. Jubb, K. V. F., Kennedy, P. C. and McEntee, K. (1970) Pa- thology of Domestic Animals, 2nd Ed. Vol. 1, 7, The Female Genital System, Granular Venereal Disease, 546-548. 46. Kendrick, J. W., Gillespie, J. H., McEntee, K. (1958) Infec- tious Pustular Vulvovaginitis of Cattle, Cor. Vet., 48, 4, 458. 47. Kendrick, J. W. and McEntee, K. (1967) The Effect of Arti- ficial Insemination with Semen Contaminated with IBR-IPV Vi- rus, Cor. Vet., 57, 1,3. 48. Kendrick, J. W., McKercher, D. G. and Saito, J. (1956) Pre- liminary Report of Studies on a Catarrhal Vaginitis of Cattle, JAVMA, 128, 7, 357. 49. Kradel, D. C., Solorzano, R. F., Dunne, H. W. and Michel, R. L. (1961) Infectious Pustular Vulvovaginitis in a Pennsyl- vania Dairy Herd, Vet. Med., 56, 8, 333. 50. Longford, E. V. (1975) Mycoplasma Species Recovered from the Reproductive Tracts of Western Canadian Cows, Canad. J. Comp. Med., 39, 2, 133-138. 51. Lein, D. H. (1982) Reproductive Disorders Associated with Ureaplasmas, Mycoplasmas, Hemophilus Somnus and Chla- mydia, (A Review), Ann. Conf. Soc. for Theriog., Milwaukee, Wise., In Press. 52. Lindley, C. C. and Hatfield, R. C. (1952) Observations on the Bacterial Flora of Infertile Dairy Cows, JAVMA, 120, 898, 12. 53. Lingard, D. R. and Hanson, L. E. (1961) Effect of Leptospira pomona on the Reproductive Efficiency of Cattle, JAVMA, 139, 4, 449. 54. Manthei, C. A. and Deyoe, B. L. (1970) Brucellosis, in Bovine Medicine and Surgery, Amer. Vet. Public, Inc., Wheaton, 111., 104. 55. Manthei, C. A., DeTray, D. E. and Goode, E. R. (1950) Bru- cella Infection in Bulls and the Spread of Brucellosis in Cattle by Artificial Insemination, Proc. A.V.M.A., 87th Ann. Meet- ing, 177. 56. Mare, J. and Van Rensburg, S. J. (1961) The Isolation of Vi- ruses Associated with Infertility in Cattle-A Preliminary Re- port, S. Afr. J. Vet. Med., 32, 2, 201. 57. McClurkin, A. W., Coria, M. F. and Cutlip, R. C. (1979) Re- productive Performance of Apparently Healthy Cattle Persis- tently Infected with Bovine Viral Diarrhea Virus, JAVMA, 174, 10, 1116-1119. 58. McIntosh, B. M., Haig, D. A., and Alexander, R. A. (1952) Isolation of Viruses Associated with Epididymitis and Vaginitis of Cattle, J. So. Afr. Vet. Med. Assoc., 23, 3, 165.478 VETERINARY OBSTETRICS 59. McKercher, D. G. (1969) Relationship of Viruses to Repro- ductive Problems, JAVMA, 154, 10, 1184. 60. Millar, P. G. (1955) Viral Infertility in Cattle, Brit. Vet. J., Ill, 7, 309. 61. Miller, F. W. and Graves, R. R. (1932) Reproduction and Health Records of the Beltsville Herd of the Bureau of Dairy Industry, U.S. Dept, of Agr. Tech. Bull, 321. 62. Nakamura, R. M., Walt, M. L. and Bennett, R. H. (1977) Stud- ies of Bovine Genital Tracts: Mycoplasma Isolations from Dairy Cows, Theriog., 7, 6, 351-355. 63. Neilsen, F. (1949) Sterility in Cattle, Especially as a Result of Uterine Infection, Proc. 14th Intemat. Vet. Congr., Section 4 (c), 105. 64. Nelson, W. A. (1958) Mass Outbreak of Necrotic Vulvitis, Jen Sal. Jour., 41, 1, 15. 65. Olds, D. (1953) Infertility in Cattle—A Review, JAVMA, 122, 913, 276. 66. Parsonson, I. M. and Snowdon, W. A. (1975) The Effect of Natural and Artificial Breeding Using Bulls Infected with, or Semen Contaminated with, Infectious Bovine Rhinotracheitis Virus, Austral. Vet. J., 51, 8, 365-369. 67. Pierson, R. E. and Hill, H. J. (1956) Necrotic Vulvitis in Feed- lot Heifers, JAVMA, 128, 2, 71. 68. Plum, N. (1926) Tuberculosis Abortion Disease in Cattle, Cor. Vet., 16, 237. 69. Roberts, S. J. (1949) Vesicular Venereal Disease, Cor. Vet., 39, 4, 435. 70. Roberts, S. J. (1971) Veterinary Obstetrics and Genital Dis- eases, 2nd Ed., Woodstock, Vt., 412-415. 71. Ruhnke, H. L., Doig, P. A., Palmer, N. C., Miller, R. B., McKay, A. L. and Waelchi, R. O. (1981) Possible Role of Ureaplasmas in Bovine Genital Tract Disease, JAVMA, 179, 3, 275- Abstr. 72. Spradbrow, P. B. (1968) The Isolation of Infectious Bovine Rhinotracheitis Virus from Bovine Semen, Austral. Vet. Jour., 44, 9, 410. 73. Stalheim, O. H. V., Proctor, S. J. and Gallagher, J. E. (1976) Growth and Effects of Ureaplasmas (T. Mycoplasma) in Bovine Oviductal Cultures, Infection & Immunity, 13, 3, 915-925. 74. Studdert, M. J., Wada, E. M., Kortum, K. M. and Graverman, F. A. (1964) Bovine Pustular Vulvovaginitis in Western United States, JAVMA, 144, 6, 615. 75. Thomsen, A. (1943) Does the Bull Spread Infectious Abortion in Cattle? Experimental Studies from 1936 to 1942, Jour, of Comp. Path, and Therap., 53, 3, 199. 76. Troutman, E. C. (1954) Granular Vaginitis as a Cause of In- fertility in Dairy Cattle, JAVMA, 124, 924, 184. 77. U.S. Livestock Sanitary Assoc. (1954) Foreign Animal Dis- eases, Rept. of Committee, Seer. Treas., Trenton, N.J. 78. Van Kruiningen, H. J., Davis, F. H., Pieper, N. W. and Dan- iels, W. H. (1968) Concomitant Granular Vulvitis, Palate Le- sions, and Respiratory Illness in Connecticut Dairy Cattle, JAVMA, 153, 12, 1581. 79. Van Rensburg, S. W. J. (1953) Bovine Sterility Caused by In- fectious Disease in South Africa, Brit. Vet. J., 109, 226. 80. Webster, W. M. (1932) Bovine Sterility in New Zealand, Aus- tral. Vet. J., 8, 6, 199. 81. Whitmore, H. L., Zemjanis, R. and Olson, J. (1981) Effect of Bovine Viral Diarrhea Virus on Conception in Cattle, JAVMA, 178, 10, 1065-1067. 82. Williams, W. L. (1943) Diseases of the Genital Organs of Do- mestic Animals, 3rd Ed., Ithaca, N.Y. HORMONAL DISTURBANCES RESULTING IN INFERTILITY Most hormonal disturbances causing infertility or ste- rility in cows and other animals are secondary to basic nutritional, hereditary and stress or work factors. Oc- casionally hormonal disturbances may be due to the ingestion or injection of exogenous steroids or other hor- mones. Hormonal diseases may include cystic ovaries, failure of estrum (anestrum) and repeat breeders due to failure of ovulation, failure of fertilization and early em- bryonic deaths. The widespread indiscriminate use of many hormones on an empirical basis by veterinarians 25 to 30 years ago has been followed in recent years by a much more selective and knowledgeable employment of the various hormones for their specific action in cer- tain limited and carefully diagnosed infertility condi- tions. The use of assays for determining the plasma or milk progesterone levels further assists these diagnoses. Cystic Ovaries Cystic ovaries in dairy cattle is one of the most com- mon conditions causing infertility, 6 to 19 percent,39b that the veterinarian is called upon to treat. Twelve to 14 per- cent of all problem breeder cows have cystic ovaries.49 A recent abattoir survey in England of 8071 bovine fe- male genital tracts revealed that 10 percent had abnor- malities. The most common abnormality was cystic ova- ries with an incidence of 3.8 percent.3 In 5083 lactations over a 60 year period the percentages of dairy cows with cystic ovaries was 1.0, 3.1, 3.3, 4.0 and 5.2 for Brown Swiss, Ayrshire, Jersey, Guernsey and Holstein breeds, respectively.30 In Holsteins the incidence of cystic ova- ries for cows having twins was 12.7 percent compared to 4.9 percent for cows having single births. Cows with metritis had an incidence of 10.4 percent cystic ovaries compared to 5.1 percent of cows without metritis.30 The more often the cow was treated for milk fever, the higher the likelihood that cystic ovaries would develop, 20 per- cent vs. 4 percent for cows with no milk fever. In 375 calving intervals in a Holstein herd cystic ovaries oc- curred in 11.2 percent. Seventy percent of the cysts oc- curred from 16 to 45 days after calving and 69 percent of these cows recovered without treatment and became pregnant prior to 300 days. Twenty-nine percent re- covered in less than 30 days.30 In 1599 Holstein lacta- tions cystic ovaries occurred in 14.5 percent with the highest rate of occurrence 3.5 percent, or about 25% of cows with cystic ovaries, between 31 and 45 days post- partum. A second peak occurred in infertile cows afterINFERTILITY IN THE COW 479 Lack of L.H. Luteal cyst (Luteinized cyst) (pathological) Follicular cyst (pathological) Figure 107. Cysts of the Bovine Ovary. 120 days.21 Thus in dairy herds cystic ovaries occur in 10 to 20 percent of problem breeders.35 This latter re- view indicated that 10 to 40 percent of all dairy cows will develop cysts once in their lifetime and 35 to 45 percent of cows having one episode will have the con- dition repeated during their lifetime. Cystic ovaries oc- curred most frequently the second to fifth lactation.30,35,62 Since 60 percent of cows developing ovarian cysts be- fore the first postpartum ovulation and 20 percent there- after spontaneously reestablished estrous cycling,396 the above estimates of the incidence of ovarian cysts are low. Thus cystic ovarian disease prolongs the postpartum in- terval to first estrus in 10 to 30 percent of dairy cows and is a serious cause of infertility. Cystic ovaries in cattle are characterized by follicular cysts or cystic degeneration of the Graafian follicle, lu- teal or luteinized cysts, and cystic corpora lutea. Follic- Figure 108. Cystic Ovaries in a Cow—bilateral follicular cysts with a flaccid atonic uterus. ular and luteal cysts are anovulatory cysts while the cys- tic corpus luteum is an ovulatory cyst. The basic cause for these cystic conditions appears to be a failure of the hypophysis to release sufficient amounts of luteinizing hormone, LH, to produce ovulation and proper lutein- ization of the corpus luteum. (See Figures 107 through 111.) Follicular cysts are anovulatory follicles that persist on the ovary for 10 days and often much longer, have a diameter greater than 2.5 cm. and are characterized by either nymphomania or continuous or frequent estrus, or by anestrus. Luteal cysts are anovulatory follicles over 2.5 cm. in diameter that are partially luteinized and per- sist for a prolonged period and are usually characterized by anestrus. Follicular cysts and luteal cysts may be hard to differentiate clinically as there is great variation in the amount of luteal tissue in anovulatory cysts. The former may be multiple on both ovaries while the latter are more often single. The follicular cyst is thinner-walled and the wall is more tense and distended than the softer thicker- walled luteal cyst. The follicular and luteal cysts have a smooth convex surface since ovulation does not occur. The luteal cyst wall is thicker due to the presence of a lining of luteal tissue. The fluid in the luteal cyst is usu- ally more amber or darker yellow or brown in color than the pale yellow clear fluid in the follicular cyst.70 Fol- licular cysts are probably more common than are luteal cysts. Thirty percent of 1191 cystic ovaries contained luteal cysts,80 (See Figures 107 through 111). Other workers have reported an incidence of 15 and 65 percent luteal cysts based on clinical examination and plasma progesterone assays.19,61 Cystic corpora lutea follow a normal ovulation but contain a fluid-filled central cavity 7 to 10 mm. or more Figure 109. A Central Luteal Cyst in a Bovine Ovary. (Courtesy K. McEntee.)480 VETERINARY OBSTETRICS 25 Figure 110. Bovine Luteal Cysts Associated with Superovulation following the Injection of FSH. (Courtesy M. R. Jainudeen.) in diameter. Cystic corpora lutea on rectal palpation feel similar to large, swollen normal corpora lutea as they have a projecting crown of luteal tissue that protrudes through the site of ovulation. Cystic corpora lutea often have a slightly fluctuating, soft consistency. This may be the most common of the cystic conditions affecting the bovine ovary with a possible incidence two and a half times greater than cystic follicles. Thirty seven cys- tic corpora lutea and 14 follicular cysts were found in 204 nonpregnant cows at slaughter.47 In 357 estrous cycles followed by rectal examinations the incidence of normal corpora lutea, cystic corpora lutea and follicular cysts were 62.4, 25.2 and 12.3 percent.54 The incidence of cystic corpora lutea was 34 to 41 percent in cycling Figure 111. A Bovine Cystic Corpus Luteum. (Courtesy K. McEntee.) cows.20,29 The total progesterone in cystic corpora lutea was about 110 ug at 7 days of the cycle compared to about 180 ug in normal corpora lutea of the same age. About 100 to 150 ug of progesterone is needed in the corpus luteum to permit normal embryo development.68 By 11 days of the cycle the cystic corpora lutea averaged 223 ug and the normal corpora lutea 295 ug of total pro- gesterone. Cows with cystic corpora lutea have normal estrous cycles and if conception occurs there is usually sufficient luteal tissue and progesterone to maintain pregnancy.29 Small central cysts less than 7 mm. in apparently normal corpora lutea are common and may be found in up to 30 percent of corpora lutea.26 These central cysts are lined by a layer of connective tissue, they become smaller late in the estrous cycle as the corpus luteum regresses and are seldom found in pregnant cows’ corpora lutea after the fourth or fifth month of gestation.26 47 For practical purposes most cystic corpora lutea are not pathological; ovulation was normal; they do not influence cycle length;47,54 they may follow a slightly longer than normal estrous period;47 and most cows with cystic C.L. usually maintain the pregnancy to term. However, they may be caused by mild faulty release of L.H. hormone and thus be caused by the same basic deficiencies producing fol- licular cysts and luteal cysts.26,47'67 Since cystic corpora lutea have a questionable path- ologic significance the term cystic ovaries will be ap- plied only to the common follicular cysts and less com- mon luteal cysts. Further detailed clinical, histological and endocrinological studies are needed to more accu- rately assess the incidence of each type of cyst since re- cent reports have indicated the incidence of luteal cysts to range from 15 to 70 percent and follicular cysts from 30 to 85 percent.19,35,61,80 Etiology—Cystic ovaries is principally a disease of all breeds of dairy cows although occasionally beef cattle are affected. While the author has observed the disease most often in Holstein cattle, it must be pointed out this is the major breed in New York State. The disease is more common in closely-confined, stabled animals dur- ing the winter months of December, January and Feb- ruary, than during the summer and fall months.32,54,62 The latter authors reported 44 and 48 percent of their cases of cystic ovaries occurring during these three months. However in New York State there is a concerted effort to have cows calve in the fall of the year. Cystic ovaries affects cows of all ages from puberty to senility but is most commonly observed following the second to the fifth parturition,24 30 or from 4-1/2 to 10 years of age.32 In 295 cases studied by the author62 41, or 13.9 percent, occurred in cattle from 1 to 3 years of age; and only 3INFERTILITY IN THE COW 481 of these were virgin heifers; 160 or, 54.2 percent, oc- curred between 4 and 6 years of age; 74, or 25.1 percent, between 7 and 9 years of age; and 20, or 6.8 percent, over 10 years of age. In a study of 64 cystic cows in a herd of 341 head over a period of 10 years the number of cows that developed cystic ovaries in any given ser- vice period after the first period was fairly constant.12 Certain cows may have repeated attacks of cystic ovaries during a service period or during different service pe- riods. Of 433 cows studied 53 suffered repeated at- tacks.24 In 341 cows 64 cows had cystic ovaries; of these, 12 were affected at 2 service periods, 4 at 3 service pe- riods, and 2 at 4 service periods.12 Thirty-five to 45 per- cent of cows with cystic ovaries had repeated attacks within a service period.32 The occurrence of cystic ovaries is closely associated with stress in the periparturient period. Twin births, re- tained placenta, metritis and milk fever were associated with an increased incidence of cystic ovaries.30,54,55 The high incidence of the occurrence of cystic ovaries be- tween 15 and 45 days postpartum coincides with peak levels of milk production and the onset of estrous cycles.21,78 ACTH, 200 IU given intramuscularly near estrus prevented the LH surge and estrus in 5 of 6 Hol- stein heifers.69 ACTH, 300 IU given daily during the follicular phase, from about day 16 of the estrous cycle caused ovarian cysts in nonlactating Holstein cows.43 Thus stress-induced ovulation failure may be a cause of spon- taneous follicular or luteal cysts. It is seen more com- monly in the higher producing cows. Affected cows have a higher quantitative milk yield than do normal cows. On the basis of the average milk yield in the herd, 45 percent of the nymphomaniac cows were excellent pro- ducers, 48 percent fair producers and only 7 percent poor producers.12,24 The occurrence of nymphomania was not associated with the level or percentage of butter fat pro- duced. There were 1280 service periods, 341 of which were in virgin heifers, during which the animals were not milked; 457 records were made during the time the cows were in the milking herd and milked twice daily, and 105 records on animals started on test but returned to the milking herd before conception; and there were 359 service periods of cows on official test being milked 3 or 4 times a day.12 In these 4 categories the incidence of nymphomania or cystic ovaries was 3.4 percent, 6.8 percent, 8.5 percent and 10.6 percent, respectively. The increased incidence of cystic ovaries in test cows might be explained either on higher production, increased feed- ing, more frequent daily milking, or all three factors.1 Many workers believe that increased feeding espe- cially of rations high in protein stimulate lactation and the development of cystic ovaries. This fact could not be confirmed but the evidence was suggestive.57 The time of onset of cystic ovaries in cattle is usually from 1 to 4 months after calving, with a peak around 15 to 45 days.21,45,54,78 This is the time when milk production is usually the highest. This condition may occasionally oc- cur following repeated services as late as 4 to 9 months after calving.21,61 Nymphomania or cystic ovaries oc- curred even in heifers that were withheld from service for a number of years.17 In 312 cases of nymphomania or cystic ovaries ob- served by the author there appeared to be a seasonal in- cidence of the disease; 151 cases, or 48.4 percent, oc- curred during the months of December, January and February. During these same months in comparable years the N.Y. State Artificial Breeders Cooperative insemi- nated only 35.7 percent of over 325,000 cattle bred those years. High feeding levels causing increased milk pro- duction, coupled with lack of exercise and sunlight might be contributing factors to the cystic condition during the winter months.54,62 There is evidence to show that nymphomania or cystic ovaries is hereditary. This conclusion has long been held by clinicians. A hereditary predisposition to nymphoma- nia existed in the Swedish Highland breed.24 In 331 Swedish Red cattle affected with nymphomania, 26 per- cent of their dams had nymphomania, 41 percent were normal, and in the remainder this information was not known. In the Friesian breed 102 cows had nymphoma- nia and of these 21 percent of their dams had nympho- mania, 45 percent were normal, and in the remainder no information was obtained.24 Of 245 daughters out of 144 dams 43 dams had been cystic; they produced 82 daugh- ters, of which 26.8 percent developed nymphomania.12 The remaining 101 dams had never been cystic; they produced 163 daughters, of which only 9.2 percent de- veloped cystic ovaries. In their data there was no evi- dence of an hereditability of cystic ovaries from cows staying in the herd for less than 4 service periods. They therefore eliminated those cows and recorded only those that remained in the herd for 4 service periods or more. Dams with cystic ovaries had 27 daughters, of which 48.1 percent had cystic ovaries whereas noncystic dams had 46 daughters, of which only 21.7 percent had cystic ovaries. Nearly all cows that suffered from a recurrent development of cystic ovaries had a genetic predispo- sition to the disease.32 Because of this factual evidence and the many observations by most practicing veteri- narians of cystic ovaries in succeeding generations of a cow family, there is every reason to assume the exis- tence of a hereditary predisposition to cystic ovaries and nymphomania. In recent years, with the increased use of artificial insemination and the increased level of pro-482 VETERINARY OBSTETRICS ductivity in our purebred and commercial dairy herds, the incidence of this condition is increasing. In a few herds the problem of cystic ovaries became so severe that the owner became discouraged and the herd was dis- persed.31 In the Ambulatory Clinic of the N.Y. State Veterinary College the incidence of cystic ovaries rose from 333 cases between 1948 to 1953, to 1530 cases between 1963 and 1968—or over a 100 percent increase for each 5 year period in an area where cow numbers declined slightly from 1943 to 1968. Some of this in- crease may be due to the farmer becoming educated, rec- ognizing the symptoms and calling for treatment: or pre- ventive herd health practices including routine postpartum examinations of the genital organs may result in earlier diagnosis and treatment with fewer cases of spontaneous recoveries occurring.78 It may be because treatment is usually successful in maintaining the cow in the herd so that the condition may recur subsequent years; or it may be due to widespread use of bulls by artificial insemi- nation that transmit this inherited predisposition toward cystic ovaries along with high milk production. Further study should be made of the hereditability of this condition. A significant sire line effect on the in- cidence of cystic ovaries in a large purebred Holstein herd was noted.50 In a recent report of 2,112 calvings over a 7-year period by 649 cows in one dairy herd 17 percent of the cows produced at least one daughter that had cystic ovaries. Two bulls sired 17.6 percent of these affected daughters significantly more than was expected since they sired only 11.6 percent of all the daughters in the herd.42b In Sweden where AI bulls siring daughters having a higher than normal incidence of cystic ovaries were culled the frequency of cystic ovaries declined from 10.8 percent in 1954 to 5.1 percent in 1961.4 Also the two abnormalities of ovulation, cystic ovaries and twin- ning, are closely associated and both are probably he- reditary. The relationship was discussed in Chapter IV. AI studs in the United States should heed with concern and action the above evidence. The actual mechanism leading to the development of cystic ovaries is not completely understood. The discov- ery that injections of gonadotropic substances rich in L.H. had a highly specific and curative effect on this condi- tion, definitely indicated that the disease was probably due to a deficiency of LH hormone normally released prior to the time of ovulation.13 The delta cells of the anterior pituitary that produce gonadotropic hormones degranulate or release their hormone shortly after the on- set of estrus in normal cows. In cows that fail to ovulate this degranulation fails to occur, or may occur later, or may not occur as completely as in normal animals.37'48 Pituitary gland gonadotropin content at estrus and four days after normal estrus and ovulation was 3.0 to 9.1 ug while in cows with follicular cysts, the pituitary glands contained 6.1 to 15.1 ug of gonadotropin at estrus and 4 days later.20 Thus in cystic ovaries the normal release of LH failed. The failure of the release mechanism or an actual deficiency of luteinizing hormone from the an- terior pituitary gland prevents normal ovulation and de- velopment of the corpus luteum. Since in cows with cys- tic ovaries plasma levels of estradiol, progesterone, FSH and LH and testosterone were the same as found in the various stages of normal estrous cycle, evidence would indicate that the cause of cystic ovarian disease is due to an abnormal time sequence of hormonal changes rather than differences in the concentration of the hormones be- tween cystic and normal cows.19 In a series of 5 cases treated by the author62 one dose of LH was given to each cow after a normal estrous cycle and estrum followed by continuous symptoms of nym- phomania, 2, 5, 5, 6, and 7 days and the presence of cystic follicles. These cows conceived to the insemina- tion or natural service on the first day of estrum preced- ing the development of the nymphomaniac symptoms. This probably indicates that enough L.H. was present to cause ovulation but not enough to cause normal lutein- ization of the follicle with the result that a number of other follicles matured, failed to ovulate and became cystic. The injected luteinizing hormone caused a rapid luteinization soon enough so that normal attachment and development of the fertilized ovum took place. If treat- ment had not been given, the fertilized ovum probably would have perished and a well-established case of nym- phomania or cystic ovaries would have developed. Oth- ers have recorded similar cases of cystic ovaries treated within 10 days after insemination and fertilization in which pregnancy occurred from that service. Cystic ovaries in cattle can be produced by the injec- tions of estrogens, especially in the latter third of the estrous cycle.23 Intramuscular injections into cycling cows of doses greater than 4 mg. of estradiol or 40 mg. of stilbestrol may result in cystic ovaries. Prolonged or high doses of estrogens have been reported1516,47 as causing cystic ovaries. Androgens could also cause this disease. Thus exogenous injection of steroids and possibly other hormones can interfere with the normal release of L.H. and produce cystic ovaries. Cystic ovaries were pro- duced experimentally583 by the injection of 5 mg estra- diol benzoate on day 16 of the bovine estrous cycle or the injection of bovine LH antiserum before the onset of estrus. The former injection caused premature release of LH and resulted in smaller cysts, 2 to 3 cm., than the latter treatment, 5 to 6 cm. cysts. In both types of cysts the plasma estrogen levels were elevated. Thus cysticINFERTILITY IN THE COW 483 ovaries may be due to premature release of LH or an insufficiency of LH at the time of ovulation. A hyperestrogenic syndrome in unrelated dairy cattle in Israel characterized by cystic ovaries, udder devel- opment in calves, increased incidence of estrus during early pregnancy, estrogenic changes in the genital or- gans, infertility, and abortions caused by feeding large amounts of alfalfa hay with a high estrogenic content was described.2 Estrogens might also be present in higher than normal amounts in red clover, pea ensilage and mold on hay and silage.1 If a herd experiences more than a 30 percent incidence of cystic ovaries and hereditary factors are not the cause, estrogens in the feed should be sus- pected.5,8,38 The pituitary gland and especially the adrenal gland were larger in cows with cystic ovaries than in normal cows. Certain cows with cystic ovaries exhibited a mas- culine behavior and appearance and had increased levels of 17-ketosteroids from the adrenal gland in the urine.24 This syndrome was called “adrenal virilism.” However, the bovine adrenal gland is a poor source of androgens.67 Many long-time nonlactating sterile cows develop a steer- like appearance. The steroid content of ovarian cysts was studied and the previous literature was reviewed.67 Although estra- diol-17B was the major steroid in normal ovarian folli- cles, the concentration of this steroid was significantly lower in follicular cysts, 50 to 75 ug. vs 20 to 30 ug. per 100 ml. of fluid, respectively. Histologically the ste- roid producing granulosa cells in the follicular cysts were undergoing atresia. Some cyst fluid samples contained large amounts of progesterone and these cysts on his- tologic examination showed atretic or luteinizing changes. Other steroids such as estrone and androstenedione were also found in the cyst fluids. The absolute concentrations and relative amounts of various steroids found differed greatly both between animals and within the same ani- mal. There was no correlation between the size of the cyst and the hormone content. The cyst itself was not the primary defect in ovarian disease.67 Cysts were de- generating structures both histologically and endocrino- logically. In normal follicles growth and endocrine ac- tivity accompanied each other while in cysts follicular growth continued but endocrine activity declined. Nei- ther the concentrations or the total amount of estradiol indicated the cysts produced increased amounts of estro- gen. However, estrogens were produced in cystic ova- ries for a longer period of time and more continuously than estrogens in a normal cycling cow. It was impossible to correlate the behavior exhibited by cystic cows with the steroids present in the cysts. This behavioral pattern was complicated since both proges- terone and testosterone can potentiate estrogens in bring- ing a cow into estrum. Progesterone in large doses can inhibit estrus in an estrogen-primed animal. Cows tend to become refractory to even high doses of estrogen and fail to show signs of estrus. Furthermore the frequency of the development of new follicles and hormonally ac- tive cysts will affect the behavior of the cystic cow.67 In 23 cows with cystic ovaries, 21 had estradiol plasma levels higher than those recorded during the preovulatory surge of estrogen in normal cows, 25 to 100 pg/ml. While 11 cows had plasma levels of progesterone over 1.5 ng/ ml, commonly seen in normal cows in diestrus. The presence of progesterone in these cows did influence the estradiol levels.64 Eight cows with ovarian cysts were studied over 30 days and LH plasma concentrations were different within and among the cows. Only one cow had a mean progesterone level above 1.0 ng/ml, but con- centrations greater than this were observed in at least one of the samples in the other 7 cows during this period. With the development of new cysts, older cystic struc- tures regressed in 6 of the cows but no spontaneous re- coveries occurred during this period in the 8 cows.39 The presence or absence of behavioral estrus, nymphomania or anestrus could not be associated with the endocrine levels in the blood plasma.64 The concentrations of es- tradiol, progesterone and testosterone from non-lutein- ized vs luteinized bovine ovarian cysts were 81.9 vs 3.5, 163.7 vs 563.4, and 4.4 vs 2.1 ng/ml, respectively.326 The concentrations of estradiol, progesterone and tes- tosterone in normal follicular fluid and ovarian cyst fluid about 10 days after treatment with 100 ug GnRH causing luteinization of the outer cells of the theca interna106 were 55.7 vs 3.9, 181.9 vs 766.0 and 5.7 vs 3.0 ng/ml., re- spectively.326 Thus physical changes in cystic structures together with the development of new cysts in the ovaries, variations in the hormonal content of the ovarian cystic fluid67 and changes and variations in the level of estradiol, proges- terone and LH in the blood plasma of cows with cystic ovaries indicate that the condition of ovarian cysts is not a stable or static but a changing one. Follicular cysts may become luteal cysts. Older luteal or follicular cysts may involute and disappear when new follicles and new cysts develop.39 Some older authors and veterinarians indicated that cystic ovaries were associated with or even due to uter- ine infections. The uterus was examined histologically and bacteriologically in 62 cows with cystic ovaries and evidence of an endometritis was found in only 4 cases. Infection of the uterus is seldom seen associated with cystic ovaries. Of the author’s cases of cystic ovaries or nymphomania, 72 cows conceived promptly within 60484 VETERINARY OBSTETRICS Figure 112. A Chronic Cystic Ovary Associated with a Unilateral Mucometra. Courtesy K. McEntee. days of treatment without treatment of the uterus. A few cases of infection were encountered. Signs—Cystic ovaries develop in cattle most com- monly from 15 to 45 days postpartum.21,45,54,78 but may occur quite commonly up to 120 days or more. Behav- ioral signs are variable for several reasons as discussed under the etiology but for general purposes cows can be divided into two groups, nymphomaniac and anestrous cattle. The cows with nymphomania exhibit frequent, ir- regular, prolonged, or continuous signs of estrum. These cows are often nervous, restless, and bellow frequently. Only very rarely does a nymphomaniac cow become vi- cious. These cows may occasionally accept the riding of another cow, or coitus by the bull at any time. Most nymphomaniac cows frequently attempt to ride other cows but often refuse to stand to be ridden. Nymphomaniac cows may be as sexually aggressive as a bull in seeking out and attempting to mount a cow approaching or in estrum. The homosexual and heterosexual characteristics of cattle are aggravated during this disease. The affected cows because of their actions are often spoken of as “bullers.” These cows, especially if on pasture are likely to lose weight during the disease because of constantly moving about, attempting to mount, and stirring up the other cows. The cows with the cystic ovaries that show anestrum are not observed in estrum for long periods of time, several months or more. In this group of cows the symptoms of estrum, if they are present, are very mild and infrequent. The owner of these cows, if they have been bred, may believe them to be pregnant. Others, about 15 to 20 percent, have had a normal estrum or two and then failed to show estrum thereafter even though they were not bred. Some of these cows may at times act as if they might be in estrum but refuse to stand for the bull or for other cows to mount them. Some cows with cystic ovaries may show anestrum initially and then exhibit nymphomania later or conversely some nymphomaniac cows may continue to have cystic ovaries but after a varying period of time exhibit anestrum. The incidence of cows with cystic ovaries exhibiting nymphomania or anestrus varies and is strongly influ- enced by the postpartum interval at which the condition is diagnosed per rectum. More cystic follicles developed from 0 to 30 days than from 31 to 60 days postpartum. About 85 percent of the cows, that developed follicular cysts prior to 60 days exhibited anestrus.45,55 A study of 187 cows with cystic ovaries in which many were ex- amined in the early postpartum period of 30 to 60 days reported a 62.5 percent incidence of anestrus.9 A study of 265 cases of cystic ovaries examined only at the re- quest of the owner from about 80 to 150 days after calv- ing reported the incidence of anestrus to be 26.4 per- cent.62 Thus as the number days following calving at which the cystic ovarian condition is diagnosed increase the in- cidence of nymphomania also increases. A constant and prominent sign of cystic ovaries is the relaxation of the sacrosciatic ligament, most noticeable at its caudal border.24 In cows showing nearly constant estrum 78 percent of the cows had highly relaxed liga- ments, 10 percent moderately relaxed and 6 percent slightly relaxed ligaments. In cows with frequent heats, 50 percent had highly relaxed 42 percent moderately re- laxed and 5 percent slightly relaxed ligaments. In a few cases because of the relaxing effect of estrogens on the pelvic ligaments constant mounting and being mounted may lead to dislocation of the hips and to pelvic frac- tures. The pelvic ligaments of anestrous cows were highly relaxed in about 40 percent of the cows, moderately re- laxed in 30 percent, slightly relaxed in 12 percent and normal in 18 percent of the cows. The genital organs are usually slightly edematous and atonic. The vulva is often increased in size, and relaxed and swollen. Prolapse of the vagina and symptoms of pneumovagina may occur especially in nymphomaniac cows. An increased amount of mucus may be present and appear as a discharge at the vulva. This mucus is thicker, more tenacious, and more opaque than the mucus of estrum. The mucus is whitish grey in color, giving it the appearance of a mu-INFERTILITY IN THE COW 485 copurulent discharge. However there are usually few leucocytes in the mucus. The external os of the cervix is usually large, dilated, and relaxed. On rectal examination the relaxation of the pelvic lig- aments is very noticeable on palpation. The cervix, es- pecially the external os, is usually large, and the uterus is also enlarged, and its walls are thickened and flaccid. In long-standing cases of cystic ovaries the uterus may be atrophied, small and flaccid. On palpation of the uterus it seldom develops tonicity or becomes erect or turgid as usually occurs in a normal uterus especially at or near estrum. One or 2 to 4 cysts varying in size from 2 to 7 cm. in diameter are felt on one or both ovaries. These cysts are usually peripheral in location, thin-walled and burst readily with pressure applied by the fingers. At times it may be difficult to differentiate between a cyst and a normal follicle. Cysts persist for 10 days up to several months or longer. No luteal tissue or corpus luteum is usually palpable in the ovaries of cows with follicular cysts. Even cystic corpora lutea are not present. Occa- sionally a thick-walled, rather fluctuating, luteal or lu- teinized cyst may be found. These are often associated with anestrous cows. Occasionally a large atretic follicle together with a normal corpus luteum may be found in a pregnant cow the first trimester of gestation. This does not affect the pregnancy. Usually the cyst is larger than 2 or 2.5 cm. in diameter whereas the normal follicle is smaller. The cyst is usually thicker-walled than is the follicle. The uterus of a cow with cystic ovaries is usu- ally flaccid, whereas the uterus during estrum is erect and tonic. The mucus of estrum is much clearer and more stringy than that in the cow with cystic ovaries. Occa- sionally cows 40 to 90 days pregnant may have a good- sized follicle and a normal corpus luteum. A cyst larger than 8 to 10 cm. in diameter may indicate the presence of a granulosa cell tumor. The size and number of ovarian cysts were similar for both nymphomaniac and anestrous cows.24 62 The inci- dence of ovarian cysts in 433 cows was as follows: both ovaries cystic 50 percent, right ovary cystic 31 percent, and left ovary cystic 19 percent.24 The author in a total of 352 cases found the incidence to be 43.8 percent, 33.2, and 23 percent, respectively. On postmortem examina- tion of the genital organs of 6286 Swedish Highland cows an incidence of 14.8 percent cystic ovarian degeneration was found, 6 percent involved only the right ovary, and 5.5 percent involved both ovaries. Thus in nymphoma- nia, as in the incidence of left- and right-horn pregnan- cies, the fact that the right ovary of cows is slightly more active or functional than the left is further illustrated. Gross examination of cystic ovaries revealed the fact that multiple cysts were more common than were single cysts and the large single cysts frequently showed evi- dence that they had been formed by the union of several cysts.24 The lining of the cyst was smooth and basal por- tions occasionally had a thin circumscribed area of yel- lowish lutein tissue. Some lutein tissue has been ob- served in many ovarian cysts by the author and his associates. The cystic fluid was clear and slightly yellow or amber in color. In large cysts the ovarian tissue was atrophied. On histologic section the granulosa layer of cells and ovum are often missing, but scanty portions of granulosa cells could be found in the basal portions of the cyst and in some cases these appeared luteinized. The theca interna was likely to be flocculent and edem- atous and show degenerative changes. Some hyaline changes in the theca interna were occasionally observed. The degenerative changes were more marked in the pe- ripheral portions of the cyst.24 The gross appearance of the uterine tube was normal in most cases.24 Sometimes the uterine tube was thick- ened and some yellow fluid could be squeezed out after incising it. Microscopically this was composed of epi- thelial cells and debris. In cows with cystic ovaries the ovarian bursa or ventricle was larger than normal and the mesometrium was more relaxed. In nymphomaniac cows the uterus and cervix usually were large, edema- tous, and flaccid. The cervical canal was dilated and re- laxed, permitting a finger or pencil to pass through. The endometrium was smooth, moist, semi-transparent, and edematous. In a few cases cystic enlargement of the en- dometrial glands was noticed as pinhead rounded ele- vations with transparent capsules. Usually the uterus was empty but the endometrium was covered with thin mu- cus. Occasionally as much as 100 ml. of mucus was found in the uterus. The vagina, clitoris and vulva were swol- len. Microscopically the greatest changes are found in the uterine mucosa. These changes, especially in nym- phomaniac cows, were characterized by marked hyper- plasia of the mucosa and cystic dilation of the endometri- al glands. In some cases cystic dilation was so marked that the endometrium developed a typical Swiss-cheese appearance on histologic section. (See Figure 113.) In some anestrous cystic cows with a small uterus the mu- cosa showed slight atrophic changes and hyperplasia and cystic dilation of uterine glands. These hyperplastic and cystic changes in the endometrium are characteristic of changes produced by long-continued action of estrogens from the cystic ovaries. In long-standing cases of nymphomania the relaxation of the pelvic ligaments produces a tipping of the pelvis and an elevation of the tail head that is made more pro- nounced by the relaxed sacrosciatic ligaments. This el- evated tail head is sometimes called the “sterility hump”486 VETERINARY OBSTETRICS Figure 113. Cystic Endometrial Glands Caused by Cystic Ovaries. Courtesy K. McEntee. because it tends to persist after recovery. (See Figure 114.) Associated with the elevation of the tail head is the elevation of the ischial tuberosities and a ventral dropping of the lumbosacral articulation. This tipping of the pelvis may result in an unsteady gait and a predis- position to injury. These changes in the pelvic ligaments are associated with prolonged low level estrogenic stim- uli and probably not due to excessively high estrogen levels in the blood plasma.19 Figure 114. A “Sterility Hump” in a Cow Associated with Chronic Cystic Ovaries and Relaxed Pelvic Ligaments. Figure 115. A Steer-like Appearance of a Cow with Chronic Cystic Ovaries and Infertility Lasting for Three Years. Hydrometra or mucometra may develop following a long-standing condition of cystic ovaries. (See Figure 112.) Cows with cystic ovaries observed by the author and his associates were initially treated apparently suc- cessfully and bred. The owners believed them to be pregnant but after 6 to 8 months the normal signs of pregnancy did not develop. Rectal examination revealed mucometra and cystic ovaries. A marked atrophy of the uterine wall or myometrium had occurred with severe cystic dilation of the endometrial glands resulting in mu- cometra with the uteri containing 100 to 1000 ml. of watery mucus. (See Figure 113.) On rectal examination in some cases the uterine wall was found to be so thin that it was difficult to palpate. Hydro- or mucometra may affect only one uterine horn or a portion of one horn. The ovaries were usually larger than normal but the cysts were multiple, small (1 to 2 cm. in diameter), and thick- walled. The cysts were extremely difficult or impossible to rupture by manual pressure. This same condition oc- curred in 3 heifers that developed chronic cystic ovaries out of 25 heifers that were withheld from breeding for 4 to 5 years.17 The cervical canal in these cases is usually closed by an accumulation of mucus and debris. In one case in which treatment was instituted by the author to relieve the mucometra by drawing off the mucus, infec- tion was established and pyometra resulted. In another cow with 100 ml. of mucus in the uterus, 20,000 I.U. of chorionic gonadotropin was injected intravenously and luteinization of the cysts and expulsion of the mucus from the uterus resulted. Most cases however fail to respond to treatment. The marked similarity of this condition in cattle to cystic degeneration of the uterine wall in horses, and to hyperplasia of the endometrium with cystic di-INFERTILITY IN THE COW 487 lation of the endometrial glands, hydrometra, and, in some cases, secondary pyometra in dogs is evident. The en- dometrial changes are probably produced in the three species by the gonadal steroids, estrogen and/or pro- gesterone. In rare cases of chronic cystic ovaries and anestrus the cervix may become greatly enlarged to 5 to 6 inches in diameter and filled with a tenacious mucus, mucocervix. The uterus in these cases is flaccid but not distended with mucus. The cause and prognosis are similar to mucome- tra. The effect of cystic ovaries on milk production is vari- able. Some authors report a drop in milk production in nymphomaniac cows. Others report good milk produc- tion until treatment is given, at which time there is a drop in production. In a careful study of 74 cows it was demonstrated that the cystic condition was apparently re- sponsible for increased production.36 The longer the cows were cystic the greater the production of milk. Cows with anestrus produced more milk than nymphomaniac cows. This indicated that the low levels of estrogen from the cystic ovaries probably stimulated milk production. Prognosis—The earlier that cystic ovaries are diag- nosed and treated, the better is the prognosis. In a series of 229 cases diagnosed and treated by the author within 6 months of parturition 79 percent conceived after 1 treatment, 10.7 percent had to be retreated, and 10 per- cent were sold because they were sterile, poor produc- ers, or for other reasons. In 46 cows diagnosed and treated between 6 and 12 months after calving, although 78.3 percent recovered, only 58.7 percent conceived after one treatment and were retained in the herd, 8.7 percent were retreated, and 32.6 percent were sold. Many were sold because it was not economical to maintain them as non- lactating cows for many months in commercial herds. There was no essential difference between the rate of recovery and conception rates between cows showing nymphomaniac symptoms and cows showing anestrus. In 124 cases of nymphomaniac cows treated within 60 days of the onset of symptoms 78.2 percent conceived and 21.8 percent were sold. In anestrous cows, symp- toms in many cases were lacking or unnoticed for an undetermined period of time. Of 46 cows, many of which had not been observed in estrum since calving, treated within 120 days of the onset of anestrum, 76.1 percent conceived and 23.8 percent were sold. The size or num- ber of the cysts bore no relation to the symptoms shown or to the rate of recovery. In some cases two or more treatments may be necessary to effect a cure. Recovery is not assured until the affected cows are safely pregnant. About 20 to 30 percent or more of cows with cystic ova- ries if they conceive will develop cystic ovaries again at subsequent service periods. Another factor to be consid- ered seriously in the prognosis is the possible furthering of this cystic problem to the future detriment of dairy breeds inasmuch as there is a definite hereditary predis- position to cystic ovaries and twinning. Cows having two or more episodes of cystic ovaries were hereditarily pre- dispositioned toward the disease.322 Bulls with an in- creased incidence of daughters with cystic ovaries should be slaughtered.4,323 The prognosis in cases of severe cystic degeneration of the endometrium and atrophy of the uterine wall in hydrometra or mucometra is poor. Most cows with mu- cometra or rare cases of mucocervix should be sold since only a very few cases respond to treatment. Spontaneous recovery from cystic ovaries frequently occurs. About 50 percent of the cases of cystic ovaries occurring within 45 days of calving recovered spontaneously before 60 days postpartum. In 42 cows with cystic ovaries, 30 of which developed between 15 and 45 days postpartum, 69 percent recovered without treatment and became pregnant before 300 days postpartum.78 In 34 cows treated for nymphomania about 15 percent were sold as sterile and the remainder required about 3 services per concep- tion after treatment; about 40 percent of the cows con- ceived on first service.73 A lowered conception rate as- sociated with early embryonic deaths following recovery from cystic ovaries was also noted.50 Treatment—Rational treatment should have as its aim the development of a functional normal corpus luteum either by spontaneous recovery or rupture of the cysts, repeatedly if necessary, administration of GnRH or lu- teinizing hormone (LH) or preventing the continuous re- lease of luteinizing hormone from the pituitary gland by the administration of progestational compounds. The bo- vine corpus luteum is formed mainly from the granulosa and thecal cells.67 Since these cells are the first cells to degenerate in the cystic follicle, treatment to be suc- cessful should be undertaken soon after cyst formation or when newer young cysts are forming on the already cystic ovary containing follicular or luteal cysts. The earliest reported treatment for cystic ovaries con- sisted of repeated manual removal or rupture of the cysts at 6- to 10-day intervals until a normal cycle and corpus luteum developed. This frequent manual massage and trauma to the ovary is not desirable if it can be avoided; moreover, repeated visits by a veterinarian for the mas- sage of the cow’s ovaries is costly. In a series of 188 cases reviewed by the author in which cystic ovaries were treated by manual removal of cysts, a recovery rate of 37.2 percent was reported.14'51,62 Of 24 cases of cystic ovaries occurring in a herd of 150 cows, 8, or 37.5 per- cent, conceived twins after treatment.14 Of 11 animals488 VETERINARY OBSTETRICS bred within 35 days after removal of the last cyst, 6, or 54.5 percent, conceived twins; only 3, or 24 percent, of 13 animals bred after 35 days following rupture of the last cyst had twins. Because of this high twinning rate following treatment it was then recommended that breeding be deferred until the second normal estrum un- less the ovaries were palpated to determine the presence of 1 or 2 ripe follicles, and the cow then bred or not bred accordingly. In cows having ovarian cysts centrally located, or thick-walled so that manual rupture was not possible, the treatment required tapping the cyst with a needle or ovarian scalpel through the vaginal wall. Stoll’s cyst aspirator70 works well in these cases. Two hundred forty two cows with cystic ovaries were treated by man- ual rupture of the cysts. Three-quarters of these cases were treated within three months of parturition. Cows with the shortest time interval from parturition to treat- ment recovered significantly more quickly; 45.7 percent or 107 cases, recovered after one treatment.65 These re- sults complement the observation that single ovarian fol- licular cysts occurring before 45 to 60 days after calving have a 50 percent spontaneous recovery rate and the ob- servations of many veterinarians that manual removal of these early postpartum cysts is often successful in re- storing a normal sexual cycle.54 Many veterinarians may manually remove cysts prior to 50 days but do not treat with LH or GnRH until 50 to 60 days or more postpar- tum. A trial on the comparative efficacy and costs of spontaneous recovery of early ovarian cysts, manual rupture of these cysts which usually is easily accom- plished, and treatment with GnRH or HCG should be conducted on cows in which ovarian cysts are diagnosed prior to 60 days postpartum. Spaying will correct nym- phomania but removing only one ovary if it is affected with cysts is useless, since the remaining ovary will promptly develop cysts. Affected nymphomaniac cows should be kept isolated from the herd so that they do not annoy or injure themselves or other cattle by excessive mounting. Although a number of authors had suggested the pos- sible value of LH in treating bovine cystic ovaries and the successful treatment of a few cases with LH (“An- tuitrin S:) in 1943 was reported,8 it was not until 1944 that successful results in the treatment of many cows with cystic ovaries, both follicular and luteal cysts, using un- fractionated sheep pituitary extracts intravenously was published.13 This report demonstrated the value of LH in curing the disease. Of 81 cows with nymphomania or cystic ovaries treated, 88 percent recovered and had a normal corpus luteum in 31 days. Of 53 cows bred after a single injection of the pituitary extract, 36 conceived. After retreatment of 16 animals 6 more became preg- nant. Thus a total of 68 percent conceived. These work- ers reported that it was not necessary to rupture cysts prior to treatment. Since then a number of reports on the treatment of cystic ovaries have recorded the successful use of pituitary extracts rich in LH, or chorionic gonad- otropin HCG.62 Injections of human chorionic gonadotropin (HCG) 50001.U. intravenously and 10,000 I.U. intramuscularly resulted in a higher incidence of conceptions than 2500 I.U. intravenously, 78.4 percent, 81.6 percent, and 73.7 percent conceptions, respectively.62 Another study re- ported 68 percent recoveries from cystic ovaries in Guernseys and 78 percent recoveries in Holsteins by the adminstration of 5000 I.U. chorionic gonadotropin in- travenously.9 Due to the cost of the product it is more economical to treat most cows with 2500 to 5000 I.U. of chorionic gonadotropin intravenously than the 10,000 I.U. dose intravenously or intramuscularly. Intramus- cular injections of 1000 to 5000 units of chorionic go- nadotropin in 14 cows resulted in a slightly lower con- ception rate of 64.3 percent.62 No difference was ob- served from year to year in the efficacy of the pituitary or chorionic gonadotropin products rich in L.H. A com- parative study reported on the treatment of 278 cows with cystic ovaries with the intravenous injection of 10 RU “Vetrophin,” a sheep pituitary gonadotropin, 65 cows with 5 R.U. “Vetrophin” intravenously, and 38 cows with 5000 and 10,000 IU HCG intramuscularly. Recov- ery and conceptions after one treatment were 65.5, 69, 78, and 71 percent, respectively, for these treatments. Thus large doses of HCG improved results only slightly. Only one case of anaphylaxis has been observed by the author. A moderately-affected case, occurred after the administration of 5000 I.U. of human chorionic go- nadotropin intravenously. No reaction has been observed or reported with the use of the sheep pituitary product, “Vetrophin.” Of 185 cows in which cysts were removed by manual pressure through the rectum at the time of treatment with either pituitary LH, or chorionic gonadotropin, 156, or 84.3 percent, recovered; 29 or 15.7 percent, did not re- cover. 133, or 71.9 percent, conceived; 20 or 10.8 per- cent, were retreated; and 32 or 17.3 percent, were sold. Of 103 cases in which the cysts were not ruptured at the time of treatment with LH, 87, or 84.5 percent, re- covered; 16, or 15.5 percent, did not recover; 79 or 76.7 percent, conceived; 11, or 10.7 percent, were retreated; and 13, or 12.6 percent, were sold. No benefit resulted from removal of cysts at the time of treatment with an L.H.-rich product.61'62 Since trauma to and adhesions of the ovary may be produced by manual removal of cysts this practice is unnecessary and contraindicated. AfterINFERTILITY IN THE COW 489 injections of LH the cysts luteinize and developing fol- licles may ovulate and luteinize79 and symptoms of nym- phomania cease in 3 to 6 days in affected cows that re- cover. Although most of the unruptured cysts luteinize, the cystic fluid may remain until a few days before the next normal estrum when the luteal tissue and the cystic fluid recede and disappear rather rapidly. A normal es- trum will occur in most cows from 15 to 30 days after treatment, with most cows exhibiting estrum 20 to 25 days after treatment. Within the last 10 years rapid advances in the study of the peptide releasing factors from the hypothalamus has resulted in the synthesis of the decapeptide gonad- otropic releasing hormone (GnRH) or luteinizing hor- mone releasing hormone or factor (LH-RH or LH-RF) or the commercial product “Cystorelin.”* This deca- peptide when injected in any manner usually intramus- cularly into cattle causes a dose related increase in plasma concentrations of luteinizing hormone (LH) from the an- terior pituitary gland. Although doses of GnRH in Eu- rope are higher, 0.5 to 1.5 mg., the dose used in the U.S. is 100 ug. (50 ug/ml) in 2 ml. For long existing cases, relapses, or slightly better response on initial treatments larger doses of GnRH may be used.35 This product is currently cheaper in price than 5000 to 10,000 I.U. of human chorionic gonadotropin. GnRH is non- toxic even in large doses and produces no side effects or anaphylactic reactions. Refractoriness to the GnRH does not develop in cows as occurs after repeated injec- tions of human chorionic gonadotropin (HCG), a foreign protein. In the normal cow the rising level of estradiol early in estrus in the absence of progesterone from the corpus luteum results in the preovulatory surge of LH in cows with a serum level of 40 to 50 ng/ml that is believed to induce proteolytic enzyme synthesis in the Graafian fol- licle that weakens its wall resulting in ovulation. Im- mediately after, or even slightly before, ovulation LH induces luteinization or a conversion of the steroidogenic activity of the granulosa and theca cells from estradiol to progesterone synthesis and within 5 to 6 days the ma- ture corpus luteum is formed that secretes progesterone to regulate the estrous cycle and, if the fertilized ovum is present, to maintain pregnancy. Progesterone has a negative feedback on the hypothalamus and the pituitary on LH release.39 Cystic ovaries in cows, as indicated earlier, are due to a failure of the normal release of LH and GnRH necessary to cause ovulation and luteinization of the ovulated follicle. * Abbott Laboratories, Chicago, 111. Recent reports indicated the treatment of cystic ova- ries with 100 ug GnRH IM caused luteinization of the cystic structures without ovulation.39b Larger doses of GnRH, 0.5 to 1.5 mg or 750 to 10,000 IU HCG given IM caused ovulation of 1 to 3 cystic or mature follicles followed by the formation of corpora lutea.39b,71b About 40 percent of ova recovered from these cows, following AI within 24 hours after treatment, were fertilized. Ovu- lation occurred about 27 hours after treatment.71b Thus GnRH and HCG may induce ovulation and CL forma- tion besides luteinizing the cystic structures. Like HCG therapy, manual rupture of the ovarian cysts is not nec- essary or recommended. Within 9 to 13 days after GnRH or HCG treatment the increased amount of lutein tissue produced in the cystic structures is producing a plasma level of progesterone that is similar to that in the estrous cycle in about 80 percent of the treated cows.41 The on- set of estrus after treatment may range from 9 to 30 days depending on the ovarian and endocrine status of the cow.10,39 In the 20 percent of cows failing to respond to treatment by the re-establishment of the estrous cycle the cause may be due to the cystic structures being unable to respond to LH release because of degeneration of the granulosa and theca interna layers.40,41 Other causes might include: unobserved estrum, the hypothalamus and/or pituitary may not be responsive in releasing LH due to elevated estradiol concentrations,41 or high ACTH and cortisol levels may be present that suppress estrus.43,69 The success or response to treatment of cystic ovaries with GnRH is about the same as with human chorionic gonadotropin (HCG).10,35 Ih 225 dairy cows with cystic ovaries treated one to three times with 100 ug of GnRH at less than 30 to more than 90 days postpartum that clinically recovered with a normal estrous cycle was 76 percent, 78 percent and 66 percent for the three treat- ments, respectively. The conception rate on first service after treatment was 49 percent and 83 percent of the cows eventually became pregnant at an average interval of 87 days from treatment to conception.78 In a controlled study 114 dairy cows with cystic ovaries were divided into four equal groups and given 0 ug, 50 ug, 100 ug and 250 ug of GnRH as an intramuscular injection.93 Recovery rates based on the development of a normal estrous cycle or conception were 21 percent, 64 percent, 82 percent and 77 percent. The mean days from parturition to treatment for these four groups was 63, 111, 89, and 94 days, respectively. Most cows came into estrus 18 to 23 days after treatment with GnRH, the range of days was 8 to 35.10,39 Other reports on the treatment of cystic ovaries with GnRH have been cited with essentially similar re- sponses.25 35 In one study there was no difference in re- sponse to 10,000 I.U. of chorionic gonadotropin (HCG)490 VETERINARY OBSTETRICS and 250 ug GnRH.61 However early diagnosis and treat- ment increased the chance of recovery as pregnancy rates within 90 days postpartum for groups treated within 59 days, 60 to 120 days, 121 to 180 days and over 180 days were 48, 39, 51 and 26 percent.61 Since the incidence of recoveries are similar for GnRH and HCG, the ad- vantages of the former are its cheaper cost and the evi- dence that refractoriness on repeated doses, due to the production of antibodies against a foreign protein, does not occur. If a normal estrous cycle has not occurred within 23 days of GnRH treatment, the cow should be reexamined and possibly treated again. This may be nec- essary in about 20 percent of the cows. In all carefully controlled studies on bovine cystic ovaries spontaneous recoveries are reported. These are most commonly observed early in the postpartum pe- riod. About 50 percent of cows developing cystic ovaries within 45 days postpartum recovered spontaneously be- fore 60 days postpartum.55 In the two studies93,78 21 and 29 percent of spontaneous recoveries occurred in cows with cystic ovaries diagnosed between less than 30 to more than 110 days postpartum. Thus early postpartum examinations77 15 to 45 or 60 days, together with early treatment of ovarian cysts will improve the rate of re- coveries. The decision for the best time to examine cows to possibly treat by rupture of cysts formed soon after calving, or treat the cows with GnRH or HCG will vary with the prevalence of cysts in the herd and the fre- quency and cost of the examinations.77 The combination of GnRH or LH (HCG) and pros- taglandins recently have been shown to have certain ad- vantages in the treatment of cystic ovaries.10,19,35'40 Treatment of cystic ovaries with GnRH or LH (HCG) results in about 80 percent of the cows developing lu- teinized cysts or CL by 9 to 13 days after the injection followed by estrus 18 to 23 days (range 9 to 35 days) after the injection. If a luteolyte dose of PGF2a is given 9 to 14 days after treatment with GnRH most cows will exhibit normal estrus 3 days later or 12 days after the injection of GnRH. This treatment aids in helping to syn- chronize estrus and shortening the time from GnRH in- jection to conception by 7 to 10 days in many cows.10,40 The second regimen is based on the facts that HCG or GnRH will effectively cure luteal cysts as well as fol- licular cysts by providing or releasing LH. From 15 to 75 percent of the cystic structures on the bovine ovary are luteal cysts as determined by palpation, abattoir stud- ied and plasma progesterone levels.10,19,35,61,80 The pro- posed and apparently successful therapy for cows with cystic ovaries consists of injecting a luteolysing dose of prostaglandin which should involute all lutein tissue in the cystic ovarian structures, followed by a dose of GnRH or HCG 3 or 4 days after the injection of PGF2a. If estrus is observed at this time, breeding is indicated. The time to the next estrus can be shortened by a second injection of PGF2a 9 to 14 days after the dose of GnRH or LH. These modifications of the usual treatment with GnRH or LH may prove valuable in the treatment of cystic ova- ries in certain cows despite the increased cost. Further studies are indicated. Many cystic ovaries in dairy cows develop between 15 and 60 days postpartum when milk production is at peak levels. Recent studies have shown that plasma and pituitary levels of LH are low at parturition and increase from 8 to 30 days later606 However the pituitary is re- sponsive to treatment with GnRH by day 14 postpartum and the resultant LH surge will cause subsequent ovu- lation, corpus luteum formation and the onset of estrous cycles. Fertility increased as the number of estrous cycles prior to 60 days postpartum increased.606 Although more studies are indicated reports have shown that when 204 Holstein cows were given 200 ug of GnRH intramus- cularly between days 8 and 23 postpartum the incidence of follicular cysts was reduced from 15.2 to 5.7 per- cent.96 However the interval to first insemination, inter- val to conception and inseminations per conception did not differ from controls also bred for the first time be- tween 80 and 90 days postpartum. In another study 100 or 250 ug. of GnRH were given to 335 dairy cows in two herds from 13 to 15 days postpartum.666 In this trial the incidence of ovarian cysts in treated and control cows was similar, about 15 to 25 percent. However in one herd given the larger dose of GnRH and insemination of cows begun at 50 days postpartum the treated cows had a shorter calving to conception interval, 81 vs 96 days, a better overall conception rate, 75 vs 56 percent and a lower number of services per conception, 1.23 vs 1.74, than the controls. If the cow has calved 50 days or more before the treat- ment of cystic ovaries and if no definite pathology of the genital tract is present requiring further rest or treatment, the author and others have recommended that the cow be bred the first estrum after the injection of luteinizing hormone. No observable increase in twinning or delayed conception has been caused by this practice. The prac- tice of breeding promptly is indicated because if cows are pregnant cystic ovaries cannot recur! If cows are al- lowed to have two or three estrous cycles after therapy for cysts relapses are more likely to occur at each ovu- latory period. In the early treatment of certain cases some veterinarians remove cysts manually without injecting LH and if there is no response they treat with LH on a return trip. In the end this procedure may be more costly to the farmer than if the veterinarian administers LH on the ini- tial call. If a case of cystic ovaries fails to respond to an in-INFERTILITY IN THE COW 491 jection of LH or GnRH and a second call is made a larger dose is indicated. The author also recommends a pos- sible change of products from a gonadotropic hormone from pituitary LH to chorionic gonadotropin, or vice versa. In 12 cases retreated with the same product 3 to 4 weeks after the first unsuccessful treatment, 5, or 41.7 percent of the animals recovered and conceived. In 31 cases of cystic ovaries in which a different product from a dif- ferent source was used for the second treatment 26, or 83.9 percent, recovered and 67.7 percent of the cows conceived.62 Since gonadotropic hormones are protein in nature and originate from a species of animal other than the bovine species, antibodies develop from the first in- jection, and neutralize some or much of the same hor- mone when reinjected. When repeated injections of go- nadotropin were used to superovulate cows the animals rapidly developed a refractoriness or inability to respond to the hormone that persisted for months. Other more recent studies have confirmed the development of anti- hormones against the injected gonadotropin such as HCG and PMSG. The more refined the gonadotropin the less antigenic it was in causing antihormones. The injection of small doses, 500 to 2000 I.U. of HCG or 0.5 to 5.0 R.U. “Vetrophin” directly into the ovarian cyst by means of a fine needle inserted through the va- ginal wall or ischiorectal fossa while the other hand of the operator in the cow’s rectum manipulated the cystic ovary has been reported upon.62 75 Although the cost of the hormones used by this technique was less, the results were about the same as other modes of administration of LH. The site of the injection by-passed the body fluids to act directly on the ovarian structures to produce luteal tissue thus avoiding possible neutralization of the LH by antihormones in repeatedly treated cows. This procedure has not proved to be popular or commonly performed. Under the influence of estrogens, early in estrus LH is released from the pituitary gland. Since progesterone and similar products suppress the release and favor the storage of gonadotropin by the pituitary gland probably by acting upon the hypothalamus to prevent the release of GnRH, these products have received attention in the treatment of cystic ovaries.36 Researchers treated 100 cows that developed cystic ovaries and remained in estrus for a few days after service with 750 to 1500 mg of Re- positol progesterone intramuscularly.7 The nympho- maniac signs terminated in most of these cows within 36 to 72 hours and 67 of the cows conceived. Ninety-eight cows with cystic ovaries were given 109 treatments of either 50 or 100 mg. of progesterone in oil daily subcutaneously for 14 days. The cysts were not ruptured.36 Normal estrous cycles and estrus resulted in 60 percent of the cows; 48.7 percent and 52.5 percent of the cows treated with 50 and 100 mg. of progester- one, respectively, conceived. Of 30 untreated control animals with cystic ovaries only 13.3 percent conceived. The average interval from treatment to conception was about 45 days with about 2+ services per conception. Presently progesterone therapy for the treatment of cys- tic ovaries is seldom used. In a discussion of the treatment of cystic ovaries in cattle the author would be remiss if he did not again call attention of his readers to the fact that this condition is frequently due to an inherited weak hormonal constitu- tion. The repeated successful treatment of affected cows simply increases the length of time these cows remain in the herd and increases the numbers of their daughters who also have an inherited predisposition for this dis- ease. In many cases the veterinarian would be doing the farmer and the breed a favor by declining to treat certain cows and to recommend their slaughter. Herds with a high incidence of cystic ovaries should be bred to bulls from lines free of cystic ovaries or by bulls shown to have daughters with a very low incidence of the disease. Failure of Ovulation or Delayed Ovulation due to a failure or delay in LH release from the anterior pituitary gland and not associated with cystic ovaries may occa- sionally be a cause of infertility in cows and heifers. This is probably a minor cause for infertility since only 3 out of 104 repeat-breeding cows failed to ovulate.71 Failure of ovulation occurred in only 3 percent of 247 cows ex- amined.11 This low incidence of failure of ovulation is further supported by other studies.6,71 Ovulation failure occurred in 13 percent of heifers on their first standing estrus and in 2 percent on their second estrus.53 Thus present evidence would indicate that failure of ovulation and atresia of the follicle with an absence of cystic fol- licles is an uncommon cause of infertility in the cow. It appears to be more common in the ewe and mare at the beginning or transitional phase of the breeding season. In a careful study of 58 cows 69 percent had ovulated by the day after estrum and 65 percent of those bred conceived. The other 31 percent of cows had ovulated by the second day after estrum and of those that were bred only 36 percent conceived.28 However in a study of 118 Friesian and 161 Afrikaner cows and heifers over a 4-year period including a total of 536 estrous periods, defective ovulations occurred in 140; 47 cases or 34 per- cent ended in anovulation and 93 cases or 66 percent had delayed ovulation. Forty-one of the 47 anovulatory fol- licles regressed, 4 became follicular cysts and 2 luteal cysts. In delayed ovulation the delay was less than 48 hours in 85 percent of the cases. In 2 cases ovulation occurred 7 and 9 days after the cessation of estrus and both cows conceived to inseminations performed the day492 VETERINARY OBSTETRICS before ovulation.74 These authors recommended that if the follicle had not ovulated by 24 hours after service the cow should be inseminated again. In 51 cows rein- seminated 24 hours after the first insemination 32 con- ceived while none of the 18 cows that had failed to ovu- late within 24 hours of service conceived. They reported that only one of 17 cows inseminated after ovulation conceived and only one of 36 cows conceived when the follicle was manually ruptured at the time of insemina- tion. They indicated that the two main causes for defec- tive ovulation were nutritional deficiencies, especially during the winter months, and an hereditary predispo- sition characteristic of certain infertile cow families in both dairy and beef breeds. Because some reports indi- cated that anovulation or delayed ovulation are rare and other reports indicated they were common, more work is necessary on the incidence and importance of defec- tive ovulation as a cause of lowered fertility. In light of the latter study it should be noted that if cows are bred early in their estrous period, which usually lasts 18 hours, range 6 to 30 hours, ovulation, which usually occurs 8 to 16 hours after the end of estrum, may not have oc- curred by the end of the 24 hour period after breeding in the normal cow. Thus breeding in the second half of the estrous period is most desirable. Delayed ovulation may result in aging of the sperm and ova and also a lowered rate of fertilization and a higher embryonic death rate. (See Repeat Breeders.) Suspected failure of ovulation, or delayed ovulation may possibly be diagnosed by the palpation of a mature follicle on the ovary more than 24 to 48 hours after the end of estrum, especially if bloody mucus is in the va- gina. The use of GnRH at breeding to assure ovulation only produced a very moderate increase in conception rates. Thus the cost benefit ratio may mitigate the regular use of GnRH. However in selected or problem cows where large follicles with delayed ovulation is suspected on the basis of repeated examinations of the ovary it may be used at breeding or six hours before or after breeding.253 Routine doses of GnRH in estrus synchronization also has not proven advantageous. It should be noted that HCG (LH) has proven superior to GnRH in the ovulation of the donor cow for embryo transfer. There is little evi- dence that failure of ovulation or delayed ovulation is often repeated at consecutive estrums. If anovulation or delayed ovulation was diagnosed, rebreeding and the in- jection of LH or GnRH may be indicated since these hormones hasten and promote ovulation in the cow. In these cases it might be advisable to rebreed the cow again 24 hours after the first service so fresh viable sperm cells would be available when the ovum was released. More work is needed to assess the importance of delayed ovu- lation and failure of ovulation without cystic follicles and to improve the diagnosis and treatment of these condi- tions. Infertility Associated with Multiple Ovulations in Cattle In a study of 294 ovulations at which breeding oc- curred, 252 were single ovulations and 42 multiple ovu- lations, as determined by rectal examination. The inci- dence of multiple ovulations was 14.3 percent. The conception rate in single ovulations was 57.5 percent, and in multiple ovulations 28.6 percent.42 Of these latter conceptions represented by 12 cows only 3 resulted in twin births. In a previous study in this same herd the incidence of multiple ovulations was 13.1 percent and the incidence of twinning was 1.92 percent. (See Dis- cussion of Twinning in Unipara in Chapter IV, and Su- perovulation in Chapter XX.) Multiple ovulation is prob- ably due to the release of increased amounts of FSH. Heredity and cystic ovaries may be associated or pre- disposing factors. Thus multiple ovulations resulted in infertility either due to defective ova incapable of fertil- ization or growth or because multiple ovulation may be a manifestation of an endocrine disturbance reflected in an abnormal transport of ova or failure of the proper at- tachment of the embryo. When twin or multiple ovula- tions occur from one bovine ovary and the fertilized ova develop in the horn corresponding to that ovary, a higher rate of embryonic death results than where twin ova are released from each ovary and each embryo develops in a separate horn, bicomual twins. This low survival rate in multiple ovulations and conceptions maybe a fortu- nate occurrence, as the harmful effects of twinning in cattle are well known. The above study may explain the occasional cases in which although on early pregnancy examination two corpora lutea are found, and twinning is therefore suspected, only a single birth occurs.42 The situation as detailed above is very similar to twinning in mares in which there appears to be a “mechanism” in the uterus that eliminates one of the twin embryos. (See Twinning in the Mare.) References for Cystic Ovaries and Other Ovulation Abnormalities 1. Adler, J. H. (1969) Personal Communication. 2. Adler, J. H. and Trainin, D. (1960) Hypoestrogenic Syndrome in Cattle, Refuah Vet. 17, 115. 3. Al-Dahash, S. Y. A. and David, J. S. E. (1977) The Incidence of Ovarian Activity, Pregnancy and Bovine Genital Abnormal- ities Shown by an Abottoir Survey, Vet. Rec. 101, 296. 4. Bane, A. (1964) Fertility and Reproductive Disorders in Swed-INFERTILITY IN THE COW 493 ish Cattle, Brit. Vet. J. 120, 431. 5. Bartlett, S., Folley, S. J., Rowland, S. J., Cumow, D. H. and Simpson, S. A. (1948) Estrogens in Grass and Their Possible Effect on Milk Secretion, Nature, 162, 845. 6. Bearden, H. J. (1954) Fertilization and Embryonic Mortality Rates for Bulls with Histories of Either Low or High Fertility in Ar- tificial Breeding, Thesis, Cornell Univ., College of Agriculture, Ithaca, N.Y. 7. Beck, C. C. and Ellis, D. J. (1960) Hormonal Treatment of Bovine Cystic Ovaries, Vet. Med. 55, 6, 79. 8. Bickoff, E. M., Booth, A. N., Livingston, A. L. and Hendrick- son, A. P. (1961) Estrogenic Activity of Fresh and Dried Red and Subterranean Clovers, J. An. Sci. 20, 1, 133. 9. Bierschwal, C. J., Garverick, H. A., Martin, C. A., Young- quist, R. S., Cantley, T. C. and Brown, M. D. (1975) Clinical Response of Dairy Cows with Ovarian Cysts to GnRH, J. An. Sci. 41, 6, 1660-1665. 10a. Bosu, W. T. K. (1980) Practical Uses of GnRH and Prosta- glandins in Bovine Reproduction, Proc. Ann. Conv. AABP, To- ronto, 137-150. 10b. Brown, E. M., Elmore, R. G., Garverick, H. A. and Kesler, D. J. (1982) GnRH Treatment of Dairy Cows with Ovarian Cysts. II Histology of Ovarian Cyst Walls., Theriog. 17, 6, 689. 11. Casida, L. E. (1953) Fertilization Failure and Embryonic Death in Domestic Animals, Paper No. 448, Dept, of Genetics, Univ. of Wise., Madison, Wise., Reprinted from “Pregnancy Wast- age” by E. T. Engle, Charles C. Thomas Co., Springfield, 111. 12. Casida, L. E. and Chapman, A. B. (1951) Factors Affecting the Incidence of Cystic Ovaries in a Herd of Holstein Cows, J. of Dairy Sci. 34, 12, 1200. 13. Casida, L. E., McShan, W. H. and Meyer, R. K. (1944) Effects of an Unfractionated Pituitary Extract Upon Cystic Ovaries and Nymphomania in Cows, J. of An. Sci., 3, 3, 273. 14. Clapp, H. (1934) Cystic Ovaries in Twinning in Holsteins, Cor. Vet., 24, 4, 309. 15. Dawson, F. L. M. (1957) Bovine Cystic Ovarian Disease—A Review of Recent Progress, Brit. Vet. Jour. 113, 112. 16. Dawson, F. L. M. (1958) Bovine Cystic Ovarian Disease: An Analysis of 48 Cases, Brit. Vet. Jour. 114, 96. 17. DeLange, M. (1950) The Influence of Delayed Breeding on the Fertility of Beef Heifers, Onderst. J. Vet. Sci. and An. Ind. 24, 1 and 2, 125. 18. Deubler, J. (1943) Personal Communication. 19. Dobson, H., Rankin, J. E. F. and Ward, W. R. (1977) Bovine Cystic Ovarian Disease: Plasma Hormone Concentrations and Treatment, Vet. Rec. 101, 459. 20. Donaldson, L. E. and Hansel, W. (1968) Cystic Corpora Lutea and Normal and Cystic Graafian Follicles in the Cow, Austral. Vet. Jour. 44, 304. 21. Erb, H. N. and White, M. E. (1981) Incidence Rates of Cystic Follicles in Holstein Cows According to 15-Day and 30-Day Intervals, Cor. Vet. 71, 326-331. 22. Eriksson, K. (1954) Genetic Analyses of Hereditary Diseases with Incomplete Phenotypic Manifestation, Royal Swedish Acad, of Agric. Scient. Sect. 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Rec., 60, 43, 513. 29. Hansel, Wm. (1964) Sterility Due to Permanent Corpus Luteum and Cystic Degeneration: Some Observations on Bovine Cystic Corpora Lutea, 5th Intemat. Congr. on An. Reprod. and Art. Insem., Trento, Italy. 30. Hardie, A. R. and Ax, R. L. (1981) A 40-Year Survey of Cystic Ovaries in Dairy Cows, J. Dairy Sci. 64, Suppl. 1, 149, Abstr. 31. Haubrich, W. R. (1954) Personal Communication. 32a. Henricson, B. (1965) Genetical and Statistical Investigations into So-Called Cystic Ovaries in Cattle, Acta, Agric. Scand. 7, 1. 32b. Hemandez-Ledezma, J. J., Garverick, H. A., Elmore, R. G., Brown, E. M. and Kesler, D. J. (1982) GnRH Treatment of Dairy Cows with Ovarian Cysts III Steroids in Ovarian Follic- ular and Cyst Fluid, Theriog. 17, 6, 697. 33. Holcombe, R. and Holcombe, R. B. (1961) Treatment of Cystic Ovarian Degeneration in Cattle, Proc. 4th Intemat. Congr. on An. Reprod. Hague, III, 654. 34. Jainundeen, M. R., Hafez, E. S. E., Gollnick, D. D. andMous- tafa, L. A. (1966) Antigonadotropins in the Serum of Cows Fol- lowing Repeated Therapeutic Pregnant Mare Serum Injections, Amer. J. Vet. Res. 27, 118, 669. 35. Jochle, W. (1978) Review: Ovarian Cysts, Animal Reprod. Rept. No. 5, Denville Twp., N.J. 36. Johnson, A. D., Legates, J. E. and Ulberg, L. C. (1966) Re- lationship Between Follicular Cysts and Milk Production in Dairy Cattle, J. Dairy Sci. 49, 7, 865. 37. Jubb, K. V. and McEntee, K. (1955) Observations on the Bo- vine Pituitary Gland, I. and II, Cor. Vet., 45, 4, 570. 38. Kallela, K. (1962) Investigations on the Occurrence of Plant Estrogens Present in Finnish AIV Silage and Hay with Special References to Red Clover, Intemat. J. of Fert. 7, 4, 358. 39a. Kesler, D. J., Elmore, R. G., Brown, E. M. and Garverick, H. A. (1981) Gonadotropin Releasing Hormone Treatment of Diary Cows with Ovarian Cysts, Gross Ovarian Morphology and En- docrinology, Theriog., 6, 2, 207-217. 39b. Kesler, D. J. and Garverick, H. A. (1982) Ovarian Cysts in Dairy Cattle: A Review., J. An. Sci. 55, 5, 1147. 40. Kesler, D. J., Garverick, H. A., Caudle, A. B., Bierschwal, C. J., Elmore, R. G. and Youngquist, R. S. (1978) Clinical and Endocrine Responses of Dairy Cows with Ovarian Cysts to GnRH and PGF*, J. An. Sci. 46, 3, 719-725. 41. Kesler, D. J., Garverick, H. A., Elmore, R. G., Youngquist, R. S. and Bierschwal, C. J. (1979) Reproductive Hormones As- sociated with the Ovarian Cyst Response to GnRH, Theriog. 12, 2, 109-114. 42a. Kidder, H. E., Barrett, G. R. and Casida, L. E. (1952) A Study of Ovulations in Six Families of Holstein Friesians, J. of Dairy Sci., 35, 5, 436. 42b. Kirk, J. H., Huffman, E. M. and Lane, M. (1982) Bovine Cys- tic Ovarian Disease: Hereditary Relationships and Case Study. JAVMA, 181, 5, 474.494 VETERINARY OBSTETRICS 43a. Lagerlof, N. and Boyd, H. 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McEntee, K. and Jubb, K. V. (1957) Functional Cytology of the Bovine Adenohypophysis in Relation to Cystic Ovaries, In- temat. J. of Fert. 2, 3, 279. 49. McKay, G. W. and Thomson, J. D. (1959) Field Observations on the Treatment of Cystic Ovaries in Cattle, Canad. J. Comp. Med. and Vet. Sci. 23, 175. 50. Menge, A. C., Mares, S. E., Tyler, W. J. and Casida, L. E. (1962) Variation and Association Among Postpartum Repro- duction and Production Characteristics in Holstein Friesian Cat- tle, J. Dairy Sci. 45, 2, 233. 51. Miller, F. W. and Graves, R. R. (1932) Reproduction and Health Records of the Beltsville Herd of the Bureau of Dairy Industry, U.S. Dept, of Agric. Tech. Bull, 321. 52. Morrow, D. A. (1969) Personal Communication. 53. Morrow, D. A. (1969) Estrous Behavior and Ovarian Activity in Prepuberal and Postpuberal Diary Heifers, J. Dairy Sci. 52, 2, 224. 54. Morrow, D. A., Roberts, S. J. and McEntee, K. 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Reprod. 7, 3, 123. 59. Nakahara, T., Yamauchi, M., Kataoka, T. and Kaneda, Y. (1962) Studies on the Antihormone Against Human Chorionic Gonad- otropin in Cattle, Jap. J. of An. Reprod. 7, 4, 137. 60a. Nakahara, T., Kaneda, Y. and Yamauchi, M. (1964) Studies on the Antihormone Against Human Chorionic Gonadotropin in Cattle, Jap. J. An. Reprod. 10, 1, 9. 60b. Nash, J. G., Ball, L. and Olson, J. D. (1980) Effects on Re- productive Performance of Administration of GnRH to Early Postpartum Dairy Cows, J. An. Sci. 50, 6, 1017-1021. 61. Nessan, G. K., King, G. J., McKay, G. W., Thomson, J. D. and Bertrand, W. (1977) Treatment of Cystic Ovarian Degen- eration in Dairy Cows with Gonadotrophic Releasing Hormone or Human Chorionic Gonadotrophic Hormone, Canad. Vet. J. 18, 33-37. 62. Roberts, S. J. (1955) Clinical Observations on Cystic Ovaries in Dairy Cattle, Cor. Vet. 45, 4, 497. 63. Roberts, S. J. (1957) A Preliminary Report on the Treatment of Cystic Ovaries in Dairy Cattle by the Injection of Gonadotropic Hormones Directly into the Follicular Cyst, JAVMA, 131, 11, 510. 64. Saumande, J., LeCoustumier, J. and Marais, C. (1979) Estra- diol-17B and Progesterone in Nymphomaniac Cows, Theriog. 12, 1, 27-31. 65. Schjerven, L. (1965) Treatment of Cystic Ovarian Disease in Dairy Cattle, Nord. Vet. Med. 17, 382. 66. Schoop, G. and Klette, H. (1952) Gehaufte Sterilitat durch Oes- trogene Stoffe im Weidegras, Rept. of the II Intemat. Congr. of Physiol, and Pathol, of An. Reprod. and of Art. Insem., Vol. II, 87. 67. Short, R. V. (1962) Steroid Concentrations in Normal Follicular Fluid and Ovarian Cyst Fluid From Cows, J. Reprod. and Fertil. 4, 1, 27. 68. Staples, R. E. and Hansel, W. (1961) Luteal Function and Em- bryo Survival in the Bovine, J. Dairy Sci. 44, 2040. 69. Stoebel, D. P. and Moberg, G. P. (1979) Effect of ACTH and Cortisol on Estrus Behavior and the Luteinizing Hormone Surge in the Cow. Fed. Proc. 38, (3) 1254, Abstr. 70. Stoll, I. V. (1969) Infertility and Draining Cysts in the Bovine, Mid Atlantic States Vet. Clinic, Baltimore, Md. 71a. Tanabe, T. Y. and Almquist, J. O. (1953) Some Causes of In- fertility in Dairy Heifers, J. of Dairy Sci. 36, 586. 71b. Tanabe, T. Y. and Brofee, R. D. (1982) Treatment of Cystic Ovarian Follicles in Dairy Cows with Chorionic Gonadotropin, Theriog. 18, 5, 497. 72. Tanabe, T. Y. and Casida, L. E. (1949) The Nature of Repro- ductive Failures in Cows of Low Fertility, J. of Dairy Sci., 32, 3, 237. 73. Trimberger, G. W. (1956) Ovarian Functions, Intervals Be- tween Estrus, and Conception Rates in Dairy Cattle, J. Dairy Sci. 39, 4, 448. 74. VanRensburg, S. W. J. and DeVos, W. H. (1962) Ovulatory Failure in Bovines, Onderst, J. Vet. Res. 29, 1, 55. 75. Vereertbruggen, W. (1957) Het Behandelen van Nymphomane Runders door Intrafolliculair Inspuiten van P. U. Hormoon, Vlaams Diergeneesk, Tijdschr. 26, 1, 19. 76. White, M. E. and Erb, H. (1980) Treatment of Ovarian Cysts in Dairy Cattle, A Decision Analysis, Cor. Vet. 70, 247-257. 77. White, M. E. and Erb, H. (1982) Optimum Postpartum Interval for Screening Diary Cows for Ovarian Cysts by Rectal Palpa- tion, Cor. Vet. 72, 137-141. 78. Whitmore, H. L., Tyler, W. J. and Casida, L. E. (1974) In- cidence of Cystic Ovaries in Holstein-Friesian Cows, JAVMA, 165, 8, 693-694. 79. Yamauchi, M. (1955) Studies on the Ovarian Cyst in the Cow. IV. The Course of Recovery From Ovarian Follicle Cyst by Chorionic Gonadotropin Therapy, Jap. J. Vet. Sci. 17, 2, 47. 80. Zemjanis, R. (1970) Diagnostic and Therapeutic Techniques in Animal Reproduction, 2nd Ed. The Williams and Wilkins Co., Baltimore, Md.INFERTILITY IN THE COW 495 FAILURE OF ESTRUM, OR ANESTRUM Failure of estrum, or anestrum, in cattle is the prin- cipal symptom of many conditions that may affect the estrous cycle (see Physiology of Reproduction). It is the most common single cause for infertility in cattle. In many instances where owners or herdsmen are negligent in ob- serving their cows closely, anestrum is reported to the veterinarians when actually the condition does not exist. Anestrum in cows is observed most commonly either after parturition as postpartum or preservice anestrum, or fol- lowing service as postservice anestrum, when concep- tion does not occur. In heifers it is frequently observed as a herd problem especially during periods of lowered nutritive intake. Because failure of estrum is due to mul- tiple causes often not directly related to the endocrine system, a complete history should be obtained, a careful clinical examination of the genital tract and ovaries per rectum and vagina by a speculum should be made, and a physical examination of the cow might be necessary so that an accurate differential diagnosis is possible. If more than several animals are affected it may be a herd problem involving management and/or nutrition in which case a careful herd survey and examination of all cows and their breeding records is indicated. Unless this is done the veterinarian has permitted the owner or farmer to make the diagnosis, and treatment will be equally unreliable and erroneous. If a hormone is injected on this empirical basis neither the farmer, the animal, or the veterinarian is likely to be benefited. Fol- lowing this essential examination, the cows or heifers that fail to show estrum may be divided into two classes, cows with a functional corpus luteum, and cows without a functional corpus luteum. Cows that are found on rectal examination to have a normal functional corpus luteum present in one of the ovaries. Since cystic corpora lutea have a normal function, these are included in this class. In this class are cows or heifers that are pregnant, those with a per- sistent corpus luteum due to uterine pathology and those that are ovulating and cycling regularly but are not rec- ognized as exhibiting estrum either because it is “weak” or “silent” or because the owner has failed to observe it. Normal cows have a functional corpus luteum in their ovary 85 percent of the time. 1. Anestrum due to pregnancy—All veterinarians performing regular rectal examination on cows have had many cases in which the owner has requested treatment for a heifer or cow that fails to show estrum, only to find on examination that the animal is already pregnant. The history or the owner’s records can often be very misleading. This finding has occurred even in well-man- aged herds where accurate records are kept. This serves to emphasize the importance of a careful rectal exami- nation, including the palpation of both uterine horns to their apices, preceding treatment of any anestrous cow. It is extremely embarrassing to remove a corpus luteum or to inject an estrogen or prostaglandin to bring a cow into estrum at the request of an owner, and have the cow abort a 40- to 120-day fetus a few days later. Usually when the veterinarian tells the owner the approximate age of the conceptus the owner can recall when or how conception occurred. Only rarely is the owner at a com- plete loss to know how the conception occurred. If the cow’s genital tract feels normal and healthy and there is a possibility of the cow having been serviced within the last 30 days, it is advisable to examine the cow two to six weeks later to determine if conception occurred be- fore any treatment is given. Thus some cases with so- called anestrum may be pregnant and the corpus luteum, if palpable, may be the corpus luteum of pregnancy. One of the most common causes for prolonged anestrum is pregnancy. However, some pregnant cows may exhibit occasional signs of estrum, especially the first three months of gestation.94 In 228 lactating cows which had milk progesterone levels determined twice a week for 120 days postpartum, 34 or 15 percent of the cows were inseminated when the progesterone levels were high.86 Of these 34 cows 20 or 59 percent were probably pregnant from a prior service. Of these 20 cows inseminated when pregnant 8 or 40 percent aborted. Therefore all inseminations after the first should only deposit semen into the cervix and not into the uterus or a trained inseminator or veterinarian should decide whether to inseminate the cow or not.86 2. Anestrum due to a retained or persistent corpus luteum—The retained or persistent corpus luteum is in- variably observed in association with some uterine pa- thology such as: pyometra, fetal maceration, mucome- tra, mummified fetus and other disease states causing endometrial damage and inability to produce prostaglan- dins. Retained or persistent corpora lutea rarely occur in cows in the presence of a normal nonpregnant uter- us.102-104 There is no evidence that cystic corpora lutea tend to persist longer than normal corpora lutea. The cor- pus luteum of pregnancy is nearly completely involuted by 7 days postpartum and it never persists.62,63 The most commonly observed “retained” corpus luteum occurs following breeding and conception and then 10 to 90 days later the embryo or fetus dies, is macerated, and ab- sorbed or expelled, and the cow previously thought to be, or even diagnosed as pregnant, comes back into es- trum or is examined and found not pregnant. This con- dition is spoken of as early embryonic or fetal death and496 VETERINARY OBSTETRICS may be due to infectious, hormonal, genetic, physical or traumatic causes. Luteal cysts, as described under cystic ovaries, may persist for a long period and cause anestrus by secreting progesterone resulting in plasma concentra- tions similar to those occurring in diestrus. (a) Retained or persistent corpus luteum associ- ated with gross uterine pathology. Retained, imbed- ded, or persistent corpora lutea are associated with pre- service or postservice pyometra, fetal maceration, mummified fetus and rare cases of mucometra.72 A few heifers have been observed that failed to show estrum and on examination had functional corpora lutea and a normal uterus. When these corpora lutea were removed the heifer came into estrum and another corpus luteum developed. (See Figure 117.) This CL also persisted for months and the heifer remained anestrus. The histo- pathological findings in these heifers after slaughter re- vealed an absence of endometrial glands and in one heifer a lack of caruncles. In heifers or cows with a uterus uni- cornis if the corpus luteum develops on the ovary cor- responding to the missing horn, a long period of anes- trum may result if there is not sufficient normal endometrium or endometrial glands in the cystic apex of the defective horn to exert a luteolytic effect on the CL on that side. (See Figure 116.) This may result in a per- sistent corpus luteum without a pregnancy occurring. Cases of anestrum associated with uterine pathology and Figure 116. Anestrus Associated with Segmental Aplasia of the Bo- vine Uterus, Mucometra, Mucocervix and a Retained C. L. Figure 117. Congenital Absence of Endometrial Glands in a Heifer with Anestrus and a Retained C. L. a functional corpus luteum, as well as pregnancy, are probably caused by the failure of the release of prosta- glandin from the endometrium or endometrial glands.36 As described previously a prolonged persistence of the CL can also be produced by hysterectomy. In these pathological cases rectal examination of the uterus will usually reveal the cause of the failure of estrum. In most of these conditions that exist for several months or more the corpus luteum becomes more centrally located in the ovary and may be more difficult to palpate. These con- ditions have been described already or will be described later under pathologic conditions affecting the uterus. Manual removal of the retained or imbedded corpora lu- tea in these cases is usually difficult and requires more pressure than do corpora lutea that have been present a shorter length of time. Injection of a luteolytic dose of prostaglandin will in most cases involute the CL, evac- uate the uterus and reestablish the estrous cycle. Without a routine pregnancy examination these conditions are likely not to be diagnosed until 6 to 8 months after breeding because the cow is believed safely pregnant. In most pyometra cases secondary to retained placenta and a postpartum metritis the condition is usually characterized by a mucopurulent vaginal discharge and a failure of es- trum following calving. Most cases of mucometra are characterized by chronic follicular or luteal cysts and anestrum and an absence of a normal corpus luteum. WhenINFERTILITY IN THE COW 497 mucometra is associated with slight or moderate ana- tomic defects of the genital tract, the estrous cycle is regular and normal developing, mature, and regressing corpora lutea are present. Mucometra with a persistent corpus luteum might rarely follow early embryonic death. Occasionally these conditions may recover sponta- neously but most would exist for months without estrum unless diagnosed and treated. In diagnosing and treating cases of retained corpora lutea an accurate breeding his- tory is often helpful. (b) “Retained” corpus luteum associated with early embryonic or fetal death—This condition is actually not a true “retained” corpus luteum but is a corpus lu- teum of a pregnancy that terminated early and was not recognized as an abortion. If because of infection or de- fective development, the embryo dies early, before the middle of the cycle, then estrum occurs at its usual in- terval; but when the embryo succumbs later, the onset of the next estrum is delayed. In many of these early embryonic deaths under 90 to 120 days, the fetus or em- bryo is so small it may not be seen when it is aborted, or it may remain and macerate in the uterus and further delay the onset of estrum until the trophoblast dies and is resorbed by the uterus. In this condition the so-called “retained or persistent” corpus luteum and anestrum al- ways follow a breeding after which conception and preg- nancy are not diagnosed or recognized. If early embry- onic deaths are suspected as a herd or individual cow’s problem, examining the uterus and ovaries and/or de- termining the concentration of progesterone in the milk or plasma 21 to 23 days after service may aid the di- agnosis. (See Pregnancy Examinations.) The cow usu- ally comes in estrum spontaneously after the embryo or fetus is expelled or resorbed. The condition has been commonly observed in trichomomoniasis, vibriosis and trauma to the early embryo by rough manipulation of the uterus. Defective sperm or ova may result in an imper- fect zygote that succumbs 15 to 90 days or more after conception and produces a similar condition of a delayed estrum following breeding. This condition of early em- bryonic deaths has been studied by workers associated with artificial insemination and is described under repeat breeder cows. There is a marked difference between the percentage of cows actually pregnant and the percentage of cows apparently pregnant on nonreturns at 28 to 35 days after artificial insemination and at 60 to 90 days after insem- ination. This discrepancy is in part due to early death of the embryo or fetus and largely due to failure to observe estrum after an infertile service. The condition has been erroneously described clinically as “persistence or reten- tion” of the corpus luteum. The following comparison has been given between re- ported nonreturns on 4,286 cows after first insemination and actual pregnancy diagnosis by rectal examination.10 Number of Days After First Insemination Reported Non-Return Percentages Actual Percentage of Cows Pregnant Percentage Difference 30-60 67.8 52.9 14.9 60-90 58.4 52.9 5.5 90-120 55.7 52.9 2.8 Thus a decline of 23.2 percent from cows supposedly pregnant at 30 to 60 days to cows actually pregnant at 90 to 120 days after the first service was reported. The figures reported may be a little higher than present fig- ures because antibiotics were not added to the semen and vibriosis was not being controlled before 1949. On data based on about 44,000 cows in 1954 the difference be- tween cows apparently pregnant according to 28 to 35 day nonreturns, and actual pregnancies at more than 180 days was about 16 percent and the difference between cows apparently pregnant at 60 to 90 days, as based on nonreturns, and actual pregnancies at more than 180 days was 6 percent.29 By employing nonreturns to service, es- trus and cyclic milk progesterone patterns, the embry- onic mortality rate between 28 and 75 days after breed- ing was an estimated 7.2 to 12.5 percent. Failure to detect estrus following an unsuccessful insemination was the major reason for the 22.9 percent delayed returns to es- trus.50 In a study of Israeli-Friesian cattle an 8.5 percent embryonic mortality was reported between 20 and 50 days postservice.76 Thus this postservice anestrus which oc- curs in 40 to 60 percent of cows in a herd103 is comprised of both a smaller component of early embryonic death and a larger component of failure to observe subsequent estrus periods.94 In a fertility study of nearly 10,000 Hol- stein cows in 125 herds in Northeastern U.S., in 1975,823 the apparent incidence of unobserved postservice anes- trus was greater than preservice anestrus confirming the reports by Zemjanis.103 The average postpartum day for the first service was 87 days for 8800 cows when 60 days was the desired time. The interval from first to sec- ond service for 4300 cows was 41 days and for second the third service for 2000 cows was 40 days. Following service many cows, 40 to 50 percent, fail to conceive; subsequently they come back in estrum after a period usually longer than the normal estrous cycle. In some instances this may be due to early embryonic death and this delayed onset of estrum or period of anestrum may be diagnosed as “persistence” or “retention” of the498 VETERINARY OBSTETRICS corpus luteum because the cows are not known to have been pregnant, have not had a history of estrum or abor- tion, and have a corpus luteum on one ovary. About 18 percent of cows bred naturally or artificially returned to service within 28 days while about 25 percent returned to service after 28 days.83 On careful clinical examina- tion at weekly intervals on 426 cows in 22 herds this investigator found 332 that failed to come into estrum within 28 days of service; 234 of these were diagnosed pregnant and of those 12 aborted, 3 abortions were ob- served and 9 were not observed. About 48 percent of return services to artificial insemination in Kentucky oc- curred after a prolonged interval of 25 days or more.67 In the experiment station herd of cattle, of 1347 cycles following service 44.8 percent were prolonged; while of 2429 cycles not following service only 26.8 percent were prolonged. Breeding cows soon after calving was not a cause for delayed returns to estrum; on the contrary there was a tendency for the cows to come back into estrum in less than 18 days when bred at 5 weeks or less after parturition.67 The study noted that 11.5 percent of the cycle lengths were 27 to 33 days for repeat services as compared to 3.3 percent of the cycles not following ser- vice. Thus early embryonic deaths after service may be the cause of so-called “retained” corpora lutea. (3) Anestrum due to subestrum, “weak” or “si- lent” estrum, occurs fairly often, according to many veterinarians on the basis of clinical observations. The cow may not show estrum for 30 to 120 days or longer after calving even though closely observed by a com- petent herdsman; but on rectal examination during this period the cow shows evidence of having ovulated by the presence of a normal corpus luteum; or occasionally the cow may be in estrum or have just ovulated, as based on the typical changes in the genital tract or ovary and by the presence of estrual mucus or metestrual bleeding. Subestrus, weak estrus, or silent estrus, occurs more frequently between calving and 60 days than it does 60 days or more after parturition. In 286 ovulations 78 or 27.3 percent were silent.47 The incidence of “silent” es- trus during the first 60 days after calving was 44.3 per- cent of 140 ovulations, but only 11.0 percent of 146 ovulations were “silent” during the period of 60 to 308 days. Of cows examined that had not come into estrus within 28 days of breeding and were not pregnant, 31 or 28.2 percent exhibited “silent” estrus or subestrum.83 Ovulation in all cows occurred at an average of 25.4 days earlier than the first postpartum estrum and 68 per- cent of the cows showed at least one “quiet” ovulation or “silent” estrus before the first clinically apparent es- trus.22 Older cows, over 5 years of age, tended to show longer intervals between parturition and estrum than did the younger cows. A high incidence of “silent” estrous cycles, when behavioral signs of standing estrus were not observed, were reported during the postpartum pe- riod in the cow.56 62 63 Seventy-seven percent of the cows at the first estrus after parturition, 55 percent at the sec- ond estrus, and 35 percent at the third estrus exhibited “silent” estrus. By 90 days after parturition over 93 per- cent of the cows had shown visible signs of estrum. Sev- enty-four percent of 53 heifers that reached puberty exhibited “silent” estrus at the time of their first ovu- lation, 43 percent at the time of the second estrus or ovulation and 21 percent at the time of the third estrus.60 About 10 percent of the ovulations during the service period were “silent.”9041 These periods were observed in 16.5 percent of the cows. From these reports it is ev- ident that “silent” estrum is probably a common cause of anestrum and loss of time in rebreeding animals. This condition is clinically characterized by failure of estrum. These animals when turned out twice a day and closely observed for 20 to 30 minutes and teased by a bull will fail to show standing estrum even though they are ovu- lating. In some cases occasional, mild signs of estrum might be shown. Of 20 cows bred artificially during “silent” estrum 65 percent conceived.91 The time of in- semination was based on repeated rectal examinations of the ovaries and palpation of the maturing follicle. Recent studies have shown that these former reports may be in- correct if cows are observed continuously 24 hours a day or by closed circuit television.48 94 In this latter study al- though the time of first, second and third ovulations after calving were similar to the above or 19.5, 44.4 and 63.7 days, respectively, an observed estrus was detected in 50 percent, 94 percent and 100 percent of the respective three ovulations. Thus “silent” estrus, a term used by the former authors, possibly should have been “unob- served or undetected” estrus. The former is more ac- ceptable to the herdsman! More postpartum silent es- trous periods occurred in nursed cows than in cows milked twice a day. The interval from calving to first estrus was 30 days longer in nursed cows than in milked cows; the interval from the formation of the first CL to the first estrus was 30 days in nursed cows and 17 days in milked cows. The interval from calving to the first CL was 53 days in nursed cows and 36 days in milked cows.97 The physiologic basis for the failure of typical symp- toms of estrum to accompany ovulation is not known but a lack of sufficient secretion of estradiol by the mature and secondary follicles or due to a need for a higher threshold of estrogen in the central nervous system of certain individuals at certain times to produce the ner- vous symptoms characteristic of estrum and acceptance of the bull is questionable since all ovulating cows haveINFERTILITY IN THE COW 499 an increased concentration of estradiol in their plasma during estrus. Progesterone can potentiate the action of estrogens in bringing a cow into estrum.77 Standing es- trus may require a regressing CL still producing some progesterone to result in good signs of estrus. A recent study showed hormone levels in plasma at the onset of estrus had no effect on intensity of estrus or on concep- tion rate. Estrous activity was greater in the morning than in the evening, in the winter than in the summer and in barn-housed cattle than those in free-stalls or on pasture. Conception rates were similar in cows bred at the time estrus detection and 12 hours later.25b Certain breeds of cattle have a hereditary predisposition for “weak” es- trums whereas other breeds exhibit more marked estrous symptoms.52 In this country the author has observed that the Guernsey and Holstein breeds are more apt to have a predisposition toward “weak” heats than is the Jersey breed.19 Certain sire lines in a herd of Holstein cows exhibited a significantly higher incidence of silent heats or quiet ovulations than others indicating that a genetic variation affects this condition.51 Cows in advanced age, arthritic cows, cows with footrot, untrimmed feet or other painful diseases may not show good signs of estrum. They may refuse to mount, or to stand to be mounted, and separate themselves from the rest of the herd. Cows on slippery concrete floors, especially during the winter months, may not exhibit signs of estrus by standing to be mounted or by mounting. Placing cows in a dirt-floor- ed lot or area greatly facilitates estrus detection. (4) Anestrum due to unobserved estrum is, on clin- ical examination impossible to differentiate from “si- lent” estrum, subestrum, or “weak” estrum. Estrous pe- riods are usually about 18 hours in length but in some cattle, especially heifers, estrum may be only 8 to 12 hours long. In tropical countries and the southern states the length of the heat periods in the English and dairy breeds is shortened to 12 to 13 hours and in Zebu cattle estrum lasts only 5 to 8 hours. A study of Canadian cows by continuous monitoring with a television camera showed the duration of “standing” estrus to be 7.5 to 10.1 hours depending on the number of cows in estrum at the same time. About 70 percent of cows exhibited signs of estrus from 6 PM to 6 AM or during the night hours.48 Since most cows are observed in estrus several or more hours after the onset of estrus and since the highest conception rate occurs near the middle or toward the end of estrus, it is recommended to breed cows soon after they are ob- served in estrus rather than 12 to 24 hours later. If a cow is still in estrus 12 hours after service she should be rebred.28 During the middle of the day, especially in hot climates or when cows are eating are poor times to ob- serve cows for estrus. When environmental temperatures were maintained at 75 to 95° F it was shown that the duration of the estrous period was 11 hours compared to 20 hours in heifers maintained at atmospheric tempera- tures of 62 to 65° F.34,89 Under the former stress con- dition the intensity of estrous signs were also reduced so that the incidence of anestrus was 30 percent when signs of estrus were watched for twice a day. In the other groups without heat stress the incidence of anestrus was only 7 to 8 percent (See Bovine Reproductive Physiology). These short periods could be missed especially if the animals were turned out of the stanchions or watched only once a day. This problem and “weak” estrums are difficulties which must be overcome in educating farmers to artifi- cial insemination. If an owner or herdsmen does not watch his cows carefully at least 20 to 30 minutes 2 to 4 times a day in a yard where the cows are free to move about, many heat periods will not be observed. In the northern latitudes artificial lighting early in the morning and late at night is necessary to adequately observe cows for es- trus. Cows exhibiting “weak” estrum or subestrum are fertile but often because of poor timing of the insemi- nation, conception rates are lower. The owner or herds- man should be acquainted with the estrous symptoms of each cow, so that if certain cows show mild or slight symptoms these can be watched for and recognized. In general the larger the herd or the greater the number of cows per man, the greater the incidence of anestrus. Due to laziness, ignorance, neglect, carelessness or inability to set priorities, some farmers cannot use artificial in- semination service because they fail to observe and de- tect estrum in many of their cows. After trying artificial insemination these farmers usually resort to the earlier method of allowing a bull to run with the herd. Anestrum due to unobserved estrum was reported in 39 percent of 5848 reproductive cycles in dairy cows, 11 percent were in preservice cycles and 28 percent were in postservice cycles.101'104 These cases were called func- tional anestrus and 90 percent of all anestrous cycles were in this category. Only 10 percent of the anestrous cycles were due to pathological or organic causes. Twenty per- cent of postservice anestrous cows were not pregnant even though the herdsman assumed them to be pregnant. The economic importance and monetary loss due to unob- served estrum was calculated to be 30 and 42 production days for preservice and postservice anestrus, respec- tively. If this loss was valued at $.50 or $1.00 per day, the annual loss for each dairy herd for the 13 dairies comprising the 2600 cattle in the study was $750 or $1500, respectively. Herds in which continuous observation, 24 hours a day, was maintained 90 to 95 percent of the cows were ob- served in estrus within a 24 day period.48'94 Only 4 to500 VETERINARY OBSTETRICS 10 percent of the cows were anestrous without detectable abnormalities. In the average fairly well-managed herd only 40 to 60 percent of the estrous periods are noted. With the advent of larger herds and fewer caretakers per herd the incidence of anestrous due to unobserved estrus continues to rise and has become the greatest single cause for infertility in large diary herds being bred artificially. The prognosis in cases of failure of estrum or anes- trum cows found to have a normal functional corpus lu- teum on repeated rectal examinations depends upon the cause. In anestrum due to a persistent corpus luteum caused by some uterine pathology the prognosis is good in fetal mummification and early embryonic deaths. While in pyometra the prognosis is fair to good and in late fetal maceration, mucometra or a congenital absence of uter- ine glands in the endometrium the prognosis is guarded to poor. The longer the condition, such as pyometra, has existed the poorer the prognosis for the future breeding life of the cow. Conception following early embryonic deaths may be delayed, especially in diseases such as vibriosis. In “weak,” “silent” or unobserved estrum the prognosis is usually fair to good as close observation re- duces the incidence of anestrus due to this cause. Treatment of failure of estrum or anestrum in cows should be based on a careful differential diagnosis, often requiring careful recordings of repeated rectal exami- nations. The treatment of retained or persistent corpora lutea due to uterine pathology such as pyometra, mucometra, mummified or macerated fetuses will be described later in this text. These conditions often respond to the injec- tion of 40 to 100 mg of stilbestrol or 4 to 10 mg of estradiol, repeated in 2 to 4 days if necessary for several injections or prostaglandins to cause an involution of the retained corpus luteum, the evacuation of the uterus, and the reestablishment of the estrous cycle. In a few cases manual removal of the corpus luteum, as described be- low, may be indicated but the dangers associated with this treatment, especially in pyometra, greatly limit this mode of therapy. The use of prostaglandin F2a (Luta- lyse), 20 to 35 mg, or cloprostenol (Estrumate), a pros- taglandin analogue, 250 to 500 ug. intramuscularly are preferred treatments over estradiol preparations such as estradiol cypionate, and possibly estradiol valerate, to cause luteolysis of the corpus luteum, evacuation of the uterus and produce normal estrous cycles. Luteal cysts causing anestrus and elevated progesterone levels in blood plasma may be treated with GnRH, HCG or prostaglan- dins as described under cystic ovaries, usually with ex- cellent results. Treatment of persistence of the corpus luteum due to long-standing pyometra and fetal maceration with the presence of bones in the uterus may occasionally result in the restoration of the estrous cycle but conception usu- ally fails to occur due to the chronic uterine damage caused by the infectious process. In some instances a laparo- hysterotomy may be necessary to remove the bones from the uterus. In the rare cases of heifers with a congenital lack of endometrial glands causing the persistence of the corpus luteum, no treatment is possible. It might be de- sirable to take an endometrial biopsy or recover the uterus at slaughter so the diagnosis may be confirmed by his- topathological methods. Treatment of anestrum due to early embryonic death is usually not necessary since the embryo or fetus and its membranes are expelled, or macerated and resorbed. The corpus luteum of that pregnancy involutes and es- trous cycles are reestablished. If the latter course is fol- lowed it may require two to six weeks following the death of the zygote before estrus occurs. Detection of anes- trum due to early or late embryonic deaths, and post- service anestrum due to “silent,” “weak” or unobserved estrums requires an early accurate pregnancy diagnosis between 35 to 45 days of pregnancy and possibly a sec- ond examination in certain cows or herds with vibriosis, trichomoniasis or a high incidence of fetal mummifica- tion at 80 to 150 days or more days of gestation. As previously mentioned, examination of the genital tract and ovaries for the presence of a corpus luteum and a lack of estrus or high progesterone levels 21 to 23 days after service can provide an early presumptive diagnosis of pregnancy and an early indication of embryonic death. Because anestrum of pregnancy is expected after service many owners fail to realize the importance of early preg- nancy diagnosis to reduce the serious losses incurred due to postservice anestrus in cows failing to conceive or af- fected with early embryonic deaths.102104 Treatment of failure of estrum or anestrum, in the common instances of “weak” or subestrum, “silent” es- trum or unobserved estrum, often requires careful, ac- curately recorded examinations of the genital tract of af- fected cows, careful assessment of herd management practices, and diplomatic education and instructions for the herdsman and cattlemen. Cows or heifers with a preservice or postparturient anestrus should be examined at 50 to 60 days postpartum or at 15 to 18 months of age, respectively, if they have not exhibited estrus by that time. A variety of treatment regimens, some already suggested under the prior discussion of the etiology of anestrum, have been used. These include: (a) Improved management practices—Owners and herdsmen often need to be trained in how to observe cows for estrum. If services per conception are low (1.2) and the average number of days open are high (150) onINFERTILITY IN THE COW 501 a herd basis, estrus detection would only be 25 percent. While another herd with 2.5 services per conception, 115 days open would have an excellent estrus detection rate of 80 percent and etc.9b The signs and degrees of exter- nal manifestations of proestrum, estrum and postestrum should be thoroughly understood.3a'94 Cows to be ob- served for estrum should be grouped or turned out to- gether and watched carefully for 20 to 60 or more min- utes twice or more times per day especially during periods of activity such as before and after milking and during the early morning, evening and night hours. Observing cows during the feeding period is not satisfactory. Ob- serving cows on pasture is better than in barnyards.94 Signs of estrus in order of their importance or signif- icance include:94 (a) Standing immobile to be mounted—This is the most important single sign and observed in 79 percent of cows in estrus. Standing heat was observed in 4.5 percent of cows not in estrus and in 7.3 per- cent of standing heats were seen in pregnant cows. (b) Mounting other cows repeatedly, exhibiting both homosexual and heterosexual activity. (c) Ruffled, scraped or rubbed rump and tailhead. These signs are misleading as they persist for 4 to 6 days. (d) Group activity of sexually active cows is impor- tant especially at night. It includes cows in estrus or proestrus and nymphomaniacs. These cows often stand close together within a few feet of each other. Moving animals and driving helps the owner ob- serve signs of estrus. Don’t isolate cows in estrus from a herd as they are excellent heat detectors. (e) Restlessness—if on pasture cows interrupt graz- ing and roam around, increased activity, can use pedometers on legs but they are often lost.93 If tied, cows often remain standing rather than lie down. By using pedometers it was determined that cows in free stalls and in comfort stalls were 4 and 2.75 times respectively more active during estrus than when not in estrus.47b (f) Vulva swollen, edematous, relaxed—This is seen in only a few cows and is unreliable. (g) Stringy mucus hanging from vulva especially after mounting or lying down. This useful but seen in- frequently. (h) Sniffing and licking of vulva, flehmen reaction, also chin resting and rubbing cow on rump. (i) Tail raising and switching, frequent urination and bellowing is also seen in cows in diestrus. Thus these are all signs of estrus but each alone, except possibly (a) are not highly dependable.3a'94 Each farm must select procedures and the men to observe, record and get cows bred early in the postpartum period so calv- ing intervals of 12 to 13 months are realized. Competent, accurate recognition of all or a high percentage of es- trous periods in cows from the time of first desired breeding until after they are diagnosed pregnant is es- sential to a satisfactory herd reproductive program. Careful records of these observations on properly and easily identified cows should be made before, during and after the breeding period. The use of heat expectancy charts are very helpful if records of previous estrous periods are accurately recorded. The use of teaser or “gomer” animals will be discussed. Some owners are incapable of properly observing cows for estrum or unwilling to spend the time to do so properly. In this instance breed- ing bull(s) should be run with the herd as an economi- cally viable artificial insemination program is impossible to accomplish. In stanchion bams it is desirable to turn cows out of the barn twice or three times a day even in the winter months and observe the cows carefully. In a stanchion bam the tails and buttocks of the cows should be carefully observed daily to detect bleeding or a clear mucous discharge. In a dark bam a flashlight might prove helpful in this examination. As an aid in stimulating closer observation of cows for estrum some owners offer in- centive payments to hired men or herdsmen detecting cows in estrus and conceiving to a service at that estrus. The economic importance of a conscientious, observant herdsman or owner cannot be overestimated in main- taining a good conception rate and a short interval be- tween calvings in a herd. Heat Detection Aids or Treatment for Anestrus that may be used to supplement, not replace, careful, fre- quent visual observation of the herd include many tech- niques or practices. (a) Cattlemen have used a cheap, plastic heat detect- ing device* that is glued to the top of the sacrum of postpartum cows due to be bred and of cows after breed- ing to assist in detecting estrous periods. When a cow in estrum is mounted by another cow or teaser bull the normally white plastic device turns red due to the release of a dye due to pressure on the device by the brisket of the mounting animal.17 These detectors may be helpful to farmers or ranchers with cattle on pasture. Cows should be examined twice a day. If a detector is only partially red that cow is often not in estrus. An Australian study on pastured cattle indicated that Kamar detectors were 90 percent effective in detecting estrus vs. 56 percent by observation alone. One drawback was that about 25 per- cent of them may be lost or rubbed off by mounting. *Heat-mount Detectors by Kamar Inc., Earl D. Smith, Box 26, Steamboat Springs, Colo., 80447.502 VETERINARY OBSTETRICS These cows were usually in estrus. Some farmers use a colored tape around the tail as well as a Kamar detec- tor.94 Other farmers will use a colored marking chalk or a water-soluble latex paste on the tailhead as an aid to detect estrus. Another alternative to a Kamar detector or chalk applied to the tailhead is to apply a green water- soluble plastic paint with a roller from the first sacral to the fourth coccygeal vertebrae from calving to confirmed pregnancy. In one large herd this aid increased the de- tection of estrus before postpartum day 60 from about 62 to 95 percent.94b Conversely a study in Northeastern U.S. indicated that visual observation was 93 to 97 per- cent accurate in detecting estrus in dairy cows compared with the 82 to 88 percent accuracy of Kamar heat de- tectors.70 (b) Teaser or “gomer” bulls, nymphomaniac cows, or cull or ovariectomized cows injected with repeated, large doses of testosterone have been used to aid in detecting cows in estrus. If bulls are only vasectomized they may spread venereal diseases in the herd. Also such teaser bulls are seldom kept beyond one year and must be re- placed and there are problems when bulls are allowed to run with the herd.94 In large, artificially-inseminated dairy or beef herds in which the detection of cows in estrum is difficult, one or more vasectomized young bulls may be allowed to run with the herd. These bulls, if used properly, are very efficient in detecting cows in estrum. Young disease-free bulls can be vasectomized in the standing position under epidural and local anesthesia or they may be cast, tied, and rolled on their backs and vasectomized under local anesthesia. Using careful clean surgical technique the operator makes separate incisions through the skin and the tunics investing each spermatic cord. The hard cord- like vas deferens is separated from the plexus of coiled veins and arteries. Two ligatures are placed on each vas about 2 inches apart and 1 inch of the vas is removed. The skin incisions are closed and antibiotics are admin- istered for 4 to 5 days. Semen should be collected once a week for 3 weeks. By this time practically no sper- matozoa are in the ejaculate and those that are present are dead. Several cases have been reported where apparently properly vasectomized bulls regained their ability to fer- tilize cows. In humans sperm granulomas following va- sectomy were common and 5 of 432 vasectomy cases recanalized.73 The cut ends of the vas deferens should be fulgurized by electrocautery and the sheath of the vas deferens should be ligated or closed over the cut end of the distal portion of the vas to prevent spontaneous re- canalization. It might also be advisable for the operator to place the removed sections of the vasa deferentia into a 10 percent formalin solution and send them to a lab- oratory for histological confirmation of the removed tis- sue to prevent possible errors and lawsuits. Other methods of preparing teaser or “gomer” bulls have been described. Epididymectomy by incising the bottom of the scrotum separating the tail of the epidid- ymis from the testis, ligating the body of the epididymis and the vas deferens with nylon and removing the tail of the epididymis was recommended.65,95 This technique is probably better than the injection of a sclerosing agent into the tail of the epididymis,14 or the crushing of the tail of the epididymis with a Burdizzo emasculatome. These above methods do not prevent normal intromis- sion and the possible spread of venereal diseases such as vibriosis and trichomoniasis. However teaser bulls pre- pared by the above methods retain a stronger sexual de- sire and drive than teaser bulls prepared by various op- erations on the penis and sheath that prevent normal intromission. Operations on the penis and sheath to prevent con- ception include: (1) cutting the penis midway between the anus and scrotum and suturing it to the skin;84 (2) placing three or four stainless steel or nylon sutures into the dorsal part of the penis cranial to the scrotum and suturing the penis to the abdominal wall;33,80 (3) making a small ventral incision in the skin and prepuce two to three inches behind the preputial office, suturing the skin and preputial membrane and inserting a 3/8 inch plastic urine drain for five days, followed by the dissecting apart of the skin and preputial membrane at the preputial ori- fice and suturing the inside membrane and outside skin to make a blind pouch to contain the penis;80 (4) and incising of the skin around the preputial orifice and su- turing the orifice so it is directed laterally instead of cra- nially, so the penis on erection is also protruded lat- erally. These operations and their modifications should be performed under good anesthesia and in an aseptic manner for best results. A male pseudohermaphrodite, a nymphomaniac cow or a cow or steer treated repeatedly with testosterone49 may also be used as a teaser animal if it has sufficient sex drive. These latter animals have not been highly successful as estrus detectors.30 (See Chap. XIX, Artificial Insemination.) Bulls selected as “teaser” or “gomer” animals should have a strong, vigorous sex drive. If possible it may be desirable to turn these bulls out with the herd only for short periods in the morning and evening and then to alternate bulls to maintain their sex drive. A New Zea- land company* has marketed a marking device for bulls *Chin-Ball Mating Device, Frank Paviour Ltd., Mahana Rd. TeRapa, Hamilton New Zealand.INFERTILITY IN THE COW 503 consisting of a small square stainless steel unit contain- ing an exposed freely rotating steel ball that is fastened securely under the jaw by a special halter. The marker material comes in a variety of colors and is placed in the steel unit where it will store indefinitely. When the bull mounts a cow the marking material is rubbed in streaks down her back. These marks will last for 2 weeks but can be washed off with a detergent. One filling of the steel container is sufficient to mark 75 to 80 cows. These chin-ball markers must be kept filled with ink to be ef- fective. Occasionally a bull on pasture with a herd will select a “harem” of cows and ignore the other cows. It was reported that smearing the brisket and inside of the legs with titanium oxide and grease was more effective than the chin-ball marker.94 Some ranchers will have a bull in a pen near water, in a corral near salt or feed, or ran their cows across a fence from yearling bulls. In these instances cows in estrum will gravitate toward the male animals and be easier to pick up. (c) Drawing a milk sample from cows at the time of breeding and submitting it, with others, to a laboratory for progesterone assay is a simple and highly effective practice to determine the efficiency of a herdsman in de- tecting cows in estrus. It is also helpful in problem cows, if samples are taken 2 or 3 times a week for 3 weeks, to tell when the cow is in estrum or whether she is cy- cling. Milk samples taken at insemination and 21 to 24 days later from over 400 dairy cows in Northeastern U.S. showed that only 5.5 percent were inseminated at the wrong time, that is, when progesterone levels were el- evated.70 High progesterone levels were found in only 2.9 percent of cows in standing estrus, 2.6 percent riding other cows, 3.6 percent with roughened tailhead and 4.5 to 7.1 percent of cows that were unusually active, bawl- ing or with clear or bloody mucus on the vulva. The Kamar heat detectors were not as accurate as visual ob- servation. High progesterone levels at insemination were recorded in 12.4 percent of cows with full red Kamars and 18.3 percent with part red Kamars.70 Besides the above uses for progesterone determination on milk, it will help monitor possible embryonic deaths, determine nonpregnant cows with good accuracy (90+ percent) but not pregnant cows (80 percent) 21 to 23 days after ser- vice.32 This test for progesterone because of time re- quired for laboratory testing is not satisfactory for de- termining the time of insemination. (d) The electronic probe measurements of electrical resistance of vaginal mucus reveals low resistance at es- trus and correlated well with low milk progesterone con- centrations, visual observations of estrus and positive Kamar heat detectors.32,42 This improved probe is in- serted into the vagina every second or third day and re- sistance readings of the dorsal and ventral vaginal mucus are recorded. The instrument is cleaned and disinfected between cows and cows must be confined for exami- nation. Conception rates after insemination were similar where estrus was detected by visual examination and where estrus was detected by the probe when the cows were not seen in estrus. (e) Other tests on bovine cervical mucus such as crys- talization pattern or “feming,” glucose content, viscos- ity and pH either require laboratory tests, are laborious or not practical.30'94 Temperature monitoring to detect estrus is not yet practical.74 In the cow body tempera- tures tend to decline slightly but noticeable with the in- volution of the corpora luteum and increase slightly dur- ing estrus because of increased activity. Good breeding records, the careful maintenance of a heat expectancy chart for each cow, and frequent examination of “prob- lem” cows by a veterinarian who can predict the ap- proximate time estrum are practices to follow in many “anestrous” cycling cows and can be helpful in control- ling this common infertility problem. Rectal palpation of the genital tract and ovaries of a number of anestrous cows in a herd can readily diagnose “inactive” or non- functional ovaries without corpora lutea due to a low plane of nutrition, debility, a negative energy balance, failure to achieve puberty or a lack of estrous cycling. (f) Frequent rectal, and if necessary vaginal, exami- nations of the genital tract by a veterinarian will deter- mine the proper time to inseminate cycling cows with “weak,” “silent” or unobserved estrum. The technique for predicting the time of estrum which is based on the physiologic and anatomical changes occurring in the genital tract of the cow during the estrous cycles have been described.46,59,85,102'104 During proestrus, days 17 to 20 of the cycle, follicular growth is occurring and culminates in the mature Graaf- ian follicle.69 The corpus luteum is regressing in size, protrudes less above the surface of the ovary and be- comes more firm in consistency. The uterus is devel- oping increased tonus. On vaginal examination the last two days of proestrus the vaginal and cervical mucosa are becoming more pink, congested and edematous. The cervix becomes more relaxed and initially a cloudy and then a clear stringy mucus characteristic of estrus comes from it and collects in the anterior vagina. The cow will be in estrus within 1 to 3 days. During estrus, day 0 or 1 of the cycle, the cow is re- ceptive to the bull, stands to be mounted, and the changes described as occurring during proestrus are more prom- inent. The vulva is often edematous and relaxed. The corpus luteum is small and firm and the follicle is nearly mature, 1 to 1.5 cm. in diameter. This is the most easily504 VETERINARY OBSTETRICS diagnosed stage of the cycle. The cow should be bred. If the cow exhibits “silent” estrum rebreeding the fol- lowing day may be indicated if ovulation has not oc- curred. During early postestrum or metestrum, day 1 or 2, the follicle may be soft and fluctuating and easily ruptures on pressure. This should be avoided. In most cases ovu- lation has occurred and the site feels like a crater-like depression 1 to 1-1/2 cm. in diameter in one of the ova- ries. The uterus is less tonic but more edematous and thick-walled. The corpus luteum of the previous cycle is difficult to detect. Metrorrhagia may be observed by the presence of bloody mucus at the vulvar lips, on the tail or buttocks or by vaginal examination. This discharge may also be observed through day 3 of the cycle. A few atretic follicles may be present. During late postestrus or metestrus, days 3 to 6 of the cycle the soft small, developing corpus luteum may be palpated and is growing rapidly, 1-1/2 to 2+ cm. in diameter, and is fairly soft in consistency. The uterus decreasingly lacks tone and loses its edema. During diestrus, days 7 through 16 or 17, the longest stage of the cycle, the corpus luteum is mature, large and liver-like in consistency. The uterus is quiescent but not atonic. During this period some growth of small fol- licles occurs and results in one or more palpable follicles at 10 to 12 days that become atretic and regress by the end of this period. During this period the vaginal and cervical mucosa is rather pale and dry. The mucus is usually scant and sticky. With practice a veterinarian can develop his skills to predict the occurrence of estrus with a high degree of accuracy. The efficacy of this method was excellent. Re- peated examinations at 2 to 3 day intervals may be nec- essary. Sixty-nine percent of the cows examined showed estrus within 23 days.104 The rate of conception on the first estrus was 10 percent better than that following re- moval of the corpus luteum, 55.7 percent vs 45.7 per- cent, respectively. Because of the dangers associated with enucleation of the corpus luteum, estrus prediction and prostaglandin injection are the methods of choice for handling anestrum due to “weak,” “silent,” or unob- served estrus in cycling cows. Thus rectal palpation can readily determine if the cow is cycling, and the approx- imate stage of the cycle. Laparoscopic examination of the bovine ovaries has been described. (g) The removal of the corpus luteum by manual pres- sure through the rectal wall was formerly, 1920 through 1960, frequently employed in the treatment of anestrus in cattle when a functional corpus luteum was present. This method consists of grasping the ovary in a fold of the rectal wall between the fingers and first knuckle of the thumb and pressing over the proximal end of the cor- pus luteum and enucleating it from the ovary. Care should be used so as not to rupture the rectal wall. The best time to remove the corpus luteum was during the middle of diestrum.3 Earlier removal of the soft C.L. may result in incomplete removal, and in proestrum the difficulty of removal increases. Some advocate squeezing through the tougher vaginal wall but this is usually not necessary since most corpora lutea are not centrally located and covered by a heavy capsule as occurs in long-standing retained corpora lutea. Although removal of the corpus luteum formerly was a common form of therapy it should seldom be used and then probably as a last resort because of the possible dangers from its practice. Manual removal of the corpus luteum in cows with pyometra or other uterine infections is dangerous due to adhesions and ovaritis that may fol- low. In a removal of the corpus luteum the cow should not be pregnant or abortion will usually occur. After the corpus luteum is removed it should be dropped into the abdominal cavity and not into the ovarian bursa, where it may cause extensive adhesions. Adhesions of the ovary and, especially the fimbriated portion of the oviduct on the medial free border of the ovarian ventricle frequently follow rough manipulations even though bleeding may not be severe. Ovarian adhesions due to rough manip- ulation of the ovary was a common cause of permanent sterility.25'57'58 After removal of the corpus luteum ex- cessive bleeding may take place from the ovary and cause a large hematoma around the ovary, permanent adhe- sions, and sterility. Fatal bleeding from the site of an enucleated corpus luteum has occasionally been re- ported. The incidence of fatal hemorrhage has been re- ported to be 1:1000 to 1:9000 removals of the corpus luteum.87 The author has not been so fortunate as in his experience fatalities occurred at a rate of 1 to 300 to 500 enucleations. The method of expression of the corpus luteum had no influence on the fatalities. Removal of the corpus luteum can result in a loss of as much as 7 liters of blood into the peritoneal cavity.58,59 The removal of an embedded corpus luteum resulted in a loss of one liter of blood. In 22 to 25 cases in which the corpus luteum of the estrous cycle was removed, bleeding of one to three liters of blood was reported. In some cases the cow will temporarily develop a rapid pulse, tym- pany, and anorexia after removal of a corpus luteum. The manual ovarian treatment for anestrum was discon- tinued in experiments because the percent of conceptions showed no improvement over the controls, and further- more removal of the corpus luteum produced permanent damage in a number of cases. Manual compression of the ovary for at least 5 minutes after removal of a corpusINFERTILITY IN THE COW 505 luteum was recommended as a means of controlling bleeding. It is doubtful that epinephrine or other drugs administered parenterally will effectively prevent bleed- ing and the former drug may even be contraindicated. Many workers have reported that removal of the corpus luteum seldom results in any permanent trauma or adhe- sions; their observations were, however, only clinical. Because of these observations the author does not rec- ommend removal of the corpus luteum in cows except in rare selected cases or only as a last resort. Properly used estrogen or preferredly prostaglandin therapy will result in the involution of the corpus luteum without the dangers present in manual removal. Enucleation of the corpus luteum was followed by the same pattern of hor- mone secretion as that following the administration of a luteolytic dose of various prostaglandins, namely a sharp decline in plasma progesterone levels and a rise in LH levels.723 Because manual removal of the corpus luteum is possible only in the cow of our domestic animals, this is not a sufficient reason to employ this mode of treat- ment in the bovine species. In cows of lesser value or in cows in which the production of milk is more im- portant than the value of their offspring, the amount of damage or risk may not be great enough to prohibit the enucleation procedure. The following reports from the literature summarize the results of manual removal of the corpus luteum. (See Table 19). From this table it appears that removal of the corpus luteum usually results in observable estrum in about 50 to 80 percent of the cases within 2 to 7 days, with conceptions in 25 to 70 percent of those cows bred on the induced first estrum. In the author’s experience re- moval of the corpus luteum from normal cows will result in about 50 percent conceptions at the next service a few days later. Most cows show estrum the third or fourth day after removal of the corpus luteum. A number of workers reported that the induced estrum frequently was “silent,” or unobserved, and the animal should be watched closely for signs of estrum. Possibly this condition of “silent” estrum was the reason for the diagnosis and re- moval of the “retained” corpus luteum. If estrum is not observed the cow may be bred three to four days after the manual removal of the corpus luteum if conception is desired. If the cow shows estrum on the fifth day she should be rebred. Nearly 50 percent of normal cows thus treated will conceive. If the cow has a normal genital tract and is in anestrum due to “silent,” or unobserved heat, removal of the corpus luteum should result in a higher rate of conception on the first estrum than if the retained corpus luteum was due to an embryonic death caused by vibriosis or some other infection in which a mild endometritis may be present. These same factors would also influence the conception rate obtained after the use of hormones. (h) Hormonal therapy for anestrus—Estrogens have been shown to cause regression of the corpus luteum.20 29 The effect of estrogens on the corpus luteum is not so marked in hysterectomized heifers as in intact heifers so there is probably an interreaction with the luteolytic mechanisms in the endometrium or endometrial glands. Estrogens probably induce regression by also decreasing the level of circulating LH.20 Five mg. of estradiol val- Table 19. Summary of Selected Reports of the Manual Removal of the Corpus Luteum in Nonpregnant Cows Author Number of cows Cows observed in estrum Days estrum occurred Conceptions Wright99 51 No. 36 Percent 70 1 to 5 18, or 50% of those in estrum Hofstad44 332 203 61.1 2 to 9 59, or 29.1% of those in estrum Stalfors81 105 3 to 10 38, or 35.6% of the total treated Hancock39 70 35 50 2 to 7 10, or 28.5% of those in estrum Lindley55 54 27 50 13, or 24.1% Gibbons35 155 98 64.9 1 to 15 51, or 52.1%, on first service Teige and Jakobsen 2746 62.5 1 to 7 49.7 to 58.7%506 VETERINARY OBSTETRICS erate given as a single dose intramuscularly on the third or fourth to eighth or ninth day of the estrous cycle caused luteal regression in 17 to 20 heifers with 15 showing estrum before day 17 of the cycle.96 Seven of 10 heifers injected on days 15 or 16 of the cycle developed large cystic ovaries and many developed signs of nymphoma- nia. Other forms of estrogen caused a similar regression of the corpus luteum. The author has confirmed the ef- fects of 5 to 10 mg. of estradiol valerate in inducing regression of the corpus luteum. Estradiol cyclopentyl- proprionate (ECP) as a single intramuscular dose to cause luteolysis has not proven to be as effective as estradiol valerate or the prostaglandins.752 He has also produced luteal regression with 40 to 100 mg. of diethylstilbestrol but this tends to require a second or third injection at 48 hour intervals. One or possibly two injections of 3 to 10 mg. of estradiol at three day intervals or estrone, 5 to 15 mg., in a similar manner also will induce luteal regression either during metestrus or diestrus or in cases of retained corpora lutea associated with pyometra, mummified fetus or mucometra. In pyometra high and prolonged doses of estrogens such as 100 mg. of repos- itol stilbestrol may result in abnormal motility or peri- stalsis of the oviduct resulting in the introduction of in- fectious organisms from the uterus to the area of the ovarian bursa or fimbria of the oviduct causing ovaritis and adhesions even in cases where no ovarian manipu- lations were made. Cystic ovaries may occasionally fol- low estrogenic therapy. These occur most commonly when estrogens are given in late diestrum or in proestrum. They are rare in cases of retained corpora lutea. Large doses of greater than 4 mg. of estradiol and 40 mg. of stil- bestrol are more apt to result in cystic ovaries than are smaller doses of estrogens. Most earlier studies on the use of estrogens for the treatment of anestrus were uncontrolled and empirical. Factors that were not considered in most studies were the cause for the failure of estrum or the type of anestrus; the high rate of spontaneous recoveries and conceptions in cows with normal estrous cycles and genital tracts but having “silent,” “weak” or unobserved estrous periods; the time following treatment that estrus and conception occurred, and whether normal ovulation occurred at that estrus or whether the signs of estrus that immediately followed the injection were due to the estrogenic hor- mone. Even spayed cows will exhibit estrus after an in- jection of an estrogen! Estrogenic hormones do not pro- duce ovulation except low doses in late proestrus or very early estrus that simulate the rise in blood concentrations due to production of estrogens from the Graafian follicle causing the LH surge. The use of low doses of estrogens or estrogens and progesterone a day or two before an expected estrus to improve the external signs of estrus has not proven of value and may lower the conception rate. Although estrogens have been widely used in the past in an empirical and haphazard manner for the treat- ment of anestrus, reports indicate that this type of ther- apy is of no, or questionable, value and may actually reduce the conception rate compared to heat prediction, removal of the corpus luteum or injection of a luteolytic dose of prostaglandin. Although prostaglandins either Lutalyse (PGF2a) 20 to 30 mg., or Estrumate, cloprostenol (a prostaglandin analogue) 250 to 500 ug or others are commonly used to produce luteolysis or involution of a functional or ma- ture corpus luteum from day 6 to day 16 of the estrous cycle, or a persistent C.L. associated with uterine pa- thology such as pyometra or mummified fetus or for a luteal cyst. The use of such products in lactating cows have now been approved in the U.S. Fortunately the prostaglandins are shortlived and are rapidly broken down so the drug or its metabolites are only present at very low levels in the milk by the second milking. An ade- quate dose of prostaglandin or its analogue will act rap- idly in involuting the C.L., causing a rapid cessation of progesterone production. The onset of the next estrus, as with the manual removal of the corpus luteum, occurs within 3 to 5 days, range 2 to 7 days. Giving two doses of prostaglandin or its analogue 10 to 12 days apart will cause nearly all healthy, cycling cows to come into es- trum within 3 to 5 days. As mentioned earlier in this Chapter treated cows may be artificially inseminated when estrum is detected or by breeding twice AI at 72 and 90 hours or once about 80 hours after the injection. (See Estrus Synchronization.) If routine rectal examinations are performed by a veterinarian in cows during the post- partum period and anestrum due to unobserved estrum in cycling cows is a problem, selected animals may be treated during diestrus. Estrus is thus synchronized so artificial insemination and early conception is possi- ble.75c (See Estrus Synchronization with Prostaglandins.) A more desirable procedure than this is to establish an effective breeding program including careful observa- tions and properly timed breeding of cows rather than relying on hormones for the detection of estrus. Re- peated treatments of prostaglandins in a cow have not been shown to be contraindicated as is manual removal of the corpus luteum. Administration of prostaglandins prior to day 6 after estrus or in cows with follicular cysts or with “inactive” ovaries due to debility will be inef- fective in establishing a normal estrous cycle. Estrus synchronization by using progesterone, pro- gestogens, estradiol valerate, prostaglandins F2a, clo- prostenol (a prostaglandin analogue) or a combination ofINFERTILITY IN THE COW 507 these drugs as described earlier in this chapter may aid in the detection of estrum in a similar manner as removal of the corpus luteum. With estrous synchronization good management is still necessary to detect estrus for proper timing of artificial insemination. Conception rates im- mediately following estrous synchronization are usually lower than normal if progesterone or progestogens have been employed unless the hormone can be removed from the body promptly (See Estrus Synchronization). Since so-called “anestrous” cows with normal uteri and corpora lutea on the ovaries are probably cycling regu- larly most or all treated or untreated cows will show an observable normal estrus within 30 days. This probably accounts for the many early reports of successful treat- ments for anestrum in cattle. At present it appears that most types of anestrum except possibly underfeeding and gross pathology of the uterus, cervix, or ovaries are self- limiting and that recovery is usually spontaneous. For this reason the author firmly believes that hormone treat- ment or removal of the corpus luteum for correction of most cases of anestrum is of secondary importance to an accurate diagnosis. During the past 25 years the author has seldom relied on endocrine therapy to relieve anes- trum which is a symptom most commonly associated with unobserved estrums. Hormones are used to correct uter- ine pathology associated with a persistent corpus luteum and for treating luteal and follicular cysts causing anes- trum. Anestrus cows with small or inactive ovaries with no functional corpus luteum palpable per rectum. These cows together with pregnant cows and cows with retained corpora lutea associated with uterine pathology are non-cycling cows. These non-cycling dairy cows comprise about 10 percent of all anestrous cows.104 In beef cattle herds on range this percentage may be larger due to nutritive deficiencies especially in postpartum heifers. (1) Due to “silent” or subestrum, or due to unob- served estrum, cycling cows may during the period of one to two days before, during, and one to three days after estrum, have only a small corpus luteum that might lead one on a single rapid examination to a diagnosis of anestrum due to failure of ovarian activity or nonfunc- tional ovaries. Careful examination usually reveals the uterus to be tonic and erect, a condition not seen in true anestrum or failure of the estrous cycle. If the ovaries are examined before ovulation the mature follicle and the regressing firm C.L. may be palpated, or if soon after ovulation the site of ovulation or a slight crepitation characteristic of an early developing corpus luteum may be felt. The corpus luteum of the previous estrous cycle is usually palpable but small. A vaginal examination with a speculum and light is often essential since the presence of hyperemia, relaxation of the cervix, and typical va- ginal mucus of estrum is indicative of estrum; and the presence of blood in the vaginal mucus indicates that ovulation occurred one to two days previously. It is not unusual in examining a number of normal, well-nour- ished cows that have a history of failure of estrum to find one or more of these cows approaching, in, or just over, estrum. This fact may be missed by a hasty ex- amination especially if a speculum examination of the vagina is omitted. Cows in proestrum, estrum or very early metestrum should be bred. Cows in metestrum after ovulation has occurred should be noted on the heat ex- pectancy chart and watched closely 18 to 20 days later. Cows in anestrum due to a failure of the estrous cycle caused by nutritive deficiencies or debility from other causes; cows with cystic ovaries; and occasionally cows with such miscellaneous conditions including freemar- tinism, hypoplasia of the ovaries, ovarian tumors, and pituitary disturbances comprise this group of cows. (2) Anestrum secondary to debility or marked loss in weight. Any severe and chronic adverse or stress con- ditions that affect the animal’s body will produce an ef- fect on the reproductive system, usually by causing a cessation of the estrous cycle and anestrum if the animal is not pregnant; or in more severely debilitating condi- tions, possibly causing abortion if the animal if preg- nant. Reproduction is a “luxury” function of the body. If “stress” due to any cause is severe enough, estrous cycles and reproduction cease. The adverse debilitating conditions that suppress or stop the estrous cycle and produce anestrum are: (a) A low plane of nutrition due to a lack of suffi- cient intake of carbohydrates, proteins, and other ele- ments necessary to maintain body weight may cause a failure or delay in the onset of puberty or the onset of the estrous cycle following parturition. Energy defi- ciency or negative energy balance is common in high- producing cows the first 20 days after calving. Ovulation and luteinization occurred about 10 days after the energy balance was returning to a positive balance. To prevent longer calving intervals in high-producing cows, feeding of large amounts of energy is essential early in the first third of lactation.230 Cows exhibiting estrus before 30 days postpartum were more fertile with fewer services per conception, 2.29, than cows with no heats in this period, 2.63.89c (See Nutritional Causes for Infertility.) This condition is seen most often in heifers maintained on poor hay or on poor pasture or range. The incidence of “win- ter sterility” in England characterized by anestrum var- ied from 5 percent around Cambridge to 50 percent in the Yorkshire Mountains, where cattle were kept in cold,508 VETERINARY OBSTETRICS dark bams and fed poor hay.38 Heifers fed on a high level of nutritive intake reached puberty and developed estrum at an average of 9 to 10 months of age, whereas heifers fed on a lower nutritive level did not reach pu- berty and estrum until 16 months or more of age.13,78 These latter heifers were maintained at optimum envi- ronmental conditions except for the level of feeding. The various nutritive factors that adversely affect the estrous cycle may also include severe nutritive deficiencies of phosphorus, cobalt, iron, copper and possibly other trace elements. When these substances are lacking, anorexia and debility, with impairment or suppression of the se- cretion of the gonadotrophic hormones by the pituitary, may develop. It is well known in humans that starvation causes amenorrhea and a cessation of the menstrual cycle before other body disturbances appear. In rats a loss of 15 percent in body weight may stop the estrous cycle. This was illustrated in cows during an experiment on the effects of a sodium chloride deficiency.1 When this com- mon element was withheld for long periods the effects became very evident after calving. Lactation caused rapid loss of weight because the appetite was poor. Milk se- cretion declined and ceased. The cows became cachectic and failed to show estrum. On examination the ovaries were found to be small and inactive; an occasional small 1 cm. follicle was palpated. Estrum did not return until salt was supplied and the appetite, nutritive state, and body condition improved. Most practicing veterinarians have observed anestrum on farms where cows and heifers are thin and poorly fed. In a survey of 1533 cows in 28 herds in New York State, carotene, vitamin A, calcium, phosphorus, and iodine deficiencies did not contribute to sterility.40 Inasmuch as reduced hemoglobin, below 9 gm. per 100 ml. of blood, was noted in all anestrous cows, cobalt and copper de- ficiencies may have been a factor. In heifers or cows that are in a fair state of nutrition but are exhibiting anes- trum, the condition may be due to a simple phosphorus deficiency, or a phosphorus and a protein or carbohy- drate deficiencies. A herd of dairy cattle deficient in phosphorus intake was described but anestrus was not observed in the deficient cattle in this herd.61 Blood lev- els below 3 mgm. percent usually indicate a phosphorus deficiency.61,92 Failure of estrum with non-functional, in- active or “smooth” ovaries is observed most often during the winter months in the northern part of the country in cows on poor and inadequate amounts of feed. In the southern and western part of the country where the an- imals are on pasture most of the year the condition is observed most commonly during the dry, late summer pasture season when available feed is greatly reduced. It may also be observed under drouth conditions. A de- lay in the occurrence of estrus after parturition especially in range beef heifers on a low level of TDN or energy intake prior to or after parturition has been report- e(j 4,13,21.97,98 j^is was also associated with a lower con- ception rate after estrus occurred. Heavy lactation, with or without ketosis, will often result in the rapid loss in body weight and if this is extreme, cessation of the es- trous cycle will occur. If the loss in weight after calving is more gradual, an estrum or two may occur before anestrum develops. In lactating cows showing anestrum of nutritional origin, milk production is usually lowered. Anestrum due to low nutritive intake is usually charac- terized by the fact that a large number of cows or heifers on a farm show the same symptoms. Examination of 4 or 5 animals that fail to show estrum will usually reveal small, atrophic, inactive ovaries. (See Figure 117.) No corpora lutea are palpable. The uterus is usually small, lacks tone, and is doughy and flaccid. On vaginal ex- amination the mucosa of the vagina and cervix is pale and dry. Repeated examinations reveal no change in the reproductive organs. The affected animals are usually thin and have rough hair coats and dry feces. (b) Chronic or debilitating diseases, by causing a de- creased appetite, may result in failure of estrum due to a marked reduction of body weight. Examples of these diseases or conditions include severe mange, lympho- cytoma, severe chronic traumatic gastritis, chronic se- vere pneumonia, Johnes disease, actinomycosis that in- terferes with eating, either severe external or internal parasitisms, including liver fluke infection,333 severe suppurative processes such as suppurative arthritis sec- ondary to foot rot with a secondary severe debility, ad- vanced tuberculosis, hyperkeratosis, anaplasmosis, and other similar diseases and conditions. If the cow re- covers from the disease or its effects are alleviated and appetite and body condition returns,^the estrous cycles will be reestablished. (c) Senility or old age with loss of teeth and inability to masticate properly, especially in older lactating cows, is a cause of loss of weight, debility, and anestrum or failure of estrum. In extremely old cows, 16 years and older, anestrum may rarely be associated with a severe reduction in the number of oocytes in the ovary as in menopausal women. (d) Seasonal influences—especially environmental temperatures, sunlight, and exercise apparently play a lesser role than does nutrition on the estrous cycle and estrum. Failure of estrum or anestrum in cattle has often been observed in cows and heifers closely confined in dark stables and allowed little or no exercise. This may be compounded by a lack of observation and a lack of proper care and nutrition. In the northern part of theINFERTILITY IN THE COW 509 country where cows are confined during the winter months, even though the cow is polyestrous the best con- ception rates occur in May, June, and July whereas the poorest breeding months are December, January, and February. This is undoubtedly a reflection of the amount of sunlight and its effect on the pituitary as well as the feeding levels, amount of exercise, type of feed avail- able and closeness of observation for estrum. During the cold winter months additional nutritive energy is re- quired by animals to maintain body temperature and in heifers an added requirement is necessary for growth. Excessive heat stress over long periods of time may cause anestrum, a shortening in duration and intensity of estrus and an increase in incidence of “silent” heats.89ab Five of 6 two-year-old heifers developed anestrus and cessation of the estrous cycle after being kept for 5 weeks at a temperature of 90° F and 60 percent humidity. Be- sides these effects on the estrus cycle and periods, ex- cessive heat and humidity greatly lowers conception rates and production in dairy cows in tropical climates during the summer months. The use of shade, evaporative cool- ing and partial air-conditioning greatly reduces or alle- viates these adverse effects of heat stress.89b (3) Cystic ovaries, as reported previously, are char- acterized externally by failure of estrum or anestrum in about 25 to 75 percent of the cases. On rectal exami- nation one or more follicular or luteal cysts are found. The uterus is usually doughy and flaccid and may be atrophied. The mucus in the vagina is tenacious, and varying degrees of edema of the vulva and relaxation of the pelvic ligaments occur due to prolonged estradiol concentrations in the blood plasma. Treatment consists of injecting luteinizing hormone (LH) or GnRH or pros- taglandins for luteal cysts. Some cases of mucometra are associated with cystic ovaries and long-standing anes- trum. This condition might be confused with pregnancy unless a careful examination is made. Another rare con- dition the author considers as also associated with pro- longed cystic ovaries and anestrum is characterized by a greatly enlarged and dilated cervix filled with copious amounts of tenacious, tough mucus similar to the mucus of a cervical seal of pregnancy. This latter condition may also have mucometra along with the cervical lesion. (4) Miscellaneous conditions characterized by anes- trum or failure of normal estrum with no corpus luteum are generally uncommon and sporadic in the United States. These may include occasional cases of: (a) Non-functional or “smooth” ovaries may occa- sionally be observed in apparently well-nourished older cattle in good condition the first 2 to 4 months after parturition when the level of lactation is high. Cows stressed at the period of calving by the occurrence of a disease process such as retained placenta, dystocia, milk fever, ketosis, mastitis, twins and other debilitating dis- eases had a delayed onset of the estrous cycle of an av- erage of 34 days compared to 15 days for cows with a normal parturition. Seven percent of the cows and 3.99 percent of the estrous cycles studied were characterized by a varying period of anestrum with “smooth” or non- functioning ovaries.91 The uterus is flaccid and lacks tone. Spontaneous recovery usually occurs. This condition is probably due to a reduced level of nutrition associated with a definite loss in weight. When production and en- ergy intake are equalized, the estrous cycle will occur. (b) Freemartinism may be a rare cause of anestrum in heifers purchased from unknown sources or raised by farmers who did not know that 90 percent of heifers bom cotwin to bulls are sterile. These freemartins are usually steer-like in appearance. They have a small vulva with a coarse tuft of hair and a prominent clitoris. On rectal examination the uterus and ovaries usually cannot be palpated except as thin or small remnants of the normal structures. Vaginal examination will reveal an undevel- oped vagina cranial to the vestibule. (c) Congenital bilateral hypoplasia of the ovaries is rarely observed in the United States. Several related cat- tle were described with a complete absence of gonads.27 In rare instances, heifers may have a fairly normal but small infantile genital tract but very hypoplastic, small, flattened, slightly corrugated ovaries the size of a bean or smaller 0.5 to 2 cm. long and 0.25 to 0.5 cm. in diameter. (See Figure 118.) These hypoplastic ovaries may be observed either unilaterally or bilaterally. Heif- ers unilaterally affected or those with partial hypoplasia of an ovary usually have normal estrous cycles. Small, inactive, immature ovaries 0.5 to 1.5 cm. in diameter; especially in prepubertal heifers, may erroneously be di- agnosed as hypoplastic ovaries. Heifers should be in good physical condition with no obvious cause for the small inactive ovaries and be old enough to have estrous cycles before a diagnosis of congenital hypoplasia should be considered. In a few of these congenital or hereditary cases of hypoplasia, the uterus and oviducts on one or both sides may also be hypoplastic. In the United States congenital, or possible hereditary, bilateral total hypo- plasis of the ovaries is rare and sporadic. In Sweden, widespread hereditary ovarian and testicular hypoplasia were formerly present in the Swedish Highland breed of cattle.26,53 Inbreeding has been associated with the de- velopment of this defect as with other hereditary anoma- lies of development. (d) Tumors of the ovary are rarely noted as a cause of anestrum or failure of estrum. In the cow the most common tumor is the granulosa cell tumor that may cause510 VETERINARY OBSTETRICS Figure 118. Bilateral Total Hypoplasia of the Ovaries in a 3-year- old Holstein. occasional symptoms of either nymphomania or anes- trum. The early stages of these tumors usually pass un- noticed and by the time clinical symptoms of pelvic re- laxation, edema of the vulva, and others are evident, rectal examination will reveal the nature of the condition by the presence of an abnormally large ovary, 7.5 cm. or more in diameter, usually pulled forward and downward in the abdominal cavity. The ovarian artery to the dis- eased ovary is usually enlarged. Removal of the diseased ovary may be indicated in some cases. Several authors have reported finding granulosa cell tumors in related cattle. Rarely chronic tumors, abscesses and cysts in the ventral area of the brain affect the pituitary gland by causing pressure atrophy and a deficiency of gonado- tropic hormones, thus producing cessation of the estrous cycle and atrophy of the gonads. Large and prolonged doses of the gonadal hormones, estrogens, progesterone and testosterone, whether taken orally or by injection will suppress the release of gonadotropic hormones and result in smooth, inactive, nonfunctioning, atrophied ovaries. Anestrus due to this cause is also rare in cattle. Treatment of anestrum in cows that have no pal- pable functional corpora lutea and in which the plasma progesterone levels are continuously low, or occasion- ally high as in luteal cysts, will vary with the clinical findings. Anestrous cows with cystic ovaries containing follicular or luteal cysts should be treated in ways de- scribed under cystic ovaries. Heifers or cows with free- martin genital tracts, bilateral total ovarian hypoplasia, which should not be confused with infantilism or failure to reach puberty, very rare absence of the gonads, ovar- ian tumors, or rare lesions of the pituitary gland or the hypothalamus should be slaughtered as treatment is not indicated or successful. Removal of one ovary affected with an ovarian tumor, especially a granulosa cell tumor, may rarely restore fertility to the heifer or the cow. In the case of unilateral ovarian hypoplasia the strong pos- sibility that the condition is genetic in nature should be seriously considered. If ovarian atrophy or cystic ovaries are due to exogenous estrogens, or possibly progester- one, testosterone or progestagens, these should be re- moved from the diet or the ration changed or injections of the same should be stopped. It may take from a week to several months or more before the estrous cycle is reestablished. Treatment of anestrum due to debility, cachexia or a lack of TDN (energy), protein, or other minerals should follow a careful clinical examination and diagnosis often requiring an analysis of the feed. If the cause is due to chronic debilitating diseases these must be corrected or alleviated so the female returns to a good condition with near normal body weight. Additional levels of TDN and other nutrients need to be fed to these animals. Therapy may require a number of months. In senile animals the prognosis is poor but occasionally pelleted, easily di- gested feed may be helpful. Treatment of anestrum due to a low level of nutrition is obviously corrected by greatly increasing the nutritive levels. Since many farmers refuse to recognize they are underfeeding and mismanaging their stock, particularly heifers, this is a difficult or impossible problem to cor- rect in some herds. Frequently nature corrects it in the spring when the animals are turned out to pasture where the feed is excellent and unlimited; the weather is warmer; the days longer; and exercise is plentiful. Occasionally a farmer or owner can be persuaded to accept your di- agnosis and suggested treatment on a trial basis by taking several anestrous heifers with small functionless ovaries and placing them in the bam with the milking cows andINFERTILITY IN THE COW 511 feeding them as if they were cows producing 50 lbs of milk a day. In 3 to 6 weeks these heifers usually come into estrum while their less fortunate companions—fed less and on a poor quality feed and usually kept in a colder and less favorable environment—remain anes- trous. This same problem may be observed in certain areas of the country and in certain beef herds where there are deficiencies of either one or more minerals such as phosphorus, cobalt, iodine, copper, salt, iron, and oth- ers, and/or of total digestible nutrients. Often nutritional deficiencies producing cessation of the estrous cycle are multiple. In some high producing old cows that are very thin and poor and are persistent milkers, it may be ad- visable to stop lactation to enable them to gain enough body reserves so that estrous cycles will begin again. Good pasture is desirable. Estrum will not occur in these debilitated animals until they receive feed over and above the requirements for maintaining life and are in a posi- tive energy balance. In heifers or cows in a fair to good nutritive state but failing to show estrum because of a phosphorus deficiency, steamed bonemeal or dicalcium phosphate should be fed free choice. Complex mineral supplements or specific mineral supplements may be necessary, free choice or incorporated into the salt or feed in anestrous, mineral-deficient cows with a low blood hemoglobin level. In range beef heifers and cows the delay in the onset of puberty or estrus after calving, especially in nursing two-year-olds and the lowered conception rates have been described.13,79'97'98 These studies have demonstrated the importance of feeding proper supplemental levels of nu- trients, especially energy and phosphorus to heifers and two-year-old cows after calving. The value of vitamins for the treatment of anestrus in range cattle is question- able. Miscellaneous Infertility Conditions Possibly Associated with Hormonal Disturbances Hormonal therapy for cows that are cycling regularly but fail to conceive has been used empirically in the past by many veterinarians. If the therapy has not been cou- pled to a careful diagnosis of the etiology of the repeat- breeder cow which is difficult, results are usually un- satisfactory or conception occurs despite the treatment. The use of luteinizing hormone (HCG) or GnRH to pro- mote ovulation has been described but failure of ovu- lation or delayed ovulation only occurs occasionally. HCG may also be used about the third or fourth day after es- trum to promote the growth and increase the size and Figure 119. A “Smooth,” Inactive Ovary Seen Bilaterally in De- bilitated or Thin Heifers and Cows and Causing Anestrus. progesterone production of the corpus luteum but its value has not been evaluated in controlled studies. Veterinar- ians have also suggested the use of repositol progester- one, 500 mg. a few days after breeding71 but controlled studies are also lacking. The use of small doses of es- trogen or GnRH early in estrus to promote the release of LH and ovulation has not proven to be of value except possibly in a few special cases in cows in which early embryonic deaths apparently occur. F.S.H. is not indi- cated in cycling infertile cows or in non-cycling cows. Thyroid therapy in the form of iodinated casein (Pro- tamone) 1 gm. per 100 lbs. body weight orally daily, 5,000 to 15,000 mg. triiodothyronine (Cytomel, Smith Kline and French) in pellet form subcutaneously or 2 to 5 grains of thyroid orally daily has been used for anes- trum. It has also been used empirically for infertile cows or heifers, especially those that are obese or have be- come steer-like in appearance. Thyroid preparations should not be used in thin cattle in which anestrum is due to a lack of T.D.N. or energy intake. A possible abnormal steroid metabolism in inbred Jersey cattle characterized by delayed puberty, a short estrus, irregular cycles, fail- ure of conception and decreased secretion rate of sex ste- roid and cortisol has been described.24 Controlled studies in infertile cattle with the above hormones is probably indicated to prove or disprove their value. 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C., McGillard, M. L. and Lineweaver, J. A. (1981) Interrela- tionships with Estrous Behavior and Conception in Dairy Cattle, J. Dairy Sci., 64, 2409. 26. Eriksson, K. (1938) Investigations Respecting the Heredity of Genital Hypoplasia in Cattle, Skand. Vet., 28, 7, 409. 27. Fincher, M. G. (1946) Methods of Increasing Fertility in Do- mestic Animals, Trans, of the Amer. Soc. for Study of Sterility, 1. 28. Fogwell, R. (1980) Inseminate Cow Close to When She First is Seen in Heat, Hoard’s Dairymen, 125, 3, 169. 29. Foote, R. H. (1978) Reproductive Performance and Problems in New York Dairy Herds, Search (Agriculture), 8, 2, 1-18. 30. Foote, R. H. (1975) Estrus Detection and Estrus Detection Aids, J. Dairy Sci., 58, 2, 248-256. 31. Foote, R. H., Oltenacu, E. A. B., Kummerfeld, H. L., Smith, R. D., Rick, P. M. and Braun, R. K. (1979) Milk Progesterone as a Diagnostic Aid, Brit. Bet. J., 135, 550-558, (A Review). 32. Foote, R. H., Oltenacu, E. A. B., Mellinger, J., Scott, N. R. and Marshall, R. A. (1979) Pregnancy Rate in Dairy Cows In- seminated on the Basis of Electronic Probe Measurements, J. Dairy Sci., 62, 69-73. 33a. Foreyt, W. J. (1981) The Role of Liver Fluke in Infertility of Beef Cattle, Proc. 14th Ann. Conv. AABP, Seattle, 99. 33b. Forgason, J. L. (1963) Winrock Farm Beef Cattle Improvement Program, Vet. Med., 53, 3, 211. 34. Gangwar, P. C., Branton, C. and Evans, D. L. (1965) Repro- ductive and Physiological Responses of Holstein Heifers to Con- trolled and Natural Climatic Conditions, J. Dairy Sci., 48, 2, 222. 35. Gibbons, W. J. (1954) Reproductive Problems in Cattle, Vet. Med., 49, 8, 323. 36. Ginther, O. J. (1968) Utero-Ovarian Relationships in Cattle: Physiologic and Applied Veterinary Aspects, JAVMA, 153, 12, 1656 and 1665. 37. Hall, J. B., Branton, C. and Stone, E. J. (1959) Estrus, Estrous Cycles, Ovulation Time, Time of Service, and Fertility of Dairy Cattle in Louisiana, J. Dairy Sci., 42, 6, 1. 38. Hammond, J. (1949) Personal Communication. Lecture at Cor- nell Univ., March 8, 1949. 39. Hancock, J. L. (1948) The Clinical Analysis of Reproductive Failure in Cattle, Vet. Rec., 60, 43, 513. 40. Hansel, W. (1953) Field Observations on the Relation of Nu- trition to Sterility in Dairy Cattle, JAVMA, 122, 911, 126. 41. Hays, R. L. and Carlevaro, C. H. (1959) Induction of Estrus by Electrical Stimulation, Am. J. Physiol., 196, 899. 42. Heckman, G. S., Katy, L. S., Foote, R. H., Oltenacu, E. A. B., Scott, N. R. and Marshall, R. A. (1979) Estrous Cycle Pat- terns in Cattle Monitored by Electrical Resistance and Milk Pro- gesterone, J. Dairy Sci., 61, 1, 64-68.INFERTILITY IN THE COW 513 43. Herrick, J. B. (1953) Progesterone Therapy in Repeat Breeding Heifers, Vet. Med., 48, 12, 489. 44. Hofstad, M. S. (1944) A Study of the Breeding Records of One Large Herd of Dairy Cattle, Cor. Vet., 31, 4, 379. 45. Humick, J. F., King, G. J. and Robertson, H. A. (1975) Estrus and Related Behavior in Postpartum Holstein Cows, Appl. Anim. Ethol., 2, 55. 46. Ireland, J. J., Murphee, R. L. and Carlson, P. B. (1980) Ac- curacy of Predicting Stages of Bovine Estrous Cycle by Gross Appearance of the Corpus Luteum, J. Dairy Sci., 63, 155-160. 47a. Kidder, H. E., Barrett, G. R. and Casida, L. E. (1952) A Study of Ovulations in Six Families of Holstein Friesians, J. Dairy Sci., 35, 5, 436. 47b. Kiddy, C. A. (1977) Variation in Physical Activity as an In- dication of Estrus in Dairy Cows, J. Dairy Sci., 60, 2, 235. 48. King, G. J., Humick, J. F. and Robertson, H. A. (1976) Ovar- ian Function and Estrus in Dairy Cows, During Early Lactation, J. An. Sci., 42, 3, 688-692. 49. Kiser, T. E., Britt, J. H. and Ritchie, H. D. (1977) Testosterone Treatment of Cows for Use in Detection of Estrus, J. An. Sci., 44, 6, 1030-1035. 50. Kummerfeld, H. L., Oltenacu, E. A. B. and Foote, R. H. (1978) Embryonic Mortality in Dairy Cows Estimated by Nonreturns to Service, Estrus and Cyclic Progesterone Patterns, J. Dairy Sci., 61, 12, 1773-1777. 51. Labhsetwar, A. P., Tyler, W. J. and Casida, L. E. (1963) Ge- netic and Environmental Factors Affecting Quiet Ovulations in Holstein Cattle, J. Dairy Sci., 46, 8, 843. 52. Lagerlof, N. (1950) Personal Communication. Lecture, April 27, 1950. 53. Lagerlof, N. (1951) Hereditary Forms of Sterility in Swedish Cattle Breeds, Fert. and Steril., 2, 3, 230. 54. Laing, J. A. (1955) Fertility and Infertility in Domestic Ani- mals, Williams and Wilkins Co., Baltimore, Md. 55. Lindley, D. C. (1953) Comparison of Treatments for Anestrum in Dairy Cattle, Vet. Med., 48, 7, 263. 56. Marion, G. B. and Gier, H. T. (1968) Factors Affecting Bovine Ovarian Activity After Parturition, J. An. Sci., 27, 6, 1621. 57. McEntee, K. (1954), (1968) Personal Communication. 58. Moberg, R. (1954) Disease Conditions in the Fallopian Tubes and Ovarian Bursae of Cattle, Vet. Rec., 66, 6, 87. 59. Moberg, R. (1964) Infertility Due to a Persistent Corpus Lu- teum, 5th Intemat. Congr. for An. Reprod. and Art. Insem., Trento, Italy. 60. Morrow, D. A. (1969) Estrous Behavior and Ovarian Activity in Prepuberal and Postpuberal Heifers, J. Dairy Sci., 52, 2, 224. 61. Morrow, D. A. (1969) Phosphorus Deficiency and Infertility in Dairy Heifers, JAVMA, 154, 7, 761. 62. Morrow, D. A., Roberts, S. J., McEntee, K. and Gray, H. G. (1966) Ovarian Activity and Involution of the Uterus and Cervix in Dairy Cattle, 1, Ovarian Activity, Cor. Vet., 59, 2, 173. 63. Morrow, D. A., Roberts, S. J., McEntee, K. and Gray, H. G. (1966) Postpartum Ovarian Activity and Uterine Involution in Dairy Cattle, JAVMA, 149, 12, 1596. 64. Newman, L. (1968) Personal Communication. 65. Oehme, F. W. (1968) Resection of the Bovine Epididymis, A Procedure for Preparing Teaser Bulls, Vet. Med., 63, 6, 603. 66. Olds, D. and Seath, D. M. (1951) Repeatability of the Estrous Cycle Length in Dairy Cows, J. of Dairy Sci., 34, 626. 67. Olds, D. and Seath, D. M. (1954) Factors Affecting Repro- ductive Efficiency of Dairy Cattle, Kentucky Agr. Exp. Stat. Bull. #605. 68. Phillips, S. (1967) Personal Communication. 69. Rajakoski, E. (1960) The Ovarian Follicular System in Sexually Mature Heifers, Acta Endocrinol., Suppl., 52, 34, 7. 70. Reimers, T. J., Newman, S. K., Cowan, R. G., Smith, R. D., Lein, D. H. and Rounsaville, T. R. (1981) Survey of Estrus Detection and Early Pregnancy Rates in Dairy Cows of the Northeast, J. An. Sci., 53, Suppl. 1, 361, Abstr. 71. Risley, H. B. (1969) Personal Communication. 72. Roberts, S. J. and Fox, F. H. (1968) An Unusual Case of Bo- vine Mucometra Associated with a Persistent Corpus Luteum, Cor. Vet., 58, 1, 116. 73a. Schams, O. and Karg, H. (1982) Hormonal Responses Follow- ing Treatment with Different Prostaglandin Analogues for Es- trous Cycle Regulation in Cattle, Theriog., 17, 5, 499. 73b. Schmidt, S. S. (1966) Technics and Complications of Elective Vasectomy. The Role of Spermatic Granuloma in Spontaneous Recanalization, Fert. and Steril., 17, 4, 467. 74. Seawright, G. L. (1976) Remote Temperature Monitoring in Animal Health Management, Proc. 80th Am. Mtg., U.S. An. Health Assoc., Miami, 214-230. 75a. Seguin, B. E. (1979) Comparative Luteolytic Activity of Estra- diol Cyclopentylproprionate and Prostaglandin F2a in Diestrus Cows, Theriog., 11, 6, 445-452. 75b. Seguin, B. E. (1980) Role of Prostaglandins in Bovine Repro- duction, JAVMA, 176, 10(2), 1178-1181. 75c. Seguin, B. E. (1981) Use of Prostaglandin in Cows with Unob- served Estrus, Acta. Vet. Scand. Suppl., 77, 343. 76. Shemesh, M., Ayalon, N., Shalev, E., Nerya, A., Schindler, H. and Milguir, F. (1978) Milk Progesterone Measurement in Cows: Correlation with Estrus and Pregnancy Determination, Theriog., 9, 4, 343-352. 77. Short, R. V. (1962) Steroid Concentrations in Normal Follicular Fluid and Ovarian Cyst Fluid From Cows, J. Reprod. and Fert., 4, 27. 78. Sorensen, A. M., Hansel, W., Hough, W. H., Armstrong, D. T., McEntee, K. and Bratton, R. W. (1959) Causes and Pre- vention of Reproductive Failures in Dairy Cattle, Bull. 936, Cornell Agr. Exp. Stat., N.Y.S. College of Agric., Ithaca, N.Y. 14850. 79. Sprague, J. I. (1963) Range Cattle Nutrition, Coop. Ext. Ser- vice, An. Sci. Dept., Colo. State Univ., Ft. Collins, Colo. 80. Smith, L. C. (1963) Surgical Procedures to Make a Bull a Heat Detector, A. I. Digest, 9, 1. 81. Stalfors, H. (1930) Some New Observations and Experiments Concerning Sterility in Cattle, Cor. Vet., 20, 1,1. 82a. Spalding, R. W., Everett, R. W. and Foote, R. H. (1975) Fer- tility in New York Artificially Inseminated Holstein Herds in Dairy Herd Improvement, J. Dairy Sci., 58, 5, 718-723. 82b. Stevenson, J. S. and Britt, J. H. (1977) Detection of Estrus by Three Methods, J. Dairy Sci., 60, 1994-1998. 83. Stewart, D. L. (1952) The Suppression of Oestrus in Dairy Cat- tle After Mating, Vet. Rec., 64, 303. 84. Straub, O. C. and Kendrick, J. W. (1965) Preparation of Teaser Bulls by Penectomy, JAVMA, 147, 4, 373. 85. Studer, E. (1975) Palpation of the Genital Tract for Prediction of Estrus in the Cow, Vet. Med/Sm. An. Clin., 70, 11, 1337— 1341. 86. Sturman, H., Oltenacu, E. A. B. and Gengenbach, D. (1981) Incidence and Consequences of Inseminating Dairy Cows with a High Milk Progesterone Level, J. An. Sci., 53, Suppl. 1, 202- 203. 87. Teige, J. (1955) Hemorrhage Following Expression of the Cor- pus Luteum in the Cow (Trans.), Nord. Vet. Med., 7, 9, 747. 88. Teige, J. and Jakobsen, K. R. (1956) Investigation on the Effect514 VETERINARY OBSTETRICS of Enucleation of Corpus Luteum in Dairy Cattle, Proc. Third Intemat. Congr. on An. Reprod., Cambridge. 89a. Thatcher, W. W. (1974) Effects of Season, Climate and Tem- perature on Reproduction and Lactation, J. Dairy Sci., 57, 3, 360-368. 89b. Thatcher, W. W. and Roman-Ponce, H. (1980) Effects of Cli- mate on Bovine Reproduction, in Current Therapy in Theri- ogenology, edited by D. A. Morrow, W. B. Saunders, Co., Philadelphia, 441-448. 89c. Thatcher, W. W. and Wilcox, C. J. (1973) Postpartum Estrus as an Indicator of Reproductive Status in the Dairy Cow, J. Dairy Sci., 56, 5, 608. 90. Trimberger, G. W. (1955) Unpublished Data. 91. Trimberger, G. W. and Davis, H. P. (1943) Conception Rate in Dairy Cattle by Artificial Insemination at Various Stages of Estrus, Univ. of Nebr., Agr. Exp. Stat., Res. Bull. 129. 92. Wagner, W. C. and McEntee, K. (1960) Herd Approach to In- fertility Problems in Cattle, Cor. Vet., 50, 2, 198. 93. Williams, W. F., Yver, D. R. and Gross, T. S. (1981) Com- parison of Estrus Detection Techniques in Dairy Heifers, J. Dairy Sci., 64, 1738-1741. 94a. Williamson, N. B., Morris, R. S., Blood, D. C., Cannon, C. M. and Wright, P. H. (1972) A Study of Oestrus Behavior and Oestrus Detection Methods in a Large Commercial Dairy Herd, I & H, Vet. Rec., 91, 50-62. 94b. Williamson, N. B. (1980) Tail Painting as an Aid to Detection of Oestrus in Cattle, Austral. Vet. J., 56, 98. 95. Wiltbank, J. N. (1961) A Technique for Sterilization of Bulls, The Southwest Vet., 14, 3, 194. 96. Wiltbank, J. N. (1966) Modification of Ovarian Activity in the Bovine Following Injection of Oestrogen and Gonadotrophin, J. Reprod. and Fertil. Suppl., 1, 1. 97. Wiltbank, J. N. and Cook, A. C. (1958) The Comparative Re- productive Performance of Nursed Cows and Milked Cows, J. An. Sci., 17, 640. 98. Wiltbank, J. N., Rowden, W. W., Ingalls, J. E. and Zimmer- man, D. R. (1964) Influence of Postpartum Energy Level on Reproductive Performance in Hereford Cows Restricted in En- ergy Intake Prior to Calving, J. An. Sci., 23, 4, 1049. 99. Wright, J. G. (1945) Observations on the Clinical Aspects of Reproductive Disorders in Cattle, Vet. Red., 57, 26, 313. 100. Yamauchi, M., Nakahara, T., Kaneda, Y. and Inui, S. (1967) Effects of Uterine Distension on the Oestrous Cycle of the Cow, J. Reprod. and Fertil., 13, 379. 101. Zemjanis, R. (1961) Incidence of Anestrus in Dairy Cattle, JAVMA, 139, 11, 1023. 102. Zemjanis, R. (1970) Animal Reproduction, 2nd. Ed. Williams and Wilkins Co., Baltimore, Md. 103. Zemjanis, R. (1972) Diagnosis and Treatment of Anestrus, Proc. 5th Ann. Conv., AABP, Milwaukee, Wise., 51-54. 104. Zemjanis, R., Fahning, M. L. and Schultz, R. H. (1969) Anes- trus, The Practitioners Dilemma, Vet. Scope (Upjohn), 14, 1, 14. Infertility Due to Nutritional Causes During the past 30 years a great mass of knowledge has accumulated about the effects on animals of various nutrients and their deficiencies. Since much of the early work was done on the rat and on laboratory animals, some nutritional fallacies have developed in so far as they pertain to domestic animals. The effect of nutrition on reproduction, sterility, and infertility has not been discussed but the relation of nutrition or nutritive defi- ciences to abortion and anestrus has been reviewed in Chapters VIII and XIII. Excellent reviews on this field have been published. 1'20-25’30,3l-37-4'~44 Only a few nu- trients have a direct effect on fertility. Some infertility conditions blamed on nutrition may in reality be due to other related or nonrelated causes. Most field cases of reduced fertility or of sterility of nutritional origin are usually due to multiple deficiencies. Underfeeding may be accompanied by poor quality of feed and by defi- ciencies of protein, phosphorus and vitamin A. A protein deficiency is usually accompanied by a phosphorus de- ficiency, and a vitamin A deficiency by a protein and phosphorus deficiency. Sometimes reduced fertility be- lieved to be of nutritional origin may be caused by the amount of light, environmental temperature, amount or type of work, or some other environmental influence. More work is required in this field as much of our pres- ent data is based on poorly controlled experiments and too few observations. It has been found that nutritional data accumulated on one species of animal does not al- ways apply to other species. Symptoms of a certain de- ficiency in one species may differ from those in another species. At one time or another claims have been made that every known food factor is indispensible for normal reproduction.41 In so far as reproductive performance is based on the general health of the animal this may be true. Malnutrition leads to lowered vitality and lessened resistance to disease but proof of such effects on the re- productive system are few and all too often not conclu- sive. If disease is complicating the malnutrition then cor- rective efforts must be directed at both conditions. Lactation, however, places a heavy drain on an animal already deficient especially in certain minerals and in the general level of feeding. Specific deficiencies seldom cause specific lesions in the reproductive system. Infer- tility or sterility due to nutritional causes is usually char- acterized by a cessation of the estrous cycle and only under certain conditions is it characterized by a failure of conception or early embryonic death. Reproduction is a “luxury” function of the body. When body functions and needs are severely compromised, reproduction usu- ally is the first system affected and if adverse influences are continued, reproductive functions cease. Underfeeding, inanition, or starvation has been shown to delay sexual maturity in heifers30-37'44 and to inhibit estrous cycles in mammals of all ages. When dairy heifers were fed various levels of TDN from birth to firstINFERTILITY IN THE COW 515 calving equivalent to 62, 100 and 146 percent of the upper level of Morrison’s Feeding Standard, the average age at the onset of puberty was 88, 49, and 40 weeks. The body size at the time of puberty was the same for all feeding levels. When the energy intake in the adult animal is low, follicles fail to develop to maturity and follicular atresia results, along with a loss of sexual de- sire, anestrus and cessation of the estrous cycle. Re- stricted food intake may have an effect on the early em- bryo but starvation after this period does not necessarily interrupt gestation but may cause stillbirth or birth of small, weak young.31 It is nearly impossible to conduct an experiment on a single food deficiency without en- countering a partial inanition in animals. Under-feeding or inanition is seen in cattle most commonly during the winter months when they are confined and/or the quality and quantity of the feed is limited or reduced. In older cattle irregular estrous periods and anestrum are mani- fested as a result of underfeeding. Inanition reduced the secretion of gonadotropic hormones and other hormones by the anterior pituitary although the gonadotropic levels in the pituitary were normal.31,37 The fact that the ovaries remain responsive to stimulation by gonadotropes during under-feeding does not mean that normal estrous cycles and pregnancy could be maintained by administration of hormones, since undemutrition probably exerts a direct effect on the reproductive tract although the major effect is on the endocrine glands. It has been shown in primiparous beef heifers that en- ergy intake levels before and especially after calving and during lactation have a marked effect on the occurrence of postpartum estrus and conception rates.57 In beef heif- ers fed high TDN, 9 lbs. and low TDN, 4.5 lbs. daily before calving and then high TDN, 16 lbs., and low TDN, 8 lbs. daily after calving the conception rate for 20 heif- ers in each group was High-High 95 percent, High-Low 77 percent, Low-High 95 percent and Low-Low 20 per- cent. The percentage of cows cycling by 60 days post- partum was 80, 81, 45 and 17 respectively in the four feeding groups. Thus it is more important that cows suckling calves receive more energy than pregnant ani- mals.56,58 The birth weight of calves from cows on the low energy ration during pregnancy was 10 lbs. lower on the average than the weight of calves from cows on the high energy ration, 67 lbs. vs 78 lbs. Beef heifers should be fed to gain one pound a day from weaning through the breeding season.57 Heifers of the English breeds of cattle should weigh 650 lbs. at the start of the breeding season. Beef cattle should be in good condition at calving and should be fed to gain 0.5 to 0.75 lbs. per day after calving until the end of the breeding season to avoid low reproductive performance. In a herd of 327 beef cattle free of infectious causes for infertility the conception rate dropped from 87 percent to 41 percent, 28 percent in lactating and 76 percent in nonlactating cows, under drouth conditions.9 Injections of vitamins A, D, and E during the breeding season failed to im- prove the conception rate. A higher incidence of dys- tocia in heifers was reported on a below normal energy intake during the gestation period.44 Retarded early growth in cattle due to a low plane of nutrition was associated with a prolongation of the life span.43 Evidence indicates that animals come into estrum and conceive most readily when their body weight is rising due to an increased plane of nutrition and conversely a low pregnancy rate occurs in beef and dairy cattle losing weight during the breeding season.12 13,21,23,30,3611,57 In 179 Ayrshire cows on 3 farms that were weighed every 4 weeks and serviced not less than 56 days postpartum, 98 cows whose body weight increased after calving had a 77.6 percent conception rate on first service while 81 cows whose body weight decreased had a 16 percent conception rate on first service.23 There was no corre- lation between conception rate and milk yield. New Zea- land studies showed that cows gaining weight had sim- ilar conception rates to those that lost only a modest amount of weight after calving.34 It was also noted in Israel that a positive energy balance if achieved fairly promptly after calving resulted in an improved concep- tion rate.21 They suggested that weighing cows at inter- vals after calving might be helpful in determining the need for increased energy intake and in determining the time for insemination. (See Anestrum.) The dairy and beef herd infertility syndrome associated with a negative energy balance and loss of weight was described12,30 to include: (1) low first service nonreturn rates; these are seldom below 30 percent, (2) spontaneous recovery but many cows are not pregnant by the third month after the first service, (3) affected cows lose an excessive amount of body weight, 5 to 10 percent, between calving and first service; such a loss is often not obvious, and (4) low blood glucose, hypoglycemia, is frequently ob- served in infertile cows at the time of the first service. The estrous cycle length was increased from normal to 34 days when cows were given insulin daily from day 17, but not day 18, through day 20 of the cycle.29 In 11 cows mated 0 to 2 days after the last dose of insulin only 2 or 18 percent were pregnant at 8 weeks, and of 16 cows given insulin, 400 units daily the first four days after mating only 6 or 38 percent were pregnant at 8 weeks. While 15 of 20, or 75 percent, of the control cows were pregnant. Thus it is possible that a hypogly- cemia at estrus and shortly after service may exert a harmful effect on conception. This effect may be brought516 VETERINARY OBSTETRICS about by a lowering of the glucose or glycogen levels in the mucosa of the genital tract resulting in a lack of en- ergy for spermatozoa and embryos. Further study of these interesting observations are needed. Reproduction in Herefords was more severely affected by low levels of TDN intake after calving than in Angus cattle.13 Weight gain in yearling heifers during the prebreeding period caused by “flushing” or feeding high energy rations was more important in its effect on age at puberty than was the gain during the wintering period.7 Thus it appears important that feeding practices in dairy and beef herds be such that, despite the stress and energy requirements of lactation, cows to be bred should be in a positive en- ergy balance and gaining weight as soon after calving as is possible to realize the best breeding results. Obesity due to overfeeding has been considered by many practicing veterinarians to be a cause of infertility in cattle. This is observed particularly in the beef breeds and has often been reported to affect valuable show cat- tle. Early references indicated erroneously that in these overly-fat animals the ovaries are small and estrus may fail to occur.156 Obese, over-conditioned dairy cows are prone to the “fat cow syndrome” at calving (see post parturient diseases). The diseases associated with this syndrome have an adverse effect on fertility and often greatly prolong the period from calving to conception.36b Obesity and sterility might arise from the same cause such as hypothyroidism or from a pituitary lesion. Fat deposits in the ovaries and ovarian bursae were sus- pected of interfering with normal ovulation and transport of ovum to the oviduct. Recent nutritional research has not confirmed the observation in cows that obesity and infertility are associated. Reid stated, “It is as logical to assume that sterility is the cause of high condition as it is to assume the reverse.”43 In a rather large controlled experiment animals kept on a high plane of nutrition their entire life had fewer calves and a higher percentage of culling due to infertility than did the animals fed at nor- mal and low levels of nutrition.38 Swedish data, New Zealand reports, and experiments at Cornell,44 indicated that heavy feeding hastened the onset of puberty, caused a slight increase in number of services per conception if heifers were withheld from breeding for a number of months after reaching puberty; and resulted in lower milk yields and a shorter life. Cattle reared on a high plane of nutrition had more breeding difficulties later in life and thus had a shorter productive life than cattle reared on a low energy intake.43 A high level of grain feeding of up to 4790 kg per lactation over a period of years in dairy cows had no significant effect on conception rate.6 Fat heifers and cows with large deposits of perivaginal fat may have more difficulties at parturition. The prob- lem of the effects of overfeeding on reproduction in cat- tle is not settled and more controlled experiments are needed and indicated. Protein deficiencies of either quality or quantity un- der the usual conditions of management of cattle are not common. Although the quality and quantity of protein might be important for reproductive functions, deficient amounts are seldom encountered except in severe inani- tion or underfeeding when vitamin A and phosphorus deficiencies are often complicating factors. The effect of a low level intake of protein on reproduction may be to reduce the total intake of feed, resulting in a delay in estrus.56 The high content of phosphorus rather than pro- tein may explain why cottonseed meal is a better sup- plement for beef cattle in the Southwest than is grain during the winter months.24 Pelleted alfalfa fed at a rate of 2 to 5 lbs. daily per animal is an excellent protein supplement. The level of energy intake is more impor- tant for reproduction than is protein. Vitamin deficiencies in cattle are mainly limited to vitamin A. Deficiencies of the other vitamins are not likely to cause reproductive failure. Vitamin A deficiency adversely affects reproduction in most species. The effects occur during the latter half of gestation and are characterized by abortion or by the birth of weak or dead calves (See Abortion, Chapter V). It seems remarkable but it is nevertheless true that vi- tamin A deficient animals have normal estrous cycles, ovulate and conceive, and early fetal development oc- curs even though epithelial and other tissue changes have developed. Infertility in cattle and other domestic ani- mals has not been associated with vitamin A deficiency or with a deficiency of the other vitamins. In the mid to late 1970’s many articles were published in Europe on the beneficial effects of beta-carotene on bovine fertility. Beta-carotene and vitamin A are defi- cient in com silage.10 20 Supplementing such diets with 200,000 IU vitamin A and 300 mg. beta-carotene per head per day reduced the time from calving to concep- tion, reduced the incidence of ovarian cysts and reduced embryonic deaths, early abortions and disease prone calves.20 27 The bovine CL contains beta-carotene but no vitamin A. The former can be converted into vitamin A. Evidence would indicate that vitamin A provided by good hay, especially alfalfa, and pasture should provide the vitamin needs for reproduction.19 The present require- ment for vitamin A in dairy cattle is 3,400 IU or 8.5 mg of carotene/100 lbs. of body weight.10 Experiments are now being conducted to determine whether greatly in- creased amounts of beta-carotene are needed for repro- ductive efficiency. Recent reports do not support the early claims for beta-carotene supplementation.586 Vitamin A requirements during pregnancy are higher than in the nonpregnant animal and higher for the femaleINFERTILITY IN THE COW 517 than the male animal. Vitamin A deficiencies are char- acterized by changes in the epithelial tissues, such as keratinization and degeneration of the placenta. Fetal death, abortion, dystocia, retained placenta, and septic metritis are likely to result. Vitamin A deficiency has been described in cattle grazing dry, bleached pastures and grain fields where possibly protein, phosphorus, and carbohydrate intake were also deficient. When green feed became available, night blindness, lacrimation, anorex- ia, diarrhea, loss of condition and other general symp- toms of vitamin A deficiency, as well as abortions and stillbirths, ceased. The liver has the ability to store con- siderable amounts of vitamin A for some time; therefore symptoms of vitamin A deficiency take months to de- velop. Good timothy hay has a much lower content of vitamin A than does alfalfa hay. Under most conditions where roughage is of average quality, vitamin A defi- ciency is very unlikely to occur and even then the re- productive effects are not those causing infertility in the cow. Vitamin B or B-complex deficiencies have been demonstrated in animals as producing the same inhibi- tory effects on reproduction as reduced food intake or starvation. This is not unexpected, as deficiencies of B vitamins are usually accompanied by a reduced appetite. By virtue of ruminal synthesis of these B-complex vi- tamins, cows are in no danger of suffering from vitamin B deficiencies. One of the B-complex vitamins, vitamin Bn, requires cobalt in its synthesis; cattle in cobalt-de- ficient areas may develop severe inanition due to lack of sufficient intake of feed occasioned by a cobalt and B12 deficiency and a lack of appetite. Vitamin C deficiency does not occur in cattle; only man, monkeys, and guinea pigs manifest symptoms of vitamin C deficiency, or scurvy, and even in these spe- cies no reproductive disturbances are produced when se- vere scurvy is present. Vitamin D deficiency probably seldom occurs, due to the presence of vitamin D in roughage of almost any quality. If the animal gains access to sunlight or green pasture, adequate amounts are available. An uncompli- cated vitamin D deficiency does not interfere with re- production in mammals.31 Vitamin E deficiency, like vitamin A deficiency, does not affect the estrous cycle or ovarian function. In de- ficient rats pregnancy is interrupted after midterm by re- sorption of the fetuses. In the male rats vitamin E de- ficiency irreparably damages the seminiferous epithelium giving rise to its early name—the “antisterility” vitamin. In herbivorous animals it is doubtful that a need for vi- tamin E for reproductive purposes is greater than the quantity liberally present in the natural feed. Cows can reproduce on a vitamin E deficient diet. Heifers and bulls receiving vitamin-E-deficient diets were fertile.15 In the past, extravagant claims have been made for the use and value of vitamin E supplementation of rations in the treatment of all types of reproductive disorders in cows and bulls. These claims and reports, largely commer- cially-developed and exploited, were uncontrolled. The use of wheat germ oil in cases where spontaneous re- coveries of infertility are known to be high resulted in a great number of apparent “cures” with this product. Re- ports on more carefully controlled data and experiments using wheat germ oil or sprouted oats showed no dif- ference in results between the treated and the control groups of cattle. At the present time vitamin E therapy for infertility cannot be recommended since it is of no known value. Mineral deficiencies causing infertility in cattle are limited mainly to phosphorus and occasional trace min- erals. Trace minerals in cattle nutrition have been re- viewed.5 Phosphorus deficiency usually tends to occur when diets low in protein are fed, under range conditions when the grass is dry and dead, in areas where the soil is de- ficient in phosphorus, and in borderline phosphorus-de- ficient areas when the cows are lactating and are not fed sufficient protein or mineral supplements to maintain the necessary body levels of phosphorus. Until clinical symptoms of the deficiency, such as inanition, poor hair coat, and depraved and decreased appetite are evident, reproduction usually does not suffer. In some phospho- rus-deficient areas cows had calves only every 2 years, and heifers failed to show estrum until over 2 years of age. The condition was most severe in the late winter and spring after a dry summer and fall. Some cows would have one or two periods of estrum after calving and then if they failed to conceive would not show estrum until the end of the lactation period. “Silent” or irregular es- trus periods may occur in heifers. Thus the usual symp- toms of phosphorus deficiency are delayed onset of pu- berty in heifers, and failure of estrum in cows. The relationship between phosphorus deficiency and infertil- ity in dairy cattle was reviewed.36 With proper phospho- rus supplementation the number of services required for conception declined from 3.7 to 1.3 in dairy heifers suf- fering from a phosphorus deficiency. The Ca:P ratio, especially excess Ca to P., could influence fertility but this was not confirmed.17'18,26 The phosphorus requirement for reproduction is about 10 to 12 gm. daily except during lactation when an ad- ditional amount is required.1 Blood levels of phosphorus below 4 mg. per 100 ml of blood serum usually indicate a phosphorus deficiency; normal values are 4 to 8 mg. per 100 ml. Phosphorus levels are much lower in tim- othy hay than in legumes. In states where phosphorus518 VETERINARY OBSTETRICS deficiency is common, the feeding of mineral supple- ments or cotton seed meal has resulted in marked im- provement or increases in the yearly percentage of calves bom. Mineral supplements to supply phosphorus include dicalcium phosphate or bone meal and these should be available free-choice together with trace mineralized salt for all cattle. Adding 1 percent sodium tripolyphosphate or monosodium phosphate to the grain ration will also increase the phosphorus intake.36 Calcium deficiency does not cause reproductive failure in cattle. Other trace element deficiencies, that may affect re- production indirectly, are: Manganese—In cattle there are few reports of naturally-occurring manganese de- ficiencies. It appears nearly impossible to devise an otherwise normal ration for cattle that is deficient in manganese.4*'43 However, reduced conception rates and anestrus in cattle deficient in manganese that was corrected by manganese supplementation was re- ported.30'4554 Cobalt deficiency in certain areas may cause a lack of appetite, depraved appetite, inanition, secondary fail- ure of estrum, and delayed onset of puberty in cattle. Low hemoglobin values were observed in many anes- trous animals. Cobalt is necessary for normal bacterial growth in the rumen. It is concerned in the production of vitamin Bi2, which is an important factor in main- taining the appetite. In cobalt-deficient soils, legumes usually contain sufficient cobalt; but timothy hay pro- duced on these soils is deficient in cobalt. Copper and iron deficiencies in some areas of the United States re- sult in, or are complicated by, anemia, debility, lack of appetite, and consequently a reduced intake of feed. As with cobalt deficiency a secondary inanition, a failure of estrum, and a delayed onset of puberty may occur. The apparent association of anemia with hemoglobin values below 10 gms, especially in the range of 8.0 to 8.5 gms, per 100 ml of blood, and anestrus, delayed postpartum breeding and possibly repeat breeding have been re- ported upon in dairy cattle.2’52 In some cases this anemia has been related to low iron or copper levels in the for- age. In certain areas such as some locations in Florida, a high molybdenum content in the feed results in severe scouring and loss of condition when copper is not added as a supplement in the feed. This loss of condition may be reflected in failure of estrum in cows or in the delayed onset of puberty in heifers. Copper-deficient cat- tle in New Zealand, England, South Africa and Aus- tralia,3115053 have marked general effects of lowered body health, loss of condition, slow growth and rough hair coat with secondary reproductive symptoms of failure of estrum, delayed conception, and infertility. Iodine deficiency especially in the northern and north- western parts of the United States may cause the birth of weak, premature or dead calves affected with goiter. Iodine is not known to affect reproductive processes. However, a lack of iodine can depress thyroid func- tion.31 Hypo- or hyperthyroidism may reduce the secre- tion of gonadotropic hormones by the pituitary. An in- crease in conception rate was reported on first service and reduced irregular breeding intervals in herds in Fin- land receiving supplementary iodine compared to control herds.33 In iodine-deficient areas iodine is usually pro- vided in the salt. Severe salt deficiency over a long pe- riod of time, especially during lactation, will result in severe loss of body weight and anestrus.46 Zinc and se- lenium has been shown to be closely associated with reproduction in laboratory and other animals but defi- ciencies in the large domestic animals have not been de- scribed. Treatment of cattle with nutritional deficiencies is es- sentially one of prevention. In most deficiency areas these deficiencies are known and should be provided for by supplementing the ration. In most areas where cattle raising is profitable, deficiencies are usually uncommon in cattle fed near-normal or balanced rations. Usually general inanition, debility, and other symptoms are ev- ident before reproductive symptoms develop. In most herds expensive mineral supplements are not necessary. Mineral supplements are added to the grain ration at a usual rate of 1 to 1.5 percent for dairy cattle. In certain mineral-deficient areas and in heavily lactating cows ad- ditional amounts or specific mineral supplementation such as magnesium may be necessary. A suitable mineral sup- plement for dairy areas in the northeast and middlewest consists of 86 lbs. of steamed bone meal or dicalcium phosphate, 12 lbs. of anhydrous ferrous sulfate, and 1.4 lbs. of copper sulfate and 1 ounce of cobalt sulphate or cobalt chloride. This can be fed free choice or added in small amounts, 1 ounce daily, to the grain ration.2 If rock phosphate is used it should be carefully defluori- nated to prevent possible fluorine poisoning. Chronic subclinical flourine poisoning induced by feeding 5 to 12 ppm flourine in the drinking water caused anestrum, reduced conception rates and a drop in the pregnancy rate.51 In some cases subcutaneous injections of 1 to 6 mg. of vitamin B12, 10 ml of iron dextran or 300 mg of copper glycinate may be given as needed if feed sup- plements are difficult to provide. There are few nutri- tional factors other than underfeeding that have been shown to have a widespread serious influence on repro- ductive functions. Trace elements had little if any effect on repeat breeding cows.8 Additional work, adequately planned and controlled, might profitably be applied to this problem of nutrition and fertility.INFERTILITY IN THE COW 519 Miscellaneous nutritive, reproductive problems, es- pecially infertility, may be associated with the con- sumption of excess estrogens from pasture plants espe- cially during lush growing season. High estrogenic content of red clover, of alfalfa, subterranean clover and of ladi- no clover and other phytoestrogens have been reported upon.4,14,20'22'49,59 Infertility in cattle consuming such for- age has been reported in isolated areas. Heavy kale feed- ing caused a reduced conception rate and prolonged in- tervals between estrous periods after service.32,39,40 No estrogens were found in kale but evidence of a goiter- ogenic factor was noted. Blood copper and hemoglobin were lower in kale-fed cows.32 Estrogenic mycotoxins or fungal metabolites may be a cause of infertility in cattle as they are in swine (See Chap. XVI) but evidence for this in the veterinary literature is scanty.8b,45b References 1. Asdell, S. A. (1949) Nutrition and the Treatment of Sterility in Dairy Cattle: A Review, J. Dairy Sci., 32, 1, 60. 2. Adams, R. S. (1969) New Mineral Problems, Cornell Nutrition Conference, January, Mimeographed Material, Penn. State Univ., University Park, Pa. 3. Alderman, G. (1963) Mineral Nutrition and Reproduction in Catde. Vet. Rec., 75, 40, 1015. 4. Adler, J. H. and Trainin, D. (1960) A Hyperoestrogenic Syn- drome in Cattle, Refuah Vet., 17, 2, 115. 5. Ammerman, C. B., Thomas, J. W., Miller, W. J., Hogue, D. E. and Hemken, R. W. (1970) Symposium on Trace Minerals— A Review, J. Dairy Sci., 53, 8, 1097. 6. Armstrong, D. V., Brown, L. D., Thomas, J. W. and Getty, S. M. (1966) High Level Grain Feeding and Herd Health, J. Dairy Sci., 49, 6, 730. 7. Bellows, R. A. (1966) Improving Reproductive Efficiency in Beef Cattle, Vet. Scope, 11, 3, 2. 8a. Bentley, O. G., Quick, V. G., Kastelic, I. and Phillips, P. H. (1951) Certain Trace Elements in the Feeds, Organs and Tissues of a Selected Group of Repeat Breeding Cows in Northeastern Wisconsin, J. of Dairy Sci., 34, 363. 8b. Blankenship, L. T., Dickey, J. F. and Bodine, A. B. (1982) In vitro Mycotoxin Binding to Bovine Uterine Steroid Hormone Receptors, Theriog., 17, 3, 325. 9. Carroll, E. J. and Hoerlein, A. B. (1966) Reproductive Perfor- mance of Beef Cattle under Drought Conditions, JAVMA, 148, 9, 1030. 10. Chase, L. E. (1981) Vitamin Nutrition in Cattle, Proc. Cornell Nutr. Conf. for Feed Manufacturing, Syracuse, N.Y., 64-68. 11. Donaldson, L. E., Harvey, J. M., Beattie, A. W., Alexander, G. I. and Bums, M. A. (1964) Effects of Copper and Cobalt Supplementation on the Growth Rate and Fertility of Shorthorn Heifers in Northern Coastal Queensland, Queensland J. of Agr. Sci., 21, 167. 12. Downie, J. G. and Gelman, A. L. (1976) The Relationship Be- tween Changes in Bodyweight, Plasma Glucose and Fertility in Beef Cows, Vet. Rec., 99, 210-212. 13. Dunn, T. G., Ingalls, J. E., Zimmerman, D. R. and Wiltbank, J. N. (1969) Reproductive Performance of Two-Year-Old Here- fords and Angus Heifers as Influenced by Pre- and Post-Calving Energy Intake, J. An. Sci., 29, 5, 719. 14. Green, John (1965) Tasmania, Personal Communication. 15. Gullickson, T. W., Palmer, L. S., Boyd, W. L., Nelson, J. W., Olson, F. C., Caverley, C. E. and Boyer, P. D. (1949) Vitamin E in the Nutrition of Cattle. Effect of Feeding Vitamin E Poor Rations on Reproduction, Health, Milk Production and Growth, J. of Dairy Sci., 32, 495. 16. Hansel, W. (1955) Personal Communication. 17. Hignett, S. L. (1959) Some Nutritional and Other Interacting Factors Which May Influence the Fertility of Cattle, Vet. Rec., 71, 247. 18. Hignett, S. L. (1962) The Influence of Nutrition on the Fertility of Livestock, in Livestock Infertility, Animal Health Mono- graph #5 F.A.O. Rome, 47. 19. Hintz, Harold (1982) Personal Communications. 20. Jochle, W. (1979) Review: Reproduction and Nutrition, Anim. Reprd. Rpt., 12, Vol. 2, Old Boonton Rd., Denville Twp., N.J. 21. Kali, J. and Amir, S. (1968) The Relationship between Milk Yield, Level of Nutrition and Body Weight of Cows and their Effect on Conception, Ann. Rept. Oct. ’67-Sept. ’68 “Hash- erut” AI Center, Rishon Le Zion, P.O. Box 31, Israel. 22. Kallela, K. (1965) Finnish Investigations on Plant Oestrogens, Nord. Vet. Med., 17, 280. 23. King, J. O. L. (1968) The Relationship Between the Conception Rate and Changes in Body Weight, Yield and S.N.F. Content of Milk in Dairy Cows, Vet. Rec., 83, 492. 24. Knox, J. H. and Watkins, W. E. (1958) Supplements for Range Cows, N. Mex. Agr. Exp. Stat. Bull., 425, 3. 25. Lamond, D. R. (1970) Influence of Undemutrition on Repro- duction in the Cow, Anim. Breed. Abstr., 38, 359. 26. Littlejohn, S. I. and Lewis, G. (1960) Experimental Studies of the Relationship Between Calcium-Phosphorus Ratio of the Diet and Fertility in Heifers—A Preliminary Report, Vet. Rec., 72, 1137. 27. Lundes, A. (1981) Beta-Carotene for Dairy Cows: The Provi- tamin can Influence Reproductive Performance, An. Nutr. and Health, 36, 7, 10-12. 28. McClure, T. J. (1968) Malnutrition and Infertility in Cattle in Australia and New Zealand, Austral. Vet. J., 44, 2, 134. 29. McClure, T. J. (1968) Hypoglycemia, an Apparent Cause of Infertility of Lactating Cows, Brit. Vet. Jour., 124, 126. 30. McClure, T. J. (1970) A Review of Developments in Nutrition as it is Related to Fertility in Cattle: 1964-1969, New Zeal. Vet. Jour., 18, 4, 61. 31. Meites, J. (1953) Relation of Nutrition to Endocrine-Reproduc- tive Functions, Iowa State Col. J. of Sci., 28, 1, 19. 32. Melrose, D. E. and Brown, P. B. (1962) Some Observations on the Possible Effect of Kale Feeding on Fertility in Dairy Cat- tle, J. Reprod. and Fert., 4, 232. 33. Moberg, R. (1961) Possible Influences of Supplementary Iodine Administered by Evaporation on Reproductive Performances in Cattle, 4th Intern. Congr. on An. Reprod., The Hague, III, 682. 34. Moller, K. and Shannon, P. (1972) Body Weight Change and Fertility of Dairy Cows, N.Z. Vet. Jour., 20, 47-48. 35. Morrow, D. A. (1965) The Effect of Energy Intake on Repro- duction in Cattle—A Review, Unpublished paper. 36a. Morrow, D. A. (1969) Phosphorus Deficiency and Infertility in Dairy Heifers, JAVMA, 154, 7, 761. 36b. Morrow, D. A. (1980) The Role of Nutrition in Dairy Cattle Reproduction, Current Therapy in Theriogenology, edited by author, W. B. Saunders Co., Philadelphia, 449-455.520 VETERINARY OBSTETRICS 37. Moustgaard, J. (1969) Nutritive Influences Upon Reproduction, in Reproduction in Domestic Animals, 2nd Ed. by H. H. Cole and P. T. Cupps, Academic Press, N.Y.C., 489. 38. Olds, D. (1953) Infertility in Cattle—A Review, JAVMA, 122, 913, 276. 39. Pickard, D. W. and Crighton, D. B. (1967) An Investigation into the Possible Oestrogenic Effect of Kale, Brit. Vet. Jour., 123, 2, 64. 40. Reed, H. C. B. (1961) Relationship Between Kale and Fertility in Dairy Cattle, 4th Intemat. Congr. on An. Reprod. (Hague) m, 457. 41. Reid, J. T. (1949) Relationship of Nutrition to Fertility in An- imals, JAVMA, 114, 864, 158 and 865, 242. 42. Reid, J. T. (1956) Nutrition and Feeding of Dairy Cattle, J. Dairy Sci., 39, 6, 735. 43. Reid, J. T. (1959) Plane of Nutrition and Livestock Perfor- mance, Proc. 1959 Cornell Nutrition Conference for Feed Man- ufacturers, 56. 44. Reid, J. T., Loosli, J. K., Trimberger, G. W., Turk, K. L., Asdell, S. A. and Smith, S. E. (1964) Causes and Prevention of Reproductive Failures in Dairy Cattle, IV. Effect of Plane of Nutrition During Early Life on Growth, Reproduction, Produc- tion, Health and Longevity of Holstein Cows, Bull. 987, Com. Univ. Agr. Exp. Stat., Ithaca, N.Y. 45a. Rogas, M. A. and Dyer, I. A. (1964) Manganese Deficiency in the Bovine, J. An. Sci., 23, 2, 600 (Abstr.). 45b. Roine, K., Korpinen, E. L. and Kallela, K. (1971) Mycotoxi- cosis as a Probable Cause of Infertility in Dairy Cows, Nord. Vet. Med., 23, 628. 46. Smith, S. E. and Aines, P. D. (1959) Salt Requirements of Dairy Cows, Bull. 938, N.Y. State College of Agric., Ithaca, N.Y. 47. Sorensen, A. M., Hansel, W., Hough, W. H., Armstrong, D. T., McEntee, K. and Bratton, R. W. (1959) Causes and Pre- vention of Reproductive Failures in Dairy Cattle, I Influence of Underfeeding and Overfeeding on Growth and Development of Holstein Heifers, Bull. 936, Cornell Univ. Agr. Exp. Stat., Ith- aca, N.Y. 48. Sprague, J. I. (1963) Range Cattle Nutrition, Coop. Ext. Ser- vice and An. Sci. Dept., Colo. State Univ., Ft. Collins, Colo. 49. Thain, R. I. (1967) Evidence for the Widespread Involvement of Clover Pastures in Bovine Infertility in Tasmania, Austral. Jour. Sci., 29, 220. 50. Van Rensburg, S. W. J. (1961) Copper Deficiency Influences Animal Fertility, Farming in S. Afr., March, 50. 51. Van Rensburg, S. W. J. and de Vos, W. H. (1966) The Influ- ence of Excess Fluorine Intake in the Drinking Water on Re- productive Efficiency in Bovines, Onderstepoort J. Vet. Res., 33, 185. 52. Wagner, W. C. (1962) Improving Fertility in Dairy Cows, JAVMA, 140, 9, 939. 53. Wallace, L. R. (1949) Nutritional Basis of Fertility, New Zea- land Dept, of Agr., Ruakura Animal Research Stat., Hamilton, New Zealand 3. 54. Wilson, J. G. (1966) Bovine Functional Infertility in Devon and Cornwall: Response to Manganese Therapy, Vet. Rec., 79, 20, 562. 55. Wiltbank, J. N. (1963) Energy Level Important in Reproductive Performance in Beef Cattle, Progress Report, Univ. of Nebr. 56. Wiltbank, J. N., Bond, J., Warwick, E. J., Davis, R. E., Cook, A. C., Reynolds, W. L. and Hazen, W. M. (1965) Influence of Total Feed and Protein Intake on Reproductive Performance in the Beef Female Through Second Calving, Tech. Bull. 1314, Agr. Res. Service, U.S.D.A., Washington, D.C. 57. Wiltbank, J. N. and Faulkner, L. C. (1970) The Management of Beef Breeding Programs, Bov. Pract., 5, 23. 58a. Wiltbank, J. N., Rowden, W. W., Ingalls, J. E., Gregory, K. E. and Kock, R. M. (1962) Effect of Energy Level on Repro- ductive Phenomena of Mature Hereford Cows, J. An. Sci., 21, 2, 219. 58b. Wong, J. Y., Larson, L. L. and Owen, F. G. (1982) Effect of Beta-carotene Supplementation on Reproductive Performance of Dairy Heifers, Theriog., 18, 4, 461. 59. Wright, P. A. (1960) Infertility in Rabbits Induced by Feeding Ladino Clover, Proc. Soc. Exper. Biol, and Med., 105, 428. Congenital or Hereditary Causes of Infertility in Cows Congenital or hereditary causes of sterility or infertil- ity may be divided into those produced by definite an- atomical defects of the reproductive organs, cytogenetic defects and those hereditary forms of infertility that are obscure, possibly due to multiple factors and difficult to assess. Because of the rapid advances in recent years in the control and elimination of many infectious venereal causes of infertility the genetic causes of infertility are assuming greater importance. Excellent reviews of this subject have been made.15,18’26,36'53'72 Many breed asso- ciations and artificial insemination centers have pro- grams for monitoring and controlling undesirable genetic traits.36 Hereditary or Congenital Anatomic Defects of the Reproductive Tract Hereditary defects are usually due to single gene ef- fects. Certain genes adversely affect both cows and bulls whereas others are sex-limited in their effect. In some females because of the severity of the abnormalities, ste- rility is manifested at the time of their first service pe- riod; while in other cows, in which the defect is less severe, it may not be detected until late in life. Hypoplasia of the ovaries and testes has been well described. 9’13,131.159.223,224 jn ^ swabs soaked in sterile water or saline223,224 are taken for culture at weekly intervals for 3 or more weeks from the prepuce and penis, the urethra and the urethral fossa, around the end of the urethra, and the urethral sinus or diverticulum. In the mare sterile swabs are taken for cul- ture from the cervix, clitoral fossa, clitoral sinus(es) and uterus, early in estrus245,246 and at weekly intervals for 3 or more weeks.8 In the pregnant mare swabs of the cli- toral fossa and sinuses should be taken for culture. After the mare foals (or aborts) the placenta should be cultured as well as the prepuce, urethral diverticulum and penis of the newborn colt or the clitoral fossa and sinuses of the newborn filly, since occasionally CEMO are found in these sites.113,131’160 224,280 The latter sites on the new- born should be swabbed and cultured at weekly intervals on 3 or more occasions before the foals reach 3 months of age.109,131 Foals bom of chronically-infected mares mayINFERTILITY IN THE MARE 605 also be potential or possible long-term carriers of this organism and when bred the first time spread this infec- tion to the stallion in the case of the infected filly or to the mare in the case of the infected stallion and thus initiate a new outbreak of this disease.169 After foaling, and before breeding, the mare should be swabbed and cultured at 3 or more weekly intervals including once during early estrus. All swabs should be smeared on a sterile glass slide and placed in Amies media with char- coal or Stewart’s media, refrigerated at 4 to 6° C and transported within 24 to 48 hours to an approved labo- ratory for the special culture and identification proce- dures necessary for this fastidious CEM organism. It was further recommended that on farms previously infected with CEM or others with much traffic from visiting mares that all stallions and teasers be swabbed and cultured twice at weekly intervals before the start of the breeding sea- son.109 After the outbreaks of CEM in other countries late in the 1970’s the U.S. banned all imports of mares or stal- lions over 731 days of age from countries known to have the infection. In 1981 regulations were changed to per- mit older mares and stallions from these countries to en- ter the U.S. under quarantine and with certain restric- tions including certified routine treatment and testing in the country of origin, similar to that required of animals after they arrive in the United States, with the last swab- bing and culture within 30 days of the export date to the U.S. A clitoral sinusectomy is required in imported mares. After arrival in the U.S. horses are now consigned to an approved quarantine station in certain states with ap- proved facilities where they are examined carefully to see if all the clitoral sinuses have been removed. If not, treatment is delayed and a quarantine imposed until proper surgery has been completed. The genital organs are then treated daily for 5 days. Seven days after treatment, rou- tine weekly swabbings and cultures are conducted. Preg- nant mares are examined and cultured, quarantined until foaling and then treated followed by routine weekly swabs and cultures starting 7 days after treatment.8 Stallions, especially those with streptomycin-sensitive CEMO, must be further tested after treatment, swabbing and culturing by breeding to two noninfected test mares. These mares are then cultured repeatedly on the 2nd, 4th and 7th days after coitus and again at the next estrus and two com- plement fixation tests are conducted 15 to 40 days after service at least 7 days apart.8 A possible supplemental test for suspect carriers of CEM was described that con- sisted of the infusing of smegma from stallions or mares diluted in sterile water into the uterus of a noninfected test mare. The contaminating bacteria were eliminated from the uterus of the estrous mare and the CEM or- ganisms were recovered in pure culture from the uterus and cervix within 3 days. This technique was particu- larly useful when the CEMO was sensitive to the strep- tomycin used to control contaminants in the culture me- dia. Also the CF test could be used 15 days after the inoculation to check for CEM antibodies.273 Specimens and all samples submitted to the laboratory must be doc- umented and carefully identified. Of the serologic tests available the complement fixa- tion test is most sensitive and specific for detection of acutely infected mares from 15 to 40 days after the mare was initially infected. This test is of no value in the con- taminated carrier stallions, chronic carrier mares, carrier foals or possibly pony mares.65 66131,270 Klebsiella pneumoniae var genitalium (formerly called Friedlander’s bacillus or Encapsulatus genital- ium or “viscid rod” infection) is observed much less commonly than Streptococcus zooepidemicus as a cause for mare sterility. Klebsiella infection is characterized by a thick, viscid, tenacious, slimy exudate that may con- tain flocculi.97 The color of the exudate varies from dull- grey to yellowish-white. On speculum examination the vaginal and cervical mucous membrane is usually a dull reddish-brown color. During estrum exudation is profuse and may soil the vulva and tail and mat the hair of the tail and buttocks. These signs may develop within 2 to 7 days after infection and be able to be transmitted in a manner similar to a venereal infection, that is by a stal- lion or by contaminated equipment. This may be asso- ciated with certain highly pathogenic strains of Klebsi- ella.239 Following treatment the mare may remain a carrier as in CEM by the organism persisting in the clitoral fossa and sinuses. Since Klebsiella organisms are commonly found in sawdust and are a common cause of acute mas- titis from that source in dairy cattle, the possibility of Klebsiella infection of the mare’s genital tract from saw- dust bedding should be considered. The presence of other infections tends to increase the inflammatory response of the genital tract to the Klebsiella infection. The in- flammatory processes affect mainly the cervix and uterus and the principal changes are in the mucous membranes and the underlying structures. Often several hundred ml. of exudate is found in the uterus. On rectal examination the uterine wall feels thickened and the uterus is en- larged. If adhesions occur in the cervix, pyometra re- sults; but these advanced lesions of genital infections are less likely to occur with Klebsiella infection than with the other types of organisms. The symptoms and lesions will vary depending upon the age of the mare, the length of time infection has been present, the time of the es- trous cycle, the number and frequency of services during the breeding season. Klebsiella pneumoniae var geni-606 VETERINARY OBSTETRICS talium is a gram-negative encapsulated rod. It is readily transmitted from infected to healthy mares by the stallion at the time of service and by the hands or instruments of veterinarians or others who examine and treat mares. This infection is much more difficult to overcome than is the streptococcic infections and CEM. The sterility produced in chronic Klebsiella infections tends to be more lasting than in the streptococcic infections. This organ- ism belongs to the Klebsiella-aerogenes group, and the paracolon bacteria, that are so difficult to treat even with antibiotics in cases of bovine mastitis.123 Pseudomonas aeruginosa infection of mares’ genital tracts was studied.'35 137 239 Of 70 mares forty-two had a slight to definite hyperemia of the cervix and 15 mares had a milky-white exudate containing flocculent material that turned green, watery-grey, or yellowish-green on exposure to light. This exudate was noted from 6 to 38 days after service to an infected stallion.137 Pseudomonas infection may spread to mares by stallions with normal conception rates. Older mares are more apt to develop endometritis and clinical signs of disease. Sporadic out- breaks of Pseudomonas infection may be caused by cer- tain more pathogenic strains of the organism.239 The differential diagnosis of these and the other mis- cellaneous infections should be confirmed by bacterio- logical examination, as clinical symptoms are not suf- ficiently distinctive for an accurate determination of the etiologic agent. Routine cultures on suspicious mares should be made to confirm the diagnosis and on ob- viously infected mares to determine the etiological agent and its sensitivity to antibiotics.227’228,239 Occasionally a mixed infection may be found on culture of the cervix. This is seen more commonly in pneumovagina. The gen- ital tract of the normal mare, with the possible exception of the vulva, vestibule and caudal portion of the vagina, is free of infection or bacteria.220 A reliable culture may be obtained by culturing the cervix, or preferably the uterus during estrum since at other times of the cycle the diagnosis of infection in the tightly closed cervix causes some difficulties. Other infectious organisms, especially E. coli, may be found on culture of the mare’s cervix and uterus. The possibility of these coliform organisms, that grow rap- idly on culture, being contaminants of the genital tract should be considered. Likewise fungi or yeasts may be found as contaminants but may rarely cause endometritis and even abortion. Candida albicans has been reported following prolonged antibiotic therapy of the uterus and vagina. To establish the diagnosis of a fungal or yeast endometritis it is necessary to culture the organism from the uterus, demonstrate the presence of endometritis and demonstrate the presence of the organism in the uterine lumen or within the endometrium or endometrial glands.48144 Thus to establish a diagnosis of a true uter- ine infection that could affect fertility the causative or- ganising) must be found as well as clinical, cytological or histopathological evidence of an endometritis. The latter can be determined by a uterine biopsy. The procedures for taking endometrial biopsies and their evaluation will be described later in this Chapter. The technique for culturing contagious equine me- tritis organisms44 169 170 205 239 (CEMO), Klebsiella and other organisms from the mare, is easiest while the mare is in estrus and the cervix relaxed and dilated. Swabs should be taken from the cervix or uterus and for CEMO and possibly other organisms, such as Klebsiella, from the urethra and clitoral fossa and sinus(es). The mare should be restrained, in favorable surroundings that are well-lighted, clean and free from dusts and drafts. Stocks, hobbles, a twitch, tranquilizers and extra trained help are often desirable. A new pair of disposable gloves should be worn for each mare. The tail should be bandaged with a 3 to 4 inch sterile gauze bandage or placed in a clean disposable plastic obstetric sleeve. The external genitalia should be carefully scrubbed, similar to a surgical site, with separate pledgets of cotton or gauze saturated with a disinfectant such as Novalsan (chlorhexidine) or Be- tadine surgical scrub working from the vulvar lips and opening and radiating outward until no soil is noted on the pledgets. The area should finally be diyed with clean, moist pledgets to remove excess disinfectants. Prepare the Tiegland* or similar guarded swab44,276 by removing the red plastic cap from the end of the plastic speculum or tube while still in the protective plastic en- velope. The culture swab should be drawn into and pro- tected by the tube or speculum. The opposite end of the envelope from the swab should be cut and the enclosed paper for indentification should be shaken out. On the handle end of the swab place a pencilled circle next to the plastic tube or speculum. This mark indicates to the operator the distance the swab is passed and whether it is fully protected when removed from the mare. Using an 8-inch sterile culture swab, the clitoral fossa is swabbed after spreading the vulvar lips with the cleaned gloved hand and exposing the clitoral fossa and sinus(es). A smear on a sterile glass slide is prepared and the tip of the swab is broken into the Amies transport media. A second 8-inch sterile culture swab is passed 1 to 2 inches into the urethra after locating the urethra with a clean gloved hand. A smear of the swab is prepared on ♦Modified Tiegland Swab, Haver-Lockhart Laboratories, Shawnee, Kansas, 66201.INFERTILITY IN THE MARE 607 a sterile glass slide and the swab placed in transport me- dia. The prepared Tiegland or similar guarded swab is di- rected into the cervix or uterus, either with a disposable clean plastic sleeve on the operator’s hand or with a ster- ile vaginal speculum.276 In the former preferred method, a disposable plastic sleeve is removed from a clean pack and drawn over the hand and arm without touching the outside to any contaminating object. Sterile lubricant is placed only on the back surface of the hand and the arm, not in the palm of the hand. The prepared open Tiegland tube or speculum with contained swab is placed in the palm of the gloved hand to protect it as the hand and tube with swab are passed into the vestibule and forward to the cervix. The tube or speculum is directed by a fin- ger into and through the cervix and into the uterine body. The swab is pushed forward to the endometrium and moved back and forth and rotated. It is then withdrawn well back into tube or speculum as determined by the pencil mark on the shaft of the swab. The open end of the tube or speculum is returned into the palm of the hand and protected as it is removed from the genital tract. The swab is smeared on a sterile glass slide and the tip of the swab removed and placed in Amies media for transport. In the double sterile glove or sleeve technique204'205 the culture tube containing the swab is placed alongside the index finger between a sterile glove and plastic sleeve, or two plastic sleeves, and carried to and through the cervix, even in diestrus. The tube containing the swab is forced through the index finger of the glove, the swab extruded and rotated and withdrawn back into the tube and guarded by the hand before the tube is removed from the genital tract. A smear is made on a sterile glass slide for staining and cytological examination and the swab placed in transport media along with proper indentifi- cation and sent to the laboratory. In the vaginal speculum method239 the sterile vaginal speculum is passed through the vagina and centered on and surrounding the cervix. However this technique may carry organisms from the vestibule to the region of the cervix. The open Tiegland or similar swab in its spec- ulum is passed visually to the os of the cervix and into the cervical canal with gentle manipulation. The Tieg- land speculum should not be forced through the cervix if it doesn’t slip through easily. This is accomplished most readily during estrus. The swab is pushed forward 2 to 7 cm. into the cervix or uterus noting the pencil mark on the shaft to determine the depth of the passage of the swab. After moving the swab back and forth and rotating it, it is retracted well back into the speculum and the speculum and swab are withdrawn through the vaginal speculum followed by withdrawal of the latter. If abundant exudate is in the vagina, a sample should be aspirated with a sterile disposable plastic treatment pipette and syringe. Put about 5 ml. of the exudate in a sterile vial and chill immediately and keep refrigerated until it reaches a laboratory for culture. The technique for culturing CEMO or other or- ganisms from the stallion170 is as follows. The stallion should be adequately restrained by a stallion shank, twitch and/or tranquilization or sedation. Teasing may be nec- essary for extension of the penis. The stallion should be approached on the left side with the handler on the same side staying close to the shoulder and girth area and for- ward from the rear leg. Using an 8-inch sterile swab, swab just inside the preputial orifice or if the penis is extended the reflected preputial membrane. Use another swab to swab the orifice and fossa of the urethra after grasping the extended penis with the hand caudal to the glans. While still holding the penis, a third swab is used to swab the urethral diverticulum or sinus. After collec- tion, each swab should be smeared on a sterile glass slide and the swab broken and placed in a properly labelled vial of transport media, refrigerated and sent to an ap- proved laboratory. After washing the penis and prepuce with mild soap (Ivory) and water and rinsing with clean water and drying, pre-ejaculatory fluids may be collected in a sterile dis- posable beaker by proper teasing of the stallion. Five ml. of this fluid should be placed in a sterile vial and sub- mitted with the above samples. The procedures used to obtain satisfactory cultures of the uterine cavity and their interpretation have been dis- cussed. Smears of swabs taken immediately after re- moval from the uterus are useful when stained, espe- cially with Gram’s stain, to determine the type of bacteria present and their numbers and also the presence of neu- trophiles and their number which is indicative of the de- gree of endometritis. Culture of this swab by the veter- inarian and even sensitivity testing will give more prompt information than sending the culture sample to a labo- ratory in suitable media and under refrigeration. How- ever a good diagnostic laboratory can provide more ac- curate information on the types of organisms and their sensitivity to antibiotics than can most field laboratories. Endometritis due to the introduction of bacteria naturally at the time of service, at parturition or experimentally14'47112’134’137’220 usually results in varying degrees of distention and turgidity of the uterus with an increased blood supply, enlargement, edema and relax- ation of the cervix and a flow of flocculent pus and mu- cus through it into the vagina at any stage of the estrous cycle, luteal or estrogenic, in the young normal healthy608 VETERINARY OBSTETRICS mare. A marked invasion of the endometrium and uter- ine lumen with many neutrophiles rapidly phagocytize the infecting bacteria and eliminate the bacteria, espe- cially streptococci, within 3 or 4 to 15 days with a return of the uterus to normal. Occasionally secondary infec- tions due to organisms, such as Pseudomonas, may last through several estrous cycles before being eliminated by the well-developed defense mechanisms of the mare’s uterus. These mechanisms include hormonal factors whereby estrogens cause a significant increase in phago- cytic activity that enhanced the bacteriostatic uterine mechanisms while progesterone inhibited the immune response in ovariectomized mares. 112,303 However in in- tact mares the endometritis produced by the infecting or- ganisms caused the apparent release of prostaglandins from the endometrium and caused luteolysis of the CL with the prompt onset of estrous with a short estrous cycle. Immunoglobulins, based on a preliminary study, do not play a significant role in this uterine defense mecha- 14 msm. Chronically infected, “infection-prone” mares with a chronic persisting endometritis or recurring endometritis are usually older, barren mares or mares with a poor reproductive history which when experimentally infected with bacteria into the uterus exhibit little if any reac- tion.'34,137 220 The uterus doesn’t become enlarged and turgid but the uterine lumen continues to contain a cream- colored exudate that may occasionally be noted in the cervix and vagina during estrus. Apparently the uterine defense mechanism in these mares is disrupted, probably at the cellular level, and the marked invasion of neutro- philes and monocytes and the phagocytosis of the bac- teria does not occur as in a normal healthy often younger mare. Thus all degrees of endometritis may be observed from mild to severe, acute, subacute or chronic depending upon the pathogenicity of the organism, the numbers of or- ganisms introduced into the uterus and the degree of re- sistance or ability of the uterine defense mechanisms to overcome the infection. Endometritis is a major cause of infertility in mares because of the resulting “hostile” en- vironment for spermatozoa and the embryo. Cytological or histopathological examination may be required to de- tect endometritis as only 44 (39%) of 114 mares with endometritis showed significant bacteriologic findings on culture.239 Metritis and pyometra due to these same wound-in- fection type of organisms often results in rather pro- nounced pathological changes in the uterus especially in older “infection-prone” mares with defective uterine de- fense mechanisms.137,239 Deep red, hemorrhagic areas and intervening areas of whitish-yellow mucosa may be scat- tered irregularly in the endometrium. In severe cases the endometrium may be denuded at many points and have a dull, red, granular appearance. The amount and con- sistency of exudate present may vary from less than 100 ml. to 5 to 10 gallons and from watery, to mucoid to inspissated or cheesy. In metritis, as in cervicitis and vaginitis, the changes, depending on the stage of the cycle, the type of organism, and the predisposing causes, vary from a mild superficial involvement of the endometrium or endometritis readily cured by proper treatment or sex- ual rest to severe, advanced, and permanent pathological lesions of the endometrium with small abscesses of the uterine glands and chronic fibrotic, degenerative and proliferative changes in the endometrium and uterine wall. In cases in which the cervix is closed by adhesions or induration the uterus may contain several quarts or gal- lons of mucopus.186 In this unusual type of pyometra, or uterine abscess, the endometrium may be severely de- generated and eroded and the mare is anestrous. The uterine wall may be thin and atonic and in advanced cases the endometrium is almost completely destroyed. The mucosa in some cases becomes a tough, thick, yellow- white fibrous pyogenic or diphtheritic membrane. In the occasional pyometra case due to subinvolution of the uterus with an open or patent cervix, the endometrial pathology is not so severe although edema, degenera- tion, desquamation and sloughing of small areas of the endometrium may occur. In these cases estrous cycling may result in evacuation of the mucopus. Pyometra in the mare may be associated with a retained or persistent CL and failure of estrum up to 12 months or more as in the cow. If the endometrium is sufficiently diseased so that prostaglandin is not released to cause luteolysis, the progesterone levels remain above 2 ng/ml. in blood plasma. A neutropenia without a left shift and occasional lymphopenia with mild erythropoiesis and an increase in monocytes and eosinophiles have been reported in mares with pyometra.142 In rare cases of pyometra, or of uterine abscess due to adhesions or obstructions in the cervix it may be nec- essary to break the adhesions or to make an incisions through them to release the pus. Placing a gauze pack or plastic pessary172,190 in the opening for several weeks will allow establishment of a fistulous opening for drain- age into the vagina and prevent the uterus from refilling with pus. Prognosis for future breeding of such mares is poor. Successful removal of the uterus and ovaries, ovariohysterectomy, in mares with severe pyometra or uterine abscess has been reported.195,307 In one case ob- served by the author nearly 15 gallons of pus were drained from the uterus of a small mare with cervical and vaginal atresia due to adhesions. The mare had suffered a severeINFERTILITY IN THE MARE 609 dystocia 6 months previously. Such mares are incurably sterile. Perimetritis in the mare is apparently very rare, or else when it does occur the results are fatal due to peritonitis. In severe chronic metritis, particularly due to Klebsiella infection, a typical chronic productive inflam- mation results that may produce an atrophy and fibrosis of the uterine wall from mucosa to serosa. Cervicitis due to a variety of infections is common and injury to the cervical mucous membrane can occa- sionally be serious in nature. In cervicitis the mucosa as seen at the external os is usually congested and dark red to purple in color; the os is generally edematous, pen- dulous, and dilated. In rare cases the cervical glands be- come cystic; deep suppuration and abscess formation may occur. Fibrosis of the cervix is usually not as pronounced as it may appear clinically, nor as severe as in the cow with advanced cervicitis. The inflammatory process in- volves mainly the mucosa of the cervix. In rare cases membranous or solid, thick adhesions may completely obstruct the cervical lumen and since uterine infection is usually present, pyometra or uterine abscess is likely to develop. Severe lacerations, scarring, and malformation of the cervix may occasionally occur in the mare at the time of parturition and produce a chronic cervicitis or cause a failure of the normal closure of the cervix, or incompetency of the cervix, resulting in repeated early embryonic or fetal deaths due to recurring infection, en- dometritis and permanent sterility. The surgical repair of cervical lacerations resulting in an incompetent cervix performed a month after foaling during the diestrous pe- riod where after debridement, the cervical mucosa, the cervical muscle and the vaginal mucosa are sutured sep- arately is described.105 A simple retention or purse-string suture placed around the caudal portion of the incom- petent cervix after breeding or early pregnancy diagnosis is also described.105 This suture must be removed a few days before foaling. Repeating these surgical procedures is usually necessary after each foaling. Vaginitis and vulvitis due to a variety of infections is commonly observed. The vagina and vestibule appear to be more resistant to irritation and permanent damage caused by infections than does the cervix and uterus. In severe metritis and cervicitis with a catarrhal exudate the vagina is usually involved. Mares that develop the habit of pneumovagina or pneumovestibule usually exhibit a vaginitis and vulvitis often with a mucopurulent exudate. Fecal material and urine may occasionally be found in the cranial part of the vagina. Injuries, trauma, lacera- tions, or severe infection of the vulva and vagina at par- turition may cause chronic vaginitis, pneumovagina, and in rate instances stenosis of the vagina. A rectovaginal fistula causes a severe vaginitis. Occasionally the cloudy, turbid, light-colored urine of the mare may be confused with a vaginal discharge by the owner. In rare instances cystitis in the mare may develop but is usually secondary to a vaginitis or metritis. Urovagina, “urine-pooling” or vesicovaginal re- flux in the fornix of the vagina is occasionally noted in barren, old, pluriparous mares with a large pendulous uterus, sunken anus and horizontal vulva that allows urine to flow into the cranial portion of the vagina especially during estrus. This condition is often associated with pneumovagina and sterility. A few cases may occur around foal estrus and as uterine involution progresses urova- gina may terminate after 2 or 3 postpartum estrous cycles. In early cases of persistent “urine-pooling,” carefully douching the vagina with several liters of sterile physi- ological saline solution to which antibiotics have been added and then removing the saline just before natural service or preferrably A.I., followed promptly by the Caslick, vulva-suturing operation often results in con- ception. In long-standing cases or those in which vagin- itis and endometritis are severe, vaginoplasty or urethral extension by surgery on the caudal vaginal floor and/or vestibule can be successfully performed to prevent uro- vagina.56’197'239’301 Caslick’s operation is usually also per- formed on these mares. Salpingitis is rare in the mare. An enlarged uterine tube was never found on rectal examination of the mare.97 On postmortem examination of 83 mares with metritis, only 18, or 21.7 percent, showed evidence of salpingitis as determined by gross and microscopic examinations. Not all oviducts that showed inflammatory changes were positive on culture. Salpingitis in the mare is an ascend- ing infection from an infected uterus. Some infected uterine tubes undergo no pathological changes while most others exhibit only a slight catarrhal inflammation. In very rare cases, inflammation may be severe enough to cause fibrosis and occlusion of the lumen with inflam- matory exudates. In no cases were the uterine tubes thickened and enlarged. In 700 equine genital tracts ex- amined in Belgium all were patent and cases of hydro- salpinx were not present.288 Two cases of hydrosalpinx and one occluded oviduct were reported by other au- thors. This latter condition was due to an oviductal cyst. However infundibular adhesions, infundibulitis, and am- pullitis was commonly found in 40, 37 and 21 percent of the tracts, respectively. Endometritis was noted in 31 percent of the tracts and often associated with isthmitis that occurred in only 9 percent of the tracts. The cause of the infundibulitis was unknown but factors such as bleeding at the time of ovulation as occurs in cattle or possibly Strongylus edentatus larvae were suggested. The degree to which this common nonocclusive chronic610 VETERINARY OBSTETRICS salpingitis reduces fertility is not known. A safe, reliable accurate means of checking the potency of equine uter- ine tubes by injecting starch granules on to the ovaries and finding them in the cervix one to 7 days later has been described.4 2,9 The presence of a papilla containing a smooth muscle sphincter through which the uterine tube opens into the uterine cavity may furnish a possible ex- planation of the rarity of severe salpingitis in the mare. Ovaritis in the mare is very rare. Evidence of acute inflammation of the ovary was rare in any postmortem cases.150 97 Two cases of an ovarian abscess in which Streptococcus zooepidemicus was found in one were reported.50 97 One was secondary to the tapping of an ovarian cyst. Adhesions between the ovary and sur- rounding tissues is rare except in association with ovar- ian abscesses. Prognosis of Genital Infections in Mares. Uterine, cervical and vaginal infections in mares due to pneu- movagina or infection of the uterus after parturition, abortion or service usually respond to treatment. In many acute cases of endometritis in normal, healthy mares re- sistant to infection prompt recovery without treatment, except in cases of pneumovagina, may occur within sev- eral days or weeks as discussed previously. The sooner a persistent infection is diagnosed and the proper treat- ment given, the more favorable the prognosis. In long- standing, severe cases due to virulent pathogenic bac- teria, endometrial damage may be severe and permanent and result in sterility. Massive purulent metritis with ci- catrization causing a loss of endometrium, and extensive cervical lacerations are two conditions that may render a mare hopelessly sterile.227 Usually it is much more dif- ficult and takes longer, and may occasionally be impos- sible to correct chronic infections due to Ps. aeruginosa, E. coli and Klebsiella than streptococcal and CEM in- fections, as the former organisms are more resistant to antibiotics and other treatments and cause greater tissue damage than the latter. In early mild infections proper treatment may result in prompt recovery within 1 to 2 months. In severe or chronic cases treatment and sexual rest for 6 months or more may be necessary in order to effect a cure. In pyometra due to an obstructive lesion in the cervix causing cervical stenosis the prognosis is usually poor or hopeless for the future breeding life of the mare. In urovagina, “urine pooling,” the prognosis is guarded to poor. A uterine biopsy and a knowledgeable prognosis based on the histopathological findings in conjunction with a complete clinical history and examination of the genital tract is very helpful in the prognosis of endometritis which may vary from mild to severe and be associated with other pathology including endometrial fibrosis, atrophy, degeneration, hypoplasia or hyperplasia. The prognosis for recovery and future breeding success should be guarded in older barren mares with a history of abortion, pyome- tra, and infertility. The technique of uterine biopsy will be discussed later in this Chapter. Treatment of genital infections in mares. The su- turing of the upper part of the vulvar lips, the Caslick operation,74 sexual rest, and possibly antibiotic intra- uterine infusions enable the veterinarian to give a much more favorable prognosis in cases of uterine infections than was possible previously.58,227,240 Early detection and treatment of genital infections of mares is essential to prevent sterility, early embyronic deaths, and abortions. Most genital infections in mares can be prevented by proper hygienic handling of the mare and stallion at the time of breeding, by proper attention and hygiene ap- plied to the mare at foaling, by close observation, cul- turing, and proper sanitary procedures in examining and treating mares, if necessary, prior to breeding. The con- trol of genital infections causing sterility or infertility in mares is mainly a matter of preventative therapy and hy- giene. This point cannot be stressed too strongly. The vulva-suturing or Caslick operation, to prevent pneumovagina or the sucking of air and debris into the genital tract has been well-described239,301 and is per- formed as follows: the tail is bandaged and the perineal region and vulva carefully cleansed with soap and water. The mare is restrained by means of a twitch being placed on the nose and one foreleg being picked up. If the mare is excitable or vicious, a tranquilizer such as zylazine HCL or promazine HCL may be given intravenously for sedation. The mucous membrane of the vulvar lips is anesthetized by infiltration with a local anesthetic solu- tion such as procaine, lidocaine or carbocaine, from 1 inch (2 cm.) below the level of the floor of the pelvis or ischial arch to and including the dorsal commissure, to a depth of .5 inch (1 cm.) from edges of the lips of the vulva at the mucocutaneous junction. In the hyper- sensitive mare it is desirable to anesthetize a small area of the mucous membrane at the border of the vulvar skin by holding a pledget of cotton that has been soaked in lidocaine or a similar anesthetic that can be applied lo- cally before the 22 to 23 gauge needle is inserted. The mucous membrane elevated by the local anesthetic so- lution is removed by scissors after stretching each vulvar lip with forceps applied at the dorsal commissure. The scarified edges of the vulvar lips are brought together by separate nylon sutures placed about one-fourth to three- eights inch apart or by a continuous interlocking suture. An oily antibiotic may be applied to the suture line to prevent dry scabs and make removal easier. The sutures are not tightened too firmly inasmuch as they may cutINFERTILITY IN THE MARE 611 the tender tissues. Union takes place rapidly and the su- tures can be removed about the tenth day after the op- eration. The administration of tetanus antitoxin is prob- ably not necessary but in valuable mares not protected by tetanus toxoid, it may be a justified precaution. This operation effectively prevents pneumovagina in most barren, infected mares and should be used on any mare if this condition is present or suspected. In mares in which pneumovagina is well-established, the vulva must be kept carefully sutured for the rest of the mare’s breeding life since once this operation becomes necessary, seldom does the mare return to normal. An exception to this is the occasional young maiden mare that was sutured at the track that can be “opened” at the breeding farm and doesn’t require further suturing. If the vulvar opening is too small, the adhesion between the vulvar lips should be incised after injecting the area with a local anesthetic solution to make the vulvar opening large enough to ad- mit the penis at breeding. A stay or protective suture is usually inserted at the dorsal portion of the incised vul- var lips to prevent tearing or trauma to the vulva or intact previously sutured area at the time of coitus. If the mare is to be bred again in 2 to 3 days, this stay suture may be allowed to remain in place. The stay suture is usually made of a double thickness of one-fourth- or one-eighth- inch umbilical tape or heavy linen thread inserted into the anesthetized vulvar lips one-half to three-quarter inch, 1 to 2 cm. from the edges and tied rather tightly. A breeding or stallion roll should be used at the time of all natural covers on sutured mares.240-243 Following service in cases in which incision of the vulva was necessary, it should immediately be resutured. At the time of par- turition, or 7 to 14 days beforehand, if a veterinarian is not to be present at the time of the mare foals, the vulva is opened by a blunt-pointed bistoury or sharp scissors after local anesthesia has been administered. After foal- ing the vulva should be resutured promptly. In the mare the vulva-suturing operation is the single most important procedure in the treatment of pneumovagina and sterility due to infection of the genital tract. Once it is indicated and undertaken it usually must be continued for the breeding life of the mare. As mentioned previously the easy and successful performance of the Caslick opera- tion to greatly improve fertility in many Thoroughbred mares may be perpetuating and increasing the number of mares with poor perineal conformation that require this • 182 operation. The vulva of normal mares may be temporarily su- tured or clamped after foaling, especially if vulvar lac- erations or a retained placenta occur, to prevent pneu- movagina until the genital tract returns to normal in 1 to 2 weeks. In a few mares windsucking may occur only during estrum or after service when the vulva is relaxed. These mares benefit from temporary closure of the vulva until the vulvar tone returns. When the vulva is tem- porarily sutured or clamped, scarification is not per- formed. The vulvar lips are simply pulled firmly to- gether, usually by means of nylon sutures. Following the Caslick operation most mares overcome the infection of the genital tract within 1 to 6 months, depending on the severity of the infection, without fur- ther treatment, since reinfection due to sucking of air and debris into the vagina is not recurring. These mares should not be bred until the infection is overcome. This em- phasizes the necessity of checking and treating barren, infected mares during the fall season or a number of months before the breeding season. Although some mares with mild streptococcal infections may conceive, early or late abortion may result, or the foal may be diseased at birth, or the placenta retained at the time of parturi- tion. The use of antibiotics parenterally and locally as intrauterine and intravaginal infusions or douches in the genital tract may precede closure of the vulva and result in a greater number of cures in a shorter length of time. The Caslick operation alone, together with a proper pe- riod of sexual rest, results in a high rate of recovery.84 Of 36 infected mares on which this operation was per- formed because of vaginitis and cervicitis and evidence of pneumovagina, 22 or 61 percent became pregnant the next season. No other treatment was used. In rare cases of pneumovagina associated with a hor- izontal vulva and a sunken anus in which the Caslick operation does not correct the pneumovagina or urova- gina (urine-pooling), more extensive perineal surgery is indicated. This may require removal of skin in the lateral and caudal areas of the perineal region to draw the anus caudally, separation of the anus and vestibule to permit the vulva to assume a normal horizontal position, ure- thral extension or other procedures or combinations of “plastic” surgery to permit possible conception. In these severe cases the prognosis should be guarded to poor for future fertility. The value of sexual rest following the Caslick oper- ation, to allow the natural body defenses to overcome infection, is well proven. It has been observed frequently that apparently normal mares infected on the ninth day or foal estrus, if not bred, will in many cases free them- selves of infection by the second estrum, about 25 to 30 days after parturition. Breeding on foal estrus, should not be practiced: if the placenta weighs over 14 pounds; if the foal is weak, deformed, or dead at birth or dies soon after birth; if the mare needs assistance in foaling; if the mare has abnormal discharges either in color, quantity, or consistency during the first week after par-612 VETERINARY OBSTETRICS turition; or if the genital tract is not free from any sign of infection, inflammation, or trauma when examined152 and possibly cultured on the seventh or eighth day after foaling. In some mares even longer periods of sexual rest are required. If a mare foals late in the breeding season and is infected, it may be desirable to hold her over until the next breeding season for service. In mares having difficulties such as retained placenta, dystocia, or severe infection and metritis at or after parturition, treatment and sexual rest for 2 to 3 months or until the following year may be indicated. As discussed previously mares may be treated locally and systemically by antibiotics on foal estrus if parturition was abnormal. Some mildly af- fected mares may be treated with PGF2a, 10 mg, 7 days after foal heat and bred on the second induced cycle about a week sooner than if a prostaglandin had not been ad- ministered. Some mares suffering from one or more of these con- ditions at parturition or after an abortion have a metritis and a delayed involution of the uterus. This can be de- termined by the breeding history, by the presence of a chronic uterine infection and discharge, and by a rectal examination that reveals a large, thick-walled uterus possibly containing varying amounts of mucopurulent exudate. Frequent douching of the genital tract of the mare at estrus with a mild antiseptic solution, such as weak Betadine, or Novalsan (chlorhexidine) solution, may assist in correcting mild inflammatory conditions. Too irritating solutions should be avoided as they may cause prolonged endometrial inflammation, ulceration, and possibly adhesions in the uterus and cervix.37'184 A 10% (3 ml. in 30 ml. of saline) Lugol’s solution was irritating to the endometrium. A plastic indwelling uter- ine infusing instrument was developed165'239 permitting frequent infusions of the uterus with antibiotics or an- tiseptics. The value of such a cathether is limited and questionable. The author has experienced difficulty in having mares retain the instrument. Nevertheless douch- ing under sanitary procedures at intervals of 1 to 2 days during estrus with a very mild chlorine solution, 50 ppm, a warm physiological saline solution alone, or physio- logical saline solution to which some penicillin, strep- tomycin, or broad-range antibiotic, such as a tetracy- cline, nitrofurazone or furacin, polymyxin B and/or neomycin combinations, have been added, may aid in hastening involution of the uterus and correction of the metritis and vaginitis. If the type of organism(s) causing the infection is known and the sensitivity of these or- ganisms to the various antibiotics has been determined, select the antibiotic that will be most effective. These solutions may be pumped into or run into the uterus by gravity. If a mucopurulent exudate is present in the uterus, this should be removed by douching and siphoning from the genital tract. Some veterinarians use antibiotics in- fused or inserted in an oil or tablet form into the uterus and left there to hasten recovery. Stilbestrol or estradiol in 20- to 30-mg. doses intramuscularly may be useful. In some of these cases the Caslick operation may be nec- essary. Exercise in moderate amounts may have value in improving the tone and hastening the involution of the uterus after foaling. In recent years the use of antibiotics for uterine in- fections in mares has become widely practiced.239'243 With the large number of antibiotics and combinations of sul- fonamides and estrogens available, each veterinarian treating genital infections of mares uses his favorite in- trauterine preparations or combinations. In general, pen- icillin, nitrofurazone and the broad-range antibiotics such as terramycin or oxytetracycline, aureomycin or chlor- tetracycline, tetracycline and ampicillin are most effec- tive against streptococci and the Gram-positive organ- isms. Streptomycin, neomycin, chloramphenicol, polymyxin B sulphate, gentamicin199 and amikacin sulfate55 are most effective against E. coli, Ps. aerugi- nosa, Klebsiella pneumoniae and other gram-negative organisms.78 278 Some veterinarians put these products into oil or into saline.227'239 Amounts of 50 to 250 ml. are usually used for instillation into the uterine lumen. Most veterinarians prefer to treat the uterus 2 to 5 times at 24 to 48 hour intervals during estrum when the natural uter- ine defense mechanisms are active. Clitoridectomy and or sinusectomy as in the therapy for CEM may be nec- essary in persistent Klebsiella infections in mares. Because of official regulatory requirements for the treatment of this reportable disease of CEM, therapy is given separately from other genital infections of mares. H. equigenitalis is sensitive to a wide range of anti- biotics and antiseptics including penicillin, ampicillin, neomycin, chloramphenicol, gentamicin, tetracyclines, nitrofurazone and chlorhexidine. The latter two drugs are used most commonly in the local treatment of the genital organs of infected mares and stallions with a high per- centage of cures when properly applied. Presently it is necessary to perform a clitoral sinusec- tomy on suspected or infected mares before antimicro- bial treatment of the genital tract. Because of the small openings of the sinuses, swabbing for culture and treat- ment is difficult or impossible.8 After sedation, often with zylazine (Rompun) and restraint, 20 to 50 ml. of lido- caine or carbocaine is infiltrated in the region around and under the clitoris. Stay sutures are placed in the lower vulva and clitoris to assist in the careful surgical removal of the entire sinuses (sinusectomy) and fossa or the com- plete removal of the sinuses, clitoris and fossa (sinusec-INFERTILITY IN THE MARE 613 tomy and clitoridectomy). The use of a small probe to delineate the depth and location of each sinus is essential to its complete removal. After either type of operation the wound produced may be left open to heal or sutured to more completely obliterate the clitoral fossa.106'161 This operation could be performed on the pregnant mare but in most cases it is deferred until after foaling. Excised sinuses of possibly infected mares should be sent promptly under refrigeration to an approved laboratory for culture. Although swabbing, culturing and treatment of quaran- tined mares and stallions, along with adequate records has resulted in the apparent eradication of the disease (CEM) in the U.S., the use of artificial insemination of mares with CEM-free semen or semen from an infected stallion to which antibiotics have been added, particu- larly gentamicin230 may be of value in the future under certain extenuating circumstances. Treatment of infected or suspect stallions or mares re- quire their isolation and quarantine until the treatment and subsequent repeated swabbings and cultures are completed.8 109 159 These animals should have their ex- ternal genitals cleansed thoroughly with warm clean water. This should be followed by a thorough cleansing and “surgical” scrub with a 2 percent chlorhexidine in a de- tergent base (Novalsan Surgical Scrub, Ft. Dodge Lab- oratories) of the erect penis, prepuce, and urethral sinus of the stallion and the external genitalia, vulva, vestibule and clitoral area of the mare. This is followed by a wash of clean warm water and drying. Then 0.2 to 0.3 percent nitrofurazone ointment (Furacin Ointment, Eaton Lab- oratories) is carefully applied in and to the above areas. This treatment is repeated at daily intervals for 5 treat- ments. After a rest of 7 days, swabbing and culturing in the aforementioned manner is then carried out. The uterus, cervix and vagina may also be infused daily for 5 days with 50 ml. of a lower concentration, 0.05 to 0.25 per- cent of a chlorhexidine gluconate solution, as higher lev- els are irritating. Most open mares spontaneously elim- inate the infection from the deeper areas of the genital tract, vagina, cervix, uterus and uterine tubes after a few weeks or months. Parenteral and local antibiotic treat- ment of mares for CEM has not proven to be necessary or highly effective. Acute cases of CEM may not require treatment as the mare’s natural defense mechanisms rather rapidly eliminate the organism from the uterus of the cy- cling mare.63,66 Since CEM is a highly contagious venereal disease, spread of the disease in the breeding shed is highly pos- sible as it was with vibriosis in bull studs.234,300 Strict aseptic carefully supervised procedures in the breeding shed are essential including the use of disposable plastic gloves and plastic pail liners, careful breeding hygiene before, during and after service or semen collection, and the use of sterile individual equipment and material for cleaning the genitals, examination and insemination. Veterinarians supervising breeding shed hygiene should eliminate all possible avenues of genital contamination or spread of organisms between all animals except the two animals being bred. This requires establishing a rigid step by step procedure, training and acceptance of these procedures by the attendants in the breeding shed and the continued monitoring of these procedures by the vet- erinarian. Such a practice could also control infections other than CEM. If present control and eradication measures are not ad- equate or are ineffective, artificial insemination and the development of a vaccine might be developed to mini- mize or control the infertility associated with CEM. Vac- cination of ponies against CEM with a killed bacterin from H. equigenitalis provided a degree of immunity but did not protect them from developing the disease when challenged.1076 CEM is a reportable disease and any suspected out- breaks with signs of a genital discharge soon after ser- vice, short estrous cycles and infertility should be re- ported to the state and federal regulatory officials as well as to owners of mares and stallions possibly exposed to the infection. Because of the great mobility of equine racing, breeding and show animals within and between countries and states, most animal regulatory agencies in each country have formulated and put into law regula- tions, codes or requirements pertaining to the importa- tion and movement of horses to control or prevent the spread of CEM.1’610 and other diseases. These codes or regulations require strict adherence to testing, identifi- cation, treatment and quarantine procedures. These codes or regulations are promulgated yearly and changes in them are made as further information on CEM and its epi- demiology are developed. Most cultures positive for molds or fungi and yeasts, Aspergillus, Mucor and others and Candida, are a result of contamination of the upper genital tract and they do not cause severe inflammatory reactions with endome- tritis and are rapidly eliminated spontaneously.48 Occa- sionally they do produce a severe inflammation with in- vasion of the endometrium and a well-established infec- tion as determined by biopsy. This may occur after in- tensive prolonged antibiotic therapy for a bacterial in- fection resulting in the introduction of the opportunistic fungi or yeast into the uterus, especially in infection- prone mares. Fungi are common in the environment of mares and frequently contaminate culture swabs, plates or media and provide erroneous readings. Although weak iodine solutions, Lugol’s and Betadine, and systemic io-614 VETERINARY OBSTETRICS dide therapy have been used in the past for treatment, presently nystatin, 500,000 I.U. daily for 5 days, am- photericin B231 and clotrimazole 400 to 600 mg. uterine infusions every third day for 3 to 4 treatments have been recommended. This latter drug, a human product, is available in suppository form which may be inserted into the mare’s uterus.144 Antibiotics given parenterally are of little value in chronic uterine infections.241 Local treatment is indi- cated. Systemic treatment is indicated in acute or severe uterine infections causing a pyemia or septicemia as may occur after parturition. Autogenous bacterins have been used with some success in genital tracts infected with Klebsiella or Pseudomonas organisms in mares.26,58,59 Further controlled studies on the value of autogenous bacterins against specific infectious organisms are needed since spontaneous recoveries in mares after a period of several months or more of sexual rest are not uncom- mon. If the Caslick operation is indicated it should be performed, since antibiotic therapy alone cannot per- manently correct a genital infection due to pneumova- gina. Genital rest will aid recovery, and bacteriological and cytological or histopathological examinations of the uterus will indicate when breeding can be undertaken with an expectancy of conception. In mares with pyometra not due to an obstructed or sclerosed cervix, that are anestrous due to a persistent CL with an elevated, >2 ng/ml, plasma progesterone level should be treated with a luteolytic dose of prostag- landin or prostaglandin analogue25 to evacuate the uterus and followed by antibiotic therapy of the uterus during the induced estrous period. Infections of the genital tract secondary to severe in- juries to the perineum or from recto-vaginal fistulas re- quire the repair of the trauma-induced lesions in order for subsequent conception to occur. However, the author and others241,243 have observed rare cases of mares that have had a recto-vaginal fistula that conceived and de- livered a normal foal. Conception in mares with severe injuries involving the recto-vulvar area are not uncom- mon because of the protection provided the vagina by the vestibular-vaginal sphincter and folds of mucous membrane in that area that prevent pneumovagina. Barren older mares with a history of recurrent chronic endometritis even though they were free of infection in their genital tract at the time of service or experimental exposure to infectious bacteria such as streptococci or Pseudomonas organisms, showed a greatly reduced uter- ine and cervical reaction with an increase in polymor- phonuclear leucocytes as well as eosinophiles in the en- dometrium. These older susceptible, infection-prone mares exhibited less mucopurulent exudation and a persistence of the infection and developed a chronic endometritis. There was definite evidence that these chronically in- fected mares or those that readily become infected had a breakdown or alteration in the non-cellular defense or bactericidal mechanisms in the uterus which set them apart from the normal, healthy, often young mares which ex- hibit an excellent, prompt, highly effective defense mechanism. There apparently is a delicate balance be- tween the pathogenicity of the infective bacteria and the susceptibility of the mare to infection.134,135,137,220 Infec- tion-prone, often older, mares are highly susceptible to uterine infections or endometritis after foaling and after each service period unless preventive therapeutic pro- cedures are taken. Twelve to 24 hour postbreeding or postovulation an- tibiotic treatment of the uterus using 250 to 500 ml of an antibiotic solution reduced the uterine bacteria present from the natural service or present in the uterus at the time of service and prevented the infection from becom- ing established in many susceptible mares.163,275 This greater susceptiblity to infection and infertility after ser- vice in older pluriparous mares that often had a local dilation of the ventral portion of the base of the uterine horns or in the body of the uterus was noted.163 In these locally dilated areas the mucosal folds were flattened and the endometrium was atrophic and aglandular. The rest of the uterus was normal. In a subsequent large study employing post-breeding antibiotic uterine treatment of mares no benefit was demonstrated by such therapy.304 A review of the antibacterial drugs used in the uterus of the mare concluded that this therapy is of secondary importance to good management and breeding hygiene. But in individual mares following proper diagnostic pro- cedures, antibiotic therapy along with induced estrus, using the prostaglandins, and sexual rest could be useful in restoring fertility in certain mares.86 Many stallions may harbor Pseudomonas, as well as Streptococcus zooepidemicus, Klebsiella and other bacteria, fungi and yeasts.26,27,134,137,257 Elimination of these infections from stallions is very difficult and usually un- successful. Most of these infectious organisms in stal- lions are not highly pathogenic, but a few stallions may apparently carry and transmit virulent organisms that in- fect a large number of mares bred to him. This fact fur- ther accentuates the necessity of careful hygiene in the breeding act. As noted previously excessive use of an- tiseptics on the stallion’s genital organs such as Noval- san and Roccal, may cause the development of resistant gram-negative bacteria that cause more serious prob- lems.51,202 In breeds of horses where artificial insemination is practiced the control of the bacterial flora in the extendedINFERTILITY IN THE MARE 615 semen with antibiotics is indicated especially for the in- fection-prone mare where the infection has been elimi- nated, but coitus would probably reestablish the endom- etritis.135,239,289 These authors recommended adding 1000 units of potassium penicillin, 1 mg. of dihydrostrepto- mycin and 200 units of polymyxin B. sulphate per ml. of skim-milk or cream-gelatin diluter (see Artificial In- semination in horses) and inseminate with semen ex- tended 1:1 or 1:4. The latter report289 recommended that 1000 units of polymyxin B per ml. be added to fresh skim-milk extender to control both Klebsiella pneu- moniae and Pseudomonas aeruginosa. The warm se- men should be added to this warm semen extender con- taining antibiotics and incubated at body temperature, 38° C, for 15 to 30 minutes before it is used to insem- inate mares. In breeds permitting the registry of foals conceived by artificial insemination, the use of this prac- tice with semen extender with antibiotics, along with strict management and hygienic practices, has resulted in im- proved, 10 to 20 percent, foaling rates versus natural service and less supervised management.99 Thus for infertle, infection-prone, usually older, mares who often have a moderate degree of endometrial fibro- sis and infiltrative endometritis as determined by endo- metrial biopsy, careful breeding management and hy- giene at the time of service is imperative. Limiting the number of services in an estrous period to one or pos- sibly two and/or the use of HCG to shorten the estrous period and hasten ovulation is desirable. The use of the post-service uterine infusions of antibiotic solutions and the use of artificial insemination with extenders contain- ing antibiotics have been practices that have been proven to be of value in improving the foaling rate of these in- fertile mares. Because each of these above procedures or practices have shown merit, Kenney and Rossdale and Ricketts have developed and modified them into minimal con- tamination techniques (MCT) for breeding mares.156,239 The former study156 reported that even when the penis and sheath of stallions were carefully washed with soap and water and rinsed before service, the ejaculate from most stallions contained 4 to 36 million colony-forming units (CFU) of a variety of Gram-positive and negative bacteria. Thus this semen could readily reinfect the sus- ceptible uterus. The following minimal contamination techniques were designed for breeds which permit arti- ficial insemination and those mandating natural service. A. Minimal contamination technique for artifical breeding: 1. The stallion is trained to mount a phantom lo- cated in a clean, dust-free area and ejaculate into a clean, sterile artificial vagina. The latter is sterilized by washing in hot water and non- residue soap, rinsed thoroughly with hot water and disinfected in 70% ethanol for several hours. Before use the artificial vagina (AV) is rinsed in hot water and physiological saline solution. A thin film of a non-spermicidal lubricant such as KY jelly is spread through the AV with the arm covered by a plastic sleeve. 2. The stallion, before semen collection, is sex- ually aroused and the penis and sheath are care- fully washed with a warm soapy non-detergent water which is removed by multiple warm water rinses. (If a quiet mare is used for a mount in- stead of a phantom her tail should be bandaged and her buttocks and perineal region carefully washed and rinsed. Before permitting the stal- lion’s penis to enter the AV the penis of the mounted stallion should be drawn to the side to allow the discharge of some of the urethral gland or presperm fraction to flush and remove bacteria from the urethra. 3. After collection of the ejaculate in the AV, it is poured through a sterile in-line milk filter into a sterile warmed beaker to remove the gel fraction. The semen is evaluated for motility, number of normal spermatozoa and pH. 4. The ejaculate is “washed” by adding equal parts of a warm extender containing antibiotics fol- lowed by centrifugation at 1500 rpm at 300 Gs for 3 minutes. The supernatant is removed and the spermatozoa are suspended in warm exten- der and drawn into a sterile syringe and capped. Depending on the fertility of the stallion 200 to 500 million motile normal spermatozoa are used for each insemination. This warm syringe after being wrapped in paper towels for insu- lation is placed in a bag and put at refrigerator temperature, 4° C, for at least one hour before insemination to permit the antibiotics to elim- inate any bacteria that might be present. 5. The mare to be bred is then inseminated after wrapping her tail, and thoroughly scrubbing and rinsing her perineal and vulvar region with Be- tadine or Novalsan scrub followed by 3 warm water rinses. The inseminator uses a sterile plastic sleeve over which he places a sterile disposable rubber glove. The back of the hand is lubricated with KY jelly and with the tip of the inseminating pipette covered by the index finger, the vulvar lips are parted and the hand and arm are inserted into the vagina. The index finger guides the pipette into the cervix and then616 VETERINARY OBSTETRICS the pipette is pushed a few inches further cra- nially and the extended semen is infused into the body of the uterus. B. Minimal Contamination Technique for Natural Service:156,239 1. Both the mare and stallion are prepared as de- scribed in A above but just before service the uterus of the mare is filled, so that slight over- flowing into the vagina occurs, with 100 to 300 ml. of warm semen extender containing anti- biotics. Care should be taken so that ballooning of the vagina, pneumovagina, does not occur before service that follows immediately after the introduction of the extender. Thus the stal- lion ejaculates directly into this antibiotic con- taining extender. Satisfactory results have been reported for the use of this technique. Usually only one service per estrous pe- riod is desired so careful estimation of the time of ovu- lation or the use of HCG are indicated. These infection- prone, infertile mares in which the above MCT technique is employed should be cycling regularly and bred during the most fertile portion of the breeding season. A simple easily prepared semen extender has been described156,239 consisting of: Instant, non-fat or low-fat skimmed milk—- Glucose— (Gelatin BP) (optional)— Sterile distilled water— 2.5 gms 5.0 gms (0.5 gms) 100 ml. Antibiotics added to this extender may be either— 300 mg or 150,000 units of crystalline penicillin and 300 mg or 150,000 micrograms of crystalline strep- tomycin or 100 mg of gentamicin sulphate Other extenders with antibiotics at levels that don’t effect spermatozoan activity or fertility have been de- scribed.259 (See Chapter on Artificial Insemination.) Several authors99,156,239 have indicated that careful breed- ing management and hygiene, service to highly fertile stallions and a minimum contamination technique either by AI or natural service should be used on the infertile, infection-prone, often older, mares in Categories II and III as defined by endometrial biopsies, breeding history and clinical examination. If obvious clinical endometritis is present, correction of the pathological condition is necessary before breeding can be recommended. This therapy may require several months or more. Endometrial Biopsy Although earlier studies reported on endometrial bi- opsy techniques121,164,282 the technique for collection of a suitable sized biopsy and the variety of histopathological findings and their relation to fertility in mare were first adequately reported by Kenney154 and since corroborated by others.92,99 154 239 251 Presently endometrial biopsies are used widely as an aid in evaluating the degree of fertility in mares, particularly those barren mares without clinical lesions or infections of the genital tract.92,154 The procurement and processing of an endometrial bi- opsy specimen should be preceded by a careful physical examination of the genital tract, obtaining a detailed breeding history and a careful collection of a swab spec- imen of the uterine lumen for the detection of bacteria that has been described. The specimen is obtained by means of a sterile alligator-jawed (rounded) biopsy for- ceps 55 to 70 cm. in length with a basket 20 by 4 by 3 mm. in size. The mare should be restrained for a rectal examination. The tail should be bandaged and the feces removed from the rectum. The perineal area and vulva should be washed with soap and water and rinsed 3 times with water. The arm should be covered with a plastic sleeve and this is in turn covered by a sterile rubber glove lubricated with sterile lubricating jelly without disinfec- tants. The vulvar lips are parted and the hand cupping the punch or forcep is inserted into the anterior vagina. The biopsy forcep is guided through the cervix with the index finger. After the forcep has entered the uterine body the hand is removed from the vagina and inserted into the rectum where it guides the forcep to the area of the bifurcation of the horns, near the implantation site. The jaws of the forceps are opened and uterine wall and en- dometrium are gently pushed laterally into the jaws by the rectal hand and the jaws are shut tightly. The biopsy forcep is withdrawn from the genital tract. Care should be taken to avoid penetrating the uterine wall with the forcep, as might occur if a straight cranial bite is made. Usually the biopsy specimen is taken from the cranial dorsal portion of the uterine lumen. A single biopsy specimen has been shown to be representative of the en- tire uterine endometrium.39 However if any abnormality of the mare’s uterus is noted a biopsy specimen from that area or from several areas may be obtained. The biopsy specimen may be taken at any stage of the estrous cycle and even within a few hours after breeding. How- ever if the mare has been bred and ovulated, taking the uterine biopsy a number of days later, as discussed pre- viously may result in luteolysis or regression of the CL and the induction of estrus with a shortened estrous cycle. If biopsy specimens are taken at the end of the breedingINFERTILITY IN THE MARE 617 season from barren mares a mid-diestrous sample was recommended.239 The suitable-sized endometrial specimen is removed from the forceps with a hypodermic needle and placed preferably in Bouin’s fluid instead of 10% formalin. After 2 to 24 hours the specimen is placed in 70% ethanol or 10% formalin and sent to the laboratory for skilled his- topathological examination. The prognostic or diagnos- tic value of a satisfactory endometrial biopsy specimen in predicting the fertility of a mare not only requires an evaluation of the breeding history and a careful complete clinical examination of the mare with appropriate labo- ratory tests but also the examination of the biopsy spec- imen by an individual who has experience and training to interpret the lesions observed. These endometrial lesions have been reviewed and categorized.92'99'154’155’239 They include varying degrees and combinations of histopathological conditions of: (a) periglandular fibrosis, either focal or widespread, often associated with cystic distention of the uterine glands, slight to severe, (b) inflammation or endometritis which may be acute, chronic, infiltrative degenerative, wide- spread or focal, (c) lymphatic stasis with lacunae, (d) hypertrophy and hyperplasia, focal or diffuse, (e) atro- phy and hypoplasia, focal or diffuse. The many variable lesions observed in these histologic sections, especially during various stages of the estrous cycle, require skilled experienced observers to assess their significance. Atrophy of the endometrium is commonly associated with seasonal anestrus and inactive ovaries. Hypoplasia is noted in postpuberal fillies and mares with congenital or chromosomal abnormalities.49,57 Inflam- mation if mild or moderate may not be associated with uterine infections. The stage of the estrous cycle also importantly influences the findings observed. It is pos- sible that degeneration of the endometrium and infertility as discussed earlier in cattle associated with delaying service until heifers were 4 or 5 years of age (DeLange) and in unspayed nulliparous dogs (Dow and others) may be implicated in the decline in fertility in nulliparous mares of middle or older age and be an important factor in sus- ceptibility to endometritis in older mares as it has in older dogs. Most pathologists and others92,99’251 trained and ex- perienced in noting the endometrial histologic or path- ologic changes have followed the general three cate- gories outlined by Kenney.154 However Ricketts233 239 has listed 14 histopathological groups of various combina- tions of lesions for predicting the fecundity of mares. The three categories outlined by the former154 are: Category I—the endometrium is essentially normal with no pathologic changes or if a few are present they are slight and widely scattered, Category II—frequent scattered mild to moderate fi- brotic changes and light to moderate diffuse infiltrations or scattered but numerous foci of inflammatory changes. Widespread lymphatic lacunae or atrophy of the endo- metrium may be present, Category III—widespread severe periglandular fibro- sis of the endometrium and widespread severe inflam- matory changes with moderate to heavy infiltration of plasmacytes. Lymphatic lacunae are extensive causing the uterine wall to be edematous or flabby- or jelly-like on palpation. Endometrial hypoplasia due to chromo- somal anomalies and severe chronic pyometra should also place mares in this category. Ricketts238 has shown the poorest post-biopsy breeding performance of mares is associated with endometrial atrophy not associated with winter anestrus, chronic in- filtrative endometritis, chronic degenerative endometritis and endometrial hyperplasia and especially combinations of these pathologic changes. Categorizing mares based on endometrial biopsies to- gether with clinical examination of the genital tract, the mare’s age, and the breeding history, number of years barren, has been shown by a number of studies92,99,154,239 to be of value in estimating and predicting the future fecundity of mares. Although the time of and diagnostic methods for de- termining pregnancy or conception and the time interval from biopsy to the termination of the study varied, preg- nancy loss from mare categories I, II and III were 10, 24 and 44 percent, respectively.92,251 This indicated that endometrial disease is probably an important cause of embryonic or early fetal death. Further, more continuing and refined studies should be conducted. In 92 clinically normal infertile mares only 30.4% (28 mares) were pos- Foaling Rates Based on Endometrial Biopsy Kenny (244 Mares)154 de la Concha-Bermajillo and Berme Kennedy (79 Mares)92 Doig et al.1 (403 Mares)99 Shideler et al. (332 Mares)251 Category I 68% 78% 82% 61% II 51% 55% 74% 48% III 11% 36% 46% 35% 'Of 4 categories listed the last was omitted as 8 mares none foaled.618 VETERINARY OBSTETRICS itive on culture and only 18% of the 28 mares, had evi- dence of endometritis on biopsy examination." Further- more in this study 75 percent of the mares had varying degrees of endometrial fibrosis and although exceptions occurred generally older mares were in the lower cate- gories. Thus endometrial biopsy is only one of the aids in predicting the fertility of a mare.155 No mare should be classified as incurably sterile except in exceptional, severe, advanced and obvious pathologic conditions that would prevent conception or a normal termination of pregnancy. Other Infectious Diseases of the Genital Organs of Mares Coital vesicular exanthema, genital horse pox or equine venereal vulvitis or balanitis, is a viral disease of horses reported worldwide. The causative agent is equine herpesvirus 3 (EHV3).45,62,216,217,267 This virus does not cause abortion. It may cause a mild nonclinical upper respiratory infection if inoculated intranasally. The dis- ease is rather uncommon in the United States. It is gen- erally believed to be transmitted by coitus but the virus apparently may be readily transmitted by other means as it spreads very rapidly through a band of mares. In rare cases even young foals may be affected.287,305 The in- cubation period is short, 2 to 10 days. No fever, anor- exia, or other signs of a systemic reaction are present. The disease appears suddenly, and often the source of infection is unknown. The disease is characterized by the early appearance of many papules, vesicles and pustular scabby erosions 1 to 3 mm in diameter that may become confluent of the skin of the vulva, penis and pre- puce.62 216 217 These lesions exude serum that dries and forms crusts. (See Figure 147.) When these crusts are rubbed off, a punched-out, irregular ulcer or erosion 0.5 to 1.0 cm. in diameter is observed. These erosions en- large and coalesce and become filled with exudate and dried scabs. The duration of the acute disease is about two weeks. Intranuclear inclusion bodies may be seen in the cells obtained from scraping the vulvar or preputial lesions. Lesions on the skin of the vulva heal leaving small nonpigmented spots. Antibodies to EHV3 are found in the blood serum. Occasionally lesions may be noted on the nose, lips and conjunctiva as well as the vulvar and vaginal mucosa resulting in a purulent dis- charge.216,267 The duration of the persistence of this virus is not known. In stallions coital exanthema develops on the penis, glans and prepuce. Some stallions may be re- luctant or refuse to cover a mare due to pain until the lesions heal. Occasionally a secondary bacterial infec- tion may occur. Some veterinarians will use mild astrin- Figure 147. Coital Vesicular Exanthema or Genital Horse Pox in a Mare. (This is due to a herpes virus.) (Courtesy T. Clark, Iowa State Univ.) gent protective preparations such as calamine lotion or other similar products on the lesions. Healing is usually rather rapid within 10 to 14 days even without treatment. Breeding activities should be suspended for 3 to 4 weeks or more until the infection has subsided and the lesions have healed. The disease does not affect fertility or cause abortion, but may cause a reduced libido in the stallion during the acute phase of the disease.216 One attack does not confer permanent immunity. Affected animals should be quarantined for 60 days. Dourine is a disease of horses due to Trypanosoma equiperdum, and is transmitted almost entirely by co- itus. This was the only trypanosome disease of impor- tance in domestic animals in the United States. Dourine is widespread throughout the world in temperate as well as tropical countries. It was first recognized in the United States in 1885 by W. L. Williams in Illinois, where it was believed to have been spread by a Percheron stallion imported from France. By the use of the complement fixation test and the destruction of all reacting animals, the disease was apparently eradicated from the states west of the Mississippi to which it had spread. In 1939 and 1940 another outbreak occurred in Nevada, California, Colorado, Arizona, New Mexico and apparently Mex- ico, affecting mainly the wild horses and horses of In- dians living in rather isolated areas. Vigorous efforts at eradication were again undertaken and it is believed atINFERTILITY IN THE MARE 619 disappear within a few hours or days and are replaced by others. These plaques are said to pathognomonic of the disease. Occasionally abortion may occur.305 Depig- mentation of the mucosa and skin of the vulva, penis, and prepuce may occur. There are irregular periods of fever in the late stages of the disease and symptoms of paralysis, involving the facial muscles, the limbs, and the penis gradually develop. Emaciation progresses until death occurs. Mortality is estimated at 50 to 75 percent. The course of the disease may be a few weeks to several years with recurrent attacks or it may remain subclinical. Infected animals are spreaders. Treatment is expensive and impractical as results are poor. This is a reportable disease in the U.S. Miscellaneous Pathological Factors in Infertility of Mares Tumors of the genital tract in mares are uncommon. On examination of over 2,000 mares only 6 true tumors Figure 148. Granulosa Cell Tumor of the Mare’s Ovary. (Note the hemorrhages interspersed throughout the tumor.) (Courtesy K. McEntee.) present that dourine is probably eradicated from the United States.24’45 Dourine is transmitted at coitus as a venereal disease. Members of the horse family are the only animals that contract the infection and therefore no other reservoirs of infection exist. Except in Europe the disease is chronic and the onset is slow. The incubation period is 1 to 8 weeks, or occasionally it may be much longer.45 The dis- ease may exist in the animal for months or years with the affected animal alternately improving and relapsing. In the terminal stages emaciation and nervous symptoms develop, rendering the animal worthless and it is usually destroyed. The early symptoms of the disease are characterized by swelling of the vulva and vagina of the mare with a mucous discharge containing trypanosomes. The af- fected stallion’s penis, prepuce, and scrotum become swollen and reddened and paraphimosis may develop. The swelling may vary in size. There may be a muco- purulent urethral discharge. On palpation the swollen area is nearly free from heat and pain. In mares genital irri- tation caused by this organism is evidenced by frequent urination and tail switching. After the acute genital symptoms subside, peculiar raised plaques appear in the skin over the body. These are often called “dollar” plaques because of their similarity in size to a silver dollar, though some may be much larger. They appear suddenly and Figure 149 Squamous Cell Carcinoma of the Vulva of the Mare.620 VETERINARY OBSTETRICS were reported.97 Of these 6, 3 were in the ovary. Equine ovarian tumors, especially granulosa cell tumors are more common than tumors of the tubular genital tract82'83'97'107’186'187'200'221 Beta-cell adenoma in the pars intermedia of the pitui- tary gland in mares over 13 years of age causes a syn- drome characterized by weight loss, muscle wasting, thin abdominal walls, poor, long hair coat that persists into the summer months with excess sweating, and often polydipsia, polyuria, hyperglycemia, glycosuria, poste- rior weakness or paresis, and elevated plasma levels of adrenocorticoids (Cushing’s syndrome).94,104 These de- bilitated mares are usually anestrous. The condition be- comes terminal within 6 to 18 months. Rarely adreno- cortical tumors may produce similar signs. Ovarian Tumors The granulosa-theca cell tumor is the most common equine ovarian tumor. These tumors occur unilaterally and on palpation are greatly variable in size with a smooth, firm or lobulated surface with large fluid-filled cysts. On incision these granulosa cell tumors are yellow to white in color. Solid tissue and cysts along with areas of hem- orrhage and necrosis are observed. Mares with repro- ductive failure, changes in sexual behavior or tempera- ment and signs referrable to abdominal discomfort should have their ovaries examined by rectal palpation. The granulosa-theca cell tumor should be differentiated from an ovarian hematoma that can reach a size of 20 or more cm. and persist for months. Mares with hematomas usu- ally continue to cycle normally with no behavioral changes and the hematoma will regress in size while the tumor will gradually increase in size. Affected mares may have a history of anestrus or continuous estrus like a nym- phomaniac mare. Others may exhibit stallion-like be- havior of teasing or mounting mares along with squeal- ing or roaring and the development of a heavy neck. Occasionally these animals may be hard to handle and aggressive toward other horses. Enlargement of the cli- toris occurs in some cases. The ovary opposite from the affected ovary is usually small and inactive probably due to suppression of its activity by the steroid hormones from the tumor. As in cattle the mare may rarely become pregnant even with a granulosa cell tumor in its early stages of development when cycling is still regular.50 All of the granulosa-theca cell tumors and probably related arrhenoblastomas194,263 produce hormones. Male-like be- havior was associated with testosterone levels over 100 pg/ml that declined to about 20 pg/ml after removal of the granulosa cell tumor.263 Granulosa tumor cells do not produce progesterone. Meagher et al. reported that 29 of 63 mares, nearly 50 percent, with ovarian neoplasms manifested male behavior. Anestrous behavior may also be due to high testosterone levels observed in 9 of 10 mares. Endocrine patterns in mares with granulosa cell tumors and exhibiting anestrus or estrus were similar al- though the latter had higher estradiol levels. Following removal of the affected ovary in 12 mares the unaffected ovary that was small and firm without any follicular growth returned to cyclic activity and ovulated a follicle 83 to 392, average 209, days later. Eight of the 12 mares did not show estrus until the next breeding season. One mare did not show cyclic activity following removal of the affected ovary before being killed 524 days later.263 The 78 mares with granulosa-theca cell tumors ranged from 2 to 20 years with an average age of 10 years.192 Mares that had foaled previously and maiden mares were equally affected. All tumors were unilateral with equal numbers affecting the left and right ovary. The tumor diameter ranged from 6 to 40 cm. with most in the 10 to 20 cm. range. Only 1 of the 78 granulosa-theca cell tumors metastasized; thus metastasis is much less com- mon than in cows and humans. Only 6 of the 78 mares died from surgical complications. Normal behavior oc- cured postsurgically in most of the mares with regular estrous cycles developing in about 75 percent of the mares. Thirty, 77 percent, of 39 mares bred, conceived and pro- duced live foals. The tumors may be surgically removed using the ventral midline, paramedian or flank ap- proach.192,249 Great care is used to control hemorrhage and to invert the serosa over the ovarian stump to pre- vent adhesions.192 Other uncommon equine ovarian tumors or cysts that have been reported are:^82'83'9731^2577578^187'!^.2*)^!,^ Melanoma Teratoma50,111,186,1926 Lymphosarcoma175,206 Arrhenoblastoma194 Cystadenomas and cystodeno- carcinomas50,83,107,125,187,200,206 Hemangioma186,187 Occasionally small masses or “rests” of adrenal cor- tical tissue are found in or near the equine ovary.157,187,210 Germinal inclusion cysts or “fossa-cysts” are formed by peritoneal fragments that become imbedded in the ovary following ovulation. These “serosal” cysts may be large enough or numerous enough to be of clinical sig- nificance by possibly interfering with ovum transport in older mares.141,186,187,210 A case report described a 7 cm. ovarian cyst containing a bot, G. intestinalis.100 Hematomas of the ovary are common.50,141,187 210 Hemorrhage into the ovarian follicle regularly occurs at ovulation and in anovulatory follicles.2,210 HematomasINFERTILITY IN THE MARE 621 may vary in size from 5 to 20 or more cm. in diameter and persist for weeks or months. Normal cyclic activity usually continues in most cases.50,141 Depending on the age and stage of development of the hematoma repeated rectal examinations may reveal they are decreasing or increasing in size. The author observed a 20-year-old mare that bled to death from a follicle that ovulated during the third month of pregnancy. Histologic section did not re- veal evidence of an early or small granulosa-theca cell tumor. These latter tumors may contain blood or rarely rupture and bleed intraabdominally. Varicosities of ves- sels in the equine ovary are common and may become large enough to palpate on rectal examination. Heman- giomas and hamartomas of the ovary have been de- scribed.187 232 Removal of large hematomas by unilaterial ovariectomy has been described where an absence of normal ovarian tissue was observed.50 Parovarian cysts are common in the mare and may vary in diameter from a few mm. to 5 to 6 cm. They are often found in the fimbria as small fimbrial cysts, hydatids of Morgagni, that usually cannot be palpated. The larger parovarian cysts originate from other rem- nants of the mesonephric or paramesonephric tubules or ducts and are located in the mesovarium near the ovary.187,210,234 The epoophoron, a cystic remnant of the mesonephos is about 0.5 to 2.0 cm. in diameter and located in the ovarian capsule at the dorso-cranial-medial pole of the ovary. These cysts have no effect on the reproductive cycle or fertility. Large pedunculated parovarian cysts that caused strangulation of the rectum have been re- ported.305 Cases of ovarian hypoplasia and/or gonadal dys- genesis with chromosomal abnormalities associated with infertility, a phenotypic small to normal-sized mare, absence of an estrous cycle or only occasional estrus of a passive type, a small flaccid uterus, a flaccid cervix with an open os and small to very small ovaries, have been described with increasing frequency in recent years in many breeds of horses.64,49,57,133,141,143 The older re- ports of bilaterial ovarian hypoplasia were probably as- sociated with gonadal dysgenesis.210,234 Unilateral hy- poplasia of the ovaries should be diagnosed with great caution, especially in nulliparous mares. Repeated ex- aminations during the breeding season in these mares is indicated. As noted above small inactive ovaries are often associated with a granulosa-theca cell tumor in the op- posite ovary. The most common chromosomal abnormality found in 28 or 58%, of 48 mares133 with gonadal dysgenesis was the 63,XO karyotype. This karotype is similar to that found in women with Turner’s syndrome but some phys- ical differences exist. Affected mares have very small but palpatable ovaries and a few germ cells may be in the ovaries.46,47,57 No sex chromation or Barr bodies were found in these XO mares.46,49 57 Other chromosomal ab- normalities included 63,XO/64XY, 64XY, 63XO/64XX and 64XO/64XY, 65XYY/64XX, 65XXY/64XX and 65XXX.46,57141 Because of a lack of germ cells in the ovaries follicles usually don’t develop and the ovaries are small, smooth and firm. It is likely that chromosomal abnormalities may be an important cause of infertility in mares. Cytogenetic studies are indicated in infertile mares showing some or all of the above signs. The relatively high incidence of mosaicism in sex chromosome an- omalies of mares may reflect, as in women, that aging of the ovum and post-fertilization errors of mitosis may be fairly common in horses because of the long estrous period and variable time of service and ovulation.46 Clinical effects of the XO anomaly in mares is limited to the abnormal development of the primary or second- ary sex characteristics which may be difficult to recog- nize in mares.57 Since mares with chromosomal abnor- malities are nearly always sterile their detection by cytogenetic techniques would save considerable ex- pense. Lesions of the uterine tube in the mare are rare. As discussed previously, mild salpingitis associated with endometritis may be fairly common but obstruction of the uterine tube is rare. Infundibulitis with small fibrous adhesions in the fimbria around the ovulation fossa is common in the mare.288 Pyosalpinx has not been de- scribed in mares. Hydrosalpinx is also very rare although two cases; both unilateral, were described.9 The author is unaware of any reported genetic defects or arrests in development of the equine uterine tube. Rare cases of small under-developed fimbriae that might have diffi- culty in picking up ova have been reported.210 Tumors of the Uterus, Cervix, Vagina and Vulva: Uterine tumors include leiomyomas, which are usually small and 1 to 2 inches in diameter or they may be mul- tiple or rarely large, fibromas, rhabdomyosarcomas, and carcinomas which are rare.82,83,97,119,187,200,284 These tumors may also be found in the cervix and vagina. Squamous-cell carcinomas often in pintos, melanomas that frequently “metastasize” in white horses, and pap- illomas are the three most common tumors of the vulva of mares.82,83,107,200,221,266 Other Pathological Changes in the Equine Uterus include: Ventral uterine enlargements hear the bifurcation of the body and uterine horns in older pluriparious mares have been described 157,163 due to mucosal atrophy or fo- cal myometrial atonia. The former probably follows the622 VETERINARY OBSTETRICS latter and may be a natural consequence of the anatomy of the uterus and its supporting ligaments and the site of implantation and fetal development. Myometrial lym- phatic lacunae or varicosities in this area may also con- tribute to this uterine enlargement. Lymphangiectasis of the myometrium or lymphatic la- cunae and possibly cystic endometrial hyperplasia153'157187 with a flaccid, edematous, soft, thick, doughy or spongy uterine wall which in the opened uterus shivers like a gelatinous mass when jarred. Numerous submucosal cysts, 1 to 5 cm. in diameter under the glistening, moist mu- cosa may bulge into the uterine lumen. Advanced cases especially in older mares may have a mucometra with the uterine contents having a milky, gray to dark-brown color.911’157'187’277,310 If this condition is severe the mare is usually hopelessly sterile.97’227 Knudsen162,163 de- scribed 24 mares with lymph stasis of the endometrium in which lymphocytes predominated in the endometrial biopsy smears. Most of these mares had poor fertility; in 2 cases pregnancy terminated in early fetal death. These mares cycled normally and appeared normal on specu- lum examination. On rectal examination the uterus was large and edematous. Only 3 of 24 mares were positive on bacteriological culture of the uterus. On postmortem examination the endometrium was very edematous. Knudsen indicated that rarely these mares recovered without therapy, and conceived after being barren for one to two years. There is no specific treatment for lymph stasis but uterine massage and hot saline infusions have been recommended. If persistent CL with high plasma progesterone levels are a possible cause, injections of prostaglandins or a uterine infusion might be helpful in a few cases but the prognosis is poor. Endometrial cysts in large numbers have been de- scribed and may be associated with periglandular fibro- sis and cystic distention of uterine glands. Some indi- vidual cysts or lymphatic lacunae may be small, 1 or 2 mm. or large, up to 4 or 10 cm. in size that may be found by careful palpation especially if the uterine wall is atrophied.9 11237 They may be mistaken for a chorionic vesicle and pregnancy on palpation or ultrasonography early in gestation, 20 to 35 days.157’1688’187 These may be differentiated from pregnancy by repeated examination and finding that the chorionic vesicle grows rapidly while endometrial cysts enlarge very slowly. Segmental aplasis of the equine uterus is rare.195 247 Lesions of the cervix and vagina are rare in the mare. The most common lesion is an acquired occlusion of the cervix with adhesions due to severe irritation of the cer- vix at the time of foaling, from severe infectious cer- vicitis, or from the use of irritating procedures and drugs that produce a severe cervicitis. Mild obstructions may be broken down and a pessary introduced and left in place for 2 to 4 weeks until healing has occurred.172 190 A re- currence of the adhesion across the cervical lumen is not uncommon. A double cervix and vagina and a band in an incomplete double cervix in 2 mares was described.291 A segmental aplasia of the paramesonephric duct re- sulting in a missing cervix and a small uterine horn was reported.247 In this case the ectopic ureter entered the antero-lateral wall of the vagina. The author has ob- served a young Standardbred filly with an ectopic ureter that opened into the lateral wall of the vestibule and re- sulted in constant dribbling of urine from the vulva. Also rarely seen in the cervix of the mare are ampullary diver- ticula or cysts, homologues of glands of the male am- pulla.6'210 A condition described as a congenitally short incom- petent or hypoplastic cervix has been described to the author by a number of veterinarians and reported in the literature.43 These young 2-year-old fillies, usually Thor- oughbreds, have a severe persistent pneumovagina de- spite a correctly performed Caslick operation. These fil- lies have normal-sized ovaries with follicular activity. The cervix is very short, 1-2 cm. compared to a normal cervix of 5 to 8 cm. and is relaxed and widely dilated allowing the examiners hand to enter the uterus, which was normal on fiberoptic examination and on culture and biopsy although a slight endometritis was present.43 The blood progesterone level was 7 to 8 ng/ml. indicating an active CL. The prognosis in these cases is poor for the future breeding life of the filly particularly if the con- dition is congenital. A somewhat similar condition of a dilated cervix has been reported in fillies with chromo- somal abnormalities and in occasional mares during the winter anestrous period. Further study on this condition is indicated. Cysts of Gartner’s duct or remants of the mesoneph- ric or Wolffian duct in the floor of the vagina are rarely observed.6’210 Previously mentioned was the severely lacerated, scarred or incompetent cervix that cannot close properly; affected mares are infertile or sterile. Persistence of a Portion of the Hymen is not unusual in maiden mares. It is usually ruptured at the time of service. (See Figure 150.) Some veterinarians advise rupturing it with a vaginal speculum 1 to 2 months be- fore service so it is healed before a natural service.124 227 In rare cases an imperforate hymen is noted in a maiden mare and requires incising to release the mucus and ep- ithelial debris trapped in the vagina and uterus. Occa- sional tenesmus may be exhibited in these mares, with a slight protrusion of the distended hymen between the vulvar lips. Occasionally a severe vaginitis or vestibu- litis may result in a stenosis of the vulvovaginal border.INFERTILITY IN THE MARE 623 Figure 150. Persistent Hymen in a Filly (Note the urethral orifice caudoventral to the hymen.) It is not uncommon to note on speculum examination varicose veins in the hymenal folds. Occasionally one of these may break down and a chronic slow dripping of blood may be observed from the vulva. This is most commonly seen in late gestation in fat old mares after exertion. Bleeding is slight and not serious. These mares despite the owner’s concern do not abort. Cautery of ul- cerated varicosity or ligation may be performed. Usually the intermittent bleeding ceases after foaling. Congenital Defects, Developmental Arrests, and other anomalies of the reproductive system of the mare are rare. Hermaphroditism has occasionally been described and is usually characterized by a large, protruding cli- toris and irregular sexual symptoms. (See Figure 37.) McEntee cited Levens (1911) who described 15 cases of male pseudohermaphroditism in stallions descended from the same sire. There is some evidence to show that certain Thor- oughbred female lines, as in cattle, are characterized by infertility of a hereditary nature resulting in a particular mare’s female descendants being “shy breeders.” The relative importance of this factor requires more scientific appraisal. Evaluation and Assessment of a Mare for Fertility This evaluation is routinely required of barren mares at the end of the breeding season on all farms. It may also be requested by a prospective purchaser of a brood- mare or a maiden mare.22'120,128,130,132'239 This evaluation examination should be thorough and detailed. The inter- pretation of many of these assessment procedures and final decision requires experience, skilled training, ex- cellent laboratory support, careful observation, excellent records and common sense. Generally one should assess or predict the fertility of a mare in a percentage range or as excellent, good, fair or poor. The veterinarian should seldom indicate a mare is hopelessly sterile unless the severity of the pathological lesions warrants such an ex- treme opinion. Furthermore the number of examination procedures and their cost should be considered in ref- erence to the value, economic or sentimental, of the mare and the expected breeding costs, such as service, board- ing and transportation fees. All mares to be examined for fertility should be carefully identified and all speci- mens taken from them for laboratory tests should be carefully labelled. A routine procedure of evaluation should be followed and conducted in a professional very clean or sterile manner that poses no danger to the mare or the operator. Careful, complete records should be kept during the examination. The various factors to consider in this fertility evalu- ation or assessment include: 1. Reproductive history—This should include the animal’s age, use, prior illnesses, surgical oper- ations, nutrition, worming and vaccination, prac- tices, and drug therapy, especially the steroids. The pertinent information on number and date of foalings and foaling problems, number of live offspring, and if the mare is barren should be noted. The length of this latter condition, history of ser- vices either by AI or natural to what stallions, prior possible exposure to venereal diseases like CEM or infected stallions, history of uterine infection and treatment, teasing and service records, en- dometrial biopsy report, history of early embry- onic deaths or abortions and possible causes, ge-624 VETERINARY OBSTETRICS netic or hereditary background of familial infertility and etc. should be recorded. 2. Physical or clinical examination—The mare’s physical condition, obese or thin, state of health, presence of an infectious disease(s), examination of the body systems such as teeth, eyes, hair coat, locomotor, circulatory, respiratory and nervous systems for conditions that could affect her fer- tility or ability to carry, deliver and nurse a foal are necessary to carefully ascertain. 3a. Genital organs—Visually examine the mare ex- ternally for the presence of a vulvar discharge, the length, thickness and angle of the vulvar lips and conformation of the perineal region and tailhead that might indicate the presence of or need for a Caslick’s operation for pneumovagina. Examine for vulvar or perineal scars, or tumors. Visual or speculum examination of the vestibule, hymenal region, vagina and cervix for the presence of a hymen in maiden mares, scars, stenoses, vaginal or cervical exudate, color and condition of the va- ginal mucosa, pale, pink, red or inflamed moist, dry and character of mucus, and the external cer- vical os, the relaxation or edema of the latter should be conducted. These changes may indicate the stage of the estrous cycle or indicate the presence of intrauterine infection (See fibroscopy). 3b. Manual palpation per vaginam and rectum of the mare’s genital organs is necessary. The for- mer examination should further check the exter- nal tubular genitalia. The index finger should be gently inserted into the cervix to determine cervi- cal competency and the possible presence of adhesions, scarring or stenosis. The rectal ex- amination should be performed carefully and thoroughly noting and recording the size of the ovaries, presence and size of follicles, the ovu- lation fossa and any abnormalities such as par- ovarian cysts, adhesions, tumors, hematomas, varicosities and etc. The uterus should be pal- pated for pregnancy, or twin conceptuses. If non- pregnant the size, shape, tone, thickness, width and any irregularities or abnormalities of the uterus such as adhesions, endometrial cysts, uterine di- lations, edema, atrophy, excessive small size, or mucometra, or pyometra should be noted. The cervix should be palpated for size, width, length and tone. The uterine tubes are seldom palpable in the mare. The size and shape and any abnormal conformation of the pelvic cavity or pelvic bones should also be noted. 4a. Bacteriological culture of the uterus of barren mares should be taken, especially if a uterine dis- charge is observed, to determine the organism and its sensitivity to various antibiotics. This test is complementary to the endometrial biopsy exam- ination if evidence of an endometritis is noted on the latter test. This examination should be per- formed in such a manner as previously described so a true evaluation of the presence or absence of infection is determined. Occasionally repeated cultures may be required. The uterine culture is superior to the cervical culture. In mares with a history of a chronic infection with Klebsiella or pseudomonas or to check for CEMO (Hemo- philus equigenitalis), the urethra and clitoral fossa and sinuses should also be cultured, possibly re- peatedly. 4b. Cytological examination for the presence of leu- cocytes can be performed on smears from the uterine culture swab. 5. Biopsy examination of the endometrium re- quires a suitable-sized specimen, properly pre- served and sectioned, examined and evaluated by a skilled, experienced pathologist or veterinarian trained in this area. The interpretation of the re- sults of both the endometrial culture and biopsy requires an understanding of the findings and their limitations. 6. Other examinations or tests that may be helpful or necessary include: a. Fiberoptic or endoscopic examination (fi- broscopy/hysteroscopy) of the cervix and uterus for the presence of adhesions, cysts, tumors, fluid accumulation, fibrosis and etc.22,184,239 b. Ultrasound examination of the uterus and ovaries for pregnancy, cysts, follicles or ex- udate or mucometra. c. Endocrine assays for progestins, estrogens, luteinizing (LH) and follicle stimulating (FSH) hormones and prostaglandin metabolites. The former is used most often to determine a per- sistence of the CL associated with prolonged anestrus. d. Chromosome analysis or cytogenetic study of the mare’s karyotype is a definite value in certain infertile maiden mares. The final prediction or assessment of a mare’s future reproductive status should also consider the managerial factors and competence of the breeding farm personnel as well as the fertility of the stallion to whom the mare will be bred.INFERTILITY IN THE MARE 625 Infertility, “Repeat Breeding.” Early Embryonic Deaths and Early Fetal Loss or Early Pregnancy Wastage in Mares Since infertility and “repeat breeding” in cattle has been studied intensively, much information of general value from these studies can be utilized in developing hy- potheses to explain early losses in horses. Limited stud- ies of this area of concern, other than those of a statis- tical or retrospective nature have been made on mares. In a large survey of Quarterhorse and Thoroughbred farms the pregnancy rate for the first service period was about 45 to 50% and the cumulative rate for the breeding season was 75 to 85 percent.64,268 If only healthy fertile mares were bred to healthy, highly fertile stallions these percentages would probably rise about 10 percent con- sidering the limited length of the breeding season of mares. It is estimated that early embryonic or fetal losses after pregnancy is established as 5 to 8% before the fourth month and 8% thereafter including stillbirths.64 On cer- tain farms in certain years early pregnancy loss may oc- cur in 10 to 30% or more of the mares and the cause is seldom ascertained.18,52,64,251 In an excellent retrospective study18 of 639 Thorough- bred mares on one farm with 2466 coverings in 1528 mare years, the fertilization failure and early embryonic death rate based on a return to estrus within 30 days of a previous cover was 31.7%. While the late embryonic death rate of 26.5% was based on a return to estrus after 30 days after a previous cover (9.4%) and a diagnosis of nonpregnancy at 42 days, often after the end of the breeding season (17.1%). In this study evidence was presented that indicated few “missed” or “silent” estrous periods occurred. But the data suggested that prolonged persistent CL, together with the short breeding season, may have played a significant role in the high incidence, 26.5%, of late embryonic deaths diagnosed at the time of pregnancy examination at or after 42 days post ser- vice. The average live foal per cover rate on this farm was 39.8% and the observed late abortion rate was 2.3%. Mares bred late in the breeding season after May 15th had a slightly better foaling rate per cover than mares bred before that date, 44.4 vs 39.0%. Mares bred before 16 days postpartum or on foal heat had a fertilization failure and early embryonic death rate of 40% and a foal- ing rate of 29% compared to the next or second normal heat of 25.5 and 49%, respectively. Statistics for lac- tating and nonlactating mares were nearly similar. Foal- ing percentage for mare age groups of 2 to 4, 5 to 7, 8 to 13, and 14 years and over was 85, 71, 63, and 45%, respectively. This decline in fertility as mares became older was reflected in the foaling rate per cover, 57 to 25%, combined fertilization failure and early embryonic death rates, 27 to 37%, late embryonic death rates, 15 to 34%, and observed abortion rates 1.2 to 3.1%, re- spectively, for the youngest and oldest groups of mares.18 Infertility or “repeat breeding” in cattle is probably due to three major categories, failure of fertilization, early embryonic death and uterine disfunction (See Chapter XIII). Failure of fertilization is characterized by the oc- currence of regular intervals between estrous periods while early bovine embryonic death if it occurs after 14 to 16 days postservice often results in a prolonged interval be- tween the time of service and the next estrous period. In mares a similar effect may be noted or the CL may per- sist even if failure of fertilization of the ovum or very early embryonic death occurred before day 12 post ser- vice. This phenomena of persistence of the CL is com- mon to the mare and increases the need for early accu- rate pregnancy diagnosis. Furthermore, mares that abort after 40 days of gestation when the endometrial cups have developed usually fail to show estrus for a number of months and often not that breeding season. Early em- bryonic or fetal loss or abortion in mares prior to 90 to 120 days of gestation is seldom observed and may be due to resorption of the embryo or the early fetus within the genital tract. The efficient natural mechanism in most mares that eliminates one of twin embryos early in ges- tation greatly minimizes the infertility associated with twinning. (See abortion in mares.) In the mare the round to oval small chorionic vesicle of early pregnancy may be expelled rapidly and unseen compared to the cow that has an elongated vesicle that may occasionally be seen hanging from the vulva between 20 to 80 days of ges- tation. No discharge or blood is observed at the vulva in most mares that abort early. Thus in the mare a regular postservice teasing routine should be followed for sev- eral months or more. Errors in early pregnancy diag- noses causes an apparent elevated early embryo or fetal loss. When a pregnancy diagnosis is in doubt repeated examinations either manually or with ultrasonography or even blood tests for PMSG should be conducted as too early incorrect pregnancy diagnoses may contribute, along with inadequate teasing procedures and disease inci- dence, to an apparent increase in pregnancy losses on certain farms. Thus management including improper teasing and breeding procedures and erroneous pregnancy diag- noses251 may contribute significantly to an apparent in- crease in early pregnancy wastage. Other management factors may include nutrition since one study showed that restricted energy intake between 25 and 31 days of626 VETERINARY OBSTETRICS gestation caused a high incidence of early embryonic loss.292 This loss may be related to the losses of embryos and fetuses caused by stress factors discussed under causes of abortion in mares (Chapter V). In cows and ewes heat stress particularly around the time of fertilization of the ovum and a few days thereafter cause definite large em- bryo losses and “repeat breeding.” This factor has not been studied in mares. Another managerial factor in broodmare management that results in a probable in- crease in early embryonic losses is the breeding on foal estrus. In two studies conception rate on foal estrus was 39 and 41 percent compared to the second estrus after foaling which was 55 and 65 percent.18,173,268 However, the abortion rates after the two breedings were similar 16.5 and 13.8 percent, respectively in one of the stud- ies.173 A uterine infection, such as CEM, and occasionally Klebsiella, Pseudomonas or even Streptococci, intro- duced into susceptible mares at the time of service by the stallion may cause an acute endometritis and a “hos- tile” environment for the spermatozoa and fertilized ovum. The estrous cycle may also be shortened due to luteolysis of the CL by the released prostaglandin. These uterine infections must be prevented or controlled to avoid early embryonic deaths and infertility. Endometritis resulting from the introduction of miscellaneous organisms at the time of service particularly in the infection-prone, usu- ally older mare18 may also cause early embryonic or fetal deaths. Endometrial pathology particularly periglandular fi- brosis, lymphatic lacunae, large endometrial cysts, en- dometrial atrophy, hyperplasia and degrees of endome- tritis often in older mares as revealed by a biopsy of the endometrium is a cause of infertility and early embry- onic death. Pregnancy losses in three studies were 10 to 20 percent in Category I mares with essentially a normal endometrium and 35 to 44 percent in Category III (ab- normal endometriums).92,154,251 Chromosomal abnormalities as a cause for early em- bryonic loss in the horse is probably the same as in other animals and man. In sows about 10 percent of all ova or 30 percent of released ova that fail to develop had chromosomal anomalies, mainly triploid blastocysts probably due to polyspermy.188 A similar incidence of chromosomal anomalies, 36 percent, occurs in sponta- neous abortions in women.72 Although further studies, which are difficult in the mare, are indicated evidence has been presented46 of the probable role of chromo- somal abnormalities in early embryonic or fetal deaths in horses based on the relative frequency of chromo- somal defects in adult horses. The high incidence of mo- saicism in sex chromosome anomalies in mares133 indi- cates that aging of the ovum before fertilization, which is probable in certain mares due to the long estrous pe- riod and uncertainities in the time of ovulation and breeding, results in post-fertilization errors of mitosis.46 Also the maternal age effect on the incidence of chro- mosomal anomalies of the embryo, fetus and newborn commonly seen in women may also be a factor in the incidence of this condition in horses. In 39 attempts at recovery of embryos from infertile older (16 to 28 years) mares only 10 embryos (26%) were collected compared to an embryo recovery rate of 76%, 119 embryos in 156 attempts in fertile younger, 3 to 15 year-old mares. Since pregnancy rates from em- bryo transfers from infertile and fertile mares were sim- ilar, the lowered reproductive efficiency in the infertile mares appeared related to failure of fertilization and transport through the uterine tube, probably due to re- tention of unfertilized ova in the tube which is common in mares.148 Although further studies are needed clinical evidence has been presented that certain infertile stallions may have twice the early abortion rate of fertile stallions used on the same group of mares.52,53 In some instances as cited previously this may be due to certain genital in- fections carried by certain stallions but it may also be due, as in bulls, to chromosomal defects in the fertilized embryo. Apparently normal semen from infertile bulls has been shown to result in a much higher rate of failure of fertilization than similar appearing semen from fertile bulls (See Repeat Breeding in Chapter 13). A similar condition might exist in horses. Two further causes of early embryonic or fetal deaths are twinning and trauma to the chorionic vesicle and embryo by rectal palpation for the early diagnosis of pregnancy. This latter occurrence is probably uncom- mon in mares over 40 to 45 days of gestation when pal- pated in a careful gentle manner. However palpation at 15 to 30 days should be done very gently by an expe- rienced operator to avoid possible damage to the embryo or chorionic vesicle. Twinning has been discussed by Ginther.1176 Although further studies are needed, it is ev- ident that the mare, in which double ovulations of fertile ova are common, has a well-developed biological em- bryo-reduction mechanism for the elimination of excess embryos early in the gestation period. Thus factors that contribute to a mare’s (or a band of mares) failure to conceive or produce a live foal include the follow- ing:130,132 A. Factors over which the veterinarian often has lim- ited or no control: 1. Selection of broodmares and stallions is usu- ally based on athletic ability rather than repro- ductive performance. 2. The breeding season starts before the physio-INFERTILITY IN THE MARE 627 logic breeding season of mares and is short- ened by human mandate. 3. Culling of aged, relatively infertile mares and stallions. 4. Possibly non-selective breeding of mares on foal heat, especially late in the breeding season. 5. Use of artificial insemination. B. Factors over which the veterinarian should have supervisory or direct control: 1. Teasing procedures and practices including vi- sual and manual palpation of the genital organs to overcome behavioral anestrus or continuous or long estrus and prolonged or persistent CL with anestrus in mares; and aberrant sexual be- havior in stallions. 2. Abnormal or pathologic conditions of the re- productive organs including endometritis, pneumovagina, other genital infections, en- dometrial fibrosis, adhesions, tumors, chro- mosomal defects and etc. in both mares and stallions. 3. Nutrition, housing and breeding practices as well as worming and vaccination programs for mares, stallions and foals. 4. Accurate, complete up to date reproductive and preventive health recording system. Breeding Farm or Stud Management Management practices on breeding farms are basically similar to those described for cattle. The veterinarian and stud manager and/or owner must work closely together in a program designed for the farm to secure the highest number of mares pregnant at the end of the breeding season. These pregnant mares should be handled so that they will produce normal, live, strong foals. A goal of over 80 percent conception in the band of mares is con- sidered a satisfactory goal on most farms raising racing stock where the breeding season is short and some of the stallions and mares being used as sires and dams are not highly fertile. Conceptions below 60 to 70 percent are definitely unsatisfactory and require remedial measures. In a study of reproductive efficiency on 14 horse farms encompassing 6 breeds and a total of 1876 mare-years, conception, foaling, and weaning efficiency averaged 80.1, 73.8 and 70.8 percent, respectively. It was sig- nificant that on 2 farms using pasture breeding, concep- tion rates were 94 and 100 percent. The conception rates were very low in February, 27.8 percent, and rose in May through July to a peak of 57 to 59 percent and de- clined thereafter. Conception efficiency in young mares fluctuated until age 7, reached a peak at age 9 of 89.6 percent, remained on a plateau above 70 percent until age 15 and declined thereafter. Conception rates on 5 Thoroughbred farms ranged from 53 to 80 percent and on 5 Quarterhorse farms from 72 to 92 percent.146 Every effort should be made in the Fall to examine, assess or evaluate the reproductive status, treat, if nec- essary, and outline a plan of breeding of all barren mares for the coming spring season. Infected mares should be treated and cured or eliminated well before the breeding season. Infertile mares and especially maiden mares should be booked to the most fertile stallions. Barren mares that have failed to conceive in a number of years should be culled. The use of increased lighting for barren mares should be considered to prolong the physiologic breed- ing season. Incorporating artificial insemination using extender containing antibiotics in breeds premitting reg- istration of foals conceived in this manner and using a program similar to the described minimal contamination technique has been helpful in getting more barren mares to foal. If a stallion’s conception rate is low his semen should be examined carefully on a number of occasions during the breeding season or preferably before the sea- son. If a stallion is of low fertility, his book should prob- ably be reduced and close attention should be paid to having the mare bred within 24 hours before ovulation. The time of breeding may be determined by careful rec- tal palpation or the use of HCG. Foaling mares should be properly cared for during foaling, given exercise and examined critically before being permitted to breed on the foal estrum. Teasing all barren, foaling or recently bred mares on a regular daily or every other day basis before and during the breeding season is essential. If this is not done regularly a veterinarian should examine the mare’s ovaries for the presence of a mature Graffian fol- licle and impending ovulation on the same frequent 48- hour schedule. Frequent speculum examinations or ser- vices should be avoided especially on the infection-prone mare. Breeding shed hygiene and restraint should be thor- ough and on a routine basis. The external genitals should be carefully washed and rinsed. Excessive use of dis- infectants on a stallion’s genitals should be avoided. Care should be taken not to have disinfectant on the stallion’s penis at the time of service. Mares with Caslick opera- tions should be carefully supervised and the number of services should be reduced to the bare minimum con- sonant with good conception rates. The use of HCG to promote and hasten ovulation may be helpful in these and other older, infection-prone mares. The stallion’s se- men should be examined to determine if ejaculation oc- curred and to observe the quality of the semen. If arti- ficial insemination is employed this should be carefully628 VETERINARY OBSTETRICS supervised, monitored and performed in a clean, sanitary manner. Careful, continuous and complete daily and even life- time records on all animals and aspects of the breeding program must be kept up-to-date, accurately and in an easily accessible form. These records should be analyzed for each stallion and for the mares during and at the end of the breeding season. All the breeding history, treat- ments, services, teasing, pregnancy and genital tract ex- aminations must be recorded. A variety of breeding rec- ord forms have been devised and used by veterinarians and managers of stud farms. Daily record and permanent record forms are essential. Satisfactory record forms may be purchased from The Lifetime Horse Record Com- pany, 6060 South Broadway, Littleton, Colorado. Rec- ords used by Andrews and McKenzie and Beeman were excellent. The mares and stallions must be on a balanced ration248 and maintained in good condition being neither too fat nor too thin. Mares at the time of breeding should be in a positive energy balance on a rising plane of nutrition. Daily exercise is essential for all breeding stock. It has proven to be a helpful practice, if it is possible, to allow a fertile stallion to run at pasture with barren or infertile mares if infection or other contra-indications are not present. As in cattle careful and constant attention to many and all details by the veterinarian and the farm manager are essential to a successful reproductive program. Vacci- nation, worming and other measures are essential for a good foaling rate and the limiting of losses of newborn animals. It is “unfortunate” that the breeding season of racing mares does not extend from April 15 to September 15, instead of the present February 15 to June 15 in the northern latitudes. The conception rates on many farms would probably rise 10 to 20 percent by this accomo- dation to the physiologic breeding season of the mare. References 1. Adams, S. B. 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L., Loomis, P. R., Shideler, R. K., Voss, J. L. and Pickett, B. W. (1981) The Ovumeter in Relation to Ovu- lation in the Mare, Eq. Vet. Sci., 1, 2, 57 (and Proc. 27th Ann. Conv. AAEP, 199, New Orleans). 259. Squires, E. L., McGlothlin, D. E., Bowen, R. A., Bemdston, W. E. and Pickett, B. W. (1981) Use of Antibiotics in Stallion Semen for the Control of Klebsiella Pneumoniae and Pseu- domonas Aeruginosa, Eq. Vet. Sci., 1, 2, 43. 260. Squires, E. L., Stevens, W. B., McGlothlin, D. E. and Pick- ett, B. W. (1979) Effect of Oral Progestin on the Estrous Cycle and Fertility of Mares, J. An. Sci. 49, 3, 729. 261. Stabenfeldt, G. H., Hughes, J. P., Cole, H. H. and Cupps, P. T. (1977) Reproduction in Domestic Animals, 3rd Ed., Academic Press, New York, San Francisco, London, pp. 401-427. 262. Stabenfeldt, G. H., Hughes, J. P., Evans, J. W. and Neely, D. P. (1974) Spontaneous Prolongation of Luteal Activity in the Mare, Eq. Vet. Jour. 6, 4, 158. 263. Stabenfeldt, G. H., Hughes, J. P., Kennedy, P. C., Meagher, D. M. and Neely, D. P. (1979) Clinical Findings, Pathological Changes and Endocrinological Secretory Patterns in Mares with Ovarian Tumors, J. Reprod. Fert. 27, 277. 264. Strangroom, J. E. and Weevers, R. de G. (1962) Anticoagu- lant Activity of Equine Follicular Fluid, J. Reprod. and Fertil. 3, 269. 265. Stowe, H. D. (1967) Reproductive Performance of Barren Males Following Vitamins A and E Supplementation, Proc. 13th Ann. Conv. AAEP, New Orleans, 81. 266. Strafuss, A. C. (1976) Squamous Cell Carcinoma in Horses, JAVMA, 168, 1, 61 (A Review). 267. Studdert, M. J. (1974) Comparative Aspects of Equine Her- pesviruses, Cor. Vet. 64, 94. 268. Sullivan, J. J., Turner, P. C., Self, L. C. and Gutteridge, H. B. and Bartlett, D. E. (1975) Survey of Reproductive Effi- ciency in the Quarterhorse and Thoroughbred, J. Reprod. Fert. Suppl. 23, 315. 269. Swenson, M. J. (1977) Duke’s Physiology of Domestic Ani- mals, 9th Ed., Cornell Univ. Press, Ithaca, N.Y. 270. 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AAEP, Newsletter, #2, June. 278. Threlfall, W. R. (1980) Interuterine Therapy in the Brood- mare, Proc. 26th Ann. Conv. AAEP, Anaheim, Cal., 155. 279. Timoney, P. J., McArdle, J., O’Reilly, P. J. and Ward, J. (1977) Contagious Equine Metritis (Letters), Vet. Rec. 101, 491. 280. Timoney, P. J. and Powell, D. G. (1982) Reported commu- nication (D. Lein). 281. Timoney, P. J., O’Reilly, P. J., Harrington, A. M., Mc- Cormack, R. and McArdle, J. F. (1979) Survival of H. equi- genitalis in Different Antibiotic-Containing Semen Extenders, J. Reprod. Fert. Suppl., 27, 377-381. 282. Tobler, E. E. (1966) Collection of Uterine Fluid and Uterine Biopsy, Vet. Med./Sm. An. Clin. 61, 8, 779. 283. Tolksdorff, E., Jochle, W., Lamond, D. R., Klug, E. and Merkt, H. (1976) Induction of Ovulation During the Postpartum Pe- riod in the Thoroughbred Mare with a Prostaglandin Analogue, (Synchrocept), Theriog., 6, 403. 284. Torbeck, R. L., Kittleson, S. L. and Leathers, C. W. (1980) Botryoid Rhabdomyosarcoma of the Uterus of a Filly, JAVMA, 176, 9, 914. 285. Trum, B. F. (1950) The Estrous Cycle of the Mare, Cor. Vet. 40, 17. 286. Turner, D. V., Garcia, M. C., Webel, S. K. and Ginther, O. J. (1981) Influence of Follicular Size on the Response of Mares to Allyl Trenbolone Given Before the Onset of the Ovulatory Season, Theriog., 16, 1, 73. 287. Udall, D. H. (1954) The Practice of Veterinary Medicine, 6th Ed., Published by the author, Ithaca, N.Y. 288. Vandeplassche, M. and Henry, M. (1977) Salpingitis in the Mare, Proc. 23rd Ann. Conv. AAEP, Vancouver, 123. 289. Vandeplassche, M., Henry, M. and Coryn, M. (1979) The Mature Mid-Cycle Follicle in the Mare, J. Reprod. Fert. Suppl. 27, 157. 290. Vandeplassche, G. M., Wesson, J. A. and Ginther, O. J. (1981) Behavior, Follicular and Gonadotropin Changes During the Es- trous Cycle in Donkeys, Theriog., 16, 2, 239. 291. VanLoen, A. 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(1975) Effects of Teasing, Rec- tal Palpation and Ovulation Control on Subsequent Fertility in Mares, Proc. Ann. Mtg. Soc. forTheriog., Cheyenne, Wyo., 1. 298. Voss, J. L. and Pickett, B. W. (1975) The Effect of Rectal Palpation on the Fertility of Cyclic Mares, J. Reprod. Fert. Suppl. 23, 285. (and J. An. Sci. 41, 3, 829, (1975)). 299. Voss, J. L., Wallace, R. A., Squires, E. L., Pickett, B. W. and Shideler, R. K. (1979) Effects of Synchronization and Fre- quency of Insemination on Fertility, J. Reprod. Fert. Suppl. 27, 257. 300. Wagner, W. C., Dunn, H. O. and Van Vleck, L. D. (1965) Incidence of Vibriosis in an A.I. Stud. Cor. Vet. 55, 209. 301. Walker, D. F. and Vaughan, J. T. (1980) Bovine and Equine Urogenital Surgery, Lea and Febiger, Philadelphia, 254. 302. Walt, M. L., Stabenfeldt, G. H., Hughes, J. P., Neely, D. R. and Bradbury, R. (1979) Development of the Equine Ovary and Ovulation Fossa, J. Reprod. Fert. Suppl. 27, 471. 303. Washburn, S. M., Klesius, P. H., Ganjam, V. K. and Brown, B. G. (1982) Effect of Estrogen and Progesterone on the Phag- ocytic Responses of Ovariectomized Mares Infected in Utero with Beta-hemolytic Streptococci, Amer. J. Vet. Res. 43, 8, 1367. 304. Wearly, W. K., Murdick, P. W. and Hensel, J. D. (1971) A Five-Year Study of the Use of Post-Breeding Treatment of Mares in a Standardbred Stud, Proc. 17th Ann. Conv. AAEP, 89. 305. Williams, W. L. (1943) Diseases of the Genital Organs of Do- mestic Animals, 3rd Ed., Ithaca, N.Y. 306. Witherspoon, D. (1982) New Kentucky CEM Outbreak, Eq. Vet. Data, 3, 7, 100. 307. Wolff, A., Dunderman, T. A. and Dunderman, B. J. (1963) Surgical Correction of Pyometra in a Mare, JAVMA, 143, 9, 1004. 308. Woods, G. L., Scraba, S. T. and Ginther, O. J. (1982) Pros- pects for Induction of Multiple Ovulations and Collection of Multiple Embryos in the Mare, Theriog., 17, 1, 61. 309. Zafrakas, A. (1964) Treatment of Anestrus Mares by Intra- uterine Irrigation with Saline Solution, Bull. Soc. Vet. Hell. 14, 75. 310. Zebracki, A. (1962) Hyperplasia of the Endometrium of the Horse Diagnosed by Uterine Biopsy, Wien Tierartzl. Mon- atschr., 49, 1, 135.Chapter XV INFERTILITY IN FEMALE SWINE The incidence of infertility in sows may approach that seen in cattle. Because of their lower value and the dif- ficulties of diagnosis and treatment, sterility in sows has not been studied as much as has infertility in cattle or horses. The farrowing rates in over 50,000 matings of sows and gilts in the Midwest was about 72 percent.81 The incidence of sterility in a herd where brucellosis was present was 21.9 percent in 382 sows over 1354 breed- ing seasons. This varied from 13.9 to 36.9 percent in various breeds.119 Currently the incidence of brucellosis in swine herds in the U.S. is greatly reduced. Five per- cent of sows and gilts were sterile, another 5 percent were hard to settle, and another 10 to 15 percent showed some impairment of fertility by a small litter size due to high intrauterine death rate of the embryos or fetuses.104 On postmortem examination 1.4 percent of 1000 sows and gilts were completely sterile and another 2.2 percent had lowered fertility.63 Because swine are multiparous or polytocous, complete sterility in swine is lower in in- cidence than in cattle but reduced fertility is common.83 In 250 sows, 42, or 16.8 percent, failed to conceive or farrow. Of the rest, 84 percent conceived on 1 service, 12 percent after 2, 2.5 percent after 3, and 1.5 percent after 4 services.119 Several studies showed that litter size rose to a peak at the fifth to sixth litter and then de- creased. Ten percent of female swine were sterile.105 The most common causes of sterility were hydrosalpinges and cystic ovaries; these two pathological lesions accounted for about one-half of the obvious failures to conceive. Stillborn pigs were classed as a form of infertility.83 Stillbirths occurred in 259, or 23.1 percent, of 1121 lit- ters. Litters of over 12 pigs had an incidence of 11.7 percent stillbirths, while medium-sized litters had an in- cidence of only 3.9 percent.98 The birth weight of still- born pigs was higher than that of normal pigs. An in- cidence of 6 percent stillborn, occurring usually in large litters, old sows and in spring farrowings, was reported.6 Stillborn pigs were more common in the latter half of the litters as they were born or in those fetuses nearer the apex of the horns. Attempts to hasten parturition with oxytocin gave inconclusive results. According to the lit- erature the incidence of stillborn pigs is 8 to 9 percent. The mortality in the two sexes was about equal.6 Sow productivity or piglets per sow per year weaned is based on ovulation rate, fertilization rate, embryo loss and fetal and newborn losses. The farrowing interval, as in cattle, is based on conception rate and lactation length and other possible genetic and environmental factors.29 76 Physiology of Porcine Reproduction Puberty occurs in gilts at 6 to 7 months of age with a range of 4 to 9 months. Spring bom gilts reach puberty 1 to 3 weeks later than gilts reaching puberty during the winter months. High environmental temperatures result in delayed puberty and an increased incidence of anes- trus. In contrast to other species the age of the gilt was more important than weight, nutrition or “flushing” on determining the onset of puberty or number of ova re- leased.76'80'81 Puberty may be delayed slightly by in- breeding or severely restricting the TDN or protein in- take to one-half recommended amounts. It may be hastened by crossbreeding and by allowing boars to con- tact the gilts.169 Moderately cold temperatures, and transport or environmental stress also hastened the onset of puberty. Certain breeds of swine such as the Landrace reach puberty earlier, 160 to 180 days, than other breeds, 200 to 230 days. Length of daylight or exposure to ar- tificial lighting had no effect on reproductive cycling or puberty in sows or gilts.816 Gilts that have not reached puberty by 240 days of age should be culled. Exogenous hormones were of limited value in promoting estrus in prepubertal gilts.76 Total confinement significantly re- duced the proportion of gilts attaining puberty by 9 months since about 25 percent were noncyclic and of these one- third were prepuberal and one-half were behaviorally anestrous.23'24,81 The greater the number of estrous cycles after puberty and before service in gilts, the greater is the ovulation rate.33a There is enough FSH and LH in the pituitary gland of gilts for several weeks before puberty to cause the onset of the estrous cycle. If prepubertal gilts are stressed by transport or by a marked change in environment, estrus will often occur within 4 to 7 days after the stress in- dicating the release of FSH. This same period of time is required to produce estrus in prepubertal gilts after the 636INFERTILITY IN FEMALE SWINE 637 injection of PMSG. Recurrent estrus may not follow this early induction of estrus and ovulation in gilts. In gen- eral, increased amounts of PMSG injected to induce fol- licle formation and estrus and HCG to induce ovulation results in a greater number of ova released at the induced ovulation. However, there is a great inconsistency in the number of ova released by exogenous gonadotropins in- jected into different gilts in various seasons, herds and years.-33* Gilts that reach puberty and conceive at an early age and have 9 or more piglets in the first litter should be retained as brood sows.22 The estrous cycle—The sow is polyestrous the entire year. Estrum usually does not occur during lactation or for at least 30 days after farrowing. Estrus usually occurs 3 to 7 days after weaning. After 6 to 10 years of age senility may affect the estrous cycle. The estrous cycle averages 21 days in length and may vary from 18 to 24 days.--’3,29’42'76’144 The estrogenic phase of the cycle is 6 to 7 days and the luteal phase is 14 days with CL regres- sion beginning on day 16. The duration of estrum is 1 to 4 days, with an average of 2 to 3 days, or about 60 hours. Ovulation usually occurs between 24 to 42 hours, or an average of 36 hours, after the onset of estrum. Nearly all sows examined had ovulated by 40 hours. Older sows have a slightly longer estrous period and cycle than gilts. Failure of ovulation results in a longer estrous pe- riod, and premature ovulation will shorten the period. Ovulation is spontaneous in sows. It takes about 4 to 6 hours from the rupture of the first follicle to the rupture of the last follicle. The LH surge in gilts and sows is about 20 hours long and peak LH plasma levels imme- diately preceded or were coincident with the onset of behavioral estrus in 60 to 70 percent of the sows. How- ever in about 20 percent of the sows the LH surge was delayed for 18 to 24 after the onset of estrus. This vari- ability may explain the lowered fertilization and con- ception rates in certain sows where frequent checks for estrus and services per estrus are limited. Sows should be checked for estrus 2 or more times per day and bred every 18 to 24 hours after the onset of estrus for 2 or more services.1536 Ovulations are slightly more frequent, 51 to 55 percent on the left than on the right ovary. The size of the follicles at ovulation is 0.7 to 1 cm. in di- ameter.1 Small follicles are present in the porcine ovary during diestrum, but during proestrum and estrum although ap- proximately 15 to 40 follicles approach maturity only about 10 to 20 ovulate. From 7 to 16 days after ovulation the corpora lutea are at their maximum size, about 1 cm. in diameter.1 The weight of the ovary during diestrum may reach 8 to 10 gm. Degeneration of the corpora lutea is rapid just before and during the next estrum and a few days before and after parturition. The symptoms of estrum in the sow are definite and usually marked.2’3,7’29,42'58’59’76’142 The sow has a reduced appetite and is restless and nervous, often pacing back and forth by the fence. Salivation, champing of the jaws, and frequent grunting may be pronounced. The sow, if suckling, may ignore her pigs; may try to escape, or if free will seek out the boar and stand for service. During estrum the vulvar lips become swollen and congested and the mucous membrane is pinkish-red in color. Some mu- cus may be present at the vulva. The most noticeable feature of estrum in the sow is her grunting and standing motionless for long periods in a position for service. This peculiar, immobilizing reflex or stance can be produced in over half of the estrous sows by the pressure of the hands on the sow’s back or by straddling the sow. In the presence of the boar with his characteristic odor, his grunts or acoustic signals, and his pushing and lifting of the rear parts of the sow by placing his snout between her rear legs, this sawhorse-like immobile stance and ac- ceptance of the boar will be induced in nearly 100 per- cent of estrous sows. In late estrum or early metestrum, a whitish mucous discharge composed of mucus, cellular debris and leucocytes may be seen on the vulva.7 The vaginal smear or the body temperature do not produce an accurate indication of the stage of the estrous cycle.85 As in the other domestic animals changes in the con- ductivity of vaginal mucus will predict the time of estrus but will not pinpoint the time of ovulation in gilts.39 The vaginal epithelium in the sow undergoes cyclic thick- ening during estrus when it has 8 to 15 cell layers. Dur- ing diestrus this will decrease to 4 to 5 layers and during pregnancy to 2 to 3 layers. This permits vaginal biopsies to be utilized for the diagnosis of pregnancy in swine.33,1 The musculature of the uterus and oviduct is most active during estrum. The endometrium and especially the re- gion where the uterine tube enters the uterus is quite edematous. In healthy sows and gilts 90 to 100 percent of ova are fertilized and 80 to 90 percent of sows farrow after service to a fertile boar. Plasma hormone concentrations or levels during the estrous cycle have been determined by radioimmunoas- says (RIA).76 Estrogens are fairly low, 8 to 12 pg/ml except during estrus, days 18 through day 1 of the next cycle when they peak at about 30 pg/ml. Plasma pro- gesterone levels are 1 ng/ml or below during estrus but rise rapidly after ovulation to 20 to 30 ng/ml from days 7 to 16 of the cycle and then decline. Prostaglandin lev- els in the uterine vein rise to 6 ng/ml between days 14 to 16 of the cycle. Plasma LH has a number of lesser small peaks during the cycle but rises to the highest peak or preovulatory surge of 4 ng/ml at the onset of estrus638 VETERINARY OBSTETRICS between days 20 and 1 of the next cycle. Plasma FSH concentrations are about 6 to 7 ng/ml during the cycle but rise slightly on days 21 to day 4 of the next cycle. Estrus and ovulation are inhibited by estrogens and pro- gesterone. Prostaglandin F2a can induce luteolysis of CL but swine CLs are refractory to prostaglandins until day 12 of the cycle.70 So the use of prostaglandins to syn- chronize estrous cycles in sows or gilts is impractical because they are only effective days 12 through 15 of the cycle. The value of PMSG to increase ovulation rate is negated by the high prenatal loss of embryos so litter size is relatively unaffected.42'76 HCG and GnRH if ad- ministered late in proestrus or at the onset of estrus will induce ovulation in about 40 hours.42 The principal uri- nary estrogen in sows is estrone. The peak in urinary estrone excretion occurred just before estrus. Estrous signs can be induced by estrogen injection in ovariectomized sows or in sows without functional cor- pora lutea. However, if estrogens are injected into sows with mature corpora lutea during the luteal phase of the cycle, estrus does not occur. In fact, even a single in- jection of estrogen into sows at this period will prolong the life of the corpus luteum causing anestrus that may persist for a number of weeks. Thus, indiscriminate use of stilbestrol or estradiol in sows to promote estrus is to be avoided.338,60 About 60 to 90 percent of sows will exhibit signs of estrus 2 to 3 days, range 1 to 5 days, after farrowing and will accept the boar.2'42 If sows are bred at this estrus they do not conceive because ovulation rarely oc- curs.8160 Furthermore if a few ova are shed and fertilized they do not develop. This estrus might be due to estro- gens from the ingestion of the placentae at parturition.- The older usual or traditional lactation period in sows was 56 days (8 weeks). This period is being shortened to improve sow productivity. The uterus of the sow is completely involuted within 21 to 28 days after partu- rition. The uterine weight decreased from 2.8 kg on the day after farrowing to 0.2 or 0.3 kg at 21 to 28 days.113 Most sows that are suckled go into a lactational anestrus that lasts for 6 weeks or longer or until the pigs are weaned. Sows whose litters were weaned at 10 days after parturition came into estrum more than 9.4 days later, 2 sows developed cystic ovaries, and only 12.8 ova were released at the first estrum. Sows whose litters were weaned at 21 days came into estrum at an average of 6.2 days later, and ovulated an average of 15.2 ova. Sows whose litters were weaned at an average time of 56 days, came into estrum an average of 4 days later and ovulated an average of 16.6 ova.66 The earlier after farrowing pig- lets were weaned to produce early cycling and concep- tion the longer the time from weaning to estrus and the lower the conception rates and smaller the litter size. However if pigs were weaned at 21 to 28 days,816 or possibly 35 days39 sow productivity for the year was maximized. Sows came into estrus sooner after weaning than gilts and white breeds sooner than black breeds.76 About 60 percent of primiparous sows returned to estrus the first week after weaning compared to 85 percent of multiparous sows. During the summer, postweaning anestrus, up to 4 months, in the former is increased; only 65 to 75 percent of sows were in estrus the first week after weaning. This delay was more apparent in primi- para. Shade and evaporative cooling had little effect. Weaning to estrus interval was shorter because of re- duced stress in crossbred sows and in crated sows than in sows penned in groups.80,81ab Synchronization of Estrus—During lactation and suckling estrum does not occur. But after the pigs are weaned estrum usually develops in about 4 to 9 days or an average of 5 to 7 days.338'42'76'85 139 Under some cir- cumstances, when it is desirable to synchronize the breeding and farrowing dates, estrum may be produced in a lactating sow by removing her pigs each night for 4 to 5 nights and allowing the pigs to nurse during the day,133 or by weaning the pigs at 3 to 5 weeks of age. Lactation may be suppressed by the former practice. Some sows, if fed well and with a boar nearby come into es- trum 5 to 7 weeks after farrowing even with pigs still suckling.164 Synchronization of estrus in gilts and sows can most practically be accomplished by management procedures. Introduction of boars into close contact with gilts along with transport or a change in the environment to produce stress will usually initiate estrus within a week in puberal gilts. In sows synchronization can also be accomplished readily by weaning pigs after 3 to 5 weeks of lactation and the introduction or close contact with boars. Increas- ing the nutritive level or “flushing” for 4 to 8 days with 3 to 4 kg/day of a well-balanced ration may slightly im- prove the ovulation rate.76 Vasectomy for heat-check boars has been described where artificial insemination is de- sired.62 Teaser-gilts to be used for detecting sows in es- trus could be produced by long-time injection of testos- terone propionate135 as has been demonstrated in cows and ewes. Over the past twenty years much research has been conducted with progestins, the gonadotropic hormones, PMSG and HCG, methallibure and recently GnRH alone and in various combinations to induce synchronized es- trus in gilts and sows to aid in artificial insemination at a specific time to progeny-tested boars. The results haveINFERTILITY IN FEMALE SWINE 639 varied widely.74 131 162 The routine use of PMSG in the U.S. is negligible because of its limited availability even though it has been shown to induce ovulation in lactating sows. Recent studies indicate that estrus synchronization in the future might be possible.74,127 1463 Altrenogest (al- ly 1-trenbolone) fed orally at a dose level of 15 to 40 mg./ day for 14 or 18 days to gilts effectively synchronized estrus. Low doses of this progestin caused cystic folli- cles.903,1463 Ovulation, Fertilization and Ova Transport—The rate of ovulation is 10 to 15 ova and 12 to 20 ova for gilts and sows, respectively. A slightly higher rate of ovulation may occur in certain breeds, in crossbred gilts and in sows 2 to 4 years of age. Very low ovulation rates, 4 or below or very high ovulation rates as in su- perovulation may result in the loss of the entire litter.166 Markedly restricting the energy intake will decrease the ovulation rate but this can usually be promptly restored by feeding a high level of TDN, or “flushing” for a week or more depending on the condition of the sow. High rates of ovulation result in larger litter size at 25 days of gestation. But at farrowing the litter size is not in- creased by higher than normal ovulation rates.333 In Wrathall’s review it was shown that the greater the ovulation rate the lower the prenatal survival rate. Losses of embryos in the pre-attachment stages, before days 15 to 17 of gestation, are mainly due to inherent limitations within the embryos themselves. While in the post-at- tachment stages losses are due mainly to limitations im- posed on the conceptuses by the uterus basically involv- ing uterine length or capacity and the evenness of dis- tribution and spacing of the blastocysts. Those concep- tuses with inadequate attachment areas for the diffuse porcine placenta either die or are growth retarded. About 10 percent fetal loss from 30 to 40 days to term is due to uterine space limitations.166 Thus even though ovu- lation rates might be elevated by various means, litter size remains fairly constant for the breed and age of the sow or gilt.333,76,166 If large litters of over 12 pigs are bom the death losses in these litters prior to weaning are higher. Most embryonic or prenatal losses occur before 25 to 30 days of gestation when the blastocyst begin to elongate rapidly at 11 to 18 days and when attachment is occur- ring at 18 to 40 days. Thus there is about a 65 to 75 percent embryo survival in most porcine pregnancies based upon ovulation rates of 10 to 22 ova and 8 to 12 pigs bom per litter.76 Included in these losses are lethal ge- netic factors causing up to 50 percent of the losses in the blastocyst stage95,96 and losses due to possible ma- ternal effects including abnormal uterine secretions (“milk”) between days 9 to 16 of gestation. The admin- istration of progesterone or progesterone and estrogens to augment early embryo survival has not resulted in a conclusive or consistent beneficial response.336,76 High levels of energy or TDN during gestation is not neces- sary or desirable as early in gestation it may increase embryo loss and late in gestation cause increased size of the fetus, and birth and postpartum problems. The best time to breed or inseminate sows or gilts is 24 hours apart on the first and second day of estrus or about 12 hours before ovulation which occurs about 40 hours after the onset of estras.42,78 Sows bred the day before heat, the first day of heat, the second day of heat and the third day of heat had 9.8, 68.8, 98.2 and 15.2 percent fertilized ova, respectively.72 The average num- ber of fertilized ova in sows mated at the proper time was 95.5 percent. Factors affecting the fertilization and conception rate are boar fertility, timing of service and seasonal conditions, or heat stress.76 Sperm cells were present in the uterine tubes of sows within 15 minutes of breeding. Thirty minutes after breeding, although 30 to 60 billions of spermatozoa were in the uterus, only about 90 to a few hundred spermatozoa were in the uter- ine tubes.53-56,76 Seminal plasma and spermatozoa were rapidly lost from the uterus and phagocytosis of sperm calls began within a few hours after mating. Although both live and dead cells may enter the uterine tube, the live sperm cells remain motile in the tube for 24 hours while those in the uterus showed a greatly reduced mo- tility after 2 hours. A mass of live sperm cells accu- mulate at the uterotubal junction in the apices of the uter- ine horns for 24 hours and then decline during the next 24 hours thus providing a steady flow of sperm cells through the junction into the uterine tube. The fertilizing ability of swine spermatozoa lasts only 25 to 30 hours in the sow.85 The best time to breed sows was 10 to 25 hours after the onset of estrus. If the sow is bred the first day of estrus she should be rebred the second if she is still in standing estrus. When ovulation time was controlled by an injection of HCG during proestrus and gilts were inseminated 2 hours before ovulation and 2, 6, 10 and 14 hours after ovulation, the proportion of CL represented by normal embryos at 25 days of gestation were 73, 61, 53, 28 and 32 percent, respectively. In control gilts bred 6 hours before ovulation, 88 percent of the CL were represented by normal embryos at 25 days of gestation.773 Aging of ova and spermatozoa significantly affected the number of surviving embryos at 25 days.56 Twenty-six percent of sows bred 44 hours after the onset of estrus had het- eroploid embryos 17 days later probably due to polysper- my. Four percent of heteroploid embryos were observed.640 VETERINARY OBSTETRICS Fertilization in female swine must take place in the am- pullae before 60 hours after the onset of estrus to cause conception and before 50 hours to produce cytologically normal embryos.15 The block or zona reaction in the vi- telline membrane in the ova to polyspermy is highly ef- fective when the sow is mated the first half of es- trus.333'76'78 Thus, it would appear from the above data that ca- pacitation of spermatozoa must occur before fertiliza- tion. Fertilization can occur within 2 to 3 hours after insemination. The corpus luteum develops steadily re- quiring a full week for development.- Fertilized ova in swine pass through the first half of the uterine tube very rapidly and remain near the ampullary-isthmic junction for 24 to 39 hours or until 60 to 75 hours after the onset of estrum. The fertilized ova at the 4-cell stage of de- velopment pass into the uterus about 44 to 54 hours after ovulation or 66 to 90 hours after the onset of estrus.42112 Thus swine ova enter the uterus sooner than in the other domestic animals. The morula stage develops and the zona pellucida is shed in the apices of the uterine horns 6 to 8 days after the onset of estrus.33a The blastocyst grows very rapidly from 4 mm. in diameter on the 9th day of gestation to 110 cm. in length on the 16th day.117 Intrauterine migration of fertilized zygotes occur during days 9 through 12 just before the rapid elongation of the blastocyst or blastodermic vesicle42'78,159 in sows and has been confirmed by comparing the number of CL in each ovary with the number of embryos in the cor- responding horn. Although 55 percent of the CL were on the left ovary, each horn contained 50 percent of the fetuses.92 In sows that are unilaterally ovariectomized before mating or sows in which one uterine tube is li- gated, equal numbers of embryos implant in each horn.159 It has been estimated that 40 percent of the zygotes mi- grate from one horn to the other. This was also shown by ova transplantation.41'44 This is apparently accom- plished by the motility and activity of the uterine mus- culature to assure both efficient distribution and equi- distant spacing of each embryo. The pig blastocyst syn- thesizes estrogens from about day 12 of pregnancy. This is apparently responsible for the maternal recog- nition of pregnancy in this species as estrogens increase blood flow to the uterus and have a luteotropic effect on the corpus luteum. This increased blood flow may ex- plain why luteolysis is not produced by the uterine pros- taglandin in early pregnant sows.57b Litter size—Much study has been conducted on causes of reduced litter size. The prenatal mortality in swine has been estimated to be about 45 percent.143 Most of these losses of zygotes occur during the first 25 days of ges- tation. About 6 percent of these losses occur in late ges- tation and at parturition resulting in stillbirths. Gilts bred the first, second and third estrum after puberty have 6.9, 8.0 and 9.4 pigs per litter, respectively. In another trial this difference was not significant in well-grown gilts.168 Farrowing rates also increased from 83 to 94 percent from the first to third estrum after puberty.80 81 168 There is an increase in prenatal mortality with increased age of the sow and parity because the increased ovulation rate in sows is not associated with a similar increase in litter size. The peak in litter size occurs about the 5th to 7th litter or 2 to 4 years of age.5'332,137'138 The decline in litter size in older sows is due to an increase in embryonic death rate. Heritability of litter size is low, 10 to 15 per- cent.16333 Litter size will differ between breeds by an av- erage of 3 to 4 pigs per litter. This difference in litter size between breeds may be associated with an increased ovulation rate in certain breeds.47 Inbreeding of the dam causes a decrease in litter size and crossbreeding an in- crease in litter size due to heterotropic effects. 13'33a'80,81 Embryonic mortality may also be a characteristic of the individual sow. The sire of the sow is also an influencing factor.115 Each of 27 boars in two studies141’1476 were mated with about 10 gilts and it was found that boars exerted a sig- nificant effect on conception rate ranging from 30 to 100 percent. The number of live embryos at 25 to 30 days of gestation ranged from 3 to 17 with an embryonic sur- vival rate of 24 to 84 percent. If a boar had a conception rate below 65 percent this could be an important cause of reduced litter size.114 Thus culling boars with low con- ception rates would improve fertility in the herd and in- crease litter size.141'1476 Chromosomal abnormalities have been described in a significant percentage of embryos from normal sows as a cause of infertility or reduced litter size.95 One boar was reported that had normal se- men volume, sperm cell numbers and progressively mo- tile spermatozoa but had a zero impregnation rate when mated to 12 sows.1476 In this instance nuclear or sperm head defects or chromosomal abnormalities might be suspected. Litter size is usually larger in spring farrowings than in fall farrowings. One disadvantage to multiple farrow- ing in sows is the lowered fertility in the summer months. Hurtgen reported that farrowing rates are 15 percent, range 2 to 40 percent, lower in the summer, July through Sep- tember, than in the winter months. Many infertile mat- ings had a delayed interval or return to estrus indicating possible early embryonic death or abortion and mimick- ing viral reproduction failure.80,81 Sows stressed by ex- posure to 85 to 100°F. heat from days 1 to 5 or 15 of gestation had an increase in embryonic death rates.45'80'81,154INFERTILITY IN FEMALE SWINE 641 If the sows were stressed by heat before breeding or from 15 to 30 days of gestation, there was no effect on em- bryonic death rates. Thus, cooling sows with sprinklers on hot days may be indicated the first week or two after breeding. Severe cold stress did not affect litter size.1473 Stress due to transportation or change or environment has not been reported to effect fetal mortality. Confinement of gilts had no effect on the farrowing rate compared to those bred and maintained in outside lots. Furthermore mated gilts maintained in gestation crates in one study had a 13.8 percent higher farrowing rate.81 There is no evidence that exposure to light over a range of 6 to 18 hours has any effect on ovulation or concep- tion rates in female swine. Mating on 2 consecutive days of estrus by the same boar improves farrowing rates by 10 to 25 percent in sows and 10 to 13 percent in gilts. When a different boar is used for the second mating farrowing rates increased an additional 4 to 8 percent, respectively, but litter size only increased 0.2 pigs/sow.28,80 Sows bred once during an estrum had a 68 percent conception rate and sows bred twice had a 78 percent conception rate. Two ser- vices produced 0.5 to 0.7 more pigs per litter than once service.147 There was no significant difference in the number of ovulations and litter size in sows bred the first or second estrus after weaning their pigs.137'138 The quantity of uterus affected the uterine capacity to maintain fetuses. When one horn and ovary was re- moved from 59 gilts the litter size at 25 days of gestation was similar to the intact control gilts, but at 105 days of gestation the treated gilts had 5.5 fetuses in the single horn compared to 9.4 fetuses in the intact gilts. In a large number of gilts it was demonstrated41'42'44 that intrauter- ine crowding was not important in early embryo survival at 25 days or 30 days and only when a gilt had 14 or more oversized embryos did it appear likely that uterine crowding was a possible limiting factor in embryonic survival. After transferring 16 to 28 fertilized embryos to gilts, the litter size was similar to control gilts, 8 to 10 pigs.10 Thus, uterine capacity is an effective factor in limiting litter size. This effect apparently occurs after day 40 of gestation. A high level of nutrition or energy intake in gilts and sows for several weeks prior to breeding and during the breeding period results in slightly higher ovulation rates.89 The level of feeding has no effect on fertilization but a high level of energy intake for four weeks after concep- tion results in a variable but greater embryonic mortality depending upon the amount of energy given. This may possibly be related to heat or other stresses. Limited feeding of female swine is indicated following breed- ing.73 The number of pigs born is not affected by the plane of nutrition as long as it is adequate during the latter two-thirds of gestation. The level or quantity of protein is not as critical as energy in its effect on repro- duction. Most swine nutritionists recommend 5 to 10 percent alfalfa in the ration during gestation to promote normal farrowing of healthy well-grown pigs. Sows should be kept in lean or moderate condition during gestation for economic reasons and to avoid dystocia or farrowing problems common in fat sows or gilts. Although both progesterone and estrogen are needed to produce a proper intrauterine environment for the growing embryo, there has been no evidence that im- plants or daily injections of progesterone and estrogen at a ratio of 2000:1, or single injections of either hormone have any beneficial effect on embryonic mortality.33b’34 It has been suggested that uterine infections during the breeding period and shortly after conception may ac- count for a reduction in litter size. The evidence sup- porting such a factor limiting litter size is present but not conclusive.35,100'131140 Feeding chlortetracycline and tet- racycline continually or only during the breeding period produced no significant benefits.35'140 The author and others29 recognize the contradictory reports on the effects of antibiotics fed at the time of breeding on reproduc- tion, but recognize that in a herd acutely-infected with leptospirosis or a similar bacterial infection, antibiotic treatment during the gestation period may be beneficial in reducing fetal mortality and stillbirths. (See Chapter V). The 30 to 40 percent deaths of fertilized ova or early embryos characteristic of pregnancy in swine, and the other species, may well be nature’s way of eliminating some unfit or abnormal genotypes at a low biologic cost. The incidence of genetic or congenital abnormalities in the newborn is low because most are eliminated early in pregnancy. The utero-ovarian relationship in swine is similar to cattle and sheep. Hysterectomies performed in sows the first half of the estrous cycle caused prolonged anestrus and the maintenance of corpora lutea for the approximate duration of gestation, about 110 days. If the operation is performed late in the cycle, ovulation occurs and the subsequent corpora lutea produced persist for a similar period. If nearly all of the uterus is removed from non- pregnant sows leaving only a portion that is less than one-fourth the length of the horn, then the CL will re- gress only on the side of the retained small portion of the horn; the CL on the opposite side will persist. If the portion of the uterine horn left in place is one-fourth the length of the uterine horn or longer then the CL will regress on both sides because sufficient amount of pros- taglandin is released from the endometrium to cause in-642 VETERINARY OBSTETRICS volution or regression of the corpora lutea. Thus in swine if there is a blind horn due to a localized segmental apla- sia involving only a portion of the horn so that zygotes are present only in one horn, then prostaglandin released in the nonpregnant horn or segment of that horn will cause CL regression and prevent implantation and pregnancy. If one horn is ligated near its base, and the sow is bred at estrum, the developing zygotes will not be present in that horn and the prostaglandin will be released resulting in a regression of the CL and the onset of estrum ter- minating the early, unicomual, pregnant state. If one horn and its corresponding ovary are completely removed then pregnancy can occur in the remaining horn. Thus an in- tact, but nonpregnant horn will cause CL regression on both ovaries in swine but not in cattle. 4,36“38’61’97 Once pregnancy is established with zygotes through- out the uterus the prostaglandin release is suppressed and cycling ceases and corpora lutea persist.121 By day 14 to 15 at least 4 viable embryos or more are necessary in gilts to suppress prostaglandin and maintain luteal func- tion during early pregnancy.78 122 When all the fetuses or embryos in one horn were killed between 4 and 50 days of gestation, that pregnancy was maintained in gilts so treated between 12 and 50 days, but was not maintained in gilts so treated from 4 to 10 days of gestation.37 38110 In these latter gilts the CL regressed on both ovaries. Thus after day 13, pregnancy will continue even if all of the fetuses in one horn die or become mummified. The author has observed a sow with all of the fetuses mummified except one and pregnancy was maintained. (See Figure 74.) Anatomical, Congenital, and Possibly Genetic Ab- normalities of the genital tracts of female swine are oc- casional causes of failure of conception which can be explained by the close utero-ovarian relationship previ- ously described that results in early regression of the CL induced by the release of prostaglandins before day 12 of gestation in the uterine horns not containing devel- oping embryos. Of 19 “repeat breeding” sows and 44 “repeat breeding” gilts 5, or 11.4 percent of the gilts had a unilateral missing segment of the uterine hom, or uterus unicornis.161 Nineteen, or 43.2 percent, of the gilts and 2, or 10.5 percent, of the sows had bilateral tubal ab- normalities; 2, or 4.5 percent, of the gilts had bilateral missing segments such as a missing vagina, cervix, or body of the uterus. Animals with bilateral tubal abnor- malities were included with those having hydrosalpinx, “pyosalpinx”, and bursitis. Present in the broad liga- ments of some of the gilts were structures that appeared to be rudimentary ducts or remnants of the mesonephric or Wolffian duct system. With so many abnormalities affecting gilts, the logical conclusion was that they were developmental defects or arrests. Of 79 female swine that had been bred an average of 2.8 services without con- ception,105107165 a unilateral missing segment was found in 1 gilt and 1 sow, or 2 percent and 3.6 percent, re- spectively. A unilateral blind segment was present in 4, or 7.8 percent of the gilts, and 1, or 3.6 percent, of the sows. A blind uterine body was found in 1, or 2.0 per- cent, of the gilts, in many cases the blind hom was dis- tended with mucus. One gilt had a missing cervix. An- other 354 day-old gilt had infantile reproductive organs with a complete lack of estrous periods. In several cases one uterine hom, uterine tube and ovary were missing. In cases in which one hom, usually the left hom, and the adjacent ovary were missing, pregnancy occurred normally in the other hom but the litter size was reduced by about one-half. A partial doubling of the uterine horns was observed in 5 of 500 gilts.36 Some of these became pregnant and farrowed. This might be genetic in nature. In Belgium it was reported that 2.2 percent of 1000 fe- male swine examined had missing segments of the uter- ine hom; 3 percent of the gilts had hydrometra; there were 4 cases of a uterus didelphys (double cervix); and 1 had a missing uterine body.63 A case of uterus didel- phys and other cases of a double cervix and median sep- tums of varying lengths in the vagina located most com- monly near the hymen and extending cranially were described.102 150 158 After examining 2967 gilts and 1288 sows, the following incidence in slaughter house mate- rial of missing and double parts of the genital tract was reported.163 Percent Missing uterine hom 0.3 Missing segment of uterine hom 0.3 Missing vagina, cervix, and uterine horns (with male ducts in broad ligaments) 0.02 Missing cervix 0.02 All reproductive organs missing except vulva 0.04 Double cervix 0.04 Double uterine hom 0.02 Total 0.74 There were 1.8 percent of the open gilts, 0.6 percent of the pregnant gilts, and 1.2 percent of the open sows— or a total of 1.5 percent of 5088 sows and gilts—with tubal abnormalities. None of these abnormalities, except possibly a missing vagina or cervix, could be diagnosed in the living animal by practical methods. Thus it was emphasized by the above figures that anatomic arrests in development were not uncommon.163 Of these anomalies hydrosalpinx was the cause of the greatest amount of sterility. Anatomic defects were found in 21.5 percent of the sterile female swine exam- ined.105107165 Thirty three percent of “repeat breeding”INFERTILITY IN FEMALE SWINE 643 swine had bilateral tubal abnormalities.161 The incidence of defects in sterile gilts in these reports was 31.3 per- cent and 43.2 percent, respectively. In sows the inci- dence was much lower, only 3.6 percent and 10.5 per- cent, respectively. Of 142 or 3.3 percent genital tract anomalies in 9250 gilts and 9 or 1.8 percent anomalies of the genital tract in 476 sows, about one half were either segmental or total aplasia of the paramesonephric ducts.150 Thus in swine, especially gilts, anomalies of the genital tract are not uncommon. The incidence is definitely higher than in other species of farm animals. Hermaphrodism in swine is seen occasionally and the affected animals are usually male pseudohermaphrod- ites, (See Chapter III). Tubal abnormalities are common in swine in the U.S. as noted above but uncommon in Europe.105,107 150 They are usually bilateral and probably genetic in origin and result in hydrosalpinx or “pyosalpinx.” In sterile female swine, usually gilts, 35 percent had obstruction of the uterine tubes. In hydrosalpinx, which was by far the most common lesion, there appeared to be an obstruction in the lumen of the uterine tube about two-thirds of the dis- tance from the ovary to the horn, causing an accumu- lation of fluid.161,165 They reported that bursitis, or adhe- sions between the fimbria and ovary occur commonly in cases of hydrosalpinx. These adhesions were probably secondary to mycoplasmosis, polyserositis, peritonitis or intraperitoneal injection of an irritating substance in pig- lets.11 Twenty or 2 percent of the 1000 female swine examined had bursal adhesions. These apparently are not so common or serious as the hydrosalpinx that may be associated with them.63 Occasionally “cysts” of the bursa developed secondary to severe adhesions. In hydrosal- pinx, which was very common, 97 percent of the cases were bilateral and usually the uterine third of the tube was involved or obstructed.165 In some cases the uterine tube was patent and a light yellow bacteriologically-neg- ative material was flushed with some force from the lu- men. This would effectively prevent the passage of sper- matozoa and ova. In most cases of hydrosalpinx or “pyosalpinx,” adhesions of the fimbriae to the ovaries were present. There was some evidence that these hy- drosalpinges and “pyosalpinges” might have been caused by the obstruction of the uterine tube by embryonal rests of the Wolffian duct system.105,107 The condition was in- variably bilateral and showed some tendency to be in- herited. It appeared almost entirely in nulliparous gilts. Attempts were unsuccessful to reproduce this condition experimentally in normal females by inoculating their uterine tubes with contents from affected tubes. Whether hydrosalpinx and adhesions are due to disease, to con- genital lesions, or to some other factors is not definitely known. More work is needed on this problem. Pathological Lesions or Diseases of the Reproduc- tive System in swine, besides those mentioned, are cys- tic ovaries and inflammations of the genital tract. The former will be discussed later under hormonal causes of sterility. Nonspecific postpartum or postservice metritis is not considered as common in the sow as in the cow and mare; retained placenta is of less frequent occur- rence; delayed involution of the uterus with endometri- tis, a common cause of postpartum sterility in cattle, is not common in sows. Only two cases of pyometra have been described.63,165 On examination of 5088 sows and gilts, no gross uterine infections were reported.163 In Chapter XI the mastitis-metritis-agalactia (MMA) syndrome or “milk fever” in sows was discussed. This acute condition occurs soon after parturition and has been the subject of much recent intensive research. The dis- ease MMA has largely been described as a clinical entity characterized by a degree of lactational failure or aga- lactia also associated with signs of anorexia, stiffness, fever, swollen mammary glands and the usual postpar- tum mucoid vaginal discharge. Infertility has not been described following this MMA syndrome.5130 The post- partum vaginal discharge is usually not associated with a uterine infection. Specific Infections of the Genital Tract causing ste- rility in swine include brucellosis caused by Brucella suis. The uterine lesions of brucellosis in swine are well described.151 Often the only recognized symptom of bru- cellosis in swine is an increased incidence of infertility.83 In one brucella-infected herd 37 of the first 100 sows bred failed to conceive. Eight naturally infected sows studied over a 2-year period farrowed only 14 litters, even though bred for 2 litters a year. Of the 129 pigs bom in these 14 litters, 44 were stillborn and 17 were weak and died within 2 days of birth, a loss of nearly 50 percent. In another herd, having 80 percent reactors to the brucellosis test and much sterility, 3 gilts were slaughtered; all had a purulent cervicitis and metritis from which Br. suis was recovered. In “repeat breeding,” brucella-positive, female swine the incidence of embry- onic death was 87.5 percent as compared with an inci- dence of 46.5 percent in brucella-negative females.161 When sows infected with Brucella were serviced by a fertile boar the pregnancy rate was only 35 percent com- pared to 90 percent in uninfected gilts.157 This infertility was due to macroscopic and microscopic lesions of the endometrium causing early embryonic deaths with pro- longed periods between heats. When infertility is a prob- lem in a herd of swine, the brucellosis status of the herd should be determined. A boar with Staph, aureus infection of the vesicular glands bred 18 females and only 4 conceived, 3 con- ceived subsequently to another boar, 3 were sold as ster-644 VETERINARY OBSTETRICS ile, and the remaining 8 sows developed an acute me- tritis with a vaginal discharge. Two of these 8 sows were rebred later and aborted.51 On postmortem all showed a chronic metritis resembling that due to brucellosis. Dur- ing a 3-week period 8 of 209 7-month old virgin gilts developed an acute severe metritis due to Staph, aureus with an elevated body temperature and copious vaginal discharge.49 There is no evidence that leptospirosis causes sterility in swine, even though there is much evidence that it may cause abortions. A high incidence of defec- tive pigs and early embryos and mummified fetuses were reported in non-immune sows vaccinated against hog cholera with the modified virus vaccines 10 to 16 days after conception.40 167 Other viruses described in Chapter V including picoma viruses, Aujeszky’s disease (Herpes) virus, parvovirus (“SMEDI”) and several other viruses described in Japan will cause heavy pre-natal mortal- ity.40 Coital vesicular exanthema, or vesicular venereal disease, may in rare cases affect the caudal portion of the genital tract of sows and gilts.-'84 This has not been described, and if present is probably rare, in the United States. Several cases of a ruptured cul-de-sac of the cranial and lateral portion of the vulva after copulation were de- scribed.165 These lesions were apparently caused by pen- etration of the vulvar mucosa by the penis. They were inflamed bulb-like structures containing coagulated blood. Intromission was apparently painful and was resented. In many instances the affected females, even though in estrum would often refuse to accept the boar. Sometimes the female would have a normal service followed by evi- dence of pain at subsequent services. These lesions did not cause permanent sterility and did not affect the more cranial portions of the genital tract. Vulvovaginitis, characterized by swelling of the vulva with a mucous discharge, enlarged mammary glands and occasional prolapse of the rectum has been described in Chapter V. This condition is due to the feeding of moldy com or barley in which estrogenic compounds, zeara- lenone, were present. Zearalenone (F-2) is an anabolic estrogen-like mycotoxin produced naturally by Fusarium growing in grains stored under high moisture conditions. Feeding of this mycotoxin caused infertility with small ovaries and atretic follicles and no corpus lutea and squa- mous metaplasia of the epithelium of the genital organs. It also caused nymphomania, pseudopregnant sows with persistent corpora lutea, juvenile hyperestrogenism in nursing piglets, malformations and possibly fetal resorp- tion.21 Swollen reddened vulvas were reported in pigs consuming a poultry feed containing dienestrol. These animals exhibited estrous behavior. The isolation of a mycotoxin from F. graminearum (Gibberella zeae) that caused vulvovaginitis, vaginal prolapse, perineal relax- ation and ovarian atrophy in young gilts was de- scribed.91'146 The action of the mycotoxin was identical to estradiol. When the estrogenic metabolite, zearale- none, of Fusarium roseum (Gibberella zeae), a com- mon mold of com is present at high enough levels in grain this mycotoxin causes testicular atrophy and rectal prolapse in boars, vulvar reddening, swelling and va- ginal prolapse in gilts and nipple enlargement in both sexes. In some nonpregnant gilts zearalenone will cause persistence of the CL, pseudopregnancy and anestrus with edematous uterine horns. Moderate doses fed to preg- nant gilts caused decreased weights of the uterus, pla- cental membranes and fetuses.486 High levels of moldy feed fed 3 to 34 days of gestation caused inhibition of fetal development and decreased numbers of fe- tuses.92b'1686 Other trichothecene mycotoxins such as deoxynivalenol produced by F. roseum have also been associated with reproductive disorders, infertility and abortion in sows.926 Hormonal or Endocrine Disturbances are described as being responsible for about 4 percent of the infertility in female swine or 20 to 50 percent of infertile sows. This is the second most common cause of infertility in swine. A 24 percent incidence of cystic ovaries in 821 sows was described and 83 or 10 percent of these sows were sterile.116 Occasional follicular or luteal ovarian cysts were found in all stages of pregnancy, as well as in non- pregnant sows and gilts.105,106 In pregnant sows, cysts apparently developed or persisted after conception in- asmuch as ovulation in nonpregnant, cystic females rarely if ever, occurred. The presence of these cysts in preg- nant sows was not related to litter size and did not in- terfere with gestation. Estrus and service may occur dur- ing pregnancy in sows possibly associated with the development of follicles or the presence of high levels of estrogen. Cystic ovaries in pregnant female swine could invariably be produced by a single injection of a small dose of 200 to 400 IU of PMS. Cysts on ovaries in preg- nant sows was not observed.116 About twice as many cysts, 35 percent were noted during the spring months as in the fall months, 15 percent. The incidence of cystic follicles in ovaries with cor- pora lutea was 1.1 percent and cystic follicles alone was 0.6 percent of 5088 female swine.163 Cystic ovaries were reported with corpora lutea in 7.6 percent and with no corpora lutea in 2.5 percent of 79 infertile or sterile sows.165 Six percent cystic ovaries with corpora lutea and 3.2 percent cystic ovaries with no corpora lutea were observed in 63 “repeat breeding” sows.161 Cystic ovaries in nonpregnant swine were of 3 types—INFERTILITY IN FEMALE SWINE 645 single cysts, multiple, large cysts, and multiple, small cysts.104-106 Single cysts were found in 2 percent of 1751 pairs of ovaries. In these cases only 1 or 2 cysts were present on the ovary. They were 2 to 3 cm. in diameter, whereas a normal follicle is only .7 to 1.1 cm. in di- ameter. The reproductive tract and behavior of these fe- male swine were normal. These single cysts were found during the luteal phase of the cycle with normal corpora lutea present. These were probably atretic follicles that failed to rupture when ovulation occurred and were not associated with sterility.104-106116 Multiple cysts were always associated with permanent or temporary sterility. Three to 4 percent of non-preg- nant females were affected. It is usually impossible to differentiate clinically between sows with large or small multiple cysts as estrous cycles in both are irregular and characterized by anestrous periods of varying length. Large multiple luteal cysts were most common. These measured 2 to 10 cm. in diameter and an average of 5.6 cysts were present on each ovary. Thus the number of these cysts was nearly the same as the normal number of follicles. The walls of these large cysts were either heavily luteinized or contained lutein patches. The uter- ine endometrium in these cases showed progestational changes. The external symptoms manifested by these sows were extreme irregularity of the estrual cycle with in- tervals of 2 to 90 days between estrous periods. The heats were of greater intensity but of the same duration as those in normal noncystic females. In 60 percent of the af- fected female swine the clitoris was larger and longer, up to 1 to 2 cm. in length, than the clitoris of normal females, 1 to 2 mm, in length. The amount of estrogen present in these large cysts was less than in normal ovar- ian follicles. Androgens were not present. Although pro- gesterone was present, the amount could not be mea- sured. It was believed that progesterone, or progesterone converted into androgens, was the probable cause of the enlarged clitoris. There was no significant difference be- tween the gonadotropic activity of the hypophysis in cys- tic and noncystic sows. In sows with large cysts given injections of LH, neither ovulation or further luteiniza- tion of the cysts resulted. This does not mean that LH deficiency might not be the cause of the condition, as the animals treated had been affected for a long pe- riod.104-106'116 Small multiple follicular cysts were observed only oc- casionally. They resembled a cluster of grapes and were always present in numbers exceeding the number of fol- licles found normally. These cysts were about 1 cm. in diameter. An average of 22.5 small cysts per ovary was reported.104-106 The walls of these small cysts were lined by normal granulosa cells. The uterus showed an estro- genic type of endometrium and the clitoris was not en- larged. These animals showed marked irregularities in the length of the estrual cycle. Symptoms of estrum were intense, similar to the symptoms produced by the larger cysts. In neither large nor small multiple cysts was nym- phomania, or continuous estrum, observed. These small cysts were found to be as rich in estrogen per unit weight as the normal follicles, but because of the large number of small cysts the total concentration of estrogen was 4 to 5 times that of the normal ovary just before ovulation and several hundred times that of sows affected with large luteal cysts. The pituitary assays showed no increase in gonadotropic hormones over that seen in normal sows. A single small dose of 250 to 400 PMS always produced cystic ovaries in nonpregnant swine but the cysts never reached the size of large luteal cysts. Thus it appeared that multiple cysts may be due to lack of luteinizing hormone necessary to cause ovulation and normal corpus luteum formation. It is doubtful that sows once they develop cystic ovaries recover sponta- neously.116 Whether there is a genetic basis or cause for cysts in sows as in cows is not known. Further work is required to determine the actual cause and possible ther- apy of cystic ovaries in swine. Porcine ovarian abnormalities other than cysts in- clude: ovotestes in hermaphrodites, ovarian abscesses, rare parovarian cysts, and aplastic or missing ovaries.116 Anestrus is common in prepuberal gilts and post- weaning SOws.24'46’79’81a b’82'86 The incidence of anestrus is most common in the summer months but varies from 20 to 40 percent in both gilts and sows.82 In 54 anestrous gilts 10 to 11 months of age examined at slaughter 19 gilts or 35.2 percent had no luteal tissue in the ovaries and were prepuberal. Forty two percent of the gilts had ovaries with active corpora lutea indicating cyclic activity but the external heat signs either were missed or were too weak to be observed. The remaining 10 gilts, 18.5 percent, had normal corpora lutea and/or luteinized cysts.46 In another study of anestrous gilts 7 to 9 months of age, 50 percent exhibited behavioral anestrus and would not mate even when exposed con- tinuously to a boar. These were confinement-reared gilts and estrous cycling was occurring based on plasma pro- gesterone levels at frequent sampling periods. This study also showed that exogenous ACTH and glucocorticoids inhibited estrous behavior and shortened the duration of estrus. Further studies on confinement-rearing stress and managerial practices to reduce this stress is indicated.24 In a third report from Japan86 192 sows or 70 percent of 274 sows with ovarian “disease” were anestrus or failed to exhibit estrus based on rectal palpation of the ovaries under thiamylal sodium anesthesia, 20 ml IV. Thirty646 VETERINARY OBSTETRICS percent of these 274 sows had corpora lutea and 30 per- cent had cystic ovaries. The factors contributing to anestrus in swine are prepuberal status or delayed estrus in gilts and sows due to the breed, age, nutrition, season, especially sum- mer, lack of boar exposure, confinement-rearing or man- agement problems, and failure to check frequently sev- eral times daily and observe estrus, preservice or postservice.79“81a,b To minimize to problem of anestrus and infertility in a swine herd, it is essential that all non- pregnant sows and gilts of breeding age be adequately “teased” daily by boars that have demonstrated their es- trus detection ability and libido. Postweaning anestrus in sows is most common in the summer months, especially in primiparous young sows. During the summer months 40 percent of the fertile matings was followed by a re- turn to estrus in a 25 to 35-day interval. This interval is suggestive of a pregnancy that was present for 12 or more days followed by early embryonic death.80 Pregnant sows are anestrous. Boars lacking libido may be a cause of missed estrous periods. Too many sows in a pen for a boar to check efficiently may also be a cause of apparent anestrus. Excessive stress on prepuberal or postweaning females causes anestrus and short estrous cycles. Cystic ovaries, either follicular or luteal cysts may cause anes- trus but these are not as common as the other factors. Lactating sows and gilts are usually anestrous. Other causes of anestrus include: delayed puberty is seen more often in Durocs and Yorkshires; first litter gilts are more frequently anestrous than multiparous sows, 35 vs 15 percent; gilts and sows whose pigs are weaned during the summer are more frequently anestrous than those whose pigs are weaned in the winter, 40 vs 10 percent; the larger the number of sows penned together the greater the incidence of anestrus due to the loss of condition and lack of feed intake in some sows; cystic ovaries and lameness also contribute to the anestrous condition as well as inefficient management and failure to detect es- trus.81b Since anestrus is a symptom, an accurate diagnosis is desirable but may be difficult to achieve. Progesterone levels above 1.5 ng/ml on a number, 6 to 18, of affected animals would indicate estrous cycling is occurring, the sow is pregnant or a luteal cyst is present. Serial samples 5 to 10 days apart would aid in diagnosing whether cy- cling is occurring. Slaughter house or abattoir exami- nation of a selected sample of females in a herd would also be most informative.81b Costly rectal examinations of the ovaries of anesthetized sows, although difficult, could be very helpful.86,99 Treatment of anestrus in gilts and sows, as in cattle, requires as accurate and correct a diagnosis of the cause as possible.79 The history, records, physical examination of the females for pregnancy by ultrasonography at 30 to 35 days of gestation or other means, nutritional status, age, season, managerial practices, disease factors, and other tests as noted above should be carefully reviewed. The use of PMSG for treating anestrous sows was re- ported in 1953.125 Estrogens and HCG gave poor results. Later trials with PMSG also proved promising.43,90 In gilts stressing by trucking, movement or mixing of fe- males, introduction of a boar and giving PMSG (500 IU) or PMSG and HCG (250 IU) if no corpora lutea are on the ovaries frequently induces estrus within 3 to 5 days at which time breeding should take place.81b If corpora lutea are present prostaglandins 5 to 10 mg of PGF2a or 1 mg (100 ug) of a prostaglandin analogue might be used.86 They are ineffective except between days 12 and 15 of the estrous cycle or in cases of persistence of the corpus luteum or luteal cysts and could cause abortion in early gestation.17,876 Prevention of seasonal postweaning anestrus in sows during August through October was accomplished by ad- ministering 500 IU of PMSG at weaning. This study re- ported 52.8 percent of controls and 91.3 percent of the treated sows in estrus within 7 days after weaning during the months of August through October.816,82 Estrus oc- curred 3 days later about a day earlier than controls. Presently PMSG is not available commercially in the U.S. Further trials with other FSH products are indicated. Ovine pituitary gonadotropin showed promise for the treatment of cystic ovaries in sows.86 Repeated daily doses of 5 to 10 mg of estradiol for 5 to 20 days to age the luteal tissue followed 5 days later by prostaglandin to involute the CL and induce estrus has been reported.17 It was recommended that gilts not in estrus by 8 or 9 months of age and sows anestrous for more than 40 days after weaning should be culled.79 A high incidence of anestrus after weaning in one herd was associated with a low packed-red-cell volume of about 20 percent and many sows serologically positive for Eperythrozoon suis.18 In a study of 63 anestrous gilts over 7 months of age and 28 sows that failed to show estrum within 5 weeks of weaning less than 10 percent of the gilts and more than 40 percent of the sows had corpora lutea indicating the presence of an estrous cycle.114 After the stress of transporting the gilts to the study center and changing their environment 68 percent of the gilts and 25 percent of the sows came into estrum within 10 days. Daughters of late maturing gilts were also late maturing so a genetic factor was involved in this type of anestrus that might be susceptible to improvement by selection for early pu- berty. Rare cases of infantile or hypoplastic ovaries and genital tracts in well-grown gilts have been described.165 Repeat Breeders in female swine, as in other ani-INFERTILITY IN FEMALE SWINE 647 mals, are caused by high embryonic death rates and low fertilization rates. These are also causes for reduced litter size. Embryonic death was of more importance than was the ovulation rate in controlling litter size in swine.8 Be- tween 10 to 25 percent of sows and gilts fail to con- ceive.104-107163 In these sterile swine, gross abnormalities of the reproductive tract were the cause of sterility in 25 to 50 percent of the gilts and 25 percent of the sows. In the rest of the sterile females there was no apparent cause for the failure of fertilization or early embryonic deaths. Failure of reproduction due to embryonic deaths ap- peared less common in gilts than in sows. In an experiment modeled after those made on “repeat breeding” cattle, 63 “repeat breeding” female swine were assembled.161 These had previously been bred 2 to 4 times without conceiving. They represented 5 breeds and in- cluded both gilts and sows. Part of the 63 were killed 4 days after service to a fertile boar and the rest were killed at 25 days. Those that came in estrum again before 25 days were rebred and killed 4 days later. Gross abnor- malities were found in 63.7 percent of the gilts and 31.6 percent of the sows. Some of these were unilateral and permitted conception. In the percentage of reactors to the blood test for brucellosis there was no significant dif- ference between either the gilts and the sows, or between those with gross abnormalities and those with no gross abnormalities. The difference in percentage of fertilized ova between brucella-positive and brucella-negative an- imals was not significant but the incidence of embryonic death was 87.5 percent in the positive animals, and 46.5 percent in the negative animals. This experiment showed the importance of the role of brucellosis in infertility in swine. These workers161 concluded that “repeat breed- ing” was due to failure of fertilization in 53.4 percent of the gilts and 32.6 percent of the sows. Gross abnor- malities accounted for failure of fertilization in 50 per- cent of the gilts and 16.8 percent of the sows. Thus ac- countable failures of fertilization occurred in 3.4 percent of the gilts and 16.8 percent of the sows. Embryonic death caused “repeat breeding” in 23.9 percent of the gilts and 67.4 percent of the sows. “Repeat breeding” swine with normal embryos 25 days after the one ad- ditional breeding included 22.7 percent of the gilts and none of the sows. Therefore, the major cause of “repeat breeding” in gilts was genital abnormalities causing fail- ure of fertilization. In sows the major cause of “repeat breeding” was embryonic deaths. In another study 79 “repeat breeding” sows and gilts that had been bred 3 to 10 times previously were assem- bled.165 All brucella-positive females were eliminated from the experiment. After being bred to a fertile boar on the first estrum, 53.2 percent conceived. They considered that this high conception rate in infertile females may have been due to breeding an average of 3.9 times per estrum as compared to only 1.4 times per estrum pre- viously. There was some indication that these animals might have ovulated early. Only 5 to 10 percent of these animals could be considered to have experienced em- bryonic deaths.165 This is in marked contrast to the 20- to 70-percent rate of embryonic deaths reported in the previous study.161 The 5 to 10 percent of the animals exhibiting extreme embryonic mortality were apparently fertile but a reduction in litter size occurred soon after implantation. Some of these losses were probably due to segmental aplasia and defects of the uterine horns and genital tract resulting in early and complete loss of em- bryos. Repeat breeders could also be due to poor manage- ment and infertile boars.114 Of 75 female “repeat breed- ing” swine brought to the study center and bred the next estrus to a fertile boar, 49 females conceived. The con- ception rate experienced by “travelling” boars on first service was 62 percent for gilts and 56 percent for sows; in herds using their own breeding boars the respective percentages were 82 and 77. The lower conception rate in “travelling” boars may have been due to overuse, the presence of genital infections, or poorly timed services. Tumors of the genital tract in female swine are rare, possibly because most swine are slaughtered at a rela- tively young age. Leiomyomas and a fibroma of the uterus in sows and one case in which a lymphoblastoma in- volved one ovary have been described.50 The author has observed a 12 X 7 X 4 cm. hamartoma on the ovary of a sow. A rare teratoma of the porcine ovary was re- ported.103 Embryonal nephromas and sarcomas of the va- gina and cervix have been described.101 Two heman- giomas, a papillary cystadenoma and a granulosa cell tumor of swine ovaries were found.109 Other reports on ovarian cystadenomas, sarcomas, teratomas and a fi- broma have been cited.109 Nutrition may have a definite effect on fertility in fe- male swine.29 Except for a few important differences, the same general principles apply to swine as to the other farm animals. As in all animals, inanition due to a low plane of nutrition in swine results in a delay in the onset of puberty, and failure of estrum, or irregular estrum after weaning. The detrimental effects on embryonic survival of overfeeding and a high energy intake immediately after breeding have been discussed. The beneficial effects of a temporary high plane of nutrition to promote early pu- berty and a higher ovulation rate have also been de- scribed. Gilts on a protein-free diet failed to cycle nor- mally or conceive.1 A protein deficiency acute enough to cause severe retardation of growth in sows did not affect the incidence of fetal atrophy.31 The presence in newborn swine of embryonic defects648 VETERINARY OBSTETRICS and abnormalities caused by a vitamin A deficiency in sows during early pregnancy has been reported.12-69 These anomalies included eye defects or the absence of eyes. Evidence was cited to indicate that deficiencies of vitamin E, C, B, complex and D are seldom, if ever, the cause of infertility in the sow or other farm ani- mals.128129 Evidence of severe deficiencies in phospho- rus, calcium or other minerals affecting reproduction in swine have not been reported in recent years. Reproductive management in swine herds, as in cat- tle herds, requires close cooperation between the owner and/or the manager and the veterinarian. The success of a reproductive program lies in its day to day efficiency and effectiveness which is primarily the responsibility of the manager and/or owner.29-81*-6 The results of several recent large surveys of swine fertility in the U.S. re- vealed that overall farrowing rates were only 72 percent in over 50,000 sows and gilts. Some well-managed herds achieve an 85 percent farrowing rate. Infertility, sterility and small litter size may be due to a variety of infectious agents and boar infertility discussed in this chapter and in Chapter XVIII, respectively. Other factors contribute to low fertility and should be recognized. Farrowing rates during the summer months, June through September, av- erage about 15 percent lower than in the winter months of November through March in the northern hemisphere. This high seasonal loss of pregnancies is apparently not due to failure of fertilization, boar fertility or infectious agents. The nature or cause of this apparent loss of preg- nancies is not known.816 The farrowing rate of gilts is lower than first-litter gilts which is lower than multipa- rous sows. Crossbred females are more fertile than pure- breds. Although high ambient temperatures reduce con- ception rates and embryonic survival its role in the summer infertility problem is equivocal.816 As the number of fe- males in a pen increases, fertility decreases due to heat detection, nutritional, infectious disease and stress prob- lems. Sows and gilts should be bred twice during estrus at a 24 hour interval and to two different boars for high- est fertility. Females should be tested for estrus starting 17 days after mating and checked for pregnancy at 30 to 40 days of gestation with an ultrasonic detection in- strument. In diagnosing or preventing reproductive failures or inefficiencies a number of requirements are essential in- cluding: 1) Breeding records, necessary to monitor and ana- lyze the monthly (seasonal) and yearly programs and results including the inventory, costs and net income. 2) An evaluation and understanding of the standard of management including training and capability of personnel and herd management procedures, in- cluding buildings, animal comfort, degree of stress and techniques for estrous observations and breed- ing both females and males, and pregnancy testing. 3) An evaluation and understanding of the nutritional program including adequacy of TDN, protein, minerals and the delivery of the rations to the herd. 4) A good preventive disease control program is es- sential including vaccinations, parasite control, feed additives, quarantine and isolation facilities and practices, supervision of farrowing and vector con- trol. 5) The genetic program and goals of the owner and/ or manager should be understood and integrated effectively to improve herd productivity. To further these goals the veterinarian and owner and/ or manager should have a good veterinary diagnostic laboratory and consulting service that also includes a nu- tritionist, a geneticist, an accountant, and if the herd is large a computer would be desirable. If artificial insem- ination is to be used in a swine herd excellent manage- ment of the female herd, very competent estrous detec- tion, careful control of the boar, semen collection and insemination and complete records are essential. Standards of production that are recognized as nec- essary for a successful swine herd operation are:29 Litters / sow / year 2 to 2.25 Pigs/sow/year 20 to 21 Stillbirths (%) 5 Farrowings (%) 88-90 No. of live pigs/litter 10-11 Weaning to service interval 7 (days) Repeat breedings (%) 6-8 Abortions (%) 1.0 No. of pigs weaned/litter 9.5 No. pigs marketed/sow/year 18.0 If these standards or goals are not closely approached or met then it is necessary for all concerned to properly assess their deficiencies, correct the problems and work toward achieving these standards in order to insure the success of the enterprise. References General l. Asdell, S. A. (1964) Patterns of Mammalian Reproduction, 2nd Ed., Cornell Univ. Press, Ithaca, N.Y.INFERTILITY IN FEMALE SWINE 649 2. Cole, H. H. and Cupps, P. T. (1977) Reproduction in Domestic Animals, 3rd Ed., Academic Press, N.Y.C. 3. Hafez, E. S. E. (1980) Reproduction in Farm Animals, 4th Ed., Lea and Febiger, Philadelphia, Pa. 4. Leman, A. D. (1981) Diseases of Swine, 5th Ed., Iowa State Univ. Press, Ames, Iowa. 5. McDonald, L. E. (1975) Veterinary Endocrinology and Repro- duction, 2nd Ed., Lea and Febiger, Philadelphia, Pa. 6. Nalbandov, A. V. (1964) Reproductive Physiology, 2nd Ed., W. H. Freeman and Co., San Francisco, Calif. 7. Swenson, M. J. (1977) Duke’s Physiology of Domestic Animals, 9th Ed., Cornell Univ. Press, Ithaca, N.Y. 8. Williams, W. L. (1943) Diseases of the Genital Organs of Do- mestic Animals, 3rd Ed., Ithaca, N.Y. Specific I. Adams, C. R., Becker, D. E., Terrill, S. W., Norton, H. W. and Jensen, A. H. (1960) Rate of Ovulation and Implantation in Swine as Affected by Dietary Protein, J. An. Sci. 19, 4, 1245. 2. Adams, W. W. (1970) Hormonal and Anatomical Causes of Infertility, Colloquium on Effect of Diseases and Stress on Re- productive Efficiency in Swine, Iowa State Univ., June. 3. Akins, E. L. and Morrissette, M. C. (1968) Gross Ovarian Changes During the Estrous Cycle of Swine, Amer. J. Vet. Res. 29, 10, 1953. 4. Anderson, L. L. (1966) Pituitary-Ovarian Relationships in Pigs, J. Reprod. and Fert. Suppl. 1, 21. 5. Armstrong, C. H. (1970) Bacterial Flora of the Porcine Uterus, Colloquium on Effect of Diseases and Stress on Reproductive Efficiency in Swine, Iowa State Univ., June. 6. Asdell, S. A. and Willman, J. P. (1941) The Causes of Still- birth in Swine and an Attempt to Control It, J. Agr. Res. 63, 345. 7. Backstrom, L. and Curtis, S. E. (1981) Housing and Environ- mental Influences on Production, in Diseases of Swine, 5th Ed., Edited by A. D. Leman, Iowa State Univ. Press, Ames, Iowa, 737-753. 8. Baker, L. N., Woehling, H. L., Casida, L. E. and Grummer, R. H. (1953) Occurrence of Estrus in Sows Following Partu- rition, J. of An. Sci., 12, 1, 33. 9. Bauer, H. R. (1950) Piglet Mortality and Blind-Bom Piglets Due to Avitaminosis of Vitamin A (Trans.), Tierarztl. Um- schau, 5, 366. 10. Bazer, F. W., Robison, O. W., Clawson, A. J. and Ulberg, L. C. 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(1970) Discussion in Colloquium on Effect of Diseases and Stress on Reproductive Efficiency in Swine, Iowa State Univ., Ames, Iowa, June.Chapter XVI INFERTILITY IN EWES AND DOES Infertility or sterility in ewes and does is uncommon when compared with the incidence of these conditions in other domestic animals. This is probably true for two reasons: first, there has been less study of the infertility or sterility occurring in these animals; and second, the incidence of disease or infertility apparently is much lower in these species because of their lower economic value and prompt elimination if they are infertile. Fertile mem- bers of the species have been selected and perpetuated over many years. In examining the genital tracts of 90 ewes, no structural defects or other abnormalities that would be a barrier to fertilization were found.37b There are many similarities between the genital tracts, the ova- ries, the reproductive hormones and other facets of re- production between ewes, does and cows. The structure and functions of the various portions of the genital tracts of ewes and does are similar to that of the cow, and treatment of pathologic conditions is similar to that used in the cow except for the fact that the smaller size of the ewe and doe renders impossible the use of certain pro- cedures and types of therapy employed in the cow. Be- cause of the differences between the ovine and caprine species in reproductive physiology and to avoid confu- sion, the author is separating the discussion in this Chap- ter into two sections—Infertility in Ewes and Infertility in Does. INFERTILITY IN EWES Reproductive Physiology Puberty occurred in spring lambs at a mean age of 249 to 293 days, 8 to 9 months; Rambouillet or crossbred lambs bom in the fall had their first estrus at 316 days range 199 to 577 days.43,54 159 About 90 percent of the lambs had ovulated before the first standing estrus, as noted by laparotomy and the presence of a corpus lu- teum. In lambs that were not bred, it was noted that over 53 percent ovulated after the last standing estrus of the breeding season. Many lambs only exhibit one or a few estrous periods their first breeding season. Sexual ma- turity varies with the breed and rate of growth. The fine- wool or Merino type sheep are slow to mature and often fail to reach puberty the first breeding season. Early ma- turing breeds such as the Finn-sheep may reach puberty as early as four months of age.3,83 Merino sheep mature more slowly than the Hampshire or Suffolk breeds. Crossbred lambs generally mature earlier than purebred lambs. A high plane of nutritution may hasten the onset of puberty and a low plane of nutrition will delay it as in cattle.143 Most ewes are bred at the first breeding sea- son after they reach one year of age. Under good con- ditions of feeding and management 60 percent or more of spring lambs of the early-maturing breeds will be- come pregnant if placed with rams in the fall. Virgin ewes were still fertile after reaching 4 years of age158 this is different from 4 to 5-year-old virgin cattle. (See DeLange.) The estrous cycle—The common coarse-wool breeds are seasonally polyestrous. The fine-wool breeds like the Merinos, Rambouillet and the coarse-wool homed Dor- set and crossbreds of these breeds may be polyestrous the year around, depending upon climatic and feed con- ditions. The coarse-wool breeds in the northern hemi- sphere usually come into estrum about September 1. If they are not bred or do not conceive they continue to come into estrum until about January 1 or slightly later. Rambouillets tend to come into estrum the earliest in the breeding season; followed by the Hampshire, South- downs and Shropshires.1 About 12 to 48 hours after parturition about 10 percent of ewes exhibited estrus.61157 After this brief estrous pe- riod probably due to the high plasma levels of estrogen and the low progesterone levels postpartum128 lactational anestrum lasting 5 to 7 weeks usually develops. After this period some ewes suckling lambs will exhibit estrus but most heats are not observed until about 2 weeks after the lambs are weaned. As determined by the fem pattern of cervical mucus, lactating ewes have one or more quiet or silent ovulations before the first estrus after lambing. It is very difficult to induce estrus unless an involuting corpus luteum is present or exogenous progesterone is given.54,55,105 In sheep, as in cattle, progesterone appar- ently is necessary to potentiate the effect of estrogen to produce signs of estrus. When rams were introduced into a flock of ewes at 654INFERTILITY IN EWES AND DOES 655 the beginning of the breeding season, 40 to 90 percent of the noncycling ewes ovulated within 65 to 72 hours. These ovulations were preceded by LH peaks about 35 hours after ram introduction.89 This study confirms prior reports that ewes ovulated within 6 days of the intro- duction of rams early in the breeding season. This first ovulation is not accompanied by signs of estrus. But the next estrus period 17 to 24 days after ram introduction is associated with estrus and fertile copulations. Thus the presence of rams at this time of the breeding season trig- gers the release of GnRH or LH causing a “silent” estrus with ovulation and CL formation. Although the duration and intensity of estrous signs were similar to ovulating puberal ewes in the same flock, 6 to 33 percent of the first estrus periods of puberal ewes were anovulatory as determined by endoscopy. The following inter-estrous period was of normal length, 16 days.48 In a recent study it was shown there are usually two peaks of estrous activity after rams are placed with ewes early in the breeding season, the first at 18 to 19 days and the second at 22 to 24 days.90 Frequent laparoscopic examinations revealed that 85 percent of ewes that were previously anovular, had ovulated within 4 days of ram introduction. Premature regression of the CL occurred in 50 percent of the ewes between days 4 and 8 and the first estrus in these ewes occurred at about 23 days after the rams were introduced. The remainder of the ewes ovulating within 4 days of ram introduction had no regression of the CL and they showed their first estrus at 19 days.90 In fall-lambing Rambouillet ewes the average interval from lambing to the start of regular estrous cycles was 72 days, range 12 to 212 days; this varied from 46 days for ewes lambing in August to 98 days for ewes lambing in January.7 The onset of estrous cycles is hastened by early weaning of lambs. The interval from lambing to breeding had a significant effect on conception but had no effect on the induction of estrus.154 Apparently, as in cattle, a 40 to 60 day interval postpartum was necessary for an optimal conception rate. Uterine involution is largely completed by 24 days postpartum.52 Thus, with the Dorset, Rambouillet, or Merino breeds or their crosses, it is possible, but very difficult on a flock basis, to obtain two lamb crops or a 200 percent or greater lamb crop each year. By alternating breeding in the spring and fall, it would be possible to get 3 lamb crops in two years.76 Over a two-year-period 539 Rambouillet ewes were mated for six weeks beginning the 21st of March, the 21st of June the 21st of September and the 21st of December in the northern hemisphere. The incidence of estrus in open ewes for the four mating periods was 84.5, 96.4, 97.2 and 99.1 percent, respectively; the ovulation rates were 105.6 140.8; 175.4 and 151.9, respectively, and the lambing rates were 83.9, 96.5, 126.8 and 135.2, re- spectively.135 The higher ovulation rates in June and September were not reflected in higher lambing rates be- cause the higher environmental temperatures during the breeding season had a detrimental or modifying effect on embryonic survival. The factors limiting the achievement of the goal of two lamb crops or a 200 percent lambing rate per year in the coarse-wool breeds was reviewed.80 The manip- ulation of light and temperature was not practical be- cause of the long latency period required to induce re- sults.80 Although ovulation rates could be increased by: (1) breeding during the middle of the breeding season instead of late in the season, (2) “flushing” the ewes by increasing the TDN or energy intake for several weeks prior to breeding, or (3) by the injection of PMSG, pre- ceded by progestin, 3 to 4 days before the next estrus, or on days 12 or 13 of the cycle, only 20 percent of the ewes with 3 CLs were carrying 3 fetuses while 75 per- cent of the ewes with 2 CL were carrying two fetuses. Thus although a combination of breeding management, including controlled lighting, and hormonal therapy makes 2 lamb crops per year feasible, much more research is needed to make it practical and a routine procedure for most breeds of sheep.9lb The presence of a ram stimulates the breeding activity or the onset of estrum in ewes in the transitional period between the anestrous period and the breeding sea- son.77'78139164 As noted previously the first ovulation thus induced is often silent and the next period associated with a regressing corpus luteum that provides some proges- terone is manifested by signs of estrus. This technique can be used to obtain a degree of synchronization of es- trus in a flock. When rams were introduced from July 1 to August 8th, the maximum conception period occurred 17 to 32 days later.139 When rams were introduced after August 8th conception rates for the first and second 16- day periods of the breeding season were similar. If a vaginal pessary containing a progestogen was placed in the vagina of the ewes for 12 days during this transi- tional period before the breeding season and then re- moved the day the ram was placed with the flock, over 90 percent of the ewes were in estrus within 4 days and 62.5 percent lambed to first service.164 165 Thus combin- ing a progestational agent and the introduction of a ram resulted in a higher level of synchronization. As with boars, the presence of a ram, the senses of smell, sight and contact all combine to produce a stimulation of the onset of the estrous cycle and ovulation in the ewe. This effect was not produced when the ram ran continuously with the ewes.77 78656 VETERINARY OBSTETRICS Photoperiodism is a characteristic of the reproductive cycle or the sexual activity in sheep and goats, and horses.-66-67,101,102,142 The onset of the estrous cycle and the breeding season in most breeds of sheep is princi- pally influenced by the reduction in the length of day- light in the late summer and fall in the northern hemi- sphere. A reduction in daylight to about 10 or 11 hours, whether it occurs naturally or whether it is induced ar- tificially by penning the ewes in a darkened area during part of the day, will induce the onset of the estrous cycle in anestrous ewes. The seasonal nature of the breeding season permits the birth of lambs at the most favorable time or in the late spring months when feed supply and ambient temperatures are nearly optimal. The breeding season of sheep tends to become shorter at latitudes near the poles.-'67 Near the equator ewes tend to have estrous cycles throughout the year and not exhibit a restricted breeding season. However irregular and prolonged in- tervals between estrous periods due to a persistence of the corpus luteum, especially in June, was reported in Niger Peulh ewes in Africa.1664 In the northern latitudes there are year to year minor variations in the onset of the breeding season as in horses. A reduction in ambient temperature occurring naturally or induced artificially also has an effect on promoting the onset of the reproductive cycle and the breeding season.39,66 There is a wide breed difference in the number of es- trous periods per year from 2 to 3 periods in a short breeding season in some breeds to estrous periods in other breeds in regions near the equator occurring all the year around.-67 The ram, similar to the stallion, does not show a restricted breeding season as does the female but there are seasonal variations in semen production and char- acteristics.3,67 (See Male Infertility.) Rams are sexually more active and produce better quality semen during the breeding season. The onset of the breeding season could be somewhat advanced by a higher energy intake before the season.123,124 Most breeds of sheep have an average cycle length of 16.5 days, with a range of 14 to 19 days.1 Most of the breeds are in estrum for a period of 20 to 40 hours, with an average of about 28 to 36 hours and ovulation occurs in estrum about 24 to 27 hours after its onset. If AI is used it is best performed about 10 hours, 2 to 15 hours, after the onset of estrus.128 The Texel ewe has two fol- licular growth waves. The first wave began on days 1 and 2 and ended on days 11 to 12 but atretic changes were evident beginning on days 5 to 6. The second growth wave began on days 9 and 10 and resulted in mature follicles at the next estrum.33 Thus these changes were similar to those reported in bovine ovaries during the estrous cycle. The follicle size varied from 0.5 to 1.0 cm. and the corpora lutea were about 1 cm. in diameter. “Silent” heat or ovulation without estrum occurs fre- quently at the beginning and after the end of the breeding season. The estrual cycles tend to be longer or shorter in duration than the average at the beginning or end of the breeding season. Short cycles are more frequent in older ewes. Cycle length does not affect fertility.162 There was no tendency for individual ewes to have an early or late onset of the breeding season, so selection on this basis is not possible. Sexual activity and signs in ewes, as in the mare, are nearly lacking in the absence of the male.2’3,67,78 Proes- trus is rather indefinite and the onset of estrus is abrupt. Cessation of estrus is gradual. The symptoms of estrus in the ewe include restlessness, seeking out the ram, fre- quent switching of the tail as if the vulva itched, teasing the ram and standing immobile to be mounted and bred. In estrum the Dorset ewe has a characteristic stance. During an average heat period a ewe penned with a ram was teased 18 times, mounted 25 times and mated 6 times.77,78 Anorexia and swelling of the vulva are usual symptoms of estrus in the ewe. Most owners allow the ram to run with the ewes during the breeding season. Painting the brisket of the rams or having them wear a harness containing a marking device, in which various colors can be placed, is a common practice. Thus by observation of the rumps of the ewes, service can be noted and the date recorded. After 17 to 20 days a dif- ferent color may be used to determine which ewes return to estrum. If many return, the fertility of the ram is prob- ably questionable. Vasectomized rams can be used as teasers and “heat detectors” for ewes that are to be bred artifically. Administration of 50 to 100 mg. of testos- terone propionate every other day for 20 days and then every 10 days or using testosterone implants resulted in producing normal male sexual behavior in treated ewes and others that could be used for estrus detection.28,97,1323 Rams can be operated upon similarly to bulls, to produce a lateral deviation of the penis at the time of erection. These surgically prepared rams were satisfactory as es- trus detectors in ewes and semen could be collected from them.6 The ewe secretes mucus from the cervical glands but not in large amounts like the cow. Smearing the estrous mucus on a slide and allowing it to dry results in a fern or arborization pattern, similar to that in the cow, due to the high salt content in the mucus of estrum.31 The vaginal smear in the ewe is of limited diagnostic value in determining the stages of the estrous cycle.3 As in the cow, increased activity of the uterine muscle and edema of the endometrium occur during proestrum and estrum. The endometrium in some ewes may be black due to theINFERTILITY IN EWES AND DOES 657 presence of melanoblastic pigment. This is not associ- ated with stages of the cycle. The cervix is somewhat dilated and relaxed during estrum. Often ewes may at- tract rams by the odor of the vaginal mucus before the ewe is ready to accept coitus.- Ewes may occasionally show estrum during pregnancy. Eleven of 50 pregnant ewes had 1 to 3 “heats” during pregnancy.162 The time of mating or artificial insemination during estrum in sheep is not as critical as in other animals.1 The optimum time to breed is about 12 to 18 hours after the onset of estrum. Ovulation is spontaneous and usu- ally occurs from 18 to 24 hours after the onset of estrum or from 12 to 24 hours before the end of estrum. In rare cases ovulation may occur after the end of estrum. In twin ovulation several hours or more may separate the time of ovulation of each follicle. Usually 1 to 3 ovu- lations take place and the rest of the follicles become atretic. Ovulation Rate—Placing ewes on a high plane of nu- trition or flushing for 2 weeks before mating increased the lamb crop by about 20 percent and flushing ewes for 3 to 5 weeks increased the rate of twinning to 40 percent or higher, compared to a 4 to 6 percent twinning rate in control, non-flushed ewes. Increasing the length of time of flushing beyond 4 to 5 weeks did not give a further ovulatory response.49 123 124 Breeding ewes fed a high plane of nutrition for 6 to 8 months before flushing resulted in a higher rate of twin ovulation than ewes fed a low plane of nutrition before flushing.53 The lamb crop of range ewes was increased from 80 to 135 percent for a 6-year period by continuously feeding on a high plane of nu- trition.104 There is no evidence that high condition pre- disposes the ewe to sterility. Ewes on a high nutritional level had a higher ovulation rate, possibly a higher fer- tilization rate, and a slightly lower embryonic survival rate than ewes on a low nutritional level.49 It was sug- gested that higher feeding levels caused an elevated plasma glucose, greater hypothalamic stimulation and release of larger amounts of gonadotropin causing greater ovarian activity and twin ovulations.76,103 The evidence that a high plane of energy intake was detrimental to embryo sur- vival in the weeks following conception was not ob- served in ewes as in sows.53,123,124 In flushing ewes a high energy or TDN intake is needed; an increased in- take of protein is not necessary.103 The lambs, especially twins, of the ewes on a high plane of nutrition, were heavier, larger and stronger.123,124 When ewes had a se- vere diet restriction during the period from weaning to breeding, about a 4 month dry period, lambing percent was 22 percent lower the first year and 52 percent lower the second year than in control ewes even when a 20 day flushing period preceded the breeding season.15 Sim- ilarly thin ewes affected with a chronic debilitating con- dition such as progressive pneumonia or visceral caseous lymphadenitis had a reduced reproductive efficiency when compared with normal ewes. The fertility and percent- age of lambs bom alive was 76 vs. 91-93 percent and 61 vs. 86 percent, respectively.60 Other factors also influence the ovulation rate and the subsequent lamb crop. Ewe lambs, yearlings and young ewes as well as old ewes produce fewer twins and have lower lamb liveability.155 The peak percent of lambs weaned was in 4-year-old ewes, range 3 to 6 years. However, a higher percentage of single lambs are viable at birth and are weaned than are twins or triplets.-137 Crossbred ewes produced 9 to 23 percent larger lamb crop than purebred ewes when bred as ewe lambs. Older crossbred ewes produced 10 to 16 percent larger lamb crops.134,135 Ovulation rates are higher in the early to middle portions of the breeding season and decline later in the season.3,6 When ewes were given a 10 hour daily light period for 9 weeks starting late in the anestrous or transition period ovulation rates and lambs bom per ewe increased about 25 percent from 1.2 to 1.65 lambs/ewe.36 Certain ewes tend to have higher ovulation rates than other ewes. Thus selection of ewes bom as twins or greater multiples from young mothers, large sheep of certain breeds, and those with open faces, free of wool, can be used to increase the lambing rate to 150 percent or greater in a flock.3 The mature ewes of the Finnish Landrace and Romanov breeds or their crosses frequently produce triplet or greater numbers of lambs.134,155 Ovulation rates in Merino, Scottish Blackface and Finnish Landrace was 1.09, 1.36 and 3.37, respec- tively.155 The breeding season midpoints for these three breeds were November 25th, December 20th and Janu- ary 23rd, respectively and the incidence of “silent” ovu- lation for the three breeds was 35.6 percent, 16.2 percent and 7.3 percent. This strongly emphasizes the genetic differences between widely different breeds of sheep studied at one location. Ovulations were slightly more frequent on the right ovary of ewes than on the left, 53 to 55 percent and 44 to 47 percent, respectively.24,80 In single ovulations 62 percent were on the right ovary. Twenty-six to 32 per- cent of embryos migrated from one hom to the other when twin ovulations occurred on one ovary; while only 0 to 10 percent migration occurred when a single ovu- lation occurred from one ovary.24 As in cattle, an in- creased embryonic loss occurred in twin ovulations es- pecially with twin ovulations from one ovary. The LH content of the anterior pituitary gland started to be discharged at the onset of estrum and was com- pleted 6 hours later when 52 percent of the LH in the658 VETERINARY OBSTETRICS pituitary gland had been released.129 The plasma surge in estradiol from maturing Graafian follicles stimulated by FSH preceded the LH release or surge. Small amounts of estrogen injected into sheep stimulated LH release.129 A recent review of ovulation reported the maturing Graafian follicle is about 0.5 cm. in diameter and the plasma progresterone level is below 0.2 ng/ml. 1 to 2 days before estrus. The estradiol produced by the follicle reaches a peak of 15 pg/ml. in the peripheral plasma 24 hours before the onset of behavioral estrus that induces the release of GnRH and LH surge about 4 to 6 hours after the onset of estrus. The ovulatory follicle enlarges rapidly to about 1 cm. in diameter at the time of ovu- lation.128 Gonadotropin levels in the anterior pituitary gland were high and constant during the nonbreeding season as were the presence of small follicles on the ovaries.-'88 Thus the onset of the estrous cycle in the late summer months associated with declining daylight may be triggered by a greater release of FSH and/or LH associated with an increased estrogen production. The ewe’s pituitary gland is about 10 times as potent as the cow’s in LH content and 5 times as potent in FSH content.- In the ewe progesterone is needed as well as estrogen to produce psychic estrus/ This probably accounts for some silent heats accompanying ovulations at the outset of the breeding season. Sixty-four ug. of estradiol was necessary to induce psychic estrus in ovariectomized ewes; if the injection was preceded by progesterone adminis- tration only 20 to 25 ug. of estradiol was needed to pro- duce psychic estrus.- During the estrous cycle 10 to 15 mg. of progesterone in oil daily inhibited estrus. After ovulation, progesterone levels in blood plasma increased from 22.2 ng/ml. to 37.6 ng. by 9 or 10 days of the cycle and then decreased to 21.8 ng/ml. about 13 to 15 days after estrus or 2 to 3 days before the next estrus.119 The highest rate of estrogen excretion in the urine oc- curred at estrus with the lowest rate of excretion two days after estrus. No estrogens were found in the urine in sheep in the anestrous season. The principal estrogen excreted was estrone but some estradiol was also present in the urine.118 If conception occurred the level of pro- gesterone in the peripheral plasma generally rose from 2 to 4 ng/ml. the first few weeks of gestation until day 60. After day 60 progesterone levels rose to 12 to 20 ng/ml. by day 110 due to increased progesterone pro- duction by the conceptus.128 Ovariectomy after 55 days of gestation in the ewe is not generally followed by abor- tion because progesterone is produced by the placenta. Following copulaton and ejaculation of sperm into the vagina of the ewe, sperm cell transport is very rapid with spermatozoa appearing in the uterine tube within 15 minutes. Dead spermatozoa were also transported at a similar rate. Although about 800 million spermatozoa are in an ejaculate of a ram, some hours after copulation less than 100,000 sperm cells were in the uterus and sev- eral thousand or less were in the uterine tube. Sperma- tozoa retain viability and fertility for about 24 hours in the genital tract of the ewe.2 The capacitation time for spermatozoa in ewes was 1.5 hours. Fertilization occurs in the uterine tube with sperm penetration of the ovum beginning about 3 hours after ovulation, pronuclei formed about 3 to 9 hours after ovulation, and the first cleavage of the ovum occurred about 20 to 30 hours after ovu- lation in the ewe.- The fertilized ovum enters the ovine uterus 3 to 4 days after ovulation.79'80 The low rate, 9 to 10 percent, of embryo migration from one horn to the other after single ovulations and the high rate, up to 60 percent or greater, after double ovulations has been dis- cussed previously.25 As in cows, estrogens injected into ewes cause a regression of the corpus luteum.14'64 Exogenous gonad- otropins (HCG or LH) protected the C.L. of the ewe from regressing after an injection of exogenous estra- diol. Developing follicles play a role in the regression of the C.L. in ewes.61 Small doses of estradiol, 39 to 150 ug, given to ewes immediately before mating did not adversely affect sperm transport, ovum fertilization or embryo survival.72 Large doses of estradiol may has- ten or delay ova transport and prevent conception. Because ewes experience about 20 percent early em- bryonic deaths, especially those mated early in the breeding season, 0.4 mg per lb. of body weight of pro- gesterone in oil was given daily subcutaneously to ewes for varying periods after breeding. This had no benefi- cial or harmful effects on fertility or embryonic deaths. Injections day 1 through 5 did tend to cause smaller C.L., but all ewes carried normal embryos.167 Ovulation could be induced experimentally in both the luteal and follic- ular stages of the estrous cycle of ewes but ova produced during the luteal phase had a very low rate of fertiliza- tion.110 When natural C.L. were removed by laparotomy on day 5, 9 or 13, ewes came into estrum at 2 to 3.5 days after removal.86'87 Transportation stress induced follicular growth and ovulation in anestrous ewes but since no declining C.L. were present no estrum was exhibited.1523 When hydro- cortisone acetate was given to ovariectomized sheep, a marked increase in FSH occurred. In intact goats hydro- cortisone stimulated the growth of luteal phase follicles and reduced the size and progesterone concentration of corpora lutea. The effect of hydrocortisone on inducing parturition in late pregnancy in ewes, cows and rabbits has been discussed previously. Parturitions in sheep lateINFERTILITY IN EWES AND DOES 659 in gestation were induced within 48 hours by the injec- tion of 10 to 20 mg of dexamethasone.2 Utero-ovarian relationships in the ewe are similar to those observed in cows. Hysterectomy from early to mid- cycle in the ewe results in the maintenance or persistence of the C.L. for about 150 days or for the approximate length of gestation.64b'86,136 Unilateral hysterectomy reg- ularly prolonged the life span of the C.L. about 17 days on the adjacent or ipsilateral ovary, but had no effect on the opposite or contralateral ovary. In one ewe with a C.L. on each ovary, unilateral hysterectomy prolonged the life of the ipsilateral C.L., while normal regression of the C.L. on the opposite ovary occurred. As in the cow the regression of the C.L. in a nonpregnant intact ewe is caused by prostaglandin released from the en- dometrium after the middle of the estrous cycle. The presence of an embryo in the uterus at 13 days of the cycle prevents the normal involution of the C.L. and the initiation of another estrous cycle by inhibiting the re- lease or formation of prostaglandin and allowing preg- nancy to proceed.136 A single embryo in one horn can maintain a C.L. in both ovaries in intact ewes because the blastocyst extends into both horns.67 Removal of the hypophysis of the pregnant ewe on day 30 of gestation caused abortion due to luteal regression because of the removal of the source of luteotrophin or prolactin.136 If the hypophysis is removed from a pregnant ewe after day 60 of gestation, no abortion occurs because progesterone and possibly a luteotrophin are secreted by the placenta. The presence of intrauterine plastic spirals or coils, an intrauterine device or I.U.D. causes a variety of effects in ewes that are somewhat similar to cows. A plastic coil in one horn of the ovine uterus inhibits sperm cell transport into the uterine tube and fertilization on both sides of the reproductive tract, and promotes sper- micidal conditions in the uterine lumen.70 The presence of an I.U.D. in the ewe’s uterus caused more than 75 percent of the uterine contractions to be propagated to- ward the cervix; while in control ewes over 60 percent of contractions were propagated toward the uterine tube.96 An I.U.D. introduced into a ewe’s uterus within the first 3 days after estrus would prevent the normal de- velopment of the C.L. and hasten its regression and shorten the estrous cycle.62 If the I.U.D. was inserted on the 8th day of the cycle, the cycle length was normal or slightly prolonged.62,156 In I.U.D.-treated ewes about 25 percent of the ovulations were quiet or silent apparently due to a lack of enough progesterone from the regressing C.L. to cause the normal manifestations of estrus.62 When a uterine infection was produced by injecting E. coli into a ligated horn with an adjacent C.L. on day 3, C.L. growth was suppressed and early regression of the C.L. and a shortened cycle occurred; infection at day 11 of the cycle caused a prolonged cycle. Thus infection acted in a man- ner similar to an I.U.D.18 Synchronization of estrus in ewes during the breed- ing season is possible using prostaglandins and long term suppression of estrus, 12 to 16 days, with progestagens alone, usually as vaginal pessaries impregnated with 60 mg. MAP or 30 to 40 mg. of flugestone (Cronolone), or combined with 500 I.U. PMSG on the day the pessary is removed as in anestrous ewes.87,91b93b A variety of treatments utilizing the prostaglandins have been pro- posed.144 Ewes are observed carefully for estrus for 5 days since prostaglandin is ineffective if given before 4 days after estrus. Those not in estrus during this period are given 5 to 15 mg. P.G.F2a or 100 to 125 ug. clo- prostenol and usually 50 to 80 percent of the ewes will show estrus in 2 to 5 days after the injection and accept service by the buck for a period of 31 to 52 hours. Ovu- lation rates are normal. If random injection of the flock is used then all the does are given prostaglandin and the second dose is given 9 to 11 days later with up to 90 percent or more of the flock coming into estrus within 1-1/2 to 5 days. Giving 500 IU PMSG 2 days before the second dose of prostaglandin induces an earlier onset of estrus.144 Although the evidence is somewhat contra- dictory, there is a lower fertility or conception rate, sel- dom exceeding 56 percent, on breeding the first estrus after the use of prostaglandins. This is apparently due to inhibition of spermatozoal transport in the cervix and uterus due to loss of motility and death of sperm similar to the effects of the persistence of a level of progester- one.72a73 This reduction in fertility is variable and ap- parently not as noticeable as that following long term injectable progesterone therapy to synchronize ovine es- trus. A recent study of double injection of P.G.F.2a at a 10 mg. dose at an 11 day interval in ewes in the breeding season compared to MAP vaginal sponges for 8 days with 10 mg. P.G.F.2a given at the time of withdrawal of the sponge resulted in 82 to 93 percent of the ewes show- ing estrus in 1-1/2 to 5 days, (1-1/2 to 3-1/2 days for the latter group) and a 60 to 80 percent conception rate, average 71.7 percent, after AI service 12 and 24 hours after the onset of estrus.94 Worldwide the vaginal pes- saries or sponges and PMSG are most preferred for es- trus synchronization in cycling and anestrous ewes.87 Synchronization of estrus in anestrous ewes has re- ceived much study over the past 20 years. Results of studies utilizing progestagens given orally, intramuscu- larly, intravaginally or subcutaneously as implants alone or combined with PMSG up to 1971 have been re- viewed.127 Although many of these studies were en- couraging, at present approval by the Federal officials660 VETERINARY OBSTETRICS for use of progestagens has not been forthcoming. PMSG in a standardized form is not readily available in the U.S. The estrogens have been proven to be of no value for synchonizing or inducing estrus in ewes. Fertility of ewes following the use of long-term progestogen therapy is reduced at the first estrous period due to poor sperm transport in the ewes’ genital tract.73 128 Use of vaginal pessaries containing progesterone have shown the most promise because the exogenous source of progesterone can be rapidly removed allowing the prompt develop- ment of the estrous cycle. However problems of vagini- tis, adhesion of the pessary to the vaginal wall and loss of pessaries have complicated this procedure. Prosta- glandins are ineffective during the anestrous period be- cause functional corpora lutea are not present. All of the above chemical procedures for estrus synchronization were most effective during the transitional period between the anestrous period and early in the normal breeding sea- son. Synchronization of estrus or establishing the estrous cycle in the anestrous period of late spring and early summer has been less successful and impractical because of a great variation in response and results. Furthermore inducing estrus in ewes out of the regular breeding season creates additional problems with rams as at this time libido and production of spermatozoa are at a low level.128 This can be alleviated to some extent by maintaining and introducing a large number of rams. Artificial insemination of ewes is costly because of the time and labor involved in estrus detection, inseminating at the correct stage of estrus, and the collection and ex- tension of fresh ram semen. Frozen ram semen has a reduced survival time in the ewe’s genital tract so timing of insemination is important. It is usually recommended that ewes be serviced 12 to 14 hours after estrus is first observed or 48 to 55 hours after progestogen withdrawal in synchronized ewes.128 Ewes synchronized during the anestrous season and the breeding season with progestins and PMSG had an increased ovulation rate but had markedly higher repro- ductive losses, 58 and 49 percent respectively, compared to untreated ewes bred during the breeding season, 25 percent.95 These losses were due to both increased fer- tilization failure and increased embryonic mortality. The increased fertilization failure was due to both decreased tubal numbers of spermatozoa and a decrease in number of accessory spermatozoa/ovum possibly related to poorer out-of-season semen quality and abnormal sperm trans- port.73 The increased embryonic mortality in treated ewes was associated with an increased variation in stage of embryo development within the ewes indicating asyn- chronies of timing of onset of estrus, ovulation and fer- tilization.95 The use of artificial insemination with fresh semen produced better conception rates than the much lower conception rates with frozen semen.58 Further studies on estrus synchronization and induction during the anes- trous season are continuing. (See ewe productivity at the end of this chapter.) Pathological Changes in the Reproductive System of the Ewe Anatomic defects of the genital tract of female sheep are uncommon. Intersexes may occasionally be observed in sheep. Freemartins, such as occur in twin births in cattle, are rare in sheep.93 Since other anatomic defects or arrests in development such as uterus unicornis, uterus didelphys, persistence of the median wall of the Mul- lerian duct with a fleshy pillar caudal to the cervix, other arrests in development of the Mullerian duct, and per- sistence of the hymen occur in other species, they prob- ably occur in sheep but are rarely recorded. Undoubtedly they are highly unusual. One ewe was reported with a bifurcation of the cranial part of the vagina.38 Pathological lesions or diseases of the reproductive system in sheep and goats are similar in most respects to those in cattle. Vulvitis, vaginitis, cervicitis, metritis, pyometra, perimetritis, and salpingitis may occur in sheep usually as sequelae to dystocia, difficult parturition, re- tained placenta, and delayed involution of the uterus.93 These acute or chronic infections in the ewe are handled in a manner similar to the treatment for these infections in cattle. In retained placenta, which is much less com- mon in ewes than cattle, the uterus may be treated lo- cally, preferably with a broad-range antibiotic, and the placenta is allowed to drop away. For a valuable ewe a Figure 151. Parovarian Cysts Adjacent to the Left Ovary in a Ewe. (Courtesy K. McEntee.)INFERTILITY IN EWES AND DOES 661 better treatment is to give parenteral antibiotics for 3 to 5 days and not to place any drug in the uterus or to at- tempt to remove the afterbirth. Manual removal of a re- tained placenta is not indicated due to the small size of the genital tract. A group of 25 ewes that had failed to breed for two consecutive seasons were mated a third season.111 Eleven ewes lambed after only one service. Five ewes were bred and apparently conceived, but on postmortem exami- nation showed evidence of interruption of pregnancy be- fore term, and 8 ewes were bred at several estrous pe- riods but failed to conceive. On postmortem examination 6 of these sterile ewes were found to have occluded or cystic uterine tubes and one ewe had a mummified fetus. An incidence of 8.7 percent of abnormalities in the re- productive tracts of 276 ewes was described.93 These included parovarian cysts, hydrosalpinx, bursal adhe- sions, and adhesions of the uterus to the abdominal vis- cera. These lesions apparently account for only a small percentage of the infertility in ewes.46 Extensive and se- vere changes could be produced in the genital tract in the ewe by feeding chlorinated napthalenes." These changes were characterized by an enlarged uterine horn and cervix due to marked squamous metaplasia with pro- fuse keratinization of the endometrial glands as well as keratinization and ulceration of the vulva. Naturally-oc- curring cases of hyperkeratosis or X disease have not been seen in sheep. Tumors of the ovaries and genital tract of the ewe are rare. Several leiomyomas affecting the uterus of sheep have been recorded.50 Rare granulosa cell tumors of the ovaries and leiomyomas of the uterus of sheep have also been reported.27,109 An adenoma of the pituitary gland of a ewe has been observed.27 Rare cases of lymphosar- coma or reticulum-cell sarcoma, myeloma and squa- mous cell carcinoma of the vulva of ewes have been de- scribed.106 Infections of the genital tract other than postpartum infections apparently are seldom a cause for infertility in ewes. This may be explained in part by the long period between breeding seasons, in which recovery can take place. Vibriosis and brucellosis, the latter usually due to Br. melitensis or Br. abortus are characterized by abor- tion. Infertility in ewes associated with vibriosis and bru- cellosis has not been described. The incidence of em- bryonic deaths in ewes bred early in the breeding season was about 20 percent. There was no indication of an infection associated with the condition.38,41 In observing and examining rams with various degrees of infertility, an enzootic venereal type of infertility spread by the ram to the ewe, as is observed in cattle has not been re- ported.6615'160 The infectious causes of abortion, such as listeria, rickettsial agents, and others have not been as- sociated with infertility. Ulcerative dermatosis, lip and leg ulceration or ul- cerative venereal disease due to a virus can be spread by an infected ram or buck to a susceptible ewe or doe through breaks in the skin, causing a necrotic, swollen, bleeding lesion on the cutaneous and mucous surfaces of the vulvar lips.43,46,13,146'147 The lesion usually starts at the inferior commissure of the vulva and spreads upward. Only rarely is the vagina involved. The lesion is an ulcer covered by a scab. Removal of the scab reveals a shal- low, bleeding crater containing a small amount of creamy pus. The disease is usually spread to the ewe at the time of coitus by an infected ram that has similar lesion on its penis and sheath. Occasionally the disease may spread to wethers and to ewes that have not been bred.46 This venereal disease of the external genitals should not be confused with contagious ecthyma which is due to a dif- ferent virus and the lesions are proliferative. In a recent report it was indicated that the viral agents causing these two diseases might be related since there was cross neu- tralization between the two viruses in serologic stud- ies.145 The symptoms of ulcerative dermatosis usually subside within a week or 10 days. No successful specific treatment is available. Five percent copper sulphate has been advised for use in treating these lesions but should only be applied externally. No vaccine is available. Rams with lesions on the prepuce causing posthitis should not be purchased or placed with ewes during the breeding season. This disease, although a cause for cessation of breeding until the lesions are healed, is not characterized by infertility. However in the acute phase the ewe may refuse to copulate due to irritation and pain. Ureaplasma have been isolated from the genital tracts of ewes with granular vulvitis34 and from the uterus of a few ewes that apparently suffered early fetal losses.9215 A recent report indicated that in sheep, ureaplasmosis appears to be a venereal disease possibly capable of causing infertility, low birth weight of fetuses,923 and acute vulvitis.66 The significance of infertility from this com- mon organism in the genital tract of ewes and cows must be further evaluated. Mules’ operation has been described108,166 for the prevention of blowfly strike (myiasis) caused by folds of skin on either side and below the vulva becoming moist with urine or soft fecal material resulting in an inflam- mation, bacterial growth, and an odor that attracts the blow flies to lay their eggs in the site. The moist fleece provides the hatching maggots with food, warmth and protection. Since clipping the wool in the area or apply- ing insecticides to prevent blowfly strike are short-lived practices, Mules’ operation has been used extensively in662 VETERINARY OBSTETRICS Australia to increase the area of smooth skin around the vulva and anus in Merino or other heavily-fleeced breeds. Also, the tail should be docked short so that no long wool lies against the vulva. Mules’ operation is per- formed on recently clipped sheep during the cold season in the spring or fall when there are no flies. The folds of skin ventral and lateral to the vulva are removed and healing is allowed to occur without suturing.166 The re- sulting healing and scarring eliminates the skin folds and long wool lateral and ventral to the vulva and prevents blowfly strike. A vulvitis that occurred in ewes on clover pasture sim- ilar to the noncontagious posthitis that was seen in weth- ers on lush clover pasture has been described in Aus- tralia.138 There was no evidence that estrogens in the clover were a factor in this disease. The ulceration, scabbing and scarring of the ventral commissure of the vulva in this disease led to its disfigurement or loss with a re- sulting soiling of the rear parts with urine predisposing to flystrike even in ewes on which Mules’ operation had been performed. Nutritional deficiencies in sheep and their effect on fertility have been extensively studied. The same general nutritive deficiencies affecting reproduction and fertility in cattle also affect sheep. Most deficiency diseases af- fecting reproduction in ewes on range are multiple and involve a lack of protein, and a lack of vitamin A. The effects of inanition on fertility are more pronounced in immature than in adult animals and they are character- ized by failure of estrum and delayed puberty. A low plane of nutrition in ewes resulted in subestrus with un- detected estrus, with cycles 26 to 42 days in length.85 A low protein diet is to be avoided if a high percentage of lambs is to be produced.104 The symptoms of vitamin A deficiency are similar in the ewe and cow.74,123,124 Pregnancy in vitamin A deficient ewes usually termi- nates in abortion or the birth of dead or weak young. The female is more susceptible to vitamin A deficiency than is the male. The estrous cycle, ovulation, and early fetal development are not noticeably affected in sheep even when partial night blindness due to Vitamin A de- ficiency is exhibited.123,124 In drouth years feed low in vitamin A is often also low in energy, protein, and phos- phorus. Vitamins E, C, B complex, and D are not nec- essary for reproduction in the ewe. It is possible, how- ever, that a lack of cobalt, an essential part of vitamin B12 would cause a deficiency of rumen bacteria, and an- orexia with secondary inanition. Severe deficiencies of cobalt may result in debility, failure of estrum, and the birth of weak lambs. Estrum in ewes was regular on a cobalt-deficient diet but only 48 percent of the lambs bom to cobalt-deficient ewes were strong, as compared to 92 percent of the lambs from ewes fed a cobalt sup- plement.16 Postnatal losses of lambs from ewes fed low levels of cobalt were 58 percent as compared to 17 per- cent for the lambs nursing the ewes receiving cobalt in their diet. Copper deficiency in sheep characterized by infertility and irregular estrous periods has been reported in certain areas of South Africa. Reproduction is not affected by a low phosphorus diet until the usual symptoms of phosphorus deficiency de- velop.123,124 Symptoms of phosphorus deficiency in sheep are the same as in cattle. A low protein diet was not as severe as one low in both protein and phosphorus.104 The reproductive symptoms of a phosphorus deficiency, which is usually complicated by low protein and vitamin A level, are: delay in onset of puberty and estrum, irregular es- trous periods, and a tendency to produce only one lamb every two years. Abortions are uncommon but weak or dead young may be expelled at term. Impaired fertility is unlikely when the ewe or doe is receiving protein sup- plements or minerals containing phosphorus. Other trace mineral elements such as iron and iodine may also be lacking. In several mineral and protein deficiencies, ewes may pull and eat the wool of other ewes in the flock. Ewes but not rams, require Vitamin E and selenium to have satisfactory reproduction.20,35,69 Not only could selenium deficiency in ewes in New Zealand cause neo- natal death losses due to several myocardial lesions but in selenium deficient areas, farms would experience an incidence of 10 to 30 percent barren or open ewes after service and apparent conception.69 Giving ewes 5 mg. of selenium monthly during pregnancy or 25 mg. in one dose after mating reduced the number of barren or open ewes to 2 to 4 percent compared to 30 percent open ewes in the control or untreated ewes. Although evidence would indicate that a selenium deficiency occurred in New Zea- land, it should be noted the diseases corrected by seleni- um therapy were referred to as “selenium responsive” diseases. It is possible that some other factor(s) may cause the primary or basic disease. Ewes fed kale had a short duration of estrus of about 22 hours and a slight increase in embryonic deaths.161 Kale feeding also resulted in anemia and produced a goiterogenic effect. In Australia a specific type of infertility in sheep due to pasturing on subterranean clover rich in estrogens is observed. In this condition, the incidence of sterility in ewes may be 30 percent or even greater.10 Dystocia due to uterine inertia may have accounted for 30 to 40 per- cent of the fetuses being expelled or removed dead and for the death of 15 to 20 percent of the ewes. Prolapse of the vagina was seen in approximately 10 to 12 percent of the ewes. The sterile ewes failed to conceive on re-INFERTILITY IN EWES AND DOES 663 peated services and on postmortem examination of the genital tract a cystic degeneration of the endometrium was observed that varied in severity from microscopic to gross lesions. The estrous cycles were normal and cystic ovaries did not occur. The infertility persisted and was irreversible even when the affected ewes were changed to pastures free of the subterranean clover.132,150 151 Ovu- lation occurred regularly but fertilization or implantation were prevented by the pathologic “Swiss cheese” type of endometrium. In a recent study of 49 ewes with a permanent phytoestrogenic sterility it was demonstrated that only 57 percent of the affected ewes showed estrus accompanied by ovulation vs. 90.5 percent of the control ewes, and 21 percent of the ovulations in affected ewes were not accompanied by behavioral estrus vs. only 4 percent in control ewes.1 Progesterone assays were nor- mal in 7 of 12 affected ewes that had normal length es- trous cycles. Four of 5 other ewes had prolonged estrous cycles of 21 to more than 23 days with prolonged high levels of progesterone. In 43 affected ewes with a C.L., the C.L. failed to regress in 5 of 7 ewes with hydrops uteri and 3 of 36 ewes without hydrops uteri. These ab- normal life spans of C.L. in affected ewes were consid- ered to be caused by endometrial changes in the uteri of affected ewes.1 The “toxic” principle in the Dwalganup strain of sub- terranean clover was an isoflavone derivative, genistein or 5:7:4 trihydroxyisoflavone, that was one-fifth as po- tent as estrone in estrogenic activity.30,46 Genistein may be found in amounts of 100 mg. per 100 gm. of fresh subterranean clover. Reducing the amont of subterra- nean clover in a pasture by increasing the amount of grasses controlled the disease. Possibly since the pasture season coincides with the anestrous season in sheep, when the ewe is not cycling and progesterone is not produced, the ingested estrogens may cause more severe lesions and disease in sheep than in cattle which are generally not affected by the level of estrogen in the clover pas- tures. Ewes in Australia, grazing red clover pastures were similarly affected as ewes on subterranean clover pas- tures.9,149 Estrogens have also been found but in lower quantities in other legumes such as ladino clover and birdsfoot trefoil.11,120,131 Injection of 0.03 to 0.09 mg. of stilbestrol per ewe 3 days a week for 6 months to 2 years caused a high incidence of sterility, persistent and per- manent cystic change in the endometrium.151 A few ewes with cystic endometritis developed pyometra in a man- ner resembling that seen in dogs. The estrous cycle re- mained normal. Cystic ovaries have not been described in ewes. Fertilization Rates and Prenatal or Embryonic Death Rates in Ewes. In 80 pregnant ewes there were normal fetuses equal to only 87 percent of the corpora lutea present. The numbers of atrophic fetuses and missing eggs were about equal.583 The incidence of fetal death was estimated in a similar manner and it was reported that 16 percent of the corpora lutea were not accounted for by live fetuses but early embryonic death with com- plete resorption could not be detected.715 Increased fetal deaths occurred with an increase in number of ova re- leased, 8 percent with 1 ovum, 26 percent with 2, and 43 percent with 3 ova. This fetal mortality may be more apparent than actual when these figures are interpreted to indicate that with a large number of eggs more em- bryos must die before the pregnancy is terminated.22,21 Fertilizaton rates and embryonic death rates in Western ewes bred throughout the breeding season showed the overall embryonic death rate on the basis of 18-day nonreturns was 20 percent but that on the basis of the lambing rate the embryonic death rate was nearly 30 percent.22,23 A much higher embryonic death loss devel- oped in ewes with 3 C.L. compared to ewes with 1 or 2 C.L.80-82 A 20 to 24 percent loss of fertilized eggs is normal in the ewe.130 A prenatal death loss in Merino sheep in Australia of about 25 to 30 percent from 3 weeks after conception to term was noted.1075 Ewes bred once early in the breeding season showed an embryonic death rate of 20 percent and a failure of fertilization in 38.9 percent of the ewes.38,41 Failure of fertilization was the most important factor accounting for the low lambing rate. Fifty-four of these ewes bred artificially with semen having a 20 to 50 percent spermatozoan motility rate had about a 31 percent conception rate, while 100 ewes bred with semen having a 60 percent or better motility rate had a 62 percent conception rate. The embryonic death rate in both groups was about equal. When rams from high and low prolificacy lines of breeding were used on unrelated ewes there was no difference in ovulation or fertilization rates. However pregnancy rates and lambing rates were higher in ewes bred to rams selected from the high prolificacy lines than rams from the low prolificacy lines.21 Ewes bred early, August 1 to September 15, had a fertilization failure of 64.3 percent, 16.7 percent due to defective ova and 47.6 percent due to poor sperm, with a conception rate of 25.5 percent.77 In ewes bred from September 16 to October 25, the respective figures were 34.3 percent, 29 and 31.4 percent, and a conception rate of 59.2 percent. The deaths of the embryo were high early and late in the breeding season.5 In asynchronous heats and ovulation, the eggs failed to fertilize. The high figure of 40 percent early embryonic deaths by 24 days of gestation in 65 ewes was reported.5 High ambient temperatures, especially during and664 VETERINARY OBSTETRICS shortly after estrus, have an adverse effect on fertiliza- tion and the survival of the zygote. Ewes exposed to an ambient temperature of 90° F on the 12th day of the cycle through estrus had a fertilization rate of 51.9 percent, as determined 3 days after breeding, compared to a 92.6 percent rate for control ewes kept in a cool environ- ment.38'41 Only 3.7 percent of ova from the control ewes were grossly abnormal compared to 44.2 percent of the ova from the ewes kept at 90° F. Embryo loss based on fertilized ova that died was 91.7 percent compared to 4 percent loss in control ewes at 24 days after breeding. In sheared ewes there were 32 percent abnormal ova and the rise in body temperature was 1.8° F. In unsheared ewes there were 55.6 percent abnormal ova and the rise in average body temperature was 2.6° F. Ewes kept at an ambient temperature of 90° F for 24 hours during es- trum had only a 10 percent lamb crop from service at that estrum. If the 90° F temperature was maintained for 24 hours at 3 or 5 days of gestation the lamb crop in each group of ewes was 35 and 40 percent. The control ewes produced an 85 percent lamb crop. The early ovum during the initial stage of cleavage is most sensitive to heat.42 This effect on the early zygote in ewes is similar to the effect of high ambient temperatures on cattle shortly after service (See Infertility in Cows) After reviewing the adverse effects of thermal stress in ewes on fertil- ization rates early embryonic death rates and lambing rates, one study75 showed that maintaining ewes at high ambient temperatures, 36° C, resulting in a rise of 1.4° C in body temperature caused significant decreases in the incidence of behavioral estrus, the preovulatory L.H. surge and in the plasma progesterone level between days 7 and 13 of the cycle. These endocrine imbalances may con- tribute to the decreased reproductive efficiency of heat- stressed ewes.75 Rams exposed to high ambient temper- atures, especially with much wool on the scrotum also have greatly lowered semen quality due to degeneration of the seminiferous tubules. Another study3'4 confirmed the above effects of high ambient temperatures on the early ova by ova transfer. A recent study indicated that the greatest embryonic death loss in heat-stressed ewes conducted during early pregnancy occurred from days 10 to 23 of gestation.42 Thus 90° F ambient temperatures are harmful to fertilization and early embryo survival and may be a cause of seasonal infertility in ewes. Ewes to be bred early in the season should be kept sheared and cool. Possibly early breeding in the summer months should be avoided. Ewes that were heat-stressed during the last two-thirds of the gestation period when compared to ewes kept cool, had fewer lambs, 81 vs. 100 percent, the lambs were lighter and smaller and fewer lambs survived, 57 vs. 81 percent.133 A high plane of feeding had no effect on embryonic or fetal death rates. Ewes giving birth in a hot environment had a significantly shorter gestation period. This is interesting in the light of the influence of the glucocorticoids and stress on the initiation of par- turition. Ewe Productivity—Because ewes can produce twins or triplets and have a 145-day gestation period it should be feasible to produce 3 lamb crops in 2 years. This goal has been sought by many investigators and sheep farm- ers but currently a practical way to achieve it has not been formulated.121 It is recognized that if such a goal is to be reached management of the flock must be ex- cellent. Some of the factors mitigating against such a goal is the photoperiodicity of the breeding season in sheep. Although excellent lamb crops can be obtained from fall and winter breeding seasons, the lamb crop from late spring breedings, whether produced by “chemical” or light manipulation methods has generally been low.43153 Even with the best of control and management it is dif- ficult to produce more than 2 lambs/ewe/year.91 b Of the “chemical” methods for inducing estrus and conception the prostaglandin and progestogen treatments alone can not be recommended. However, even the progestogen- PMSG controlled breeding is best in the fall breeding season.121 Progestogens and prostaglandins have not been approved by Federal agencies for use in ewes and PMSG is not readily available in the U.S. Yearling or younger ewes do not do well in controlled breeding regimens. Possibly certain breeds might be more suited to this in- tensified production scheme. Currently the best or most easily accomplished prac- tice to increase ewe productivity is to crossbreed using the Finnish Landrace on the standard breeds in the U.S.43'113 Half-bred Finn ewes gave birth to 42 percent more lambs and weaned 24 percent more kilograms of lambs than 1/4-Finns and 52 percent more lambs and 38 percent more kilograms of lamb than did Suffolk-Ram- bouillet cross ewes.113 References General L Asdell, S. A. (1964) Patterns of Mammalian Reproduction, 2nd Ed., Cornell Univ. Press, Ithaca, N.Y. 2. Cole, H. H. and Cupps, P. T. (1977) Reproduction in Domestic Animals, Academic Press, N.Y.C. 3. Hafez, E. S. E. (1980) Reproduction in Farm Animals, 4th Ed., Lea and Febiger, Philadelphia, Pa. 4a. Jensen, R. and Swift, B. L. (1982) Diseases of Sheep, 2nd Edit., Lea and Febiger, Philadelphia, Pa. 4b. Marsh, H. (1965) Newsom’s Diseases of Sheep, 3rd Ed., Wil- liams and Wilkins Co., Baltimore, Md.INFERTILITY IN EWES AND DOES 665 5. McDonald, L. E. 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(1959) Estrogenic Activity in Green Forage Crops and Its Effect on Breeding Ewes, JAVMA, 134, 5, 237. 132a. Scheffrahn, N. S., Wiseman, B. S., Nowak, R. A. and Kes- ler, D. J. (1982) Induction of Male Sex Behavior in Ewes with Silastic Implants Containing Testosterone Propionate, Theriog. 18, 1, 1. 132b. Schinckel, P. G. (1948) Infertility in Ewes Grazing Subterra- nean Clover Pastures, Austral. Vet. Jour., 24, 289. 133. Shelton, M. and Huston, J. E. (1967) High Temperature Stress During Gestation and Reproduction in the Ewe, J. An. Sci. 26, 1, 230. 134. Shelton, M. and Klindt, J. (1975) The Ovulation Rate of Fin- nish Landrace Rambouillet Ewes, J. An. Sci., 26, 168-170, 41, 1, 275, (abstr.) and Proc. Western Section, Amer. Soc. of An. Sci. 135. Shelton, M. and Morrow, J. T. (1965) Effect of Season on Reproduction of Rambouillet Ewes, J. An. Sci. 24, 3, 795. 136. Short, R. V. (1967) Comparative Endocrinology of Early Ges- tation, in Fetal Homeostasis, Vol. II, Edit, by R. Wynn, N.Y. Acad, of Sciences. N.Y.C., 224. 137. Sidwell, G. M., Everson, D. O. and Terrill, C. E. (1962) Fer- tility Prolificacy and Lamb Livability of Some Purebred Breeds and Their Crosses, J. An. Sci. 21, 4, 875. 138. Southcott, W. H. and Moule, G. R. (1961) Vulvitis in Merino Ewes, Austral. Vet. J. 37, 8, 291. 139. Smith, H. J., McLaren, J. B., Odom, J. A. and Miller, H. (1958) Influence of the Use of Sterile Teaser Rams Prior to Breeding on Subsequent Fertility of Ewes, J. An. Sci. 17, 4, 1231. 140. Stabenfeldt, G. H. (1970) Recent Advances in Bovine Repro- ductive Physiology, Bov. Pract. 5, 2. 141. Starke, N. C. (1949) The Sperm Picture in Rams of Different Breeds as an Indication of their Fertility. II—The Rate of Sperm Travel in the Genital Tract of the Ewe, Onderstep, J. Vet. Sci. and An. Ind., 22, 2, 415. 142. Thibault, C., Courot, M., Martinet, L., Mauleon, P., Du- Mesnil Dubuisson, F., Ortavant, R., Pelletier, J. and Signoret, J. P. (1966) Regulation of Breeding Season and Estrous Cycles by Light and External Stimuli in Some Mammals, J. An. Sci. 25, (Suppl.) 119. 143. Terrill, C. E. (1968) Reproduction in Sheep, in Reproduction in Farm Animals, edit, by Hafez, E. S. E., 2nd Ed. Lea and Febiger, Philadelphia, Pa. 144. Thimonier, J. (1981) Practical Uses of Prostaglandins in Sheep and Goats, Acta. Vet. Scand. Suppl. 77, 193-208. 145. Trueblood, M. S. (1966) Relationship of Ovine Contagious Ecthyma and Ulcerative Dermatosis. Cor. Vet. 56, 4, 521. 146. Tunnicliff, E. A. (1949) Ulcerative Dermatosis of Sheep, Am. J. Vet. Res. 10, 240. 147. Tunnicliff, E. A. (1960) Report of Committee on Diseases of Sheep and Goats, 64th Ann. Meeting of U.S.L.S.A., 38. 148. Uchovsky, D. (1970) Personal Communication. 149. Underwood, E. J. (1957) Personal Communication. 150. Underwood, E. J. and Shier, F. L. (1951) The Permanence of the Oestrogenic Effects of Subterranean Clover Grazing on the Ewe, Austral. Vet. J. 27, 63. 151. Underwood, E. J., Shier, F. L., Davenport, N. and Bennetts, H. W. (1959) Further Studies of the Effects of Prolonged In- jections of Stilbestrol on the Ewe, Austral. Vet. J. 35, 84. 152a. VanRensburg, S. J. (1965) Adrenal Function and Fertility, Jour. S. Afr. Vet. Med. Assoc., 36, 4, 491.INFERTILITY IN EWES AND DOES 669 152b. Venzke, W. G. (1953) Efficacy of Estradiol Cyclopentylpro- pionate (E.C.P.) in Anestrous Ewes, Am. J. of Vet. Res. 14, 52, 411. 153. Vesely, J. A. (1975) Induction of Lambing Every Eight Months in Two Breeds of Sheep by Light Control With or Without Hormonal Treatment, Anim. Prod. 21, 165-174. 154. Wagner, J. F. (1964) Hormonal Control of Reproductive Ac- tivity in the Ewe, Proc. Conference on Estrous Cycle Control in Domestic Animals, A.R.S. U.S.D.A., Misc. Public. 1005, 28 (Lincoln, Nebr.). 155. Wheeler, A. G. and Land, R. B. (1977) Seasonal Variations in Oestrus and Ovarian Activity of Finnish Landrace, Tas- manian Merino and Scottish Blackface Ewes, Anim. Prod. 24, 363-376. 156. Whitten, W. K. (See McLaren). 157. Wiggins, E. L. and Barker, H. B. (1958) Occurrence of Post- Partum Estrus in Ewes, J. An. Sci. 17, 4, 1230. 158. Wiggins, E. L., Barker, H. B. and Miller, W. W., Ill (1970) Estrual Activity in Open Rambouillet Ewes, J. An. Sci. 30, 3, 405. 159. Wiggins, E. L., Miller, W. W., Ill, Barker, H. B. (1970) Age of Puberty in Fall Bom Ewe Lambs, J. An. Sci. 30, 6, 975. 160. Wiggins, E. W., Terrill, C. E. and Emik, L. O. (1954) The Effect of Year, Breed, Age, and Number of Ewes Bred on Fertility in Range Rams, J. of An. Sci., 13, 2, 455. 161. Williams, H. L., Hill, R. and Alderman, G. (1965) Effects of Feeding Kale to Breeding Cows, Brit. Vet. Jour. 121, 2. 162. Williams, S. M., Garrigus, U. S., Norton, H. W. and Nal- bandov, A. (1956) Variations in the Length of Estrous Cycles and the Breeding Season in Ewes, J. An. Sci. 15, 4, 984. 163. Williams, W. L. (1943) Disease of the Genital Organs of Do- mestic Animals, 3rd Ed., Ithaca, N.Y. 164. Wishart, D. F. (1966) The Induction of Earlier Breeding Ac- tivity in Sheep. A Comparison Between the Use of Vasecto- mized Rams and the Use of Intravaginal Pessaries Impregnated with a New Progestin, Vet. Rec. 79, 13, 356. 165. Wishart, D. F. (1967) Synchronization of Oestrus in Sheep, The Use of Pessaries, Vet. Rec. 81, 12, 276. 166a. Yenikoye, A., Pelletier, J., Andre, D. and Mariana, J. C. (1982) Anomalies in Ovarian Function in Peulh Ewes, Theriog. 17, 4, 355. 166b. Young, R. B. (1960) 10 Points on Mulesing, Leaflet #266 Queensland Dept, of Agr. and Stock., Australia. 167. Zimbelman, R. G., Pope, A. L. and Casida, L. E. (1959) Ef- fect of Exogenous Progesterone on the Corpus Luteum of the Bred Ewe, J. An. Sci., 18, 4, 1327. INFERTILITY IN DOES Reproductive Physiology Puberty—Depending upon breed, season of birth, latitude and level of nutrition, puberty usually occurs about 6 to 8 months of age in the Swiss breeds of goats in the temperate latitudes. Young bucks and does should be separated before 5 months of age. Certain pygmy does may reach puberty by 3 months of age.22-25 Does should not be bred until they reach 60 to 70 percent of their adult weight, about 80 to 90 pounds, to assure higher conception rates and safer parturitions. Delaying breed- ing until they reach this weight often results in breeding does after they reach a year of age. Twin births are com- mon in young well-grown primiparous does. In later par- ities twin or triplet births are more common and quadru- plet births are not rare. The estrous cycle—Does and bucks in northern tem- perate climates are photoperiodic with a breeding season extending from late summer (August) to early spring (February and March) with the peak of the breeding sea- son in late fall (October) through early winter (Decem- ber). During this breeding season brought on by shorter daylight hours, the does are polyestrous with most cycles being 20 to 21 days in length.22,25 In the tropical regions near the equator the breeding season is not dependent on photoperiods and extends throughout the year.13,25 Short cycles of 5 to 12 days in length are not uncommon in young does at puberty or older does at the beginning of the breeding season. Long cycles 40 to 50 days, at the end of the breeding season are also fairly common.611,22,25 Further studies on the cause of these abnormal cycles are indicated. Estrus may occasionally, 1 to 5 percent, be observed during pregnancy.6b Between early March through May, nonpregnant does in the temperate zones are anestrous. Between May and July is the transition period from anestrus to ovarian activity and cycling. Bucks like rams and stallions do not have a restricted breeding season as do females of those species. But during the breeding season bucks are sexually more active, have a stronger “buck odor,” and produce better quality semen. Like sheep and swine placing bucks in a group of does early in the breeding season often induces estrus in many of the does within 7 to 10 days,22’25 probably due to the release of GnRH or LH (see ewes). The estrous period is variable in length depending on the interpretation of behavioral signs indicating the onset and termination of this period. It is generally given as 32 to 40 hours with ovulation occurring about 30 to 36 hours after the onset of estrus. 19,22,25 In the Angora breed estrus is about 22 hours in duration.22 Another study25 indicated proestrus lasts about 24 hours during which time the buck follows the doe but she will not stand for ser- vice. Once standing estrus occurs it only lasts 12 to 24 hours. When does are observed in estrus they should be bred then and again 12 hours later.13,26b Signs of estrus in does is detected by a teaser or breed- ing buck because does, like mares and ewes, rarely mount other females or stand to be mounted by other does as do cows.25 If a rag is rubbed over an older buck’s scent glands located caudomedially to his horns and stored in a tightly-covered jar, this “buck jar” is warmed, opened and presented daily to each doe in a small flock.25 If the670 VETERINARY OBSTETRICS doe is in estrus she will be very interested in the jar. In the presence of a buck a doe in estrus will stay close to him. Her external genitalia may be more swollen, red- dened and moist during estrus. Rapid up and down or side to side movements of the doe’s tail, flagging, is a good sign of heat along with restlessness, increased fre- quency of urination, increased bleating and decreased milk production and appetite. Vaginal smears are of limited value to identify the stage of the cycle.25 As in other domestic species a speculum examination of the vagina and cervix will show an increased reddening of the mu- cosa, a variable amount of clear mucus in the cervix and on the floor of the vagina early in the estrogenic stage of the cycle. The mucus becomes more cloudy together with a more relaxed cervix in midestrus. Metestrous bleeding, as occurs in cows, is not present in does.25 Sexual behavior in the buck usually consists of nuzzling the doe’s perineum, pushing or butting her rear parts, flehmen and flicking out the tongue, striking out with a forefoot and emitting a low-pitched sound.26b Mounting and copulation is rapid and quick. As in sheep the introduction of bucks into a flock of does at the beginning of the breeding season produces a prompt stimulation of the onset of the estrous cycle. This effect is probably caused by the combined senses of sight, smell and contact. In one study 66 percent of the does kidded between the 8th and 12th day of the kidding sea- son. This indicated that most does come into estrum about 10 days after the bucks were introduced.20,21,243 Recent reports17,27 have demonstrated rather conclusively that introduction of bucks into flocks of does in the early breeding season or late anestrous season and observing and monitoring the latter with progesterone assays of blood plasma, that a synchrony of estrus was obtainable. Six- teen of 17 does were in estrus at an average of 5.5 ± 1.3 days after the bucks were introduced, with 31 of the does showing a subsequent progesterone profile, with concentrations of 3 to 4 ng/ml., characteristic of a nor- mal diestrous period. When the bucks were introduced into the control does 15 of the 17 exhibited estrus within 7 ± 1.5 days. Short six-day estrous cycles were seen in 4 does but the progesterone concentrations between the estrous periods never rose above 1.0 ng/ml indicating the first period was anovulatory. Thus it appears that at the onset of the breeding season in goats the first estrus is usually clinically observable and ovulatory.27 This is probably related to a small, brief but significant rise in plasma progesterone levels occurring just before this first estrus.4 Occasionally a short anovulatory cycle has been reported.27 This general pattern in does of a standing es- trus and ovulation at the first estrus of the breeding sea- son apparently differs from that in ewes in which the first estrus and ovulation is “silent” or without signs of estrus. Following copulation and ejaculation of sperm into the vagina of the doe, sperm cell transport is very rapid with spermatozoa appearing in the uterine tubes within min- utes with fertilization occurring in the ampullae of the uterine tubes. Does usually ovulate 2 ova with 3 being quite common. So they are generally more prolific than most breeds of sheep or cattle.19 After ovulation it nor- mally requires about 4 days for the fertilized ova or em- bryo to reach the uterus. As with ewes, the plane of nu- trition, degree of growth and development, and freedom from disease influences the ovulation rate.22 The corpus luteum in the doe persists throughout preg- nancy as in the cow. Thus ovariectomy at any time dur- ing pregnancy will result in abortion unless progesterone replacement is instituted. The conceptus, placenta and fetus, does not produce sufficient progesterone like they do in ewes, to maintain pregnancy in the absence of the CL in the middle or latter half of gestation.19 Twice daily doses of 50 units of oxytocin given to does on days 3 to 6 of the estrous cycle shortened the cycle to 6 to 7 days. The next cycle was normal in length. This oxy- tocin stimulated uterine prostaglandin F2a release in does to cause luteolysis in the same manner as occurs in cows given oxytocin several days after estrus to cause failure of normal CL development. Synchronization of estrus in the doe has been studied outside the breeding season (during the anestrous period) and during the breeding season. In the former period plasma progesterone levels are very low, below 1 ng/ ml. and there is little or no ovarian activity. Thus pros- taglandins are ineffective during this anestrous period. PMSG at doses of 400 to 750 IU, depending on the sea- son, month of lactation and lactation rate, given intra- muscularly, or combined with HCG, have been reported to induce estrus in 2 to 3 days with about 40 to 50 per- cent conceptions.60,13,25 Progestogen impregnated vaginal pessaries have been inserted for 17 to 21 days with PMSG given 48 hours before removal. By using large numbers of spermatozoa by artificial insemination, this procedure has been reported to be highly successful. The use of 100 ug GnRH daily for 4 or 5 days may produce estrus.25 During the transition period between anestrus and the breeding season synchronization is promoted, as men- tioned previously by the introduction of bucks into the herd. Manipulation of the photoperiod to advance the breeding season by keeping both does and bucks under daylight or artificial light for 14 to 18 hours a day for 3 months or 19 hours a day for 70 days in midwinter and then reducing the amount of daylight to 6 to 10 hours per day in the spring.4,25 This will usually successfullyINFERTILITY IN EWES AND DOES 671 synchronize the herd and result in conception in over 50 percent of the does. A practical procedure to alter the photoperiod and breeding season of does so that a uniform supply of milk could be maintained throughout the year was described.3 Since most does under natural conditions freshen from January through May in the northern hemisphere, Sep- tember through November freshenings are desired. To accomplish this 40 watt fluorescent bulbs, 1 foot (12 inches) of bulb for 10.5 square feet of floor space, 9 feet above the floor were turned on by a timer for twenty hour days starting on January 1. The lights were turned off from 1 to 5 am. Continuous 24 hour lighting did not produce the desired results. From one hour after sunrise to one hour before sunset the bam light may be turned off to save energy. This regimen was continued for 60 days for both does and bucks or until between March 1 and 15. At this time normal daylight of 14 to 15 hours exists and this shortened day length initiates estrus cy- cling 7 to 10 weeks later or late in April or May and cycling continues into June with 80 to 90 percent con- ceptions during that period. Putting yearling does and bucks on a 19 hr./day-light regimen for 70 days starting in January and then introducing the bucks to the flock 42 days after the 70 day light period resulted in 79 per- cent of the does coming into estrus and ovulating within 21 to 30 days.4 Sixty three percent of all the does or 80 percent of the does ovulating conceived at this estrus. Thus the breeding season was advanced to 60 to 80 days and a degree of synchronization achieved without hor- mones. Breeding bucks need to be light-stimulated like does or their libido may be poor. If bucks are to be used in both breeding seasons their feeding and management should be excellent.3 Standing heat in light-treated does is shorter, often only 8 to 10 hours, during the artificially established breeding season and often occurs during the night hours so clinical signs of estrus are often not ob- served. Therefore handmating of all does is not possible and opportunity for pen mating is necessary. When the latter practice is used the attendant should check the does every other day for the discharge that mats the tail fol- lowing service. Often a pen of light-treated does may come into estrus at the same time. To obtain maximal milk production during November and December 16 hours of daylight should be provided by the supplemental use of lights. If the above regimen for light stimulation dur- ing January and February is provided the entire herd, it has no effect on does or bucks not bred until the natural fall breeding season.3 During the breeding season synchronization is best achieved by the injection of 1.25 to 2.5 mg. of prosta- glandin F2a or its equivalent of prostaglandin analogue, 125 to 150 ug. of cloprostenol, to produce luteolysis or involution of the CL.5,13,25 If estrous cycling is occurring a single dose should result in estrus within 2 to 3 days in about 60 percent or more of the does. Another method is to inject PGF2a in 2 doses four hours apart. In cycling does PGF2a was luteolytic as early as day 5 of the cycle and does were in estrus 50 to 57 hours after the second injection with a preovulatory peak of LH observed at 55 hours after injection.18 Similar posttreatment results were observed with 2 treatments'll days apart and 100 per- cent of 20 does were synchronized compared to 85 per- cent with a single treatment.16 The estrous period was normal and 30 of 32 does, 93 percent, conceived by nat- ural service. Although doses of 5 to 15 mg of PGF2a were originally recommended to produce luteolysis in does, smaller doses of 1.25 to 2.5 mg, were found to be equally as effective.5 Another procedure for synchronizing estrus in does during the breeding season is administering progestogens to suppress estrus and cycling in does for 20 to 22 days66 alone or usually with 300 to 700 IU PMSG at the time of progestogen withdrawal. Progestogens may be given either orally, intramuscularly, subcutaneously or as im- plants or intravaginally as an impregnated pessary or sponge. The latter method is most preferred because of the ease of administration and the rapid withdrawal of progesterone on removal of the sponge that favors a higher conception rate.25,28 In France about 45,000 does were synchronized in 1981 .fcb Does may be inseminated with large numbers of spermatozoa 31 and 48 hours after pes- sary or sponge withdrawal and PMSG injection. Further large scale field trials with various combinations of pro- gestogens, PMSG and prostaglandins are indicated. Va- ginal progestogen pessaries and PMSG are neither ap- proved nor available in the U.S. for synchronizing does. Furthermore, fertility at the first estrus after certain types of progesterone administration, oral and intramuscular, is reduced even if larger numbers of spermatozoa are inseminated.22 Pathological Changes in the Reproductive System of the Doe Anatomic defects of the genital tract of female goats are rare except for a high incidence of intersexes, or pseudohermaphrodites. This was discussed in Chapter III. Hermaphrodism was noted most commonly in polled goats of Swiss origin.2,3,78 In one Saanen herd the inci- dence of pseudohermaphrodites, was as high as 11 per- cent; in a Toggenburg herd the incidence reached 6 per-672 VETERINARY OBSTETRICS cent. The intersexes are usually male pseudoher- maphrodites. The condition appears to be inherited as a simple recessive character associated with homlessness. Homed hermaphrodites are extremely rare, if they occur at all. To eliminate hermaphrodism in a flock, the polled goats that were normal should be mated to homed goats. Freemartins, such as occur in twin births in cattle, are rare in goats.26 Since other anatomic defects or arrests in development such as uterus unicornis, uterus didel- phys, persistence of the median wall of the Mullerian duct with a fleshy pillar caudal to the cervix, other ar- rests in development of the Mullerian duct, and persist- ence of the hymen may occur in goats they are rarely recorded. Undoubtedly they are highly unusual. Pathological lesions or diseases of the reproductive system in goats are similar in most respects to those in cattle. Vulvitis, vaginitis, cervicitis, metritis, pyometra, perimetritis, and salpingitis may occur in goats usually as sequelae to dystocia, difficult parturition, retained placenta, and delayed involution of the uterus. These acute or chronic infections in the doe are handled in a manner similar to the treatment for these infections in cattle. In retained placenta, which is much less common in does than cattle, the uterus may be treated locally, preferably with a broad-range antibiotic, and the placenta is al- lowed to drop away. For a valuable doe a better treat- ment is to give parenteral antibiotics for 3 to 5 days and not to place any drug in the uterus or to attempt to re- move the afterbirth. Manual removal of a retained pla- centa is not indicated due to the small size of the genital tract. Infections of the genital tract other than postpartum infections apparently are seldom a cause for infertility in ewes and goats. This may be explained in part by the long period between breeding seasons, in which recov- ery can take place. Brucellosis, usually due to Br. mel- itensis, is characterized by abortion. Infertility in goats associated with brucellosis is not described. A granular vulvovaginitis in does has been described due to My- coplasma agalactiae.14 After an incubation period of 7 days, the lesions in the vulva which are similar to those in granular veneral disease of cattle, are observed for several months. The granular papules are accompanied by edema and a mucopurulent exudate. The granular lymphoid lesions were also noticed in the anterior vagina and on the cervix. Anestrus in does during the breeding season is oc- casionally observed and may be due to: 1. the intersex condition in naturally-polled does. 2. pregnancy or rarely pseudopregnancy with a per- sistent CL. 3. hydrometra or mucometra, probably with a per- sistent CL. 4. severe nutritional deficiencies especially in TDN and protein, or a chronic debilatating disease in- cluding external and internal parasitisms resulting in cachexia often with anemia. 5. prepuberal anestrus, usually due to restricted feed intake and anestrus in old does due to inability to chew properly, a restricted diet and heavy lacta- tion. 6. anestrus due to pyometra or cystic ovaries is pos- sible but seldom reported. 7. severe heat stress may shorten estrous periods and reduce the observable signs of estrus. 8. mineral deficiencies of copper, cobalt, phospho- rus, and selenium may have a minor role in infer- tility, delayed puberty and reduced signs of estrus. 9. failure to observe estrus particularly in small flocks without a buck is not uncommon. Hydrometra or mucometra has been described as a cause of anestrus, infertility and abdominal distention in does. The uterus is distended with up to several liters or gallons of a thin clear fluid but no membranes or fetus are present. The doe usually has a history of mating nor- mally and the owners consider her pregnant. This fluid is often expelled spontaneously about 150 days after ser- vice.246,25 The laymen often speak of this as a “cloud- burst” condition. A corpus luteum remains in the ovary during this condition and pregnancy examination with ultrasonography, not the Doppler instrument, will often erroneously indicate the doe is pregnant. There is no as- sociation in hydrometra with evidence of a fetus, cystic ovaries or an obstructed cervix. The report of a hydrops condition in ewes with permanent sterility caused by phytoestrogens and a persistent CL after mating1 would lead one to speculate that this condition in does is due to a failure of the production of prostaglandin, the uter- ine luteolytic substance, and a persistence of the CL. A plasma progesterone assay is probably indicated. If this is the case and a high progesterone plasma level is pres- ent, the administration of prostaglandins, 2 to 3 mg. of PGF2a or 100 to 150 ug. of cloprostenol should cause luteolysis and expulsion of the fluid. The prognosis for the future reproductive life of the doe is good. One doe was cited that had alternate normal and false pregnancies for 6 years.266 Cystic follicles or ovaries have not been described in does. The normal Graafian follicle is about 1 cm. in di- ameter. Larger “follicles” up to 3.7 cm. in diameter have been reported in abattoir specimens.25 These may be parovarian cysts, cystic ovarian tumors, bursal cysts, orINFERTILITY IN EWES AND DOES 673 larger than normal follicles. Short cycles in does espe- cially early or late in the breeding season are common and not an indication of a pathological endocrine prob- lem. Treatment is not indicated. Intersexes or hermaphrodites are commonly observed in naturally polled does. These intersexes are genetic fe- males and although the polled condition is dominant the hermaphroditic defect is recessive, sex-limited and in- completely penetrant. (See Chapter III.)2'3'22’25 Preven- tion of this condition is assured if either the sire or dam is homed. Most of these hermaphrodites are phenotypic females most with ovotestes and many exhibit a projec- ting vulva and enlarged clitoris. The more masculine phenotypes have a penile-like clitoris, hypospadias and hypoplastic testes often in the inguinal region. Variable development or lack of development of the mesonephric and paramesonephric ducts are seen at autopsy. The va- gina in these hermaphrodites is very hypoplastic and a small glass rod will only penetrate about an inch past the vulva." A caprine freemartin with XX-XY chimerism was described.26 It resembled a male pseudohermaphrodite with an enlarged clitoris and inguinal testis-like gonads. Goat X sheep hybrids have been produced. Does (60 chromosomes) bred to rams have greater fertility than ewes (54 chromosomes) bred to bucks. Early develop- ment of the embryo is normal but at the time of placen- tation a possible immunorejection response may occur resulting in early fetal deaths from 40 to 60 days of ges- tation.25 Reproductive efficiency in Angora goats is very low under range conditions compared to the other caprine breeds and the net kid crop per year in the U.S. is about 50 percent vs. 100 to 200 percent for the other breeds. This low rate is possibly due to poor nutrition but most likely due to selection practices and the stress of high mohair production. In range flocks predators and cold stress also reduce the kid crop.22 23 25 This condition in Angora goats has been intensively studied in South Af- rica.29-31 It is characterized by the selection of larger kids with finer hair coats that produce more high quality mo- hair until 3 to 5 years of age. This was also associated with a better breeding potential of both does and bucks the first breeding season. These selected animals usually had small adrenal glands and low plasma cortisol levels. Such selective practices would make these animals with adrenocortical hypoplasia more susceptible to nutri- tional, physical, climatic and gestational stresses. After about the fourth or fifth year of life the incidence of abortion increased markedly. Most abortions occur from 90 to 110 days of gestation and were associated with evidence of growth retardation and anemia of the fetuses and fetal adenocortical hyperplasia with excessive estro- gen secretion. This was usually preceded 10 or more days by a severe reduction in maternal plasma cortisol levels along with maternal adrenocortical atrophy. High nutri- tional levels during this period protected most habitual aborters from losing their fetuses. With our present knowledge an hypothesis might be proposed that this triggers prostaglandin release, involution of the corpus luteum and abortion similar to the sequence of events at parturition. Older habitual “aborters” tended to develop adaptive changes of enlarged pituitary glands, adrenal hyperplasia, high plasma cortisol levels and hyperadre- nocorticism, with poor hair growth, and abdominal dis- tention. In Angora goat flocks a minor peak of early abortions was noted at 34 to 46 days of gestation and in these does fetal mummification or maceration occasion- ally followed fetal death and delayed evacuation of the uterus. Controlling this problem in Angora goats re- quires careful genetic selection by eliminating aborting does and their progeny. Bucks should be selected from nonaffected strains or families. Abortion, although com- mon, was not identified as the major cause of low re- productive efficiency in Angora goats in Texas. Ade- quate nutrition including supplemental feeding, parasite and infectious disease control, shelter in inclement weather and predator control are further required management practices.23 Tumors of the genital organs of goats are rare.9 25 Granulosa cell tumor and dysgerminoma of the ovary have been reported. Uterine tumors include adenocor- cinoma, leiomyomas and fibromas. Rare adenomas and fibromas of the vagina and vulva have been described. As in cows, squamous cell carcinoma of the vulva and perineum is not uncommon in white-haired does exposed long periods to sunlight. Although lymphosarcomas are reported in goats the genital tract is apparently seldom involved. Warts and melanomas are occasionally seen on the perineum.25 Ectopic mammary tissue in the vulva of does is char- acterized by a firmness and swelling of the vulvar lips prior to parturition that regresses in several months. As- piration of milk or a biopsy confirms the diagnosis. Rarely these swellings at parturition may interfere with defe- cation and urination.25 References 1. Adams, N. R., Heamshaw, H. and Oldham, C. M. (1981) Ab- normal Function of the Corpus Luteum in Some Ewes with Phyto- oestrogenic Infertility, Austral. J. Biol. Sci. 34, 61-65.674 VETERINARY OBSTETRICS 2a. Asdell, S. A. (1944) The Genetic Sex of Intersexual Goats and a Probable Linkage with the Gene for Hornlessness, Science, 99, 124. 2b. Asdell, S. A. (1962) Personal communication. 3. Ashbrook, P. F. (1982) Year-Around Breeding for Uniform Milk Production, Proc. 3rd Intern. Conf. on Goat Prod, and Dis., Tucson, Ariz. 153-154. 4. Bon Durant, R. H., Darien, B. J., Munro, C. J., Stabenfeldt, G. H. and Wang, P. (1981), Photoperiod Induction of Fertile Oestrus and Changes in LH and Progesterone Concentrations in Yearling Dairy Goats, J. Reprod. Fert. 63, 1, 1-9. 5. Bretzlaff, K. N., Ott, R. S., Weston, P. G. and Hixon, J. E. (1981) Doses of Prostaglandin F2a Effective for Induction of Es- trus in Goats, Theriog. 16, 5, 587-591. 6a. Cooke, R. G. and Knifton, A. (1981) Oxytocin-Induced Oestrus in the Goat, Theriog., 16, 1, 95-97. 6b. Corteel, J. M., Gonzalez, C. and Nunes, J. F. (1982) Research and Development in The Control of Reproduction, Proc. 3rd Intm. Conf. on Goat Prod, and Dis., Tucson, Ariz. 584-601. 7. Eaton, O. N. (1943) An Anatomical Study of Hermaphrodism in Goats, Am. J. of Vet. Res., 4, 333. 8. Eaton, O. N. (1945) The Relation Between Polled and Her- maphroditic Characters in Dairy Goats, Genetics, 30, 51. 9. Feldman, Wm. H. (1932) Neoplasms of Domestic Animals, W. B. Saunders Comp., Philadelphia, Pa. 10. Gall, C. (1981) Goat Production, Academic Press, N.Y.C., London. 11. Guss, S. B. (1977) Management and Diseases of Dairy Goats, Dairy Goat Journal Publ. Co., Scottsdale, Ariz. 85252. 12. Hulet, C. V. and Shelton, M. (1980) Reproduction in Farm An- imals, 4th ed., edited by E. S. E. Hafez, Lea and Febiger, Phil- adelphia, 346-357. 13. Molokwu, E. C. I. and Oliveira, D. M. (1981) Reproduction and Breeding Management of Does, Vet. Med/Sm. An. Clin. 76, 10, 1473-1477. 14. Nem Singh, Rajya, B. S. and Mohanty, G. C. (1975) Pathology of Mycoplasma Agalactiae Induced Granular Vulvovaginitis (GUV) in Goats, Cor. Vet. 65, 363-373. 15. Ott, R. S. and Memon, M. A. (1980) Sheep and Goat Manual, Society for Theriog. Vol I, Hastings, Nebr. 68901 (References). 16. Ott, R. S., Nelson, D. R. and Hixon, J. E. (1980) Fertility in Goats Following Synchronization of Estrus with Prostaglandin F;,, Theriog. 13, 341-345. 17. Ott, R. S., Nelson, D. R. and Hixon, J. E. (1980) Effect of Presence of the Male on Initiation of Estrous Cycle Activity of Goats, Theriog. 13, 2, 183-190. 18. Ott, R. S., Nelson, D. R. and Hixon, J. E. (1980) Peripheral Serum Progesterone and Luteinizing Hormone Concentrations of Goats During Synchronization of Estrus and Ovulation with Prostaglandin F^, Am. J. Vet. Res. 41, 9, 1432-1434. 19. Robertson, H. A. (1977) Reproduction in the Ewe and the Goat, in Reproduction in Domestic Animals, edited by H. H. Cole and P. T. Cupps, 3rd Ed., Academic Press, N.Y.C., London, 475-498. 20. Shelton, M. (1960) Influence of the Presence of a Male Goat on Initiation of Estrous Cycling and Ovulation of Angora Does, J. An. Sci., 19, 2, 368. 21. Shelton, M. (1960) A Comparison of the Ovulation Rate at First Three Heat Periods of Angora Goats, J. An. Sci., 19, 4, 1227. 22. Shelton, M. (1978) Reproduction and Breeding of Goats, J. Dairy Sci., 61, 994-1010. 23. Shelton, M., Huston, E., Livingstone, C. H., Jr. and Whitford, H. W. (1976) Report and Recommendations Concerning the Problems of Low Reproductive Efficiency in Angora Goats, Proc. 80th Ann. Mtg. USAHA, Miami, 395-401. 24a. Shelton, M. and Morrow, J. T. (1966) Influence of Certain Ex- teroceptive Factors on the Initiation of Estrus in Angora Does, J. An. Sci., 25, 1, 252. 24b. Short, R. V. (1967) Comparative Endocrinology of Early Ges- tation, in Fetal Homeostasis, Vol. II, Edit, by R. Wynn, N.Y. Acad, of Sciences, N.Y.C., 224. 25. Smith, M. C. (1980) Caprine Reproduction, in Current Therapy in Theriog., D. Morrow, Editor, W. B. Saunders, Co., Phila- delphia, 971-1004. 26a. Smith, M. C. and Dunn, H. O. (1981) Freemartin Condition in a Goat, JAVMA 178, 735-737. 26b. Smith, M. C. (1981) Management and Diseases of Goats, Re- vised 1981, N.Y.S. Coll, of Vet. Med., Ithaca, N.Y. 11-19. 26. Smith, M. C. (1982) Personal Communication. 27. Thibier, M., Pothelet, D., Jeanguyot, N. and DeMontigny, G. (1981) Estrous Behavior, Progesterone in Peripheral Plasma and Milk in Dairy Goats at Onset of Breeding Season, J. Dairy Sci. 64, 513-519. 28. Thimonier, J. (1981) Practical Uses of Prostaglandins in Sheep and Goats, Acta. Vet. Scand, Suppl. 77, 193-208. 29. VanRensburg, S. J. (1965) Adrenal Function and Fertility, Jour. S. Afr. Vet. Med. Assoc. 36, 4, 491. 30. VanRensburg, S. J. (1971) Malnutrition of the Fetus as a Cause of Abortion, J.S. Afr. Vet. Med. Assoc. 42, 305-308. 31. VanRensburg, S. J. (1971) Reproductive Physiology and En- docrinology of Normal and Habitually Aborting Angora Goats, Ondestepoort, J. Vet. Res. 38, 1-62.Chapter XVII INFERTILITY AND REPRODUCTIVE DISEASES IN BITCHS AND QUEENS by Donald H. Lein, DVM, PhD* In the last ten years, significant studies in reproductive physiology in the bitch and queen have taken place. Learning the normal female reproductive physiology and endocrinology of both these domestic small animal spe- cies has helped understand the infertility problems that may be due to misinterpretation and lack of knowledge of the normal reproductive cycle, as well as those irreg- ular cycles that are abnormal physiological patterns. Still more research in the pituitary gonadotrophins, gonado- trophic releasing hormones, endogenous prostaglandins, influence of higher brain centers on reproductive hor- mones as well as the influence of other endocrine hor- mones on the reproductive cycle is needed. This decade has certainly noted the influence of hypothyroidism on the cycle and reproductive performance of both the fe- male and male dog and to a certain extent the queen. The genetic effect of certain breeds in both species also plays a significant role in their reproductive performance since selection, small gene pools of certain breeds, close line breeding or inbreeding are all frequently potentiated by breeders. New hormone products to treat infertility problems, especially prostaglandin F2a (PGF2a), analogues of PGF2a, gonadotropic releasing hormone, (GnRH), and the bromoergocryptine drugs have just recently began to be used in these two species to treat infertility problems. Use of hormone products to influence the cycle in both species is still largely empirical and controlled by ob- served or expected clinical effects. Use of hormones, an- tihormones, immunological measures and other unique methods for cycle and reproductive control and wide- spread inexpensive sterilization of pet populations still needs in depth research and field trials. The clinical study of infertility in the bitch and queen have been enhanced by careful methodical examinations over a period of the reproductive cycle time, with good Associate Professor of Pathology, Assistant Director Veterinary Di- agnostic Laboratory, Department of Pathology, Department of Clin- ical Sciences, New York State College of Veterinary Medicine, Cor- nell University, Ithaca, N.Y., 14853. adequate histories and clinical records. Use of veterinary diagnostic endocrinology laboratories for hormone pro- files, vaginal cytology and good veterinary clinical prac- tices including vaginoscopic examinations, sexual be- havior records, deep vaginal cultures, laparoscopic examination, hysterosalpinography, ultrasound and good client education has greatly enhanced the success of di- agnoses and treatments of infertility in these two species. The veterinary profession and several veterinary colleges and private clinics have made small animal theriogen- ology a specific service or entity much like that for our large domestic animal theriogenology services. Infections of the reproductive tract are common in both species and in recent years have been studied and char- acterized further, leading to the successful treatment of selected cases to restore fertility. Tumors of reproductive organs and mammary glands, hyperplastic and degen- erative reproductive tract lesions and their association with both exogenous and endogenous sex steroid levels have been further elucidated. Several recent excellent review articles on small animal reproductive physiology, en- docrinology, pathology and infertility have been pub- lished and the reader is encouraged to review this list at the end of this Chapter. Canine Reproductive Physiology Puberty in the bitch occurs as early as 6 months of age and rarely as late as 22 months of age with most bitches showing their first estrus between 8 to 12 months of age. The plane of nutrition and other stress or disease factors may influence the onset of puberty as in other species. In general, small breeds of dogs exhibit earlier puberty than large breeds. Confined dogs reach puberty later than free-roaming dogs and single confined dogs may reach puberty later than groups confined together. (See pages 409—411.) Onset of puberty is gradual with interrelated changes in hormone levels and reproductive development. Some bitches apparently have several abortive attempts at es- trous expression. Endocrine studies show that individual 675676 VETERINARY OBSTETRICS pubertal bitches have inadequate or sporadic elevations in estradiol-17B blood levels during the preovulatory phase of the cycle that are associated with reduced or abbre- viated LH surge blood levels and this leads to an absence or only minor preovulatory rise in serum progesterone which is also associated with a lack of sexual receptiv- ity.27139 Bitches may show vulvar swelling, bleeding and attract males because of brief elevated blood estrogen levels from early follicular activity prior to a full estrous cycle. In studies on the Beagle bitch by Anderson and Simpson, a few showed false estrus at 6 and 9 months of age with short periods of proestrus (2 to 5 days) dur- ing which time the female attracted but would not accept the male.3 These bitches usually showed estrus in the next few weeks. Puberty in these Beagle bitches oc- curred at approximately 12 months of age with the youngest being at 8 months. In one study, the mean du- ration of proestrus and estrus was significantly shorter in bitches experiencing the first reproductive cycle than in those experiencing the second. The ability of bitches to demonstrate normal sexual behavior at the first estrus appears to be a function of age and not size.139 Asdell cited Schotterer in reporting that ovaries of fe- male pups at birth contain 700,000 oocytes; at puberty there are 355,000, at 5 years of age nearly 40,000 and at 10 years of age only about 500 follicles remain.5 In another report, the ovary of a 2 month old Beagle con- tains approximately 100,000 follicles and thereafter the number progressively decreases so that at 8 years of age only about 2000 follicles are present.3 The genital ridge is first recognized in Beagle embryos of 7 to 9 mm in crown-rump (C-R) length.3 Histologic evidence of the testis and ovary are recognized in 20 mm and 30 mm embryos, respectively, By late gestation, oogonia and pregranulosa cells are present in the cortex of the ovary with no evidence of prophase meiosis until after birth. Primary follicles become more abundant as prophase meiosis wanes and ceases in Beagle pups be- tween 33 and 54 days of age. Any oogenic foci found after this time appear to be presumptive and abortive centers of oogenesis. Polyovular primary follicles, that is follicles with 2 or more oocytes surrounded by a com- mon granulosa, are first observed at 81 days of age and become a prominent feature of the dog ovary.3 Most pri- mordial germ cells, primary or vesicular follicles undergo atresia with only relatively few reaching maturity, ovu- lation and formation of corpora lutea. As the bitch ages the ovary develops surface crypts which increase and may be used to distinguish prepuberty, maturity, middle and old age.3 If a bitch is well grown, there is no reason not to breed on the first estrum. Full sexual maturity, the attainment of maximum capacity, may not be fully attained until the second or third estrum.109 Beagle bitches in one study reached a reproductive peak at 3 years of age.3 By 8 years of age, reproductive senility was present, with longer interestrous periods, increased infertility and increased preweaning mortality. The estrous cycle—The dog is considered a mones- trous animal with only one estrous cycle occuring during the breeding season. In a review by Shille and Staben- feldt, an even distribution of estrous cycles throughout the year was shown, although there is definite pattern of increased incidence of estrus from January through May.103 There are some reported breed differences, with the Ba- senjii bitch having the highest birth rate from November through January although pregnancies and estrous cycles occur throughout the year in this breed.103 Greyhounds and other large breeds may have only one estrous period a year.18 (See pages 411-415.) The interestrous interval is affected by breed differ- ences, but not necessarily by breed size. There appears to be less variability within animals than within the breed. Studies on several breeds showed interestrous interval differences for the Toy Poodle of 239 days, Cocker Spaniel, 186 days, Basset Hound, 175 days, German Shepherd, 149 days, and Rough Coat Collie, 255 days,103’115 Differences for the same breed but in differ- ent localities have also been reported: Great Britain ver- sus the United States, Cocker Spaniels, 224 vs. 186 days, Miniature Poodle 189 vs. 239 days, respectively.103 In some studies, the interestrous period appears to be lengthened following pregnancy versus a nonpregnant cycle, while other studies have shown no significant dif- ferences.27’103’115 Further studies on the interestrous pe- riod are needed on the effect of pregnancy versus non- pregnant cycles and the effect of breed, husbandry, nutrition and environment. Latitude and photoperiodicity had no effect on the reproductive activity in dogs in Great Britain.23 Age does affect the interestral period with in- creased interval time and more irregular cycles. Bums and Fraser quoted Frost in reporting that in nearly 500 bitches, 338 had an estrous interval of 5 to 7 months, over 100 had an interval of over 7 months and only 16 had an interval of less than 5 months.18 In other studies, the interval averaged between 7 to 8 months and 4 to 13 months (over 7 mo.) in a Beagle colony.27 103 Intervals longer than 13 months always had an intervening ovu- latory and luteal phase for which no sexual behavior was observed, a silent heat, but was detected by serial pro- gesterone blood levels.27'34 In the author’s experience, interestral periods less than 4 months are usually irreg- ular or abnormal cycles with no ovulations, luteinized cystic follicles or very short luteal function. The intervalINFERTILITY IN THE BITCH AND QUEEN 677 between estrous cycles is rarely 6 months, so most bitches have the ability to be in estrus or whelp in any month of the year. The estrous cycle of the dog as originally described using the four terms, anestrus, proestrus, estrus and me- testrus are still used and accepted.3,27 34,62 Metestrus was used to designate the full luteal phase. The terminology used in other domestic animals; metestrus, the period of luteal formation to maximal size or maximal progester- one production, and diestrus, the period of maintenance of the mature corpora lutea, is difficult to use in the bitch, since these stages may be looked at differently by sex behavior, estrogen and progesterone blood levels, and vaginal cytology. Concannon, et al., has shown that pro- gesterone is produced by the mature graafian follicle prior to ovulation and is responsible for initiating sexual re- ceptivity in the bitch.33 Also, the bitch is sexually re- sponsive to the male well after ovulation and into early formation of the corpora lutea with high progesterone levels. Thus, metestrus and estrus in the strictest sense overlap or occur within each other. Maximal blood pro- gesterone levels do not occur until 15 to 25 days after the LH peak and the nonpregnant bitch may continue to secrete progesterone above basal anestrous blood pro- gesterone levels for 120 to 150 days after the LH peak. Holst and Phemister observed a sharp decline in va- ginal comified cells about 3 days before the end of be- havioral estrus and suggested that this be considered the first day of diestrus.55,56 They also found in a later study that vaginal ramification was complete in 12.1 days (S.E., 0.2) from the beginning of estrus and 8 days (S.E., 0.3) from the LH peak. They considered this stage of the cycle should be diestrus. Behavioral-wise the bitch may still be in estrus, the corpora lutea are still developing, pro- gesterone levels are still rising for some days and in the strict scientific sense this stage is metestrus. Stabenfeldt and Shille suggested that the simplest ap- proach is to recognize that metestrus occurs during the latter part of estrus in the dog and to use the term diestrus for the luteal phase of cycle which begins with the loss of sexual receptivity.47 A nomenclature committee of small animal theriogenologists, endocrinologists and physiol- ogists must finally decide on an acceptable terminology for all to use. The estrous cycle of the dog is considerably longer and more variable compared to our large domestic ani- mals. In general, the four accepted phases or time pe- riods are: 9 days for proestrus (range 3-16), 9-10 days for estrus (range 4-12), 75 days for metestrus-diestrus (range 51-82), and 125 days for anestrus (range 15- 265).117 The less variable portion of the estrous cycle is proestrus-estrus which is frequently quoted as 21 days of attraction followed by loss of receptivity to the male. The most variable are metestrus-diestrus and anestrus. Vaginal cytology, If used on a routine basis in a cy- cling bitch can accurately reveal the stages of the estrous cycle. Vaginal smears examined at one- to two-day in- tervals during proestrus, estrus and early metestrus/dies- trus can be a very valuable clinical test to predict when a bitch will ovulate, when to inseminate or send to a stud for breeding, or when an irregular cycle is taking place. Couple the vaginal cytology with sexual behavior, teas- ing with a sexually active male, changes in the size and consistency of the vulva, changes in the vaginal and cer- vical mucosal folds and possible sex steroid hormone serum profiles and the strength of clinical diagnostic and management at breeding for optimum reproduction greatly increases. (Chart III) The above tests and changes are all under the influence of estrogen and its mitogenic Chart III. A schematic summary of temporal relationships between periovulatory endocrine level changes, behavioral, vaginal exfoliated cytology, vulval and vaginal mucosal changes associated with the es- trous cycle in the bitch. (Courtesy and with permission of P. W. Concannon and publisher, W. D. Saunders, Co.27)678 VETERINARY OBSTETRICS influence especially on target tissues. Several excellent reports have been published on the obtaining of speci- mens, stains and techniques for staining, interpretation and correlation of vaginal cytology to the estrous cycle, reproductive hormone changes, sexual behavior, repro- ductive tract changes and diagnostic use for infertility conditions in the bitch.2•8'22•27•42•55•64■68'87'88■98',,x,•,02'1,7•122 Specimens must be collected from the vagina and not the vestibule since cells from this area do not readily reflect sex steroid hormone changes and are always cor- nified.42 98 Thus, the use of a speculum is important to bypass the vestibule. No lubrication for the speculum or collecting instrument should be used since most cause artifacts on the smear. Specimen collection can be done with a moist clean cotton swab, metal or wood spatula, glass rod, pipette and saline flush; the author prefers a moist (saline) clean cotton swab which is rotated in the anterior vagina. Cells are less distorted if the swab is rolled on the clean glass slide instead of pulling across the slide. Several stains are available; Wright’s, Leish- man’s, Giemsa, Wright’s-Giemsa, Trichrome stains such as Sano-Pollack Trichrome,98 Shorr’s trichrome, New Methylene Blue, Toludine Blue and Diff Quick, a mod- ified Wright’s-Giemsa stain.27,87 The author prefers to use Diff Quick because it is simple, rapid and adequate and the slides can be stored for reference and studied throughout a bitch’s cycle. A drop of New Methylene Blue on a cover slip, applied to an air-dried vaginal smear can be read immediately and shows good detail, but it will not stain red blood cells and cannot be stored for reference.68,87 It is advisable to stay with one stain throughout a study of an estrous cycle because of the difference in staining detail between stains.27 An excellent study on the changes of cells and cell types with percent of changes throughout the cycles is reported by Christie, et al.22 Increasing estrogens from the developing follicles during proestrus and estrus cause the target tissue of the vagina to progress rapidly from a two cell thick epithelium in anestrus, made up of basal and parabasal cells that are small round cells containing a large distinct nucleus, to a very rapid growing epithe- lium that will become several cell layers thick as estro- gen levels increase in late proestrus. Cells as they mature from basal and parabasal cells will become larger, lose their round shape and become polyhedral or angular, still contain a nucleus (called intermediate cells) and even- tually become larger, more polyhedral and degenerate so that the nucleus now becomes pyknotic, eventually lys- ing (karyolysis) and disappears. These cells are classi- fied as superficial cells, containing a pyknotic nucleus, partly comified, or anuclear, fully comified. The com- pletely cornified superficial cells are seen with the full effect of high estrogen levels and are predominant in the smear when the height (number of cell layers) of epi- thelium is maximum. These cells are polyhedral, fre- quently “wrinkled” or “curled” and appear like “corn- flakes.”1303 The cytological change, day by day, through the early cycle (proestrus, estrus, early metestrus) is al- ways a percentage of change in types of cells. Late in anestrus, mainly scant parabasal and early intermediate cells are present. Occasionally in the last 40 or 50 days of anestrus, erythrocytes will be seen in the smears be- fore any vulvar bleeding at proestrus is noted indicating early follicular activity and estrogen production.122 Proestrus is characterized by mixtures of parabasal, in- termediate and superficial cells (cornified cells) that progress towards a higher percentage of mature or com- pletely comified cells in late proestrus to early estrus. Erythrocytes, from uterine diapedesis are quite numer- ous in proestrus, tend to decrease in estrus, but in some bitches, may be present through estrus and into metes- trus/diestrus. The presence or absence of erythrocytes in estrus or diestrus is the most variable of all cell types. Leucocytes, polymorphonuclear leucocytes, are present in proestrus, but are not present in full estrus. If they are present, it indicates an inflammatory process in the reproductive tract and they are usually degenerate leu- kocytes filled with phagocytized bacteria. Epithelial cell changes and height (number of cells thick) of epithelial layers in the vagina during proestrus and estrus follow estrogen secretion levels by approximately 1-2 days, thus maximum cornification (95-100%) follows the preovu- latory LH surge by 1-2 days.27,102 103 Near the time of the LH peak, a clearing of the background on the glass slide (lack of debris) takes place and is possibly related to a decrease in mucoprotein content of the vaginal mu- cus.27,68 This is usually an optimal time to start breeding a bitch or to send the bitch to a breeder, since LH release has taken place and destined ovulation is eminent. Ship- ping and changing of the environment of bitches prior to destined ovulation may cause a bitch not to ovulate because of inadequate LH-RH, LH release, possibly controlled and blocked by the higher brain centers. The “clearing” effect is best noticed when following a series of daily or every other day vaginal smears. By 3 or 4 days after the LH peak, fully comified superficial cells (anuclear) almost completely replace partially comified superficial cells (contain pyknotic nuclei). About 7 to 8 days after the LH peak, an abrupt decrease in comified epithelial cells takes place, confirming retrospectively that ovulation has taken place. There is a rapid loss of fully comified epithelial cells and reappearance of in- termediate and parabasal cells indicating the start of me- testrus or the onset of diestrus as described by Phemister, et al.91 This is probably the last day that an unmated bitch is likely to be fertile since it coincides with theINFERTILITY IN THE BITCH AND QUEEN 679 fertile lifespan of oviductal oocytes.27 The reappearance of leucocytes in the vaginal smear in early metestrus/ diestrus indicates the end of the fertile period and the increase of progesterone blood levels. The reappearance of leucocytes may coincide with the metestrus/diestrus shift of epithelial cells, but frequently their entrance are more variable and may be one or two days earlier or in the author’s experience, two to four days later and in many cases may not be that abrupt in appearance. If a bitch is presented at this time with no prior history of stage of cycle, by either behavior or vaginal cytology, this stage (early metestrus) may be confused with proes- trus. Study of further daily smears will determine the stage of the cycle. As the bitch procedes into late me- testrus/diestrus, the cell thickness (number of layers of cells in vagina) returns to 5 to 8 cells thick and even- tually to two or three cells thick at anestrus. In a study during metestrus and anestrus, Dore described the great increase in parabasal and intermediate cells after 30 days postovulation which increased in late metestrus/diestrus and early anestrus to mainly parabasal cells. Recognition of this stage is important when a bitch of unknown cycle status is presented for contraceptives or for estrus in- duction (Chart III). Vaginal smears for cytologic diagnosis of inflamma- tory processes of the genital tract; vaginitis, endometri- tis, pyometritis, or subinvolution of placental sites ver- sus postpartum metritis or endometritis, neoplasia, etc. are well described by Rozzel and a recent report by Ol- sen, et al.88,98 Vaginoscopy or endoscopy of the vagina of the bitch has been a very valuable procedure for pinpointing the changes from proestrus to estrus and finally metestrus/ diestrus. This procedure is also useful for breeding soundness examinations and the diagnosis of anatomical abnormalities, inflammation, neoplasia, obstetrical and postpartum difficulties.27,68'69'70 Lindsay has described the method used for postuterine endoscopy and the estrous cycle changes. Visualization of the vaginal mucosa can best be accomplished with a fiberoptoscope or a small human pediatric fiberoptic proctoscope or sigmoido- scope (Welch-Alien) in both noninflated and insufflated states. These instruments can easily be passed with ster- ile lubricant to the anterior vagina and a complete ex- amination performed with minimal restraint of the bitch. The true cervix cannot be easily viewed because of the anterior dorsal median vaginal fold which occupies the anterior 2 or 3 cm. of the vagina and narrows this portion of the vaginal cavity to a ventral slit, making it difficult to pass instrumentation in this area unless it is 4 mm in diameter. The true cervix opens on the anterior ventral portion of this dorsal fold. A paracervix, which is the caudal portion of this dorsal vaginal fold and contains the narrowed ventral lumen leading to the true cervix, is frequently mistaken for the external cervical os. ’ ’ ’ ’ The cervix can be seen easily in full estrus or at late pregnancy, at whelping or early postpartum when the area is under the influence of estrogen, is edematous and quite dilated. As estrogen increases during proestrus, the vaginal mucosal folds become progressively more edem- atous, rounded, puffy and turgid in appearance. At the time of the preovulatory LH peak, estrogens are falling, progesterone is rising, the blanched, rounded, smooth mucosal folds and prominences that completely fill the vaginal lumen quickly change and rapidly develop a wrinkled, angular, peaked or crenulated appearance that are less edematous and do not fill the vaginal lumen. It is felt that these gross changes probably reflect an abrupt withdrawal of the water retention effects of estrogen dur- ing the preovulatory decline in estrogens and the trig- gering of the LH peak. This is the start of estrus and coincides with acceptance of the male and complete cor- nification of vaginal cytology. The angular or crenated vaginal mucosal folds will continue to be present for 5 to 6 days and then are lost about the time of the metes- trus/diestrus shift in the vaginal cytology and are re- placed by flaccid vaginal folds with the paracervix area appearing as a soft “rosette.” These changes can easily be followed through proestrus, estrus and early metes- trus/diestrus by every other day examinations (Chart III). Progressive swelling and edema with turgidity of the vulva, perineum and the ventral floor of the caudal va- gina takes place with increasing estrogen levels in proes- trus. Frequently this edema is ascertained prior to vulvar bleeding in early proestrus. Since these are target tissues for estrogen and easily visualized and palpated, daily ex- amination of the vulva will give a good indication of the progression of proestrus and the change to estrus because the rapid decline in estrogen levels will cause a rapid softening of the vulva and vaginal floor at estrus. This is an ideal time to breed the bitch. Some bitches could not be naturally bred in late proestrus because the vulva and hypertrophied caudal vaginal floor are so edematous and enlarged. In some bitches, severe edema and hy- pertrophy of the vaginal floor will lead to prolapse of the hypertrophied caudal vaginal floor between the vul- var lips. Endocrinology of the estrous cycle and pregnancy— Excellent studies and reviews on the endocrinology and physiology of the estrous cycle and pregnancy of the bitch have been reported.3'20'24'26'27'30'31'33'34'35'36'37'38'40'47' 53,54, 62,70, 74, 75,77,79, 82,84 ,85 ,91,94, 95, 102, 103,106. 108, 109,116,117, 119, 120,121,.23,124,125,127,128,136,137,.39 The follicular phase, mainly proestrus and early estrus was considered an abrupt oc- curence following a quiescent anestrus. Olson, et al. has shown that in late anestrus (at least 45 days before proes-680 VETERINARY OBSTETRICS trus) concentrations of follicle stimulating hormone (FSH) in serum are high (240 to 294 ng/ml) and again at the time of the preovulatory surge of luteinizing hormone LH (297 ng/ml). During proestrus, FSH was lowest (131 to 200 ng/ml). There is sufficient FSH present during anestrus for follicular growth.82 Serum estradiol 17-B was high in late anestrus (20 to 46 pg/ml), decreased prior to proestrus (8 to 46 pg/ml), and increased through proestrus and then dropped just prior to estrus. Inhibition of FSH may be caused by elevated estrogen levels (neg- ative feedback) or, as proposed for other species, ele- vated serum levels of inhibin a follicular peptide that se- lectively inhibits FSH secretion.27 The serum LH levels were inverse to the estrogen levels, low early, higher just prior to proestrus, possibly inducing a new follicular phase, lower during proestrus, and then surging to a high level at estrus. Similar findings for LH and estrogen were found in prepuberal bitches prior to their first estrus.139 Concannon has also noted that in nonpregnant bitches in anestrus (150-180 days from last estrus) ovarian follic- ular activity, uterine and oviductal hyperemia, including enlarged fimbria and a congested red endometrium are present. He believes this represents the transition from late luteal phase of one cycle to the early follicular phase of the next cycle.27 Others have also reported this phe- nomena in pubertal and anestrous bitches.3116 From the above reports, anestrus cannot be considered strictly a quiescent state. At the onset of proestrus, several follicles, 1.0 to 1.5 mm in diameter are present on the ovaries of Beagle bitches. They increase to 2 mm by mid proestrus, 3 to 4 mm by late proestrus and 3 to 5 mm by the onset of estrus.3 Several of these follicles degenerate at any of these stages, while a few, up to 20 or more, increase to 8 to 10 mm in diameter at ovulation.137 Mature follicles are amber in color, contain several infolds of the gran- ulosa cell lined wall and coiled blood vessels can be seen in the walls. Just prior to ovulation, the oocyte becomes free-floating in the follicular fluid. The rupture site of a follicle can be recognized by a pinpoint area with very scant hemorrhage and no appreciable collapse of the walls.3 The released oocytes promptly pass to the am- pullary region of the oviducts. The turgid fimbria effec- tively close the ovarian bursa (ventral slit) at ovulation to prevent the loss of ova. During the follicular phase, estrogens cause the in- creasing evidence of external signs of proestrus: edema, hyperemia and enlargement of the vulva, vaginal dis- charge of uterine blood (endometrial diapedesis), edema and hypertrophy of the caudal vaginal floor, secretion of sex phermones from the vaginal or vestibule secretions and attraction of males. Urine from bitches in proestrus and estrus will attract males at this time.43 One vaginal sexual attractant was analyzed as methyl-p-hydroxyben- zoate.51 Methyl-p-hydroxybenzoate and to a lesser ex- tent, propyl-p-hydroxybenzoate, when applied by cotton swab applicators to the vulva and vestibule of anestrus or ovariohysterectomized bitches caused intense ano- genital interest and attempts at mounting by teaser males. The use of oral administration of chlorophyll in some bitches at the first sign of proestrus appears to mask the sexual attractive odors of bitches in proestrus/estrus.103 During proestrus, the bitch will usually not permit mounting and intromission. The behavioral change from proestrus to estrus is when the bitch will stand for the male, with tail deviated laterally and the back in a lor- dosis position. This is also the time when vaginal cy- tology has changed to mostly comified epithelial cells with no leukocytes and lack of debris and variable amounts of red blood cells. At this time the vulva has come from a full swollen, turgid, edematous estrogen-primed tissue to a more flaccid, soft tissue with a rapid decrease in estrogen blood levels and increasing progesterone blood levels. The tumification of the vulva of most bitches dur- ing proestrus would make intromission by the male al- most impossible even if the bitch would stand. Daily va- ginoscopic examination at this time also shows a change in the anterior vaginal longitudinal and transverse folds and the paracervical areas from a smooth edematous rounded swollen, “pillow” type appearance to an an- gular, sharp edged or crenulated, wrinkled appearance. These changes take place when serum estrogen levels are falling and early progesterone levels are increasing and indicate the luteinizing hormone (LH) surge that will cause ovulation in the next 2 days.69'70 This abrupt change is one of the best clinical signs to indicate the LH surge and ovulation (Chart III). The endocrine and reproductive patterns during proestrus and early estrus have been well defined by several investigators.3'20'24'27'31'33'34'38'47'53'62'74'75'77'82'84'91' 94,95,102,103.106.107.109,136.139 serum estradiol jy.g leVels increased from basal levels of 2 to 10 pg/ml to peak levels of 50 to 120 pg/ml in late proestrus.27 Concurrent increases in estrone also take place with these levels being elevated during the 6 day interval both before and after the LH peak, while average estradiol-17-B levels remain elevated only during the 6 day interval preceding the LH peak.139 The release of LH to cause ovulation is initiated by the drop of blood estradiol-17B and that is facilitated by the low, but rising blood progesterone lev- els.27’31,33’34’38 Sexual receptivity in the bitch is the result of a slight preovulatory rise of serum progesterone in association with a preovulatory serum LH surge and a rapidly declining serum estradiol-17B level.27 38 The sourceINFERTILITY IN THE BITCH AND QUEEN 681 of the progesterone appears to be the preovulatory lu- teinizing granulosa cells of the mature follicles (Chart IV). Further work with ovariectomized Beagle bitches showed that the best combination of sex steroid hor- mones for inducing estrus was to administer estradiol- 17B for 8 days followed by progesterone and removal of estradiol-17B.31,33,38 The mechanism of regulating LH release in the dog appears similar to that of other spe- cies, mainly gonadotrophin releasing hormone (GnRH) from the hypothalamus which releases both LH and FSH. Exogenous GnRH causes LH release in the bitch within minutes.19 Atypical reproductive behavior and patterns are ob- served in certain bitches at estrus. These atypical re- sponses include lack of sexual receptivity and reduced or inconsistent patterns of circulating concentrations of estradiol-17B, luteinizing hormone (LH) or progester- one. It appears that inadequate or sporadic elevation in levels of estradiol-17B during the preovulatory phase of the cycle were associated with reduced or abbreviated LH surge concentration which resulted in a minor pre- ovulatory rise in serum progesterone causing a lack of sexual receptivity.139 Olson, et al. has reported that during proestrus, mean serum testosterone levels range from 106 ± 29 to 239 ± 3 pg/ml with a high concentration of 526 ± 225 pg/ ml occurring the day of the preovulatory surge of LH. During late anestrus, levels of serum testosterone ranged from 31 ± 11 to 141 ± 63 pg/ml. The physiological or endocrinologic function of testosterone in the bitch has not been studied.84 Ovulation is spontaneous in the bitch and occurs about 24-48 hours after the LH peak with a range of 24 to 72 hours.27,34,91 136 In relation to estrus or acceptance of the male, ovulation has been reported by laparoscopic ex- amination to occur from the first to the seventh day of estrus with one bitch ovulating on the ninth day.119,136 Studies on the preovulatory LH peak and the onset of estrus indicate that the latter occurs between 7 to 8 hours Chart IV. A schematic representation of typical endocrine changes reported, or presumed to occur, during the nonpregnant canine ovarian cycle and their relation to observable stages and functional phases of the cycle. (Courtesy and with permission of P. W. Concannon and publisher W. D. Saunders, Co.27)682 VETERINARY OBSTETRICS after the LH peak with a range of 3 to 5 days before the LH peak to as late as 4 to 5 days after the LH peak.27 One bitch was reported to have been in estrus 9 days before the LH peak.136 “Early estrus” may be caused by a slight or transient drop in estrogen levels or a rise in progesterone during the follicular phase prior to the final estrogen peak. The later estrus, following the LH peak, may occur in an insensitive bitch and is seen particularly in the pubertal bitch. Occasional bitches never show es- trus, or even proestrus, and still ovulate. Some of these conditions may be the degree of knowledge, talent and time spent by the observer on canine sex behavior or the number of mating attempts, compatability of the dog and preference or experience of the pairs. Estrus in the bitch is typically 6 to 12 days, but it may be short, 2 to 3 days in those showing late after the LH peak, or it may be protracted up to 3 weeks or longer in a few females. The luteal phase of the canine estrous cycle begins before ovulation with preovulatory luteinization of the granulosa cells and theca interna. Complete transfor- mation of granulosa cells into lutein cells is not observed until 4 to 5 hours after ovulation.3 The serum proges- terone level continues to rise during estrus and reaches peak levels of 15 to 80 ng/ml or higher between 15 and 25 days after the LH peak.27 Progesterone levels will gradually decline after reaching a peak and are quite variable in concentration between bitches and in duration in the nonpregnant bitch. This may vary in the nonpreg- nant bitch from 55 to 110 days before reaching serum levels of 1 ng/ml, but may not reach basal levels of 0.3 to 0.4 ng/ml, until 120 to 150 days after the LH peak (Chart IV). Depending on the definition of metestrus and/ or diestrus, the duration can be considered to last about 2 months, as in pregnancy; 2 to 3 months until mammary development associated with physiological pseudopreg- nancy subsides or near the mean of 80 days, when mean serum progesterone levels are 1 ng/ml or lower, or when serum progesterone levels reach anestrous basal values of 0.3 to 0.4 ng/ml, or at 120 to 140 days, when the effect of progesterone on histologically examined en- dometrium is no longer evident. In the pregnant bitch, desquamation of the endometrial lining is more exten- sive and repair occurs about 2 weeks later, 140-155 days post coitus.3 One other steroid, estriol, has been found during metestrus and may play a role in the cycle. Estriol is a weak estrogen and may act as a competitive metab- olite, displacing estradiol-17B endometrial receptors. Throughout the non-pregnant cycle, LH and FSH lev- els appear to remain at basal levels. FSH rises again late in anestrus, as described earlier in this Chapter, and stimulates late anestrous follicular development. LH and prolactin (PRL) are both pituitary luteotrophic hormones for corpora lutea maintenance in the dog. Studies show that removal of the pregnant or nonpregnant uterus did not alter maintenance of luteal function in the bitch. Also that serum LH concentration appears to increase as pro- gesterone levels decline indicating that cessation of lu- teal function does not appear to result from a lack of LH.85 Prolactin also is inversely proportional to progesterone secretion. Thus serum prolactin levels rise as progester- one levels decline, which may result in overt behavioral signs of pseudopregnancy in some bitches.27,64 Pseudopregnancy—All nonpregnant bitches will undergo a pseudopregnancy in late metestrus/diestrus which may be covert or overt. The covert type will show no behavioral signs of pregnancy, but will still have en- dometrial and mammary gland hyperplasia. The overt bitch will have varying degrees of pregnancy signs from milk secretion, enlarged uterus and abdomen, nest mak- ing, restlessness and false labor, anorexia, vomiting and the caring for toys, inanimate objects or other animals’ young. In some bitches and possibly some breeds, either higher levels of prolactin are released or the dogs are more sensitive to expression of pseudopregnancy.27 Some dogs are triggered into overt pseudopregnancy when blood levels of exogenous progesterone or progestins, or pos- sibly similar blood steroids drop. A homologous radioimmunoassay for canine prolactin has been developed. Throughout the estrous cycle, basal plasma prolactin (PRL) levels of 2-4 ng/ml remain fairly constant until the end of metestrus/diestrus in non-preg- nant bitches, when a rise to 9 ng/ml was noted.40 Pro- lactin is highly lactogenic in the bitch and exogenous administration can maintain lactation indefinitely (Chart IV).62 Prolactin and thyroid-stimulating hormone (TSH) are both released following an injection of thyrotropin-re- leasing hormone (TRH). Prolactin secretion is controlled by hypothalamic prolactin releasing inhibitory factor (PLF) which may be dopamine. Dopamine agonists, such as bromoergocryptine, can reduce prolactin secretion in dogs as in other species and can reduce the severity of overt pseudopregnancy.27 Bromoergocryptine is not used clin- ically because of its unfavorable side effects, but new analogues show great promise in treating overt pseudo- pregnancy. Growth hormone (GH) is primarily a metabolic hor- mone, but is also lactogenic in some species. Hypotha- lamic somatostatin, an inhibitor of GH secretion, and GH releasing factor from the hypothalamus, regulate the secretion of GH. Growth hormone secretion can be el- evated by progesterone secretion endogenously, and also exogenously, leading to acromegaly-like changes inINFERTILITY IN THE BITCH AND QUEEN 683 bitches, and alterations in glucose and insulin levels.27,29 The most fertile period in the bitch appears to be as- sociated with the time of the LH peak to 4 days after ovulation.27,91,103 Bitches have conceived with single breedings as early as 3 days before and up to 7 to 8 days after the LH peak thus leading to gestation periods of 57 to 72 days.37128 It is usually recommended to breed early followed by services every 2 to 4 days.27,87 The best method is to utilize daily teasing with a sexually re- sponsive male and breed when the bitch shows the first good stance, with lordosis and lateral deviation of the tail (so called “flagging”). To increase the knowledge of timing or in lieu of a teasing stud, the use of vulvar changes from tumescence of proestrus to relaxation and detumescence of estrus, daily vaginal cytology and va- ginoscopic examination can be used to pinpoint the changes from proestrus to estrus, ovulation and on to metestrus. Ovulation, fertilization and implantation—Canine ova are ovulated from follicles as primary oocytes about 36 to 48 hours (24-72) after the LH peak. Maturation of oocytes take place in the oviduct and may take as long as 2 to 3 days, so fertilization probably occurs no earlier than 3 days after the LH peak.27 For this reason the im- mature ova shed by the dog, and fox, remain viable for several days after ovulation before the male and female pronuclei join and cell division begins. Thus in canine ova, sperm penetration occurs while the egg is still a primary oocyte but the sperm head remains quiescent in the vitellus until the second polar body is extruded. In one study, using laparoscopy for determining ovulation, the first polar body was extruded at 48-72 hours post- ovulation, the germinal vesicle (follicular cells) were re- tained until 24 to 48 hours and no follicular cells were seen at 68 hours. Cleavage began from 72 hours on, in the middle or distal part of the oviduct and ova were in the 2 cell stage at 96 hours, 3-6 cell stage at 120 hours, 8 cell at 144 hours, 8-16 cell stage at 168 hours and 16 cell at 192 hours in the distal oviduct. At 204 to 216 hours postovulation the ova in the morula stage were transferred into the uterus.120 (See pages 419-422.) After ova maturation, the fertile life span is not known, but may be two to three days; since in some bitches, fertilization and pregnancy occurred as late as seven days after the LH peak. Mahi and Yanagimachi found that canine oocytes mature to the stage of germinal vesicle breakdown within 48 to 72 hours of in vitro incubation following removal from follicles. Thus, this process may take as long in vivo. They also reported that dog sperm can penetrate canine oocytes after 7 hours of incubation in vitro and that they can penetrate immature or degen- erate oocytes as well as mature oocytes.71 Dog sper- matozoa can remain viable in the lumen of the uterus for 5 to 6 days and even to 11 days after copulation.27,41 Disappearance of spermatozoa coincided with the onset of metestrus. Free floating blastocysts have been observed in the uterus between 8 and 20 days postcoitum. Implantation occurs 21-22 days after first acceptance, but may have a range of 17 to 18 days (late estrus mating) to 26 days after mating (early mating, 3 days prior to LH peak).27,62 In a series of 21 bitches studied by TsuTsui, the blas- tocyst on the 16th day after ovulation (determined by laparoscope) has shed the zona pellucida and was free floating in the uterine lumen. Implantation took place 20.5 to 23.0 days postovulation in bitches allowed to mate from 54 hours preovulation to 108 hours postovula- tion, respectively. Thus the time interval between mat- ing and implantation was 18.5 to 24.0 days and if dated from the time of fertilization, 18.5 to 19 days post fer- tilization.123 Future implantation sites are noted as edem- atous areas of the endometrium (Chart V).3 The number of follicles that mature and rupture may vary from 4 or fewer, especially in small breeds, to 20 or more in the larger breeds. As the bitch ages, the num- ber of follicles maturing and ovulating, as well as litter size will decrease. In a study of 135 mongrel bitches the rate of ovulation was 6.0 ±1.7 ova (2-12), 2.9 ± 1.4 (0-8) in the right ovary, and 3.1 ± 1.4 (0-6) in the left ovary. There was no statistical seasonal affect. The fer- tilization rate of all bitches was 88.8%. Transuterine mi- gration showed a tendency for distribution to be equal between both uterine horns.121 Diagnosis of pregnancy via abdominal palpation is usually possible by day 25 of pregnancy following the last mating, but may be possible by 17 or 18 days when mating occurs late in estrus or not until 26 days after a mating occurring 3 days before the LH peak. The uterine horns are like a “corkscrew” from endometrial hyper- plasia and hypertrophy during early metestrus and may be difficult to differentiate from implantation sites or swellings of pregnancy.116 The uterine swellings are about 1.0 cm in diameter at 19 to 20 days after the LH peak, 1.5 cm at 23 to 24 days and 2.0 cm at 27 to 28 days and 3.0 cm at 31 to 32 days. The uterine swellings be- come more confluent and oblong by day 30 to 35 and are difficult to palpate as individual entities from this time on.27 The amnionic vesicle and developing embryo can be viewed by ultrasound by 20 to 22 days postmat- ing with evidence of fetal heart movement by day 22. In the author’s experience, biweekly studies with ultra- sound can be used to detect, confirm and record by pho- tography early embryonic and fetal death and resorption. Rendano, et al. demonstrated that fetal skeletons do not684 VETERINARY OBSTETRICS Chart V. Events of Canine Pregnancy Timed in Relation to the Preovulatory LH Peak and to Potential Times of Fertile Matings Event Days After the Preovulatory LH Peak* Potential Range of Days After a Fertile Mating! Onset of proestrus -20 to -3 -25 to -2 Full vaginal comification - 4 to +2 Onset of estrus - 3 to +5 Estradiol peak - 3 to -1 Decreased vaginal edema - 1 to 0 LH surge and sharp rise in progesterone - 1 to 0 LH peak 0 - 7 to +3 First mating - 5 to +10 First fertile mating — 3 to +7 Crenation of vaginal mucosa 0 to 1 Ovulation of primary oocyte 2 - 5 to +5 Oviductal oocytes Resumption of meiosis 3(?) Extrusion of first polar body 4(?) Sperm penetration 3 to 7 0 to 7 Fertilization/pronucleus formation 5 to 7 1 to 8 Degeneration of unfertilized ova 6 to 8(?) Two-cell embryo 6 to 8 Loss of vaginal crenulation 6 to 8 0 to 9 End of complete vaginal comification 6 to 9 Return of leukocytes to vaginal smear 7 to 12 Morulae (8 to 16 cells) in oviduct 8 to 10 Blastocyst (32 to 64 cells) entry into uterus 9 to 11 3 to 14 Intracomual migration (1-mm blastocysts) 10 to 13 Transcomual migration (2-mm blastocysts) 12 to 15 Attachment sites established, zona pellucidae shed 16 to 17 Swelling of implantation sites, primitive streak formation 18 to 19 Palpable uterine swellings of 1-cm diameter 20 to 25 17 to 27 Onset of pregnancy anemia 30 Reduced palpability of 3-cm swellings 32 26 to 38 Hematocrit below 40 % PCV 40 Hematocrit below 35 % PCV 50 Fetal skeleton becomes radiopaque 43 to 46 Radiographic diagnosis of pregnancy 45 to 48 39 to 50 Prepartum luteolysis and hypothermia 63 to 65 Parturition 64 to 66 58 to 70 ♦Conservative estimates based on literature reports and unpublished observations. tBased on fertile single matings from three days before to seven days after the LH peak. (Courtesy of P. W. Concannon)INFERTILITY IN THE BITCH AND QUEEN 685 become sufficiently mineralized and radiopaque for a pregnancy diagnosis until approximately 46 days after the LH peak or 19 to 20 days prior to parturition.97 Uter- ine enlargement is detectable 35 days prior to parturi- tion. Mineralization of fetuses progresses rapidly with the proximal extremities; forelegs/hindlegs/pelvis, cau- dal vertebrae/paws, and finally teeth becoming visible at approximately 17, 11, 5 and 4 days prior to parturi- tion, respectively.36,97 (See pages 32, 33.) Fetal death late in gestation or at parturition can be diagnosed if the radiographs show the following: (1) alteration of fetal skull bone alignment: overriding of the fetal skull plate bones or extreme deformity of the fetal skull; (2) intra- fetal or perifetal gas collections; (3) abnormal fetal pos- ture, “ball sign” or increased fetal flexion or straight- ening of the hind limbs.97 The endocrine patterns have been studied for the preg- nant bitch but not to quite the extent of those at estrus (Chart VI).27 The sex steroid hormones, estradiol-17B and progesterone are similar in the nonpregnant and pregnant bitch up to the time of implantation (18 to 19 days post LH surge). Secondary elevations in proges- terone levels are seen in the fourth and fifth week of pregnancy. This difference over the nonpregnant bitch cannot be used diagnostically because of the great in- dividual variations encountered. Whether the increased progesterone is caused by increased luteal progesterone secretion or by placental gonadotropic activity is un- known at this time. Hemodilution that probably accom- panies the rather dramatic anemia of pregnancy in the bitch from implantation to the end of gestation, probably effects the concentration of hormones, and if corrected, the higher progesterone levels of pregnancy versus non- pregnancy may be significant. The mean hematocrit (PCV) falls below 40% following implantation and by the end of gestation reaches 30 to 35 percent.27-35 Serum estrogen levels rise during the latter third of pregnancy but do not reach levels as high as those ob- served during proestrus. Follicle stimulating hormone (FSH) increase in pregnant bitches has also been re- ported following implantation. The two-fold increase in FSH was observed as early as 28 days of pregnancy and was present to one week prepartum. This may account for the increased ovarian follicular activity and increased Chart VI. A schematic representation of typical endocrine changes reported, or presumed to occur, during the course of a fertile canine ovarian cycle including pregnancy and lactation, and their relation to events critical to breeding protocols, pregnancy diagnosis and estimation of gestation length. (Courtesy and with permission of P. W. Concannon and publisher, W. D. Saunders, Co.27)686 VETERINARY OBSTETRICS estrogen levels in the second half of pregnancy.27 Luteal progesterone is needed to maintain pregnancy in the bitch. This has been substantiated by several re- searchers. Removal of ovaries, hypophysectomies caus- ing loss of LH and prolactin support of the corpora lutea, anti LH serum, suppression of prolactin with bromoer- gocryptine, prostaglandin F2a induced luteolysis in the last 30 days of pregnancy, all cause reduced serum pro- gesterone levels to baseline and abortion.3,27,112,126 Progesterone levels begin to drop between 30 to 35 days and 60 days of pregnancy from peak levels of 15 to 80 ng/ml to a prepartum plateau of 4 to 16 ng/ml, which is maintained for one or two weeks prior to par- turition. Formation, full development, and progressive retrogression of the corpora lutea in the dog have been fully described and each phase occupies approximately one-third of pregnancy (0-21, 22-43, and 44-63 days postcoitum).3 The corpora lutea decrease in size after 37 days of pregnancy, but not until after 45 days is there histologic evidence of retrogression. Retrogression is progressive and remnants of corpora lutea can be de- tected for 2 or 3 subsequent estrous cycles.3,62 In non- bred bitches, degenerative signs are seen about the same time (42 days) as pregnant corpora lutea, but retrogres- sion becomes more extensive at this time than in the pregnant bitch. By 5 to 6 months after the onset of es- trus, corpora lutea in both bred and non-bred bitches are approximately 2 mm in size, are located deeper in the medulla of the ovary and have similar histolological fea- tures.3 A pregnant specific two to five fold increase in serum prolactin (50 ng/ml) takes place with a rapid decline in progesterone the last few prepartum days.27,30,40 Prolactin levels remain high during lactation because of the suck- ling stimulus and decline to basal levels following wean- ing. Levels fall rapidly in bitches not nursing pups. In one study, PRL increased very rapidly during the 16 to 56 hours prepartum and reached peak levels (117 ± 24 ng/ml) at 8-32 (21 +3) hours prepartum in 6 bitches and at 24 hours postpartum in one bitch. By 36 hours after this peak, PRL levels were reduced to 37 ± 8 ng/ ml before again increasing in response to suckling. Mean PRL levels increased during the first week of lactation, peaked at 86 ± 19 ng/ml at 1.5 weeks of lactation, fell slowly to 43 ± 6 ng/ml at 5 weeks, shortly before wean- ing, and then fell abruptly to 13 ± 2 ng/ml following weaning (Chart VI).30 In the week prior to parturition maternal cortisol levels increase and are considerably increased 24 hours pre- partum at the time that progesterone levels are falling. Concannon, et al. reported that on Days -3, -2, -1,0 and 1 from parturition, mean plasma progestins were 4.2, 4.3, 1.6, 0.9, and 0.8 (±0.2) ng/ml while the mean corticoids were 19, 19, 37, 15, and 14 (±3) ng/ml.35 In another study, mean serum progestin levels at approxi- mately 120, 36, 20 and 10 h prepartum were 4.5 ± 0.6, 3.1 ± 0.4, 1.2 ± 0.4, and 0.6 ±0.1 ng/ml respec- tively. In 6 of 7 bitches, serum cortisol was elevated above mean prepartum levels of 23 ± 1 ng/ml during the day prior to the start of parturition, reached peak levels of 63 ± 7 ng/ml at 8-24 hours prepartum and fell to 19 ± 4 ng/ml at 8-12 hours postpartum. Mean serum cortisol levels remained between 22 ± 1 and 27 ± 5 ng/ml during lactation and weaning.30 Dexameth- asone treatment (2X5 mg daily for 10 days) from Day 30 of pregnancy caused, fetal death and fetal resorption, while treatment about Day 45 caused abortion or birth of dead fetuses at Days 55-59. A very accelerated de- cline of serum progesterone occurred after treatment in midpregnancy.6 By recording rectal temperature twice daily a transient hypothermia will parallel the decline in serum proges- terone prior to parturition with a delay of approximately 12 hours. Rectal temperature falls about one to two de- grees centigrade between 12 and 36 hours prepartum. During or following parturition, a rise in rectal temper- ature to slightly above normal takes place which will persist for several days.27,35 Further studies have shown that administration of prostaglandins F2a (60 ug/kg di- vided bid or tid) can cause luteolysis, serum progester- one levels to fall rapidly, and some abortions in the last half of pregnancy. Rectal temperature also dropped within 15 minutes of PGF2a administration, but only in luteal phase bitches and not in ovariectomized bitches, which suggested that the temperature drop depends on rapid drop in progesterone levels.32,35 Three bitches in this study did not abort, because progesterone levels remained at 2.1 ng/ml and after treatment of PGF2a was stopped, pro- gesterone levels returned to 5-10 ng/ml until normal prepartum decline. Progesterone serum levels must drop to baseline for parturition to take place. Exogenous pro- gesterone given prior to Day 60 caused prolonged ges- tation, with either death of pups and the bitch if caesar- ian sections were not done.35 What role prostaglandins play in natural luteolysis and parturition are not known. It has been shown that the canine pregnant uterus does produce PGE2 and PGI2 but no PGF2a. Thus the PGE2; PGF2a ratio may present a protective mechanism as it does in other species for the corpora lutea and mainte- nance of myometrial vascular tone during late preg- nancy. Possibly PGF2a is increased at the very end of gestation.27,83 Parturition—The bitch at parturition is responsive to exogenous oxytocin, but measurements of endogenousINFERTILITY IN THE BITCH AND QUEEN 687 oxytocin have not been reported. Clinically the bitch ap- pears like other species, that the neural reflex release of oxytocin occurs in response to cervical and vaginal dis- tention during delivery of pups, digital “feathering” or stroking of the vaginal wall and suckling during lacta- tion. The relaxation and dilation is probably caused by progesterone decline and estrogen increase at this time. The sharp prepartum prolactin rise may play a role in the anxiety, panting, scratching, chewing, nesting be- havior, milk secretion, and seclusion that are usually ob- served 12 to 24 hours prior to whelping. It may also be responsible for other maternal activities such as removal of fetal membranes from pups, separation of the umbil- ical cord, eating of the placenta and licking and cleaning each pup as it is bom. These same maternal behavioral signs and lactation may be seen in bitches with overt pseudopregnancy. (See pages 107-110.) It appears that relaxin or a relaxin-like hormone is also present in the bitch, since along with increased estrogens the bitch shows great relaxation and softening of the sac- rosciatic ligaments, pubic symphysis, relaxation and di- latation of the vulva, vestibule and vagina. The sequence of parturition in the bitch includes the three recognizable stages of labor. The first stage in- volves the anxiety, restlessness, nesting behavior, an- orexia, seeking seclusion, and temperature drop of 1- 2C°, 12 to 36 hours prior to whelping. The pelvic lig- aments are softened with the tail head and tuber ischii becoming more prominent and the vulva lengthened, be- coming flaccid and moist. Mild uterine contractions dur- ing this time can cause some of the restlessness. The second stage of labor is the true delivery of the pup or pups with usually one or two delivered at a time period and may consist of tenesmus and a few forceful strains similar to defecation resulting in the delivery of a pup in the non-complicated case. Over half are delivered in the anterior dorsal position, 40% in the posterior posi- tion. Usually extremities are extended, but birth in many can take place with a retained limb. Most bitches will deliver one or two pups every 30 minutes to 2 or 3 hours with the interval usually the longest following the first pup or pups delivered. Most bitches deliver their litter in 3 to 6 hours but can take up to 24 hours. Placentas are usually passed between the delivery of one or two pups since pups usually come alternately from each uter- ine horn. The third stage of labor, delivery of the pla- centa, is blended with the second stage. Most bitches will ingest the fetal membranes. Suppression of estrus or control of estrus, contra- ception or complete sterility in the bitch are subjects of great interest and research in recent years. Different populations of dogs need different forms of control. The most difficult group is the control of the stray, ownerless or homeless dogs (and cats) which require permanent sterilization of both sexes, instead of suppression or re- versible control of fertility. These are usually dogs (and cats) owned originally by irresponsible persons. Animal shelters would like to provide sterile male and female pups, (kittens) or adults with a minimum of expense. A method or methods are needed that are effective, hu- mane, permanent with one application, easily obtained by consumers, and easily provided by the health delivery system involved. Several studies and conferences have been held to provide measures to meet these needs, such as the National Conference on Dog and Cat Control, held in 1976 and sponsored by the American Humane As- sociation, American Kennel Club, AVMA, Humane So- ciety of the U.S. and Pet Food Institute.81 Several state and local societies have also studied the problem. A large part of their studies have been organizational, defining who is responsible, educational and informative to the public, setting control measures and the most difficult, finding finances for research and field trials to conduct studies on control of fertility or permanent sterilization. Studies on the pet population in the United States are interesting and appalling. In nearly two decades of effort to raise public awareness and to educate conscientious pet owners, there appears to be little improvement.61 A report by APHIS-USDA in 1981 showed that 20 million dogs and cats are annually not wanted; 5 million are abandoned and 15 million are given to animal pounds and shelters.80 Of those, 2 million are adopted and 13 million are destroyed. Faulkner’s paper on pet popula- tion problems claimed that in 1973, 4.5 billion dollars were spent on combined care and feeding of pets, 18 million neglected pets were impounded costing society nearly 125 million dollars. To maintain a zero growth in the population, 72,000 dogs and cats must be destroyed each day. He also brought out the public health hazards, zoonotic diseases, waste problems of feces in highly populated areas and the trauma and fear of bites and stray dog packs.49 Two studies in pet population control in a midwest U.S.A. college town showed that the dog population stayed stationary from 1968 to 1979 with 66% of all bitches spayed; with a people to dog ratio of 4.14:1 and a 12% population of roaming dogs with 36% of them, actually stray dogs. The cat population though was in- creasing by 18% annually. Only 59% of the females were spayed and it was calculated that 88% should be spayed to obtain zero population growth. The people to cat ratio was 5.2:1, household average was 0.508; 28% of all households had cats with 1.74 cats per household, whereas 43% of the households had dogs with 1.36 dogs per688 VETERINARY OBSTETRICS household.78 An excellent study by Schneider on the pet population in two areas of California from 1970 to 1975 showed an increase in pet owners, a reduction in the numbers of unwanted pets, increased life expectancies of pets and increased neutering of pets." The only procedure available to the humane shelters is the spay or castration clinics which are expensive and time consuming. However, Faulkner stated that surgical sterilization or any alternative contraceptive technology deals with the consequence of the problem and not with its cause, which are irresponsible owners and inadequate control of irresponsible ownership.49 Other methods cur- rently being investigated are immunological control, es- pecially with gonadotrophins, gonadotrophic releasing hormones, the ova, zona pellucida, fertilized eggs, sper- matozoa, testicular tissue; the destruction of specific cells of the pituitary or hypothalamic area with cytotoxic sub- stances, the formation of acyclic pets by testosterone sensitization of the perinatal hypothalamus and quicker methods of sterilization, utilizing laparoscopic tech- niques, electrocautery, lasers and injection of sclerotic . e . .•__ 1,13,28,48,50,59,72,73,92,104,138 or caustic agents for castration. Probably no one method will answer all needs. Popu- lation control of other wild carnivores; coyotes and foxes are being studied for possible control of the stray dog. The second population of dogs to provide estrus control are those that are owned by conscientious persons that want to produce litters, but need estrus suppression or control to avoid the nuisance of estrus while using the bitch for performance, show, work and also to avoid the problem of confinement, attraction of males and possible unwanted pregnancies. When unwanted breedings do take place, then mismating, “day after” or pregnancy ter- mination methods are needed. Options for preventing estrous cycles or pregnancy in the bitch still remain limited to veterinary practitioners in the United States compared to other countries in the world. If permanent sterility is desired, then the best method available is ovariohysterectomy. This is not without postoperative complications. In one study of 109 bitches, referred to a University clinic over a 30 month period, 28 bitches had a persistant vulvar discharge, 37 attracted male dogs, 28 showed periods of estrus, 14 had postoperative pseudopregnancy. Pseudopregnancy may occur post surgically when bitches are spayed in the lu- teal phase causing a rapid fall in blood progesterone lev- els and a release of prolactin which may simulate the same hormone sequence as parturition.27 Forty seven of these bitches had remnants of ovaries left on exploratory surgery (41 right side, 22 left side); 70% had elevated progesterone levels, 39% had cyclic vaginal smears; 19 bitches had uterine stumps infected and inflamed.812 One case report involved a bitch with a partial hysterectomy; ovarian cycles continued; three years post surgery a va- ginal discharge was discovered and on surgery the re- maining uterus and cervix contained abscesses and gran- ulomas from which B. canis was recovered. A high B. canis titer was maintained for at least one year after re- moval of ovaries, remaining uterus and cervix and ther- apy with tetracycline.402 These reports indicate that good techniques are required and that complete ovariohyster- ectomies are much preferred over tubal ligations, ova- riectomy, salpingectomies or subtotal hysterectomy which frequently lead to uterine, cervical and/or ovarian disease. There is a move to encourage spaying prepub- ertal or pubertal bitches for several reasons; the infantile tract is located and removed with minimal time and trauma. There is little or no chance of developing mam- mary gland tumors and there is no chance of several un- wanted litters before accomplishing ovariohysterectomy. Post complications of prepubertal spayings may result in a higher incidence of juvenile vulvas, perivulval der- matitis and hypoestrogenism with bilateral miliary der- matoses. Increased obesity may be seen in some bitches, but frequently the young bitch will have a greater ten- dency to exercise well and exercise and diet control will control the obesity problem. To what extent bone de- velopment, epiphyseal closure, or adult body confor- mation will change is not known and further studies are needed.28 For control of estrus, reversible contraception by phar- micologic means is available with synthetic progestins or androgens.16'28'135 One of each for use in the dog are approved for use in the United States (“Ovaban,” Scher- ing Corp, Kenilworth, N.J. and “Cheques,” Upjohn Co, Kalamazoo, Mich.). With either of these two steroids, estrus can be prevented and pregnancies postponed. Manufacturers recommendations should be followed. They are not the answer for life control for estrus nor are they meant to replace ovariohysterectomy. They are products to be used in young bitches prior to uterine or ovarian disease. Bitches that were not planned to be bred or have finished their reproductive use should be neutered. Megestrol acetate (“Ovaban”) is marketed in the United States as a canine contraceptive in 5 and 20 mg tablets for oral use. It is distributed as “Ovarid,” Glaxovet Ltd., Greenford, Middlesex, in the United Kingdom and Eu- rope. It is a potent oral progestin with a very short half life, with total elimination from the bitch in about 8 days.16 It can be administered at two times of the cycle to con- trol estrus, either in anestrus or the first 3 days of proes- trus. The recommended dose for anestrous bitches is 0.25 mg/lb (0.55 mg/kg) body weight for 32 days. The time for anestrous treatment must be selected on the basis ofINFERTILITY IN THE BITCH AND QUEEN 689 the bitches’ history of interestrous intervals and be at least one or two weeks prior to the next expected proes- trus. The return to estrus averages 4-6 months (1-7 mo. range). The proestrus dose is 1 mg/lb (2.2 mg/kg) for 8 days, which is the same total dose for the 32 day treatment. The occurrence of proestrus should be verified by ex- amination of vaginal cytology. The bitch should be con- fined for 3-8 days or until cessation of bleeding and loss of attraction for males. Usually proestrus subsides in 3 to 8 days. Again, most bitches return to estrus in 4 to 6 months (1-7 mo. range). If treatment is started too early in proestrus, the bitch may return to proestrus, if too late in proestrus, a fertile estrus may occur.28 British work on “Ovarid” reported that return to estrus can be delayed by administrating megestrol acetate at 1 mg/lb, (2.2 mg/kg) for 4 days, beginning during the first 3 days of proestrus, followed by 0.25 mg/per lb (0.55 mg/kg) for 16 days which again is the same total dosage as the other two regimes. They also recommend that if mating occurs during the first three days of treat- ment, megestrol acetate therapy should be stopped and the bitch treated for mismating. If mating occurs after 3 days of treatment, therapy should be continued at 3 to 4 mg/kg since the drug will prevent pregnancy in most cases. British work also prescribed megestrol acetate for up to 4 months following a postponement course of ther- apy for extended suppression, but these bitches should be allowed a normal cycle before being retreated.16 Precautions indicated by the manufacturer for “Ova- ban” are; not to administer for more than 2 consecutive treatment periods; do not use in bitches with reproduc- tive tract disease, pregnant bitches, or bitches with mam- mary tumors; do not use in first estrus or pubertal dogs. A report has shown that it is safe and effective in first- heat or pubertal bitches when the onset of proestrus is accurately determined and treatment administered as prescribed for proestrus.9 Clinical trials reveal suppres- sion of estrus in 92% of 387 bitches in early proestrus and 97% of 117 in anestrus with minimal adverse ef- fects.17 Treatment did not affect subsequent cyclicity and fertility. Temporary minor side effects include increased ap- petite, decrease of activity, calming effect, less aggres- sive behavior, weight gain, water retention and rarely lactation. Therapy during either the first or second half of pregnancy did not result in fetal abnormalities. Over- dosage or prolonged therapy may cause cystic endome- tritis or Cushingoid syndrome.141516 28 “Mibolerone” is a synthetic androgen-derived steroid and is approved for long-term estrus prevention in dogs as “Cheque” drops to be added to food daily in the United States and as “Matenon” in the United Kingdom. Ap- proval has been obtained in the United States to market mibolerone in canned dog food as a prescription diet. It is androgenic, anabolic, antigonadotrophic and does not possess progestational or estrogenic activity. Inhibition of estrus was over 95% successful in dogs treated for periods up to 5 years and possibly it may prove capable for life-time use.16'111 Manufacturers recommended treat- ment for up to 2 years, starting in early or mid anestrus. Treatment should start at least 30 days prior to the onset of the next proestrus to completely suppress estrus. It will not arrest proestrus or estrus like megesterol acetate, and will not interfere with conception or gestation, how- ever, female puppies were masculinized.16110113 Dosage ranged from 30 pig/day for dogs weighing 1 to 12 kg. up to 180 (jig/day for dogs over 45 lbs, Ger- man Shepherd Dogs and any German Shepherd cross- breed which for unknown reasons require the high dos- age. Undesirable side effects include: mild clitoral hypertrophy which is worse in prepuberal bitches to the point of os penis formation; vaginal or vulval discharge, especially in those with an enlarged clitoris; masculin- ized deeper voice, masculinized hair coat, especially over the neck region; anabolic effects; overdose leads to anal gland inspissation and resulting odor; increase severity of preexisting seborrheic dermatitis; and occasional el- evation of liver function test which returns to normal when the compound is removed from the diet.16'28111 Bitches that show estrus while on therapy are either receiving too low a dose, started with less than 30 days to estrus, or therapy was not reliably administered. Re- turn to estrus following cessation of administration is usually 2 to 3 months but may be as short as 7 days and up to 7 months.16 28 Bitches that are on higher doses than recommended may also have a decrease in the post treat- ment size of the first litter.111 Several other non-approved steroid hormones have been shown to suppress or inhibit normal ovarian cyclicity in the bitch. Excellent reviews on their use and side effects have been reported.16,28,60,103 The steroids used include natural steroids, progesterone and testosterone, and syn- thetic steroids including medroxyprogesterone acetate, melengestrol acetate, proligestone, norethisterone ace- tate. It is felt that all of these work by mimicking the normal feedback effects of endogenous ovarian steroids or in the case of androgens, testicular steroids, on the hypothalamus (releasing hormone and/or pituitary go- nadotrophins, FSH and LH). All of the above steroids are effective in controlling ovarian cycles in the bitch, but have undesirable side effects: progestins promote uterine disease, mammary gland hyperplasia, and other effects on pituitary and adrenal cortical functions, whereas690 VETERINARY OBSTETRICS androgens have masculinizing effects. Both progestins and androgens can cause fetal reproductive abnormali- ties if given during pregnancy.39112 Medroxyprogesterone acetate, MAP or also known as Ga-methyl 17a acetoxy progesterone, MPA (“Pro- mone,” Upjohn) was marketed as an injectable canine contraceptive in the U.S. until 1969. It was removed at that time because of the high incidence of cystic endo- metrial hyperplasia, endometritis and pyometra.4,11 This effect may be related to overdosing or administering dur- ing stages of the cycle other than anestrus since the im- portance of a synergism between progesterone and es- trogen to cause increased uterine disease was confirmed earlier.103 High doses of MAP (MPA) also cause mam- mary gland tumors, adrenal suppression and acromega- ly 29,45,101 re(juce(i amounts, (50 mg/dog) estrus was prevented and normal fertility followed,12 but later stud- ies using this dose, either single or multiple injection schedules, caused uterine disease.103 However MAP/MPA is still used widely in other countries as a contraceptive (“Depopromone,” “Perlutex,” “Anovulin”) and is mar- keted in the U.S. for human use other then contraception as “Depo-Provera” (Upjohn Co.) The minimal effective contraceptive dose is approximately 2 mg/kg every 3 months. Melengestrol acetate, MG A, another progesterone, ef- fectively prevented estrus in dogs at 200 pg/day, but levels of 4 or 8 pg/kg produced abnormal uterine changes, dystocia and pyometra.52,114 Proligestone (14a 17apropylidene-dioxyprogester- one), a progestin, is an injectable canine contraceptive marketed in Europe as “Delvosterone” (Mycofarms, Ltd. and Gist-Brokades).131 Doses of 10 to 30 mg/kg de- pending on the weight of animals, are injected subcu- taneously at zero, three and four months followed by others at 5 month intervals thereafter. Administration during proestrus resulted in signs disappearing within 5 days and retreatment of these animals within 3 months resulted in continuing persistence of anestrus in 97% of animals treated. Clinical trials showed no formation of mammary gland tumors, only 0.3% of uterine disease and none of these were in proestrus treated cases (1685 cases). There appears to be little or no restrictions on usage at any stage of the cycle.28,103,131 Silastic implants containing 169 ug/kg of testosterone controlled estrus for as long as 840 days with normal estrus cycles and litters after removal.105 Androstenedi- one, at a dose of 400 ug/day/dog was not effective in preventing estrus. No uterine disease was observed, but mammary gland development with milk secretion (4/13), clitoral enlargement of all treated and one pregnant bitch with testosterone implants in situ produced two female pseudohermaphrodites. Progesterone implants placed subcutaneously in bitches inhibited cycles for 15 to 20 months with no objection- able side effects. These implants, although effective, will probably not be made available commercially because they are not biodegradable and must be inserted and re- moved surgically.28 A 19-norandrogen, norethisterone called “Norlutin A” (Parke Davis) was used orally to suppress estrus in Grey- hound bitches. A 4 week treatment regime starting at proestrus delayed the return of estrus for 132.9 days av- erage. Four bitches had normal litters following treat- ment.103 A synthetic 19 norsteroid, 6,6, spiroethylene, 19-nor- espiroxenone, effectively suppressed the occurrence of estrus in dogs when administered orally once daily for 90 days at a dosage of 0.9 mg/kg body weight. There was no evidence of mammary gland or uterine disease during the period of treatment.76 Testosterone propionate has been used to prevent es- trus, especially in racing Greyhounds, for up to 5 years at an oral dosage of 25 mg per week. Many of these have returned to normal reproductive status. Clitoral hy- pertrophy and vaginitis are frequent side effects with cli- toral hypertrophy being so prominent in some Grey- hound bitches that they are referred to as “tail-light- ers.”16 Other side effects such as premature epiphyseal closure if immature bitches are treated and urogenital an- omalies, hermaphrodism in female pups born to treated pregnant bitches, makes testosterone objectable. The oral administration of 2 to 4 drops of a 1% so- lution of pilocarpine has been reported to suppress estrus in bitches, but the action and method of control has not been reported or investigated.16,28 Vaginal devices (“Option I”) have been marketed and used as a contraceptive but since have been discontinued because of expense, various sizes needed, problems with fitting, poor retention, vaginal discharges, rejection and loss, unacceptable failure rates and dissatisfaction on the part of owners and veterinarians. Immunization as described for population control and use in either bitches or studs may have value for tem- porary estrus suppression and control of spermatogenesis through LH or GnRH control, but a great deal of re- search is needed to find the right antigens, protocols for repeatibility of effect, evidence of any deleterious effects and overcome the disadvantage of the need for irritating adjuvants for antibody production. Luteinizing hormone, LH, given during proestrus has been reported as a possible antifertility drug for that cycle (20 units/kg-IV). This is repeated once again 2-3 days after the first injection if proestrus has not subsided. The effect is supposed to cause premature luteinization of follicles instead of stimulating further follicular growthINFERTILITY IN THE BITCH AND QUEEN 691 and maturation. The effect would depend on timing of administration so that follicles are young enough to en- sure premature luteinization and not ovulation. This would be similar to reports of premature luteinization of folli- cles when too early attempts are made to induce estrus in bitches using PMSG or FSH and following with LH or HCG resulting in preovulatory luteinization instead of ovulation.28 For years estrogens have been used as post-breeding, “day after,” misalliance and antinidatory treatment in bitches that were mismated. A variety of estrogens have been used with little scientific and experimental evi- dence of their effectiveness and side effects. Diethylstil- besterol, before it was removed from use in the United States, was the hormone of choice and continues to be used in many countries where it is still legal. Since then, several of the longer acting available estrogens are being used, especially estradiol cypionate (ECP) followed by estradiol valerate or benzoate and finally estrone. Few statistics are quoted for their success and/or for failure. One report revealed, that 1-2 mg of ECP given intra- muscularly the first 5 days following mating had pre- vented conception in 537 consecutive cases.65 Several failures had resulted when ECP was given later than 5 days after mating. It was indicated that these animals should receive a second injection of ECP five days after the first or receive oral diethylstilbesterol tablets at the rate of 1 to 2 mg daily for five days. Estrogens usually delay the transit of zygotes in the oviduct and may affect the development of zygotes directly (zygotoxic).103 Holst and Phemister have shown that oocytes remain in the oviduct until one to three days after the vaginal smear is no longer fully cornified or the beginning of metestrus/diestrus.55,56 Since a bitch can accept a male over a long period of time, late proestrus to early met- estrus/diestrus, it is very important that vaginal smears be made and the cytology studied for stage of cycle when the bitch had coitus and judge the most appropriate time for “mismating” with estrogen therapy. Concannon has given excellent guidelines on the use of ECP until more scientific evidence is presented for its use in misalliance. If the smear is still of estrous type, only a most conser- vative dose of ECP should be considered (0.1 mg/10 lbs, max. of 0.5 mg); if the smear is not fully cornified or late proestrus, a delay of 1 to 3 days before estrogen administration should be considered because the bitch probably has not ovulated. Remember, semen in the uterus can be fertile for 5-6 days or possibly to 11 days or at least until metestrus.41 If the vaginal smear is very late estrus or early metestrus, then an intermediate or less conservative dose can be given (0.2 mg/lb for a total of 1.0 mg). These doses are based on clinical impressions and published reports.28,58 Estrogen will lengthen the es- trus or attractiveness and if given in proestrus may do little but delay the LH surge and the bitch eventually reaches estrus and may become pregnant. Bitches must be confined during this prolonged acceptance period. Bitches that have received the long acting estrogens are more prone to developing pyometra in 2 to 6 weeks, which is frequently an “open” pyometra with a muco- purulent or mucosanguinous vulval discharge. Excessive estrogens can cause aplastic anemia, thrombocytopenia and a hemorrhagic syndrome with a rapid course and death.10 66 Concannon has reported on the several forms of estrogens used for mismating bitches with no scien- tific data on safety, side effects or effectiveness (Chart VII).28 An antiestrogenic compound, 3-4-trans-2,2-dimethyl- 3-phenyl-3-4-p-(B-pyrolidinoethoxy)-phenyl-7-methoxy- chroman, devoid of progestational, androgenic, or an- tiandrogenic activity, was reported to be effective when given 24 hours after mating to prevent pregnancy. It can be given orally or parentrally in a single dose to interfere with ovum development.103 Administration of two compounds, (L10492) and (LI0503) prevented pregnancy in bitches most effec- tively when administered at 20 days postbreeding, about the time of nidation. A single dose of 100-150 mg/kg was administrated. When given at 45—48 days, they caused resorption in 2 bitches and expulsion of macerated fe- tuses 1 week past the due date. Undesirable side effects include loss of appetite and diarrhea for 3-8 days be- ginning 1-3 days after the start of treatment.103 These drugs seem to work on the utero-placental complex di- rectly and do not influence pituitary or ovarian function since plasma progesterone levels remain normal post treatment. Termination of pregnancy after diagnosis has also become an alternative choice after an undesirable mat- ing. Several drugs have been used including estrogen implants, prostaglandins, bromoergocryptine (an ergot alkaloid) and dexamethasone. At midpregnancy, silastic capsules containing crystal- line estradiol, sufficient to maintain blood levels of es- tradiol of proestrous level, were inserted subcutane- ously. All bitches treated either resorbed or aborted their litters.28 Adrenal corticosteroids have the potential to terminate established pregnancies in the bitch. One study reported on the use of dexamethasone at 5 mg twice a day for 10 days with intrauterine death and resorption when started at 30 days; and birth of dead fetuses at days 55 to 59 when treatment started at day 45.6 Bromoergocryptine, an ergot alkaloid, reduces prolac- tin secretion as a dopamine agonist, is luteolytic and when administered to bitches at 0.1 mg/kg/day for 6-10 days692 VETERINARY OBSTETRICS Dosage (per bitch) Comment Reference Repositol Stilbestrol (DES) 0.4 mg/kg Within 36 to 48 hours Mann, 1971 1.0 mg/kg Safety questioned Jochle, 1975 1.1 mg/kg Within 5 days Merck Veterinary Manual, 5th ed., 1980 2.0 mg/kg Maximum dosage 25 mg Jackson and Johnston, 1980 Estradiol Cypionate (ECP) 0.25 mg/30 kg Maximum dosage 0.5 mg Okin et al., 1976 0.125 to 1.0 mg Jackson and Johnson, 1980 0.25 mg For toy breeds Merck Veterinary Manual, 5th ed., 1980 0.5 to 2.0 mg Within 5 days Merck Veterinary Manual, 5th ed., 1980 1.0 to 2.0 mg Within 5 days Jochle, 1975 1.0 to 2.0 mg If after 5 days Jochle, 1975 Estradiol Valerate 3.0 to 7.0 mg Once, days 4 to 10 Jochle, 1975 Estradiol Benzoate 0.5 to 3.0 mg every other day Three injections, days 4 to 10 Jochle, 1975 Estrone 2.0 to 5.0 mg Within 5 days Okin et al., 1976 Chart VII. Antinidatory Injectable Estrogen Treatments Indicated for Mismated Bitches Without Data on Safety or Side Effects. Refs. (1) Mann, 1971; (2) Jochle, 1975; (3) The Merck Veterinary Manual, 5th ed., 1980; (4) Jackson and Johnston, 1980; (5) Okin et al., 1976. (Courtesy and with permission of P. W. Concannon and publisher, W. D. Saunders, Co.28) it terminated pregnancy in 60% of bitches studied. Nau- sea, depression, anorexia are some of the deleterious side effects reported.27 Prostaglandins of the F series, PGF2a are used in the bitch for their luteolytic and smooth muscle effect, re- sulting in cervical dilatation and uterine contraction. This effect causes luteolysis and abortion in midpregnancy; approximately from 30 days to parturition in the bitch. The current popular clinical use of PGF2a is to treat pyometra—endometritis in the bitch and queen. Pros- taglandin analogues have also been studied in the bitch to cause luteolysis and abortion. The right analogue could become a very important drug for small animal use be- cause they usually are much more potent and long acting with lower dosage, and less side reactions. The median subcutaneous lethal dosage for PGF2a in the bitch was determined to be 5.13 mg/kg.112 Clinical signs of side reactions and toxicosis include excessive salivation, vomiting, diarrhea, hypemea, ataxia, urina- tion, anxiety, and pupillary dilatation, then constriction. Severity of side effects are dose dependent. At low dos- ages, defecation is more frequent, while at intermediate dosages, hypemea, anxiety, hypersalivation, vomiting and defecation have been observed. Higher doses have caused ataxia and slight depression.90 The clinical dose range in the bitch has been from 0.02 to 1.0 mg/kg or 20 ug to 1000 ug/kg administered usually intramuscular or subcutaneously.32 90 Side reactions are seen in 20 to 120 minutes post in- jection. Death in animals given lethal doses range from 2 to 12 hours post injection.112 Bitches seem to adapt to PGF2a with side effects diminishing by the fourth or fifth treatment. Prostaglandin F2a or analogues should not be used in dogs with asthma, liver, kidney or cardiac prob- lems. Early researchers thought that PGF2a was not luteolytic in the dog but did cause temporary lowering of serum progesterone levels for a brief time.3'7'63 Concannon was the first to show that 20 ug/kg every 8 hours or 30 ug/ kg every 12 hours for 3 days caused abortion in 4 of 7 bitches started on treatment on days 33 to 53 of gesta- tion, with abortion occurring 56 to 80 hours after initial treatment.32 Progesterone plasma levels were 0.6 to 1.4 ng/ml when abortion occurred. The 3 bitches that did not abort had a mean low value of 2.1 ng/ml of plasma progesterone during PGF2a treatment beginning on day 31 to 40 of gestation. Their plasma progesterone re- covered to 5-10 ng/ml and were maintained until nor-INFERTILITY IN THE BITCH AND QUEEN 693 mal prepartum decline. In this study, 8 nonpregnant bitches in mid or late luteal phase were also treated and all 8 had complete luteolysis with low anestrous baseline plasma progesterone levels afterwards. Two nonpreg- nant bitches in early luteal phase (days 5 and 20) were also treated and plasma progesterone levels were not drastically altered. Concannon also found a transient fall in rectal tem- perature within 15 minutes and maximal at 45-60 min- utes postinoculation that averaged 1.39 °C. No change in temperature was seen in ovariectomized bitches treated with PGF2a. It was concluded that hypothermia was due to the 20 to 45 percent fall in plasma progesterone levels within the 15 minute period postinoculation of PGF2a. Ten mated bitches were given 250 ug/kg of PGF2a bid; 5 between the first and fifth days of metestrus and 5 between 31 and 35 days of metestrus.90 Early metes- trus dogs were not affected and appeared the same as the 5 nontreated controls, whereas all 5 in midgestation had complete luteolysis, hypothermia following the initial in- jection of PGF2a and abortion following the fourth to eighth injection. Prostaglandin analogues, fluprostenol and clopros- tenol (“Equimate” and “Estrumate,” respectively, Im- perial Chemical Industries, U.K.) were administered to 42 Beagle bitches at gestational periods of 4 to 35 days at doses from 10-40 ug/kg.57 A slow releasing formula of both analogues (48 to 72 hours) and a 24 hour release intravaginal device of both analogues showed minimal acceptable side effects compared to the aqueous mar- keted form of cloprostenol. Sustained depression of plasma progesterone levels and pregnancy termination were seen in 6 of 22 bitches (27%) treated before day 25 of gestation and 16 of 20 bitches (80%) treated on or after day 25. An interesting effect was that 2 bitches whose pregnancies or corpora lutea were terminated at 14 days by the 40 ug/kg cloprostenol injection showed clinical estrus 10 to 14 days after treatment with normal mature ovarian follicles at necropsy. This suggests that a bitch could possibly be remated in a few weeks after correction of a misalliance in the first 2 weeks instead of having to wait until the next cycle at 4 to 12 months. Eleven pregnant bitches were treated with a single subcutaneous injection of 20 ug/kg of synthetic pros- taglandin analogue (TPT) in an aqueous buffer.133 Five bitches treated between days 30-43 of pregnancy aborted 5.4 ± 1.4 days following treatment. Two of 4 bitches treated on days 20-22 of gestation continued to normal term, while the other 2 appeared to resorb their fetuses following diagnosis by palpation on day 28. Two others treated on day 9 had normal pregnancies. Further work by this group utilized bitches on days 20-22 of pregnancy and administered TPT subcutane- ously in different treatments: minipump at a rate of 10 ug per hour for either 24 or 48 hours, single injection of 200 ug in either aqueous, or polyethylene glycol 400 or the methyl ester of TPT in polyethylene glycol 400.134 All treatments caused abortion or resorption with the best treatments being those that had the longest administra- tion of analogue; 48 hours minipump, 5/6 aborted and the methyl ester of TPT, 3/4 aborted. Eight bitches were given 5 to 30 mg of PGF2a on day 5-17 of pregnancy which resulted in a marked tempo- rary decrease in progesterone levels and in those given 20 mg or more deaths occurred in some or all of the embryos after implantation. Seven bitches given 5-50 mg of PGF2a in 25-51 days of pregnancy resulted in only one animal given 20 mg of PGF2 having a pre- mature birth at day 51. All others were normal. Bitches given 5-10 mg of PGF2a on days 55-58 of pregnancy resulted in induced parturition in 38.1 hours. In this study, side effects of PGF2a were intense in bitches given 10 mg or more of PGF2a and those treated during pregnancy returned to estrus about 40 days earlier than untreated control bitches.130 The above research indicates that the early corpora lu- tea are quite resistant to exogenous prostaglandin until midgestation, 25 to 30 days to term. The author has aborted 6 mismated bitches. Their ages ranged from 8 months to 5 years, gestations ranged from 31 to 60 days, and a range of 2 to 8.5 days of PGF2a therapy was needed to cause abortion. Treatment consisted of 25 to 50 ug/ kg of PGF2a (Upjohn Co., Kalamazoo, MI) intramus- cularly, given twice a day. The lower dose was given the first day or two to observe the severity of side effects and to relax the cervix. These bitches showed nesting signs 24-48 hours prior to abortion. Vaginoscopic ex- amination of 3/6 bitches revealed daily changes in the anterior vagina with increasing edema of the vaginal and cervical folds, fluid, and dilation of the cervix 24 to 48 hours prior to abortion. The two late gestation bitches, 57 to 60 days of gestation, aborted at 2 and 4.5 days of treatment, respectively, and both had live pups. The bitch at 31 days of gestation aborted 3 pups 6 days post initial treatment and abortion appeared to be complete. She was given 10 i.u. of oxytocin intramuscular the following day to enhance uterine involution. Two weeks later, two re- tained viable fetuses were noted on palpation and radi- ographs. The bitch whelped 2 normal live pups and has had 3 normal litters since. All bitches returned to estrus at normal intervals. One bitch had prolonged postpartum hemorrhage for 6 weeks that was diagnosed as subin- volution of placental sites. All bitches showed varying individual slight side effects the first 15 to 60 minutes post injection including increased salivation, diarrhea, emesis, and panting.694 VETERINARY OBSTETRICS The above work shows that PGF2a can be used to cause abortion in healthy bitches from midgestation to term. A dose range of 25-250 ug/kg, given intramuscular, BID to effect can be used. Hospitalization and close obser- vation are necessary and the later the stage of gestation the quicker the effect. More research is needed on the analogues, different routes of administration such as the intravaginal route, possible early gestation luteolysis and early return to estrus. Induction of estrus and ovulation with successful breeding is desired at times for convenience of a timed whelping for companion dogs, show or performance bitches, research dogs, infertile bitches with a history of never expressing estrus or having an abnormal long in- terestrous period (usually >12 months). The infertile bitch with this history should have a physical and reproductive tract examination, thyroid function test for hypothyroid- ism, vaginal cytology and a blood serum progesterone test to determine true anestrus or a possible missed cycle. Gonadotrophins, follicle stimulating hormone, (FSH), pregnant mare serum gonadotrophin, (PMSG), lutein- izing hormone, (LH), and human chorionic gonadotro- phin (HCG) and gonadotrophin releasing hormone, (GnRH), estrogens and some human fertility drugs have all been used, in different regimes, combinations and dosages with varying success. Several have induced es- trus with or without ovulation, normal or degenerate ova, and few have been highly successful in producing nor- mal pregnancies or having repeatable results. The in- duction of estrus in the queen is much more predictable than in the bitch 2I-43'44'46'60'64'67'68’86-89-102'103'118'129-140-141 The use of PMSG daily, utilizing either 250 IU/day, 500 IU/day or 20 IU/kg/day for 10 days with 500 IU of HCG combined on the last day of PMSG treatment resulted in successful induction of estrus and ovulation in 14/25 bitches.118 Another researcher, used these same regimes for 8 days, with successful induction of estrus and ovulation in 6/6 bitches.103 The undesirability of causing premature luteinization of follicles with HCG is important to consider. The 10 day interval from the start of treatment is about the normal interval for follicular growth in the dog prior to the preovulatory LH surge.103 Another group reported on the use of 20-50 IU/kg/day, IM for 9 days or 500 to 1000 IU/day, I.M., of PMSG, two treatments, six days apart, followed by either 500- 1000 IU/day, I.M. on the first and second day of estrus or 2 treatments of GnRH, 50 ug, IM, each six hours apart on the first day of estrus. Bitches treated with these regimes ovulated 60% of the time. Ovulation was de- termined by serum progesterone increase or pregnancies following artificial insemination.19,21 This group found PMSG more effective than FSH-P. These treatments ap- pear to work in the truly anestrous bitch and appear to be more effective when administered intramuscular in- stead of subcutaneously. If the bitch is in metestrus/ diestrus with progesterone levels above basal levels, then pretreatment with either estrone or estradiol is recom- mended. Pretreatment with 100 to 300 ug of estrone per day for 5 to 6 days produced vulval bleeding. This was followed by the regime of PMSG and HCG previously mentioned and resulted in normal pregnancies. Either PMSG or FSH-P if used indiscriminately can cause cys- tic follicular degeneration. Induced bitches should be bred every other day for three matings starting with the first day of acceptance. In another study, 4/8 bitches had fer- tilized ova or pregnancies when 200 IU of PMSG and 500 IU of HCG IM was followed by 500 IU of HCG 3 days after the vaginal smear was fully comified.129 Wright induced estrus in eleven anestrous bitches with 110 IU/ kg of PMSG given once weekly until estrus occurred or until 3 treatments had been given. Estrus occurred in 8 of 11 bitches. Three of 8 received 500 IU of HCG on the first day of estrus resulting in 7/8 bitches ovulating with those receiving HCG having a better ovulation rate (88.6% vs 46.1%). In a later study, 8 anestrous bitches were given 250 IU of PMSG per day until estrus oc- curred, or till 20 days of treatment. Then 500 IU of HCG was given on the first day of estrus or on day 21. Six of 8 ovulated, 3 with 100% ovulation rates; two showed estrus at 14 days, the rest went to day 20.140,141 Several regimes using either PMSG and HCG, sheep pituitary gonadotrophin (“Vetrophin”) or equine pituitary gonad- otropin (“Pitropin”) are reported with about 85% normal dogs induced at the proper time and 65% of bitches with prolonged anestrus showing good standing estrus after treatment with expectation of normal conception and lit- ter rates.46 One FSH and LH scheme was reported to cause fol- licular growth but not ovulation.89 Another method, uti- lized 1 mg diethylstilbesterol oral tablets daily for 4 days and on day 8 twice daily injections of 2 mg FSH sub- cutaneously, until the vaginal epithelium was 90% cor- nified (about 8 days of FSH) followed by 500 IU of HCG I.V. Most bitches accepted the male 48 to 72 hours post HCG. This regime has produced small litters in bitches with prolonged anestrus but not in normal anestrous bitches.85 The author prefers a method of weekly 25 mg FSH injections, I.M., in truly anestrous bitches, until vulvar enlargement or a bloody vulval discharge oc- curs.67 The author only gives FSH for up to 5 treatments. If estrus does not occur then one month’s rest and repeat the regime for another five weekly treatments. Most bitches will show estrus after the second and third FSH injection. At each injection day, vaginal cytology is per- formed for evidence of increased estrogens and follicular development. Once proestrus is determined, then everyINFERTILITY IN THE BITCH AND QUEEN 695 day vaginal cytology is taken and the bitch is bred at estrus every 48 hours for 3 or 4 times. 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(1976) Serum Profiles of Lutenizing Hormone, Progester- one and Total Estrogen During the Canine Estrous Cycle, Theriog., 5, 4,175-187. 78. Nassar, R. and Mosier, J. E. (1980) Canine Population Dy- namics: A Study of the Manhattan, Kansas, Canine Popula- tion, Am. J. Vet. Res., 42, 1798-1803. 79. Nett, T. M. and Olson, P. N. (1983) Reproductive Physiology of Dogs and Cats, in Textbook of Veterinary Internal Medi- cine, 2 ed, vol 2, W. B. Saunders Co., Philadelphia, Pa., 1698- 1710. 80. N.N. (APHIS-USDA) (1981) Unwanted Dogs and Cats Create Problems, Canine Practice, 8, 1, 7-8. 81. N.N. (1976) Summary and Conclusion: National Conference on Dog and Cat Control, JAVMA, 168, 12,1125-1134. 81a. Okkens, A. C., Dieleman, S. J. and Goog, I. V. D. (1981) Ovariohysterectomy in Dogs and Subsequent Gynecological Complications, Tijdschrift voor Diergeneeskunde, 106, 1142. 82. Olson, P. N., Bowen, R. A., Behrendt, M. D., Olson, J. D., and Nett, T. M. (1982) Concentrations of Reproductive Hor- mones in Canine Serum Throughout Late Anestrus, Proestrus, and Estrus, Biol, of Reprod., 27, 1196-1206. 83. Olson, P. N., Bowen, R. A., Behrendt, M. D., Olson, J. D., and Nett, T. M. (1984) Validation of Radioimmunoassy to Measure Prostaglandins F, and E2 in Canine Endometrium and Plasma, Am. J. Vet. Res., 45, 1,119-124. 84. Olson, P. N., Bowen, R. A., Behrendt, M. D., Olson, J. D., and Nett, T. M. (1984) Concentrations of Testosterone in Ca- nine Serum During Late Anestrus, Proestrus, Estrus and Early Diestrus, Am. J. Vet. Res., 45, 1,145-147. 85. Olson, N. P., Bowen, R. A., Behrendt, M. D., Olson, J. D. and Nett, T. M. (1984) Concentrations of Progesterone and Luteinizing Hormone in the Serum of Diestrous Bitches Before and After Hysterectomy, Am. J. Vet. Res., 45, 1,149-158. 86. Olson, P. N., Nett, T. M. and Soderberg, S. F. (1983) Infer- tility in the Bitch, in Current Veterinary Therapy VIII Small Animal Practice, ed. R. W. Kirk, publ. W. B. Saunders Co., Philadelphia, Pa., 925-931. 87. Olson, P. N., Thrall, M. A., Wykes, P. M., Husted, P. W., Nett, T. M. and Sawyer, H. R. (1984) Vaginal Cytology. Part I. A Useful Tool for Staging the Canine Estrous Cycle, The Compendium of Continuing Education, 6, 4,288-297. 88. Olson, P. N., Thrall, M. A., Wykes, P. M., Husted, P. W., Nett, T. M. and Sawyer, H. R. (1984) Vaginal Cytology. Part II. Its Use in Diagnosing Canine Reproductive Disorders, The Compendium on Continuing Education, 6, 5,385-390. 89. Paisley, L. G. and Fahning, M. L. (1977) Effects of Exoge- nous Follicle-Stimulating Hormone and Luteinizing Hormone in Bitches, JAVMA, 171, 2,181-185. 90. Paradis, M., Post, K. and Mapletoft, R. J. (1983) Effects of Prostaglandin F2 on Corpora Lutea Formation and Function in Mated Bitches, The Canad. Vet. Jour., 24, 239-242. 91. Phemister, R. D., Holst, P. A., Spano, J. S. and Hopwood, M. L. (1973) Time of Ovulation in the Beagle Bitch, Biol, of Reproduction, 8, 74-82. 92. Pineda, M. H. (1973) Immunologic Control of Reproduction in Dogs, in Proc. Ann. Conf. Amer. Vet. Soc. for Study of Breed Soundness, Davis, Calif., 74-84. 93. Pineda, M. H., Kaimer, R. A. and Faulkner, L. C. (1973) Dorsal Median Postcervical Fold in the Canine Vagina, Am. J. Vet. Res., 34, 1,1487-1491. 94. Reimers, T. J. and Lein, D. H. (1980) Patterns of Reproduc- tive Hormones in the Bitch, in Satellite Symposium on Dis- eases of Small Animals, XI International Congress on Disease of Cattle, Tel Aviv, Israel, 31-36. 95. Reimers, T. J., Phemister, R. D. and Niswender, G. D. (1978) Radioimmunological Measurement of Follicle Stimulating Hormone and Prolactin in the Dog, Biol, of Reprod., 19, 673- 679. 96. Rendano, V. T. (1983) Radiographic Evaluation of Fetal De- velopment in the Bitch and Fetal Death in the Bitch and Queen, in Current Veterinary Therapy, VIII, Small Animal Practice, ed. R. W. Kirk, publ. W. B. Saunders Co., Philadelphia, Pa., 947-951. 97. Rendano, V. T., Lein, D. H. and Concannon, P. W. (1984) Radiographic Evaluation of Prenatal Development in the Bea- gle. Correlation with Time of Breeding, LH Release and Par- turition, Veterinary Radiology, 25, 3,132-141. 98. Rozzel, J. F. (1975) Genital Cytology of the Bitch, Veterinary Scope, by the Upjohn Company, Kalamazoo, Mich., 19, 1,2- 15. 99. Schneider, R. (1980) Overpopulation of Dogs and Cats: De- mographic Aspects, in Current Therapy in Theriogenology, ed D. A. Morrow, publ. W. B. Saunders Co., Philadelphia, Pa., 669-673. 100. Schutte, A. P. (1967) Canine Vaginal Cytology, Small An. Pract., 8, 301. 101. Scott, D. W. and Concannon, P. W. (1982) Gross and Mi- croscopic Changes in the Skin of Dogs with Progestogen-In- duced Acromegaly and Elevated Growth Hormone Levels, J.A.A.H.A., 19, 523-527. 102. Shille, V. M. and Stabenfeldt, G. H. (1980) Clinical Repro- ductive Physiology in Dogs, in Current Therapy in Theriogen- ology, ed. D. A. Morrow, publ. W. B. Saunders Co., Phila- delphia, Pa., 571-574. 103. Shille, V. M. and Stabenfeldt, G. H. (1980) Current Concepts in Reproduction of the Dog and Cat, Advances in Veterinary Science and Comparative Medicine, 24, 211-243. 104. Shivers, C. A., Sieg, P. M. and Kitchen, H. (1981) Pregnancy Prevention in the Dog: Potential for an Immunological Ap- proach, J.A.A.H.A., 17:823. 105. Simmons, J. H., and Hammer, C. E. (1973) Inhibition of Es- trus in the Dog with Testostrone Implants, Am. J. Vet. Res., 34, 11,1409-1419. 106. Smith, M. S. and McDonald, L. E. (1974) Serum Levels of Lutenizing Hormone and Progesterone During the Estrous Cycle, Pseudopregnancy and Pregnancy in the Dog, Endocrinology, 94, 404-412. 107. Soderberg, S. F. and Olson, P. N. (1983) Abortifacient, in698 VETERINARY OBSTETRICS Current Veterinary Therapy VIII Small Animal Practice, ed. R. W. Kirk, publ. W. B. Saunders Co., Philadelphia, Pa., 945-946. 108. Sokolowski, J. H. (1973) Reproductive Features and Patterns in the Bitch, J.A.A.H.A., 9, 71-81. 109. Sokolowski, J. H. (1977) Reproductive Patterns in the Bitch, Symposium on Reproductive Problems, Veterinary Clinics of North America, 7, 1,653-667. 110. Sokolowski, J. H. (1978) Evaluation of Estrous Activity in Bitches Treated with Mibolerone and Exposed to Adult Male Dogs, JAVMA, 173, 983-984. 111. Sokolowski, J. H., and Geng, S. (1977) Biological Evaluation of Mibolerone in the Female Beagle, Am. J. Vet. Res., 38, 9,1371-1376. 112. Sokolowski, J. H. and Geng, S. (1977) Effect of Prostaglandin F2—THAM in the Bitch, JAVMA, 170, 536-37. 113. Sokolowski, J. H. and Kassen, C. W. (1978) Effects of Mi- bolerone on Conception, Pregnancy, Parturition, and Offspring in the Beagle, Am. J. Vet. Res., 39, 5,837-839. 114. Sokolowski, J. H. and Van Ravenswaay, F. (1976) Effects of Melengestrol Acetate on Reproduction in the Beagle Bitch, Am. J. Vet. Res., 37, 943-945. 115. Sokolowski, J. H., Stover, D. G., and Van Ravenswaay, F. (1977) Seasonal Incidence of Estrus and Interestrous Interval for Bitches of Seven Breeds, JAVMA, 171, 3,271-273. 116. Sokolowski, J. H., Zimbelman, R. G. and Goyings, L. S. (1973) Canine Reproduction: Reproductive Organs and Related Struc- tures of the Nonparous, Parous, and Postpartum Bitch, Am. J. Vet. Res., 34, 8,1001-1013. 117. Stabenfeldt, G. H. and Shille, V. M. (1977) Reproduction in the Dog and Cat, in Reproduction in Domestic Animals, ed. H. H. Cole and P. T. Cupps, Academic Press, New York. 499-527. 118. Thun, R., Watson, P. and Jackson, G. L. (1977) Induction of Estrus and Ovulation in the Bitch, Using Exogenous Gonad- otropins, Am. J. Vet. Res., 38, 4,483-486. 119. Tsutsui, T. (1973) Studies on the Physiology of Reproduction in the Dog II. Observation on the Time of Ovulation, Japanese Joum. of An. Reprod., 18, 4,137-142. 120. Tsutsui, T. (1975) Studies on the Reproduction in the Dog V. On Cleavage and Transport of Fertilized Ova in the Oviduct, Japanese J. of An. Reprod., 21, 2,70-75. 121. Tsutsui, T. (1975) Studies on the Reproduction in the Dog VI. Ovulation Rate and Transuterine Migration of the Fertilized Ova, Japanese J. of An. Reprod., 21, 3,98-101. 122. Tsutsui, T. (1975) Studies on the Reproduction in the Dog. Ill Observations of Vaginal Smears in Estrous Cycle, Japanese J. of An. Reprod., 21, 1,37-42. 123. Tsutsui, T. (1976) Studies on the Reproduction in the Dog. VII. Implantation of Fertilized Ova, Japanese Jour. of. An. Reprod., 22, 2,44-49. 124. Tsutsui, T. (1981) Process of Development of Uterus, Fetus, and Fetal Appendices during Pregnancy in the Dog, The Bul- letin of the Nippon Veterinary and Zootechnical College, 30, 175-183. 125. Tsutsui, T. (1982) Peripheral Plasma Gestagen Levels during the Estrous Cycle and Pregnancy in the Bitch, The Bulletin of the Nippon Veterinary and Zootechnical College, 31, 150-155. 126. Tsutsui, T. (1983) Effects of Ovariectomy and Progesterone Treatment on the Maintenance of Pregnancy in Bitches, Jpn. J. Vet. Sci., 45, 1,47-51. 127. Tsutsui, T. and Shimizu, T. (1973) Studies on the Physiology of Reproduction in the Dog. I. Duration of Estrus, Japanese Joum. of An. Reprod., 18, 4,132-136. 128. Tsutsui, T. and Shimizu, T. (1975) Studies on the Reproduc- tion in the Dog IV. On the Fertile Period of Ovum after Ovu- lation, Japanese J. of An. Reprod., 21, 2,65-69. 129. Tsutsui, T., Shimizu, T., Shimizu, K. and Matsukaki, M. (1982) Induction of Estrus and Ovulation in the Bitch, Application of PMSG and HCG., The Bulletin of the Nippon Veterinary and Zootechnical College, 31, 143-149. 130. Tsutsui, T., Takatani, H., Hirose, O. and Yamauchi, M. (1982) Effects of Prostaglandin F2 on Implantation and Maintenance of Pregnancy in the Dog, The Japanese Joum. of Vet. Sci., 44, 3,403-410. 130a. Van Arkel, B. (1984) Personal Communication on Cell Type. 131. Van Os, J. L. and Oldenkamp, E. P. (1978) Oestrus Control in Bitches with Proligestrone, a New Progestational Steroid., J. Small An. Pract., 19, 521-529. 132. Van Os, J. L. (1981) Oestms Control and the Incidence of Mammary Nodules in Bitches, a Clinical Study with Two Pro- gestagens, Vet. Quarterly, 3, 46-56. 133. Vickery, B. and McRae, G. (1980) Effect of a Synthetic Pros- taglandin Analogue on Pregnancy in Beagle Bitches, Biol, of Reprod., 22, 438-442. 134. Vickery, B. H., McRae, G. I., Kent, J. S. and Tomlinson, R. V. (1980) Manipulation of Duration of Action of a Synthetic Prostaglandin Analogue (TPT) Assessed in the Pregnant Bea- gle Bitch, Prostaglandins and Medicine, 5, 93-100. 135. Wildt, D. E. (1977) Reproduction Control in the Dog and Cat: An Examination and Evaluation of Current and Proposed Methods, J.A.A.H.A., 13, 223-231. 136. Wildt, D. E., Chakraborty, P. K., Panko, W. B., and Seager, S. W. J. (1978) Relationship of Reproductive Behavior, Seram Luteinizing Hormone and Time of Ovulation in the Bitch, Biol, of Reprod., 18, 561-570. 137. Wildt, D. E., Levinson, C. J. and Seager, S. W. J. (1977) Laparoscopic Exposure and Sequential Observation of the Ovary of the Cycling Bitch, Anat. Rec., 189, 443. 138. Wildt, D. E., Seager, S. W. J., and Bridges, C. H. (1981) Sterilization of the Male Dog and Cat by Laparoscopic Occlu- sion of the Ductus Deferen, Am. J. Vet. Res., 42, 1888-1897. 139. Wildt, D. E., Seager, S. W. J. and Chakraborty, P. K. (1981) Behavioral, Ovarian and Endocrine Relationships in the Puber- tal Bitch, Joum. of An. Sci., 53, 1,182-191. 140. Wright, P. J. (1980) The Induction of Oestms and Ovulation in the Bitch Using Pregnant Mare Seram Gonadotrophin and Human Chorionic Gonadotrophin, Austral. Vet. J., 56, 137— 140. 141. Wright, P. J. (1982) The Induction of Oestms in the Bitch Using Daily Injections of Pregnant Mare Semm Gonadotro- phin, Austral. Vet. J., 59, 123-124. Reproductive Physiology of the Queen Puberty in queens usually occurs between 7 and 12 months of age depending upon their nutritive state, breed, freedom from disease and season of the year that they are bom. Queens may have their first estrus as early as 4 months of age if they obtain the minimal body weight of 2.3 to 2.5 kg or they may be as late as 21 months ofINFERTILITY IN THE BITCH AND QUEEN 699 age. If the normal pubertal age and weight are attained during the anestrous period of October to December, cy- cling usually begins in January or February following birth. If pubertal weight is attained in early or late sum- mer then an early pubertal estrus may take place.48 Males usually reach puberty at a minimal body weight of 3.5 kg which is attainable at 9 months of age. (See pages 409-411.) Purebred cats may reach puberty later than non-pure- bred cats. Cats that are housebound versus a free-roam- ing environment, especially those that are housed with- out other cats, may reach puberty later.18 A British study of several breeds showed that puberty on the average was seen between 9-10 months of age, with consider- able breed difference; Himalayans or colorpoints were the oldest, average 13 months (9-18 mo.), while Bur- mese were the youngest, average 7.7 months (4.5-15 mo). They noted that puberty was affected by age of kittens at weaning, time of year litter is bom, natural or artificial increase of daylight and the breed of cat.30 The reproductive life of the cat is long, with both toms and queens known to continue breeding for 14 or more years, with a period of 8 to 10 years most common for continuous breeding of a queen. (See page 110, 111) Litter size is reduced with age. Most queens will have two litters of 2 to 6 kittens with an average of 4 each per year. Some will produce 3 litters per year. Siamese cats or their crosses have slightly larger litters (average 6). First litters of pubertal breedings are usually small and rearing is less successful.34,38 The estrous cycle—The queen is seasonably polyes- trous, a long day breeder, similar to the mare.29 Breed- ing season in temperate zones usually begins 20 to 60 days after the winter solstice and may end any time after the summer solstice. In the northern temperate zone, breeding usually begins in January or February and ex- tends through the early part of September with a range of August to October or early November.18,22 The first cycle usually will occur between January and March, the second from April to early July, and the last during late July through early September.18 The author has fre- quently noted the first cycles of the year will be during a January or February thaw in free-ranging cats. Again, like the mare, kittens can be bom in any month of the year.30 In conditions of artificial light or combinations of natural and artificial light, where queens receive 12L: 12D,. 14L: 10D, or 16L:8D, many will cycle throughout the year. Fourteen to 16 hours of light versus 12 hours will increase the percentage of cycles. Even in colonies with artificial light, some queens will experi- ence a winter anestrus.22 Winter anestrus was reported in 90% of long-haired cats (aver. 4 mo., 2-9 mo.) from September to January, whereas 60.8% of shorthairs re- mained cyclic throughout the year. More queens of all breeds confined indoors remained cyclic, while those al- lowed or confined outside, usually become anestrous.30 Tom cats will show depressed sexual activity during the winter period.48 The vomeronasal organ, which is a blind pouch dorsal to the hard palate and communicates with the nasal and oral cavities via the nasopalatine duct that opens behind the incisors, is thought to be used to perceive sexual pheromones from urine and glands, possibly vaginal and vulvar secretions and the scent marks in the environ- ment.24 Odor produced by intact tomcats and valeric acid, or a mixture of fatty acids, produced by the estrous queen act as sexual pheromones. Tomcat odor released during urine spraying for territorial marking is androgen-depen- dent and disappears after castration. Its source is uncer- tain, but may be part of a lipid component of the urine and/or it may be produced by the anal glands. During estrus, valeric acid is present in vaginal secretions. Tom- cats may show an open-mouth flehmen response when sniffing urine, but anosmic sexually experienced males continue to mate. In tomcats, the odor of valeric acid induces a restless and lively searching reaction, but no sexual connotations, while sexually mature intact queens respond by exhibiting typical estrous behavior, thus it may induce or facilitate estrus in other queens.4 Catnip leaves contain nepetalacetone which produced a characteristic behavior response simulating the antics of estrous queens. This is an olfactory response via the vomeronasal organ but is considered not a feline sex pheromone or pheromone-mimic but a hallucinogen which induces pleasurable behavior in cats, independent of sex or the presence of gonads. This response appears to be inherited as an autosomal dominant trait.4 Cats utilize 3 methods of territorial marking including scratching; leaving visual marks and odor marks from foot gland secretion; the cat’s human family and familiar objects are marked by cheek or head rubbing with se- cretions from glands at the cheek corners and in the su- praorbital region; and tomcat urine spraying to mark ter- ritorial boundaries.24 The author has observed tomcats spraying parked car wheels, a trait frequently displayed by male dogs. Sexual behavior of the queen is considered the most stimulatory to attracting tomcats. Proestrous signs are usually minimal, with increased affection or occasion- ally aggression and a desire to be petted. Frequent uri- nation is usually seen.60 In proestrus or early estrus, a slight amount of clear watery vaginal discharge may be present. In one study, 20% of cycling queens showed a700 VETERINARY OBSTETRICS 0.5 to 2 day proestrus in which many queens have be- havioral characteristics of estrus, attract tomcats, roll in front of them, meow, but will not allow mounting or copulation.22,35 Estrous behavior in the queen in the absence of a tom- cat usually includes persistent vocalization, rolling, rub- bing, extreme affection, and with variable incidence and intensity, treading the hind legs, lordosis, and tail de- viation. A slight anterior and lateral set to the ears is common, and an intense facial expression simulates that seen with aggression or fright. A repeated monotone howling for as long as 3 minutes at a time is common and may accompany treading and rolling. The estrous cry is given by the queen to indicate that she is in estrus and in presence of the male, an “appeasement” cry to stimulate the tomcat to mount. Restlessness, general uneasiness, pacing back and forth, may accompany any of these behavioral patterns. A general loss of appetite of both the queen and tomcat is common during the breeding season. Some queens may not exhibit typical behavioral signs at every estrus except for increased af- fection, but will when properly handled or exposed to a tomcat. Treading, lordosis and the typical copulatory stance with lateral deviation of the tail can be induced by flank stimulation, stroking the back, alternate strokes over the thigh or stroking the perineum. Rubbing or scratching the back of the neck or shoulders induce treading, but usually not the precoital stance. The ear and facial expression may be induced by all of these ma- nipulations. Handling and stroking an estrous queen may cause enough neural stimulation to induce ovula- tion. 3,22,37,49,57,58 Once the female shows good copulatory signs, the waiting and watchful male will approach usually from the side and grasp the skin of the neck in his teeth. This usually takes 5 to 50 seconds. He next will place his forelegs over her shoulders and mount, and for 0.3 to 8 minutes he will position himself by straddling her pelvic area and treading along her flanks with his legs and pos- sibly stroke or strum the queen’s thorax with his front feet. The queen at this time reflexly varies her perineal area by lordosis until her perineum and vulva are almost horizontal. Her tail will be deviated laterally. When po- sitioning is right the tomcat will start pelvic thrusting with his exposed penis and on contact, intromission and ejaculation and the queen’s coital “cry” or “scream” usually takes 1 to 17 seconds followed by the queen quickly rolling or twisting out of the male’s grasp and aggressively attacking the male if he doesn’t move away quickly; this takes 0 to 1 seconds for dismounting. Im- mediately the queen displays a postcoital “after action” consisting of disoriented rolling, stretching and genital licking and twisting, taking 1 to 7 minutes and a variable period, 0 to 5 hours of refusing attempts by the tomcat to remount. Usually the tomcat stays at some distance watching and protecting his territory. Freeroaming, other tomcats may challenge him and indeed other males may mate with this queen and if they are successful, resulting in a litter from different tomcats or superfecunda- tion.22 34 60 In one study, copulations numbered 20 to 36 during 36 hours of observation and were more frequent during the first 2 hours (3 to 6 copulations) than any subsequent 2-hour period.22 In one study, estrus aver- aged 7.1 ± 0.8 days, even though a significant level of plasma progestins were present.44 The average range of estrus is considered to be 5 to 8 days with a range of 3 to 20 days. Ten days or longer periods is considered pro- longed. Duration of estrus is not greatly influenced by mating and induced ovulation, although some feel estrus may be one or 2 days shorter in average duration in mated queens.22 Other researchers have reported the opposite effect, with mated queens in estrus for 8.3 to 8.6 days and non-mated queens in estrus for an average of 6.2 days.53 Occasionally a timid queen, low on the social scale in a colony of females and checked with an ex- perienced breeding male, will express poor estrous be- havior, have good estradiol-17B serum levels indicating active mature follicles, but not allow interested males to mount and breed.53 Relative size of the male and female may influence the success of mating. Females that are too large or too small may make it difficult for a successful rapid coital act resulting in a frustrated and unsuccessful breeding male. This is especially a problem with young males or timid males that are hand bred. The activity of the male attempting to breed a female may be enough to induce ovulation although the lack of intromission and ejacu- lation has failed to deposit semen for fertilization.18 The coital “scream” or “cry” was at some time thought to be pain caused by the penile spines, but this reaction can be elicited in queens in or out of estrus, intact or spayed, with any instrument that invades the vaginal and cervical area.18,34,48 The cat is an induced or reflex-ovulator. Either natural mating, mechanical stimulation of the cervix/vaginal wall with probes, exogenous luteinizing hormone (LH) or gonadotrophic releasing-hormone (GnRH), or in a few queens, other stimulation, such as handling, or rubbing against objects during estrus, petting or stroking, may be enough neural response to cause GnRH and LH re- lease which then appears as spontaneous ovulation.22,37,53 Experiments on the effect of genital desensitization on mating behavior and ovulation in the queen revealed that sensations from the vagina cause the appropriate behav-INFERTILITY IN THE BITCH AND QUEEN 701 ioral responses of queens to intromission. Ovulation in queens can be triggered by impulses from the vagina, as well as the cervix, received during intromission.23 Most queens in the absence of coitus will have non- ovulatory estrous cycles throughout the breeding season (Chart VIII). The cycle then consists of waves of folli- cles producing estrogen followed by atresia of these fol- licles and an interestral period with no luteal or metestrus period. The mean and duration ranges of proestrus, es- trus and the interestrous periods and cycle interval are quite variable. Proestrus can really only be characterized early by the presence of a male or possibly with vaginal cytology. A length of 0 to 3 days has been reported for proestrus. Estrus may last 3 to 20 days, but most will average 7 to 8 days. The interestrual period will last usu- ally 3 to 14 days during the breeding season, but may be as long as 30 days. The mean interestrual time ranged from 9 to 13 days. Thus the length of nonbred queens’ cycles can range from 7 to 40 days with most cycles being 12 to 22 days long with a mean of 16 to 20 days.18" In non-fertile or induced ovulation by instruments or exogenous LH or GnRH, pseudopregnancy occurs with corpora lutea persisting for 3 to 7 weeks, with a mean of about 40 days followed by 4 to 10 days of anestrus. Thus the duration of pseudopregnancy from mating to the next estrus is usually from 35 to 70 days, the average is around 45 days.22 Pregnancy in the queen lasts 64 to 69 days with an average of 66 days. Some reports have an average of 63 days with a range of 58-65 days which is probably based on timing from the last of multiple breedings.22,53 Suc- cessful litters have recorded gestation periods of 59 to 71 days. (See pages 104-107) Variations may also be due to breed difference, colony differences, litter size and possibly time of year.18,22 Occasional queens will show estrus during pregnancy and estimates of 10% of pregnant queens, typically around 21 and 42 days of pregnancy, may show sexual behavior. Possible super- fetation can occur at this time.34,48,60 Some queens will be in estrus within 7-10 days following parturition and may conceive if bred at this time while caring for the litter they just queened. Most will show lactational anes- DOMESTIC CAT 40 30 20 10 cn c Q) C o 0) Vi & o Q_ E 3 testos- terone. Testosterone is the major androgen elaborated by the testis in the bull, dog and human. In the bull testos- terone is 16 times more active than androstenedione. The latter is the major androgen in the stallion testis.— These authors reported an average androgen titer of 3.0 micro- grams per ml. in the peripheral plasma of 3 to 4-year- old bulls. In 3 of 4 bulls injected daily with large doses of HCG a marked increase in the androgen level was produced. Based on studies of prostatic fluid, 2.5 mg per kg. of body weight daily of testosterone was needed to maintain prostatic function in male canine castrates.— Androgens are excreted in the urine as androsterones. Testosterone or androgens from the testis are neces- sary for: (1) the sexual differentiation of the external male genitalia, and the descent of the testis into the scrotum in fetuses or neonates;--- (2) the keratinization of the preputial epithelium, the separation of the glans penis from the prepuce; (3) the growth and maintenance of the accessory genital glands so they can contribute their se- cretions to the semen at the time of ejaculation; (4) sex- ual desire or libido and the ability for normal erection and copulation; (5) secondary sex characteristics of hair and hom growth, male attitudes, timbre of the voice, increased bone thickness, increased muscle tissue with a different distribution of fat from the female due to pro- tein anabolic effects; (6) the maintenance of secretory and absorptive activities and structures of the efferent ducts, epididymis and ducti deferentes including the am- pullae, and (7) spermiogenesis or development and ma- turation of the spermatids and spermatozoa in the testic- ular and mesonephric ducts are largely maintained by testosterone produced by the interstitial cells which in turn are stimulated by ICSH. High levels of testosterone are present in the lymph and fluid around the seminif- erous tubules of the testis. Testosterone enables diaki- nesis and meiosis to occur. — Testosterone can restore sexual desire and copulatory ability when injected into the castrated male animal. Estradiol when administered to steers was highly potent in stimulating most male sex- ual behavioral characteristics. Testosterone may exert part of its effect on steers and normal males by conversion to estradiol in the brain or hypothalamus.— The sheath or prepuce is a modified skin membrane and not a true mucous membrane. It is rich in glands producing sebum and smegma. The preputial glands, which are under the influence of testosterone, are located in the dorsal lateral region of the preputial orifice of boars. They are modified sebaceous glands that are responsible, together with the preputial diverticulum, that fills with smegma, urine and semen from masturbation, for the typical boar odor. These preputial glands that secrete a muscone type of material, a combination of 16 andros- tenes,- may be surgically removed along with the pre- putial diverticulum to eliminate the characteristic odor of boar tissues. An immunization attempt against the boar taint steroid, androstenone A, was unsuccessful.— The highly odoriferous musk-like odor characteristic of adult intact male goats may be due in part to 6-trans nonenal- but further studies are necessary in this animal. In goats these glands are located in the caudo-medial skin at the base of the hom. By removing this area of skin, about 24 X 14 X 5.5 mm., at the time of dehorning prepub- ertal male goats, the odor characteristic of mature male goats is eliminated.--- These odoriferous chemical compounds are called pheromones that elicit either or both sex attraction or mating behavior through their ac- tion on the brain and hypothalamus.— Castration, if performed before puberty, prevents the development and function of those organs and activities requiring testosterone and if performed after puberty re- sults in the atrophy of organs and of activities that are testosterone dependent. There are no interstitital cells in the epididymis so the early belief and practice of “cut- ting a horse proud” by leaving a portion of the epididy- mis at the time of castration is fallacious.— There is no antagonism between estrogens and androgens per se. Their apparent antagonism is due to their similar effects on the hypothalamus and the anterior pituitary gland in pre- venting the release of the gonadotropic hormones. Marked abnormal antler growth in deer with severe hypogo- nadism was reported.- In the bull interstitial cells were active by 3.5 months of age and the androgen content of the testis increased through 5 years of age and from then on tended to decrease.- This decrease in plasma an- drogen concentration is reported in other animals at older ages.- Undemutrition also reduces testosterone levels by reducing gonadotropin production or release.— Occasionally male, or female, reproductive steroid hormones are produced by adrenal cells or tumors. Pres- ently all commercial veterinary sources of androgens are synthesized from cholesterol-like compounds and are sold in solution in oil or alcohol (“Repositol”), in suspension in aqueous preparations, or in pellets for implantation. Testosterone may be administered orally especially to dogsINFERTILITY IN MALE ANIMALS 763 and cats because of their simple stomachs. Oxytocin administered intramuscularly prior to ejacu- lation in a limited number of bulls has resulted in a larger volume and greater numbers of spermatozoa in the ejac- ulate. Contractile mechanisms involved in sperm trans- port in the male are in part regulated by oxytocin. (See erection and ejaculation.) Although they are essential for normal body function other pituitary hormones such as ACTH, somatotropic hormone, prolactin, thyrotropic hormone, and oxytocin and vasopressin, as well as thyroxine from the thyroid gland, the glucocorticoids and adrenaline from the adre- nal gland and others have only moderate secondary ef- fects of limited importance on reproduction in the male domestic animal. Puberty—The onset of puberty in male domestic an- imals occurs at approximately the same time after birth as puberty in females of the same species. About 4 months of age GnRH from the hypothalamus causes the episodic release of gonadotropic hormones, LH and FSH, from the anterior pituitary gland resulting in the secretion of androgenic hormones from the gonads that cause growth of the genital organs and secondary sex characteris- tics.-131517 Injections of gonadotropic hormones into prepuberal animals results in precocious sexual maturity. In the male the onset of puberty is characterized by sec- ondary sex signs, sexual desire, ability to copulate and the presence of viable spermatozoa in the ejaculate. The onset of puberty is a gradual process and is variable in time since it may be influenced within a species by the plane of nutrition, breed of animal (Bos indicus bulls mature slowly than Bos taurus bulls), cross-breeding, methods of management, presence of chronic disease processes, and individual differences.-'6 The development of puberty in bulls has been care- fully studied.1'1113^17 Primary spermatocytes appear in the seminiferous tubules by 4 to 6 months of age, spermatids by 6 to 7 months, and spermatozoa by 7 to 9 months of age in bulls. Seminal secretion from the accessory glands appears by 5 to 6 months. Separation of the penis from the sheath in bulls proceeds caudally beginning at 1 month and ending with complete separation by 8 months of age. The period from 6 to 10 months of age in bulls is char- acterized by the accelerated growth rate of the genital system, increases in GnRH and in plasma LH, external manifestations of puberty and the rapid onset of sper- matogenesis. Puberty was reached at 10 months, 40 weeks, in well-fed, healthy Swedish Red and White bulls and by 12 months, 48 weeks, when fed on a lower plane of nutrition. However others7 have reported that fertile semen with conception has been produced by well-reared bulls at 6 months of age. Puberty probably commences at 2 months and is qualitatively completed by 10 months of age in Holstein bulls.18 The onset of sexual behavior in a young male is sig- nificantly hastened by rearing with other males or fe- males and is retarded by rearing in isolation.16 The size of the testis in prepubertal bulls increases rapidly be- tween 4 and 8 months of age and then growth of the testes is at a slower rate and is correlated with the body weight. During the pubertal period it may be difficult, without repeated examinations over a number of months to differentiate between delayed testicular development due to poor nutrition and management or testicular hy- poplasia caused by genetic or congenital influences.16 The penis of newborn ruminants and swine is without a sigmoid flexure and is adhered to the prepuce. Penile growth due to androgens between 3 and 8 months of age results in the development of a sigmoid flexure and its separation from the prepuce. A scrotal circumference of 28 cm. is indicative of puberty in bulls.1314'15 The attainment of puberty does not signify full repro- ductive capacity. Highly significant increases in ejacu- late volume, output of motile spermatozoa and concen- tration of spermatozoa occur in bulls for 6 to 9 months after the onset of puberty.2'3,8 Puberty in bulls was de- fined as the age at which the first ejaculate containing at least 50 x 106 spermatozoa with 10% motility was obtained.15 Within 4 months after puberty the percentage of normal acrosomes had not yet reached mature lev- els.14 A marked reduction between 9 and 12 months in the number of proximal protoplasmic droplets on bovine spermatozoa was noted.2 The same reduction in proto- plasmic droplets and abnormal spermatozoa in ejacu- lated boar semen occurred between 150 and 200 days of age.12 The rapid growth of the testis and epididymis from 4 to 8 months of age in the boar was described.20'21 De- tachment of the sheath from the penis occurred at 4 to 6 months and sexual maturity in the boar was reached at 7 to 8 months of age. It was noted that 16 to 17- month-old stallions produced only 16.4 ml. of gel-free sperm per ejaculate with 22 percent progressive motility and 48 percent abnormal sperm cells.10 Because of the above indications of a lack of maturity after the onset of puberty and because of individual differences in libido, spermatozoan reserves, and the ability to produce large numbers of normal spermatozoa, immature male animals should be used sparingly for breeding purposes for one- half to one year or more after reaching puberty. Bulls that mature early with large testicles generally produce daughters that also mature early and may be more fer- tile.9 Scrotal size in young bulls was not highly corre- lated with sexual behavior or libido.13 The time of puberty in male animals is:764 VETERINARY OBSTETRICS Stallions—18 months (range 12 to 24 months) Bulls—9 to 12 months (range 6 to 18 months) Rams and Bucks—7 to 8 months (range 4 to 12 months) Boars—5 to 7 months (range 4 to 8 months) Dogs—7 to 10 months (range 5 to 12 months)llb Toms—8 to 10 months (range 6 to 15 months) The Scrotum and Heat Regulation of the Testes— The testicles in all domestic animals are normally lo- cated in the scrotum. In certain wild species of rodents the testes are retained in the abdominal cavity except during the breeding season when they descend into the scrotum. The whale, elephant, rhinoceros and seal have no scrotum and the testes are intra-abdominal. In the do- mestic animals the scrotum performs a vital temperature- regulating function for the testes. If the testes are main- tained at body temperature, as occurs in bilateral cryp- torchidism, spermatogenesis does not occur. High, pro- longed fevers, insulation of the scrotum or prolonged exposure to high atmospheric temperature and humidity can also seriously impair spermatogenesis. However, testosterone production by the interstitial cells or Leydig cells is not affected by temperature. The dartos muscle, by contracting in cold weather to hold the testes against the body and relaxing in warm weather is the principal thermoregulator of the testis.2 The external cremaster muscle, by raising the testis, may also play a role. In the dog, bull, boar and stallion the scrotal skin is thinner and less well covered with hair which together with increased numbers of sweat glands further assists in cooling the testes.17 Scrotal temperature in three dairy bulls varied from 93.2° F (34.1°C) to 100.4° F (37.9° C) while rectal temperature varied from 100.4° F (37.9° C) to 102.2° F (38.9° C) during the same 8-hour period.1 Scrotal tem- perature can rise rapidly when bulls recline. Fluctuations of 18° F (10° C) in environmental temperature had little effect on scrotal temperature. The testicular temperature of the ram may vary from about 85° F (28° C) to about 104° F (40° C). In animals with well-developed scro- tums the testicular temperature is usually 2 to 7° C below body temperature.- In rams blood in the coiled internal spermatic artery winding through the pampiniform plexus of spermatic veins cools 9.4° F (5.2° C) when the testicular temper- ature is about 93.2° F (34° C).3 The arrangement of the spermatic artery and vein in the region of the pampini- form plexus provides an efficient heat exchange mech- anism that, although it is not regulatory, rapidly transfers any benefit of scrotal thermoregulation to all parts of the testis. In this regard in the bull the extensive network of superficial veins in the tunica albuginea plays an im- portant role in lowering the temperature of the venous blood before it passes through the tortuous spermatic vein. The Testes, Spermatogenesis and Spermiogene- sis—The testes perform a dual function in producing tes- tosterone from the interstitial cells, and spermatozoa and “inhibin” from the seminiferous tubules. The mature male domestic animal is capable of fertile copulation at any time. However, in certain wild animals such as deer, camels and elephants there is a definite seasonal period of sexual excitement or “rut” and spermatogenesis oc- curs only during this period. In some domestic animals, such as the ram and stallion, there may be seasonal vari- ations in libido and in spermatogenesis and semen qual- ity due to environmental nutritional, length of daylight or other factors. Spermatogenesis is a highly synchronized process whereby spermatozoa are formed from the precursor dip- loid cells, type A spermatogonia.- Spermatogenesis in- cludes both spermatocytogenesis (spermiocytogenesis) or formation of primary and secondary spermatocytes from type A spermatogonia and spermiogenesis or the for- mation of mature fertile spermatozoa from the immature spermatids. Spermatocytogenesis is under the regulation of FSH from the anterior pituitary gland and conditions favorable for spermiogenesis are under the control of LH and testosterone. Under normal conditions spermatogen- esis is a very orderly continuous process. In any single small area of the seminiferous epithelium various stages of the well-organized extremely regularly occurring cycle of the seminiferous epithelium may be observed. The duration of spermatogenesis is comprised of 4 cycles (4.68 cycles if spermatogenesis is started with a dormant type A spermatogonia) of the seminiferous ep- ithelium starting with type A spermatogonia. At each cycle of the seminiferous epithelium the spermatogonia renew themselves by producing new stem cells and cells that will produce spermatocytes. Each cycle length in the bull and dog9b is 13.5 days, in the boar 8.6 days and in the ram about 12.2 days. In the boar, bull and ram and other male animals a succession of 8 highly characteristic cel- lular associations or stages occur in each cycle which takes place in the form of a spiral along a portion of the seminiferous tubule as well as at one transverse area. In each stage there are several distinct groups of cells pres- ent on cross-section of the seminiferous tubule. At stage 8, for example, nearly mature spermatozoa line the lu- men of the tubule. Spermatids at a certain stage in de- velopment, or a generation of germ cells, are always as- sociated with the same types or other generations of spermatogonia and spermatocytes. The distance between two similar cellular associations or stages in the semi- niferous tubule is called a spermatogenic wave.8,916 AINFERTILITY IN MALE ANIMALS 765 second classification of 14 cell associations forming the spermatogenic cycle has been described.-— (See Table 22.) Any agent that damages spermatogonia could lead to permanent damage of the testis; but if only differen- tiating cells are damaged, repair is possible. Spermiogenesis begins as soon as the spermatid is formed. At this stage the spermatid has a spherical nu- cleus surrounded by cytoplasm containing many mito- chondria in which a Golgi complex or zone soon forms. The acrosome and head cap of the spermatozoon arise from the Golgi complex. The cytoplasm and centrioles move to the opposite side of the nucleus. The centrioles give rise to the flagellum or axial filament and later the body and tail of the spermatozoon. The mitochondria later become arranged like a collar around the upper region of the flagellum as the mitochondrial helix forming the middle piece. At the end of spermiogenesis when the spermatozoa are in the head of the epididymis, unused cytoplasm and Golgi material, now called the proto- plasmic or cytoplasmic droplet, is located in the neck region of the sperm cell in the testis, and is cast off as the spermatozoa pass through the epididymis.2 During part of its transformation to a spermatozoon the spermatid is closely associated with “nurse” or Ser- toli cells in the seminiferous tubules. After it leaves the Sertoli cell and is “free-living” in the lumen of the sem- iniferous tubules it is moved into the rete testis and ef- ferent tubules by a large volume of secreted fluid from the Sertoli cells and cells lining the rete and efferent tu- bules.- There is little evidence of any contractile tissue and no cilia in the seminiferous tubules, straight tubules or rete testis. Spermatozoa do not develop any signifi- cant degree of motility until ejaculation. The testicular capsule apparently contains smooth muscle that contracts and relaxes and this alternate activity exerts a pumping action on the seminiferous tubules forcing the nonmotile sperm cells and “plasma” out of the testis and into the epididymis. Normal bulls and stallions produce 12 to 17 million and rams 12 million spermatozoa per gram of testicular tissue daily.--’1,8’9’16 Boar produce 25 to 30 million sperm cells per gram of testis daily because of the shorter du- ration of spermatogenesis and the larger number of sper- matozoa produced from one type A spermatogonium.10 Table 22. Outline of Spermatogenesis in the Bull, Boar and Ram Chromosome No. of** Time in Days* Complement cells Bull Boar Ram Type A Spermatogonia (dormant) 2N (diploid) 1 Type A Spermatogonia 2N 2 Intermediate Type Spermatogonia 2N 4 Type B Spermatogonia 2N 8 Primary (Preleptotene) Spermatocytes (active DNA synthesis) Leptotene stage 4N (tetraploid) 16 Zygotene stage Pachytene stage Diplotene stage Diakinesis Metaphase I Anaphase I Telophase I Secondary Spermatocytes Diakinesis Metaphase II Anaphase II Telophase II Spermatids Spermatozoa Meiotic Prophase I (long, 16 days in ram) 1st Meiotic (maturation) Division Meiotic Prophase II (very short, hours) 2nd Meiotic (maturation) Division Spermiogenesis (long, 15 days, ram) 2N IN (haploid) IN about 10-20 25-26 40-42 36-37 32 64 64 *It takes approximately 10 days in the bull and 13-15 days in the ram and boar for spermatozoa to traverse the epididymis. Thus from type A spermatogonium to ejaculated spermatozoa is about 60 to 70 days in the ram and bull and 50 to 60 days in the boar, stallion and dog. **Theoretically in the bull and ram 16 primary spermatocytes and 64 spermatozoa develop from one type A spermatogonium; boars and rats have 24 primary spermatocytes and 96 spermatozoa from one spermatogonium. However a certain loss in cells, about 25%, is experienced during meiosis and is characterized by the presence of pycnotic nuclei.766 VETERINARY OBSTETRICS Thus daily sperm cell production for a bull with testes weighing 400 gms each, a stallion with testes weighing 185 gms. each, a ram with testes weighing 250 gms. each, and a boar with testes weighing 300 gms. each would be 12 billion, 6 billion, 7 billion and 15 billion spermatozoa, respectively. About 70,000 spermatozoa are produced every second during the breeding season by the testes of an adult stallion.- Sperm numbers in the testis are highly correlated with testis weight, testis di- ameter, testis tone or consistency, and scrotal circum- ference.3,5 Testicular growth continues through puberty until complete sexual maturity occurs, which in the bull is about 4 years of age. Beef breeds, particularly Bos indicus, mature more slowly than the dairy breeds. Scrotal circumference in normal bulls is closely correlated with spermatozoa production since 70 to 90 percent of testic- ular weight is comprised of the seminiferous tubules. In most beef bulls average scrotal circumference increases from 14 months, to 26 months to 36 months of age from 33 cm. to 35 cm. to 36 cm., respectively. While in Brah- man bulls the corresponding age-related average circum- ferences are 22 cm. to 32 cm. to 37 cm. and in Holstein bulls 32 cm. to 39 cm. to 42 cm., respectively.3,5 Mea- surements are made with scrotal circumference tapes.* Other factors that influence bovine testicular size be- sides age and breed is body condition, body weight, sea- son (heat stress)- testicular pathology. Testicular size is highly heritable.5 Bulls of breeding age should have a scrotal circumference measurement of 32 to 34 cm. or more to be classified as a “ satisfactory potential breeder. ”5,6 The testes of other animals also increase in size from puberty to maturity. In the stallion under 12 months of age the total testes weight is 53 gms., at 24 months it is 209 gms., at 36 months, 232 gms., and at 4 to 10 years, 317 gms.- Testicular size in stallions may be mea- sured by calipers.- As in other animals total scrotal width is closely correlated to testicular weight and production of spermatozoa. The average scrotal width of normal stallions is 105 mm., range 80 to 140 mm. Equine tes- ticular size decreases 10 to 15 percent in the nonbreeding winter season and as stallions age the testes increase in size from 90 mm. scrotal width in 2 year old to 108 mm. in 15 year old horses. Individual testis width in Stan- dardbred stallions averaged 4.6 to 6.3 cm. with the right testis slightly larger than the left in all ages. A 9 to 18 percent reduction in size of testes of like aged horses occurred in working, stressed, or hormonally treated stallions at racetracks compared to breeding farm stal- lions.19 During the nonbreeding season in sheep scrotal *Lane Manufacturing Co., 5560 E. Pacific Place, Denver, Colo. 80222. circumference in rams was 15 percent less than during the breeding season.14 Scrotal circumference in rams varies with the weight and age of the ram. Scrotal circumference of normal, well grown rams was 26, 33, 34, 36 cm. for rams weigh- ing 100, 150, 200, 250 and 300 pounds, respectively, with a range of 20 to 43 cm.16b Heritability estimates for scrotal circumference were high and for testis consist- ency medium. These traits should be emphasized in bull evaluations.5b Four months after unilateral castration in the ram and prepubertal bull the weight of the remaining testis in- creased by about 76 percent and sperm cell production was nearly double that of a normal testis.lb'18 As in rab- bits and dogs after hemicastration the diameter of the seminiferous tubules increased greatly to produce a com- pensatory hypertrophy of the single testis. Further study of this interesting observation is needed in these and other species. The Morphology of Spermatozoa—In recent years electron microscopy has done much to elucidate the fine structure of spermatozoa. Although the size and shape of spermatozoa differ between the domestic species of animals the basic morphological structure is similar. The head length and width is about 8 to 10 microns by 4 to 4.5 microns in bull, ram and boar spermatozoa and smaller, 5 to 7 microns in length and 2.7 to 4.0 microns in width, in stallion, dog and cat spermatozoa. The head thickness is about 0.5 to 1.5 microns or less in all spe- cies. The spermatozoan body or middle piece is about one and one-half to two times as long as the head, 10 to 15 microns, and about 1.0 micron in diameter in all species. The tails of spermatozoa are 35 to 45 microns long and 0.4 to 0.8 microns in diameter. The total length of spermatozoa of domestic animals is thus about 50 to 70 microns or 1/300 of an inch.- -1,4 The head of the spermatozoon is elongated and ovoid in shape, broad and flat in one plane and narrow in the other with the thickest portion at the base and tapering to a fairly thin apex. The head is entirely filled with a nearly homogenous nuclear material containing the ge- netic material, DNA or deoxyribonucleic acid, sur- rounded by the nuclear membranes. (See Figure 163.) DNA is the amazingly concentrated coded genetic ma- terial. Each spermatozoon contains about 2.5 billion bits of information necessary to form a fetus yet it takes 300 billion spermatozoa to make 1 gram of DNA.6 The an- terior part of the nuclear membrane or the inner mem- brane of the acrosome forms the body of the acrosome. The anterior 60 percent of the nucleus and its modified membrane, is covered by the acrosome cap or head cap which is a double-walled pouch-like structure about 0.1INFERTILITY IN MALE ANIMALS 767 Neck region < Mid piece < To i I < Cell membrane Acrosomal corpuscle Perforatorium Outer membrane of acrosome ■Acrosomal substance Inner membrane of acrosome Equatorial segment. Nuclear membrane Nucleus Postnucleor cap Basal plate Basal knob ■Centriol Helix region End piece* ■Terminal n -Tail sheath Figure 163. Diagram of the Ultrastructure of the Sperm Cell. T7, 4, 10 Synonyms: 1. Acrosomal Vacuole or Apical Body 2. Galea Capitis or Sperm Cap 3. Equatorial zone 4. Mitochondrial Helix 5. Jensen’s Ring 6. Cytoplasmic or Fibrillar Sheath 7. Terminal Filament. micron thick enclosing the acrosomal substance and the denser acrosomal corpuscle, body, or vacuole.—4,10 The equatorial zone or segment is the posterior part of the acrosome or head cap around the middle portion of the sperm head corresponding to the area where the acro- somal substance is most scanty. The posterior 40 percent of the nucleus and nuclear membranes from the equa- torial zone to the base of the cell are covered by the postnuclear cap or nuclear sheath. The differences be- tween the acrosome cap and postnuclear cap explain the differences in affinity for stains observed in these two regions. The cell membrane composed of several layers completely encloses the head, body, and tail of the sper- matozoon. The membrane is closely applied to the cell at the anterior portion of the acrosome cap, the post- nuclear cap, and at Jensen’s ring. The outer membrane of the acrosome cap, is identical with the galea capitis, described in the earlier literature, that is detached either spontaneously in the tail of the epididymis by long, sex- ual abstinence, artificially in vitro, or during fertiliza- tion, probably as a step in sperm capacitation. Detach- ment occurs by rupture of the cell membrane and the outer membrane of the acrosome cap in the equatorial zone which exposes enzymes such as hyaluronidase in the acrosome that are necessary for penetration of the spermatozoa into the ovum.— 7 It was recommended that earlier term “perforatorium” be dropped as the function ascribed to it is performed by the acrosomal body.7 The detached outer membranes of the acrosome may break into two halves, or remain joined and appear as “bath- ing-cap” shaped structures in stained or India ink prep- arations of semen. The neck, centriolar region or implantation zone, about 1.5 microns long, consists of the two centrioles and their surrounding radices or implantation plates.-— The mi- tochondrial sheath originating in the basal knobs or gran-768 VETERINARY OBSTETRICS ules of the head form two counter-clockwise spiral struc- tures, the mitochondrial helices, that continue down the body or midpiece to the terminal or Jensen’s ring. The radices change into the fibrillar bundle at the posterior portion of the neck region. Most authors consider the neck region as part of the body or middle piece. The mitochondrial sheath is about 0.1 micron in thickness and surrounds the fibrils, 9 coarse or peripheral and 11 fine or central. These latter structures resemble cilia. The helix region, midpiece, middle piece, or body supplies energy for the sperm cell by metabolic processes occur- ring in the mitochondrial helix. The tail region, the long- est part of the sperm cell originates at the terminal ring of the body and extends to the endpiece. In the tail re- gion, the fibrils are surrounded by the fibrillar coil sheath or tail sheath consisting of pair of spiral coils with each of the coils making more than 400 spirals. The endpiece or terminal portion of the tail is about 3 to 4 microns in length and consists of the terminal portion of the fibrils covered by the cell membrane but the fibrillar coil sheath of the tail is absent.10 The wave-like or whip-like action of the tail originates in the neck region of the body and generates contractile force as it proceeds distally. Helical oscillations of the tail of the spermatozoon are very rapid and provide the force necessary for sperm cell motility which under optimum conditions of temperature, and medium is about 100 microns per second, range 10 to 352, in bull spermatozoa,3 9111213 or about 4.23 mm. per minute.2 The motility rates for equine, ovine and human spermatozoa were 80 to 100, 200 to 250 and 30 to 75 microns per second, respectively. Spermatozoan Transport, Maturation and Storage and Accessory Gland Secretion—Spermatozoa are car- ried in a large amount of fluid secreted by the seminif- erous epithelium into the rete testis and the tortuous ef- ferent ducts (ductuli efferentes) usually about 13 to 15 in number, located adjacent to the head of the epididy- mis and opening into the epididymal duct.-- These structures since they arise from the mesonephros have kidney-like functions in respect to absorptive and secre- tory activities. As mentioned previously contractions of the testicular capsule probably aids in forcing semen from the testes into the efferent ducts. Nearly all of the fluid, 200 ml. daily in the bull, entering the efferent ducts and head of the epididymis in the bull, as well as the boar, was reabsorbed there.—10 About 30 ml. of fluid passes daily from the rete testis into the efferent tubules of the ram.32 The sperm cell concentration in this fluid was 100 million per ml. Ligation of the efferent ducts and pos- sibly the head of the epididymis caused an accumulation of fluid or edema in the testes followed by atrophy while no accumulation occurred if the ligature was placed around the more distal portions of the epididymis.17,28 Both se- cretory cells and cells with cilia beating toward the ep- ididymis are found in the efferent ducts. The ciliated borders of these cells in the bull may become detached and excreted with the semen at the rate of one “medusa head” per 10,000 spermatozoa or about 500,000 in the average ejaculate.9 Smooth muscle activity as well as ciliary activity help transport sperm through the efferent ducts. In the epididymis peristaltic activity of smooth muscle is largely responsible for sperm transport. Microvilli are present in epididymal cells but they are nonmotile. The contractile mechanisms involved in sperm transport in the male are partly regulated by oxytocin. The epididy- mal epithelium has absorptive and secretory functions producing variations in the sodium, potassium, calcium, chlorine and phosphorus ion concentrations and in the concentrations of proteins, enzymes and glycerylphos- phorylcholine in the luminal contents in different por- tions of the epididymis.14 The composition of epididy- mal plasma is closely related to testicular function, the passage of sperm cells and the hormonal and physical testicular environment. Plasma volume in bulls was dou- bled by secretions in the caput and halved by absorption in the cauda; while in boars the epididymal content underwent continuous dilution from the caput to the cauda epididymis. The time required in the domestic animals for spermatozoan transport through the head, body and tail of the epididymis is about 7 to 15 days. Frequent ejaculations hasten the passage of spermatozoa through the tail of the epididymis.2 Although physiologic mechanisms of the epididymis are largely under the hormonal control of testosterone they are not well understood. The sperm cell undergoes maturation and other changes including the ability to be- come motile and fertilize an ovum,2— in its passage through the epididymis. An example of this maturational process is the passage of the cytoplasmic droplet from the neck region, down the middle piece and tail from which it is lost before ejaculation. This is most com- monly described in ungulates. Proximal protoplasmic droplets were present on 44% of the spermatozoa in the caput and only 2% in the cauda epididymis of bulls.4 The percent of proximal protoplasmic droplets in the caput of swine is higher. Spermatozoa removed from the tail of the epididymis were 2 to 10 times more fertile than spermatozoa from the caput apparently due to abnor- malities in locomotion of the sperm cells taken from the head of the epididymis.8,24 The percentage of motile bo- vine sperm cells in the caput and cauda epididymis were 0 and 41, respectively.16,17 Staining with an eosin or vital stain revealed equal numbers of live, unstained cells andINFERTILITY IN MALE ANIMALS 769 morphologically normal spermatozoa in both sites. Sper- matozoa removed from the cauda epididymis exhibited normal fertility. Only about 1 ml. of fluid per day flows through the ovine epididymis but the epididymis does secrete compounds such as glycerylphosphorylcholine.- The seminal fluid in bulls is concentrated as it passes through the epididymis, especially in the head region, so sperm cell concentration in the tail of the epididymis in bulls is 4,000,000 or more per cmm. In the epididymis sperm cells exhibit a very low rate of motility and are resistant to cold shock.7 In the tail of the epididymis stor- age conditions are optimal. Spermatozoa can remain vi- able and fertile for up to 60 days in the ligated epididy- mis of the bull.9 After long periods of sexual rest, however, many spermatozoa in first ejaculates may be dead or infertile. Bulls have about 70 billion spermato- zoa outside the testis proper, extragonadal sperm re- serves (ESR), with 19 billion (29%) in the head, 5 bil- lion (7%) in the body, 37 billion (53%) in the tail of the epididymides, 2 billion (3%) in the ducti deferentia and 6 billion (8%) in the ampullae.1 Thus the major storage site for spermatozoa is the tail of the epididymis. De- pletion trials in the bull, consisting of 20 or more ejac- ulates taken within several hours, removed about 53 percent of the extragonadal sperm reserves. In the ram depletion trials reportedly removed only 31 percent of the extragonodal sperm reserves. In the bull these de- pleted extragonadal sperm reserves are completely re- plenished within about 7 days and a significant replen- ishment of spermatozoan numbers in the tail of the epididymis occurred within 60 to 90 minutes after the last ejaculate. During depletion trials no increase in proximal protoplasmic droplets or abnormal spermato- zoa were noted. Unejaculated, defective27 spermatozoa or spermatozoa confined to the epididymis by resection or ligation of the ductus deferens or vasectomy have been reported to be removed from the epididymis, rete testis and efferent ductules by selective phagocytosis by macrophages and epithelial cells or resorbed.4'13'20,25'27 29 Histologic ex- amination has only occasionally shown degeneration or phagocytosis of sperm cells in the rete testis or epididy- mis.13 Many workers have reported that spermatozoa were voided in the urine.2,21 The number of sperm cells voided daily in the urine of sexually-rested rams was about the same as the total daily sperm cell production. Long term vasectomy in the bull did not abolish spermatogenesis and testis size was unaffected even after 5 years.18 Thus a mechanism must exist for the removal of sperm cells from the epididymis. Further work is needed to elucidate the fate of unejaculated or defective, dead sperm cells. Masturbation in domestic animals may cause some de- pletion of sperm cell reserves from the tail of the epi- didymis. Thus there are apparently several routes for eliminating excess, dead, or abnormal spermatozoa from the testis and epididymis. The ductus (vas) deferens is a firm muscular duct, about 2 mm. in outside diameter in the bull, that trans- ports spermatozoa by peristalsis especially at the time of precoital stimulation and ejaculation to the ampullae and the pelvic urethra. The ampulla of the ductus deferens, present in the bull, stallion and ram, is a thickening of the ductus abundantly supplied with glands that are sim- ilar to the vesicular glands. The ampullae have a limited role in the storage of spermatozoa. There is no notice- able enlargement of the terminal portion of the ductus in the dog, tom or boar. The accessory glands including the vesicular glands; (seminal vesicles), the prostate; and bulbourethral (Cow- per’s) glands are under the control of testosterone from the interstitial cells of the testis and secrete the major portion of the seminal plasma into the urethra at the time of ejaculation. The seminal plasma acts primarily as a carrier for spermatozoa and secondarily stimulates sper- matozoan activity by providing fructose, a readily avail- able energy source, and buffers. While seminal plasma is capable of influencing the fertilizing ability of sper- matozoa there is no evidence it is essential for it. In 7 vesiculectomized bulls the volume of the ejacu- late decreased as did the motility of the spermatozoa while the concentration of sperm cells increased. Five of these bulls were mated with heifers and had acceptable fertil- ity. Seminal vesiculectomy in bulls nearly eliminated fructose in semen and reduced the protein level and ejac- ulate volume.19 There was a greater loss in sperm cells after freezing in the treated bulls but the libido was not affected. The vesicular gland secretion is not essential, as the metabolic needs of the sperm cells are provided by the secretions in the female genital tract. In the bull the vesicular glands contribute slightly to the presperm semen fraction but mainly to the sperm cell rich fraction of the ejaculate.12 The vesicular glands secrete fructose, citric acid, potassium, proteins, enzymes and other sub- stances. Certain prostaglandins have been reported to be present in the seminal plasma of man, guinea pigs and rams. These have a strong pharmacodynamic effect on the smooth muscle of the genital tract of females facil- itating sperm migration.31 In certain Holstein, Hereford and Guernsey bulls, and possibly in other breeds, the semen may have a definite yellow color due to riboflavin secreted by the vesicular glands. This may be inherited as a dominant character. Upon standing in sunlight for several hours the yellow color will fade.33 In the boar, secretions from the seminal vesicle and bulbourethral770 VETERINARY OBSTETRICS glands when mixed form a gelatinous, waxy, tapioca- like material. Certain horses, especially grade animals and only occasionally Thoroughbreds, produce a thick, glairy, “egg-white,” sticky secretion from the vesicular glands.2'611 This is of interest in light of the production of a vaginal plug or coagulum in the rat and guinea pig when Cowper’s gland and the secretions from the co- agulating gland, a portion of the prostate, combine with secretions from the seminal vesicles.15 This promotes fertility in these latter species by sealing the vagina and preventing the escape of semen. No useful function of this viscous portion of the ejaculate is evident in swine or horses. About 50 percent of the volume of semen in the bull and 20 percent in the boar come from the vesicular glands. The prostate gland in the dog and tom provides most of the volume of the ejaculate as in these species the ve- sicular glands are absent and bulbourethral glands in the tom are fairly small. In the boar the prostate gland is relatively small weighing about 20 gms., compared to the other large accessory glands. A number of references appear in the literature refer- ring to urethral glands in domestic animals. As indicated previously urethral glands are not present in domestic animals; it is likely that some authors are extrapolating from the human or mistake the disseminate or diffuse portion of the prostate glands around the pelvic urethra for urethral glands. The bulbourethral (Cowper’s) glands are relatively small in all species except swine where they provide about 20 percent of the volume of the ejac- ulate. The clear watery secretions dribbling from the sheath or penis during sexual stimulation in bulls, stal- lions, and rams are considered to originate from the bul- bourethral and possibly the prostate and vesicular glands,-'912'23 and may assist in clearing and flushing the urethra before ejaculation. After castration or vasectomy, spermatozoa may be found in small numbers in the ejaculates of stallions, dogs, rams and bulls for up to 21 days, indicating the presence of residual spermatozoa in the ductus deferens and am- pullae. In geldings no motile spermatozoa were obtained after 7 or 8 days after castration.30 The numbers of sper- matozoa were very low in the ejaculate, 20 x 106 and 40 x 103 in the stallion and dog, respectively. Thus it may be prudent not to allow males to associate with fe- males for 1 to 2 or 3 weeks after castration or vasectomy if pregnancy is to be avoided.26 Erection and Ejaculation The penis has a twofold function—the expulsion of urine, and the deposition of semen in the genital tract of the female. Before the latter process can occur the penis must become erect. This is provided for by the erectile structures, the 2 large corpora cavernosa penis and the small corpus cavemosum urethrae (spongiosum) that be- come distended by blood. In the stallion the cavernous spaces of the corpus spongiosum extend into the glans penis and cause “belling,” flowering or great dilation of the glans during erection and ejaculation.- - Stimulation of the nervi erigentes composed of parasympathetic fi- bers from the pelvic and sacral nerves results in erection. Erection is accomplished by blood from the internal and external pudendal arteries to the penis and relaxation of the helicine arteries. The cavernous blood sinuses dilate with blood, the outflow of which is retarded or blocked by the contractions of the smooth muscles of the corpora cavernosa and the extrinsic ischiocavemosus and bul- bospongiosus muscles at the base of the penis.-13 4’5 The dilation and filling of the bulbous areas of the bovine penile crura under the ischiocavemosus muscle together with 4 or 5 contractions of this muscle “pumps” blood into the corpus cavemosum causing rapid penile erection with the resulting blood pressure peak in the corpus cavemosum penis averaging 14,198 mm of Hg (about 275 pounds per square inch (PSI)), range 8000 to 24,000 mm. of Hg, at the time of coitus and ejaculation in the bull.4 Thus if forced ventral angulation or bending of the erect bovine penis at the time of copulation oc- curs, a dorsal rupture and hematoma may result.2 In the stallion the highest peak of pressure in the corpus cav- emosum penis was 7,900 mm. of Hg. and the average peak pressure in the corpus spongiosum penis during coitus was 994, range 642 to 1784, mm. of Hg.3 The contrac- tions of the bulbospongiosus muscle at the time of ejacu- lation forced about 8 waves of blood distally in the cor- pus spongiosum moving the semen down the urethra.2'3 In the buck the corpus cavemosum penis peak pressure during coitus was about 10,000 mm. of Hg and the peak pressure in the corpus spongiosum penis was 750 to 1250 mm. of Hg.1 Since the high blood pressure in the corpus cavemosum is maintained for only a short period of time, it is suggestive that full erection only persists as long as the ischiocavemosus muscle is contracted and forcing and holding the blood in the penis. The mechanism of the erection in the dog which is aided by the contraction of the vulvar sphincter muscles after intromission12 has been well-described.5 78 A similar pumping action to that in the bull and buck is noted in the dog and ram.12 This “pumping” action of the pelvic urethral muscle and the bulbocavernosus muscle causes an intermittent increased blood pressure or wave in the corpus cavemosum spon- giosum to compress the urethra to expel semen. The anatomic structure of the male penis influencesINFERTILITY IN MALE ANIMALS 771 the precoital and coital sexual behavior of the animal.7b The vascular penis in the stallion and dog is slow to erect and foreplay before copulation is essential. The fibro- elastic penis of the bull, ram, and boar, containing much less vascular erectile tissue, erects rapidly and there is less foreplay in these species. The acts of erection and ejaculation are reflex, with the centers being located in the lumbar region of the spinal cord.— Normally the ner- vous paths responsible for erection and ejaculation also involve the cerebral cortex of the brain. Erection can take place, however, even if the spinal cord is divided in the thoracic region. Reflex stimulation from the testicles, urethra, prostate, or penis, especially the glans penis, causes erection. Sectioning of the sensory pudendal or dorsal nerve of the penis prevents ejaculation when the glans penis is stimulated. Erection is predominantly un- der the influence of the parasympathetic system and ejaculation is controlled by the sympathetic system.- Animals such as the stallion, dog, and boar, which ejaculate large amounts of semen have a prolonged pe- riod of coitus. The bull, ram and tom ejaculate small amounts of semen and their period of coitus is short. The duration of coitus or copulation in the domestic animals, including erection, mounting, intromission, ejaculation, withdrawal and dismounting is approximately as fol- lows: Stallion 1 to 3 minutes Bull 5 to 10 seconds Boar 4 to 6 minutes Tom 10 seconds Dog 5 to 45 minutes Ram Buck 3 to 5 seconds 3 to 5 seconds Although copulation initiates ejaculation by sensory stimuli from the glans penis, certain stimuli are more important than others in the various species.7b In the bull and ram the warmth of the vagina is most important and pressure and friction less important as stimuli for ejacu- lation. In the stallion, boar and dog pressure on the penis is relatively more important than temperature. The non-erect penis of the stallion is about 50 cm. long and 2.5 to 5.0 cm. in diameter and when erect it doubles in length and thickness and the glans penis en- larges 3 to 4 times.2 In the bull penile extension from the sheath was about 55 cm. or 22 inches.10,11 The in- terval of time from contact of the glans penis with the vulva to ejaculation averaged 1.0 second. Semen emis- sion time averaged 0.29 seconds. During more than half of the ejaculations by 8 Holstein bulls a twisting of the glans penis was observed ranging from a slight bending to a 360° counterclockwise coil 6 cm. in outside diam- eter. In the ram the urethral or vermiform process en- gorges with blood, the urethral dilatation in the base of the process fills with semen and the semen is forced through the narrow orifice at the end of the urethra under considerable pressure producing a back and forth spray- ing or “fire hose” effect at the time of ejaculations.9 In the boar the corkscrew glans engages in the thick-walled, spiral, transverse ridges of the sow’s anterior vagina and cervix that are erect and edematour at estrus. The por- cine penis becomes “locked” in the cervix by further erection and dilation of the corpus cavernosum before ejaculation commences. In the dog two stages of coitus have been described.73 The first stage which lasts several minutes is character- ized by intromission without erection, which is made possible by the large os penis, followed by the marked enlargement of the bulbus glandis which is rigidly an- chored to the os penis that prevents the withdrawal of the penis from the caudally constricting vestibular struc- tures of the bitch. During this first stage the sperm-rich fraction of the semen is ejaculated. The second stage of coitus lasting 5 to 45 minutes is characterized by the male dismounting and facing in the opposite direction from that of the bitch. This results in an 180° bending of the penis in the middle of its body caudal to the os penis. This act delays detumescence by causing venous occlu- sion. The major portion of the seminal volume is ejacu- lated during this stage into the “closed” vagina. This may possibly assist in forcing the semen cranially into the uterus. Human restraint to impose the first stage posture during the entire act may result in reduced fertility.73 The process of ejaculation starts in the epididymis and travels along the ductus deferens. At the same time the walls of the accessory glands contract and force their contents into the urethra. Sexual stimulation in the bull and possibly males of other species may involve oxy- tocin release as an increased volume and total number of spermatozoa of the ejaculate followed oxytocin injec- tion.6 It would seem logical that oxytocin might be in- volved in the transport of semen in the epididymal tail and the ductus deferens. The urethra is emptied by the rhythmic contractions of the urethral, ischiocavemosus, and bulbocavemosus muscles.— The stallion, for ex- ample, requires about 10 seconds for complete ejacula- tion, and about 10 pulsations of the urethra occur ap- proximately a second apart. Semen and the Ejaculate Semen or sperm is the entire seminal discharge of the male during normal ejaculation. It consists of cellular elements, or spermatozoa produced in the seminiferous tubules, and seminal plasma or the liquid portion of the772 VETERINARY OBSTETRICS semen produced by secretions of the seminiferous tub- ules, epididymis, ducti deferentes, and ampullae, vesic- ular, prostate, and bulbourethral glands. Sperm cells constitute about 10 percent of bull semen by volume. Two to 5 percent of boar semen is made up of sper- matozoa and epididymal secretions. The amount of se- men and concentration of spermatozoa varies greatly be- tween species and individuals. (See Table 23.) In species having photoperiodic breeding and nonbreeding seasons variations in semen volume, concentration of sperma- tozoa, testosterone and LH plasma concentrations and libido occurred between these seasons.-’33 Environmen- tal influences had little or no effect on semen output in AI bulls.11 By “teasing” bulls before service the amount of semen and the numbers of spermatozoa per ejaculate can be increased.15b In stallions such “teasing” may in- crease semen volume but does not increase spermato- zoan numbers.23b Some bulls producing a small volume of semen with a low total number of sperm cells in either collection with the artificial vagina or electroejaculation may produce larger ejaculates with much greater sperm cell numbers if given 50 to 100 units of oxytocin intra- muscularly 5 to 10 minutes before collection. Frequent ejaculation reduces the amount of semen and the concentration of spermatozoa and if carried to ex- tremes, as in depletion or exhaustion trials, marked re- ductions may occur. These trials have been used exten- sively as a method of estimating sperm reserves in the live animal. In 44 depletion trials in 21 adult bulls where 20 consecutive ejaculations were collected in an artificial vagina from each bull within 1-1/2 to 7 hours, the av- erage volume of semen declined from 4.2 ml. to 2.1 ml. between the first and twentieth ejaculate. The concen- tration of spermatozoa decreased from 1.35 billions per ml. to 0.3 billions per ml. and the total average number of spermatozoa per ejaculate decreased from 5.8 billion to 0.65 billion. Except for a slight reduction in semen volume, semen characteristics including concentration of sperm cells had returned to normal within 7 days.5 Weekly output of spermatozoa was increased 112 percent in 10 Table 23. Semen Characteristics in Domestic Animals Semen Constituent Bull Stallion Ram (Buck) Boar Dog Tom Volume (ml) 4* (1-15)** 70 (30-250) 1 (0.7-3.0) 250 (125-500) 10 (1.0-25.0) 0.04 (0.01-0.12) Spermatozoan Concentration (millions/ml) 1200 (300-2500) 120 (30-600) 3000 (1000-6000) 150 (25-1000) 125 (20-540) 1730 (96-3740) pH 6.8 (6.2-7.5) 7.4 (7.0-7.8) 6.8 (6.2-7.0) 7.4 (7.0-7.8) 6.7 (6.0-6.8) 7.4 Total Spermatozoa per Ejaculum (billions) (Approx.) 4.8 8.4 3.0 37.5 1.25 0.057 Fructose (mg/100 ml) 530 (150-900) 2 (0-6) 250 13 (3-50) 0 — Glycerylphosphorylcholine (mg/100 ml) 350 (100-500) (40-120) 1650 (1100-2100) (110-240) 180 (110-240) — Potassium (mg/100 ml) 140 (80-210) 60 90 (50-140) 240 (80-380) — — Sodium (mg/100ml) 230 (140-280) 70 190 (120-250) 650 (290-850) 90 (50-124) — Phosphorus (Total in mg) 80 17 375 66 13 — Citric Acid (mg/100 ml) 700 (300-1100) 25 (8-60) 140 (110-260) 80 (60-100) Trace — Inositol (mg/100 ml) 35 (25-46) 30 (20-47) 12 (7-14) 530 (380-630) — — Sorbitol (mg/100 ml) (10-140) 40 (20-60) 92 (76-120) 12 (6-18) 0 — Ergothionine 0 (40-110) 0 (6-23) — — Other substances found in seminal plasma include calcium, magnesium, chloride, carbon dioxide, proteins (1-7 gms/100 ml), amino acids (cattle and sheep), lipids, urea, uric acid, lactic acid, ascorbic acid, phosphatase, muco-proteins, fatty acids, vitamins (riboflavin), peptides, other enzymes, hormones, and water (85-98%), * = average, **( ) = Range.INFERTILITY IN MALE ANIMALS 773 bulls by collecting six ejaculates per week instead of two. Bovine semen collected daily showed no difference in ability to store or freeze, fertility, abnormalities of sper- matozoa, motility, or pH from semen of bulls collected only once weekly.1617 The volume of semen, concentra- tion of spermatozoa, percent motility and total sperma- tozoa per ejaculate for bulls collected one time per week vs bulls collected 6 times per week were 9.5 vs 6.2 ml., 1.9 vs 0.8 billion/ml., 63 vs 69 percent and 17.8 billion vs 4.8 billion per ejaculate, respectively. Deficiencies in the quality of semen of abnormal bulls may be revealed by a high frequency of collection but are not caused by a high frequency of collection.3,4,5 Semen characteristics were most severely affected by a high frequency of ejac- ulation in young immature bulls and with sexual rest they took longer to return to normal.34 A study of 350 beef bulls and 870 dairy bulls from 1958 to 1966 indicated that beef bulls comprised a dif- ferent “population” than dairy bulls.10 Beef bulls had lower sperm cell production, lower post-freeze motility and higher numbers of abnormal sperm cells (50 percent of beef bulls had above 10 percent abnormal cells). Beef bulls reached puberty one to three months later, and their libido was generally lower than dairy bulls. The period of recovery after ejaculation was not evident in beef bulls as in dairy bulls. Once a beef bull was sexually stimu- lated 4 or 5 successive ejaculates could be collected in nearly the same time as required to obtain the first ejacu- late. Sexual preparation did not significantly increase sperm cell output in the following ejaculate in beef bulls.11 A stallion performed 12 normal services or covers within 72 hours. Two days previously he had ejaculated 50 ml. of semen containing 8 billion spermatozoa. On the twelfth ejaculate 90 ml. of semen containing 4 billion spermatozoa were delivered.18 In a recent depletion trial in which 5 ejaculates were collected at hourly intervals from 2 to 3 year-old, 4 to 6 year-old and 9 to 16 year- old stallions the sperm cell numbers per ejaculate de- clined from 4.5, 9.5 and 11.4 billion to 0.5, 1.1 and 1.2 billion respectively in the first and fifth ejaculate.—33 In depletion trials with stallions an average of 20.8 billion spermatozoa were obtained in each trial. After one day of sexual rest 11.8 billion of spermatozoa were obtained in a second depletion trial. With 5 days of sexual rest after the first depletion trial 25.7 billion spermatozoa were collected. Only 2 to 4 collections could be made in each depletion trial with stallions due to a lack of libido.86 Stallions ejaculated daily during the breeding seasons produce about 5 billion spermatozoa per day. In an exhaustion test a ram ejaculated 42 times in 9 hours and still delivered a total 100 million spermatozoa in the last ejaculate.24 In dogs libido remained high with one to two ejacu- lations per day. The total sperm cell count per ejaculate dropped from 580 and 548 million in dogs collected 2 and 3 times per week to 286 million and 147 million in dogs collected daily or twice daily, respectively. The to- tal number of spermatozoa per ejaculate returned to nor- mal after 2 to 3 days of sexual rest.9 In boars collected once every 4 days and once a day for 20 days the average ejaculate volume dropped from 286 to 193 ml., the sperm cell concentration from 275 to 143 million per ml. and total average daily sperm cell numbers from 55 to 24 billion. No changes were noted in percent motility, percent abnormalities, or pH in the same boars on the two frequencies of ejaculation.15 There may be a great variation between males in the same spe- cies in respect to their ability to copulate frequently and produce a satisfactory ejaculate. (See Table 23.) In the pig, horse and dog the seminal plasma placed in the uterus during coitus is in contact with the sper- matozoa for a period of time in the uterine lumen before some of the latter enter the tubes. While in man, cattle, cats and sheep the sperm cells are in contact with the seminal plasma in the vagina, after ejaculation a rela- tively shorter period of time before the cells migrate into the cervical canal. In all animals however the seminal plasma is not necessary for sperm cell metabolism or prolonged survival in the female genital tract. The pos- sible role of seminal plasma in the various species has been reviewed.25 Fructose is the normal sugar providing a source of en- ergy for spermatozoa in the semen of the bull, ram and buck, but is low in the boar, very low in the stallion and absent in the dog. It is produced mainly by the vesicular glands. The rate of fructolysis in semen is generally cor- related with the concentration of spermatozoa. It is also related to the availability of oxygen and the buffering capacity of the seminal fluid. Spermatozoa can utilize glucose for energy as well as or better than fructose. Sorbitol is a sugar alcohol that can be oxidized to fruc- tose and provide a source of energy. Lactic acid in se- men increases as fructose is broken down and may reach levels in the bull and ram where it immobilizes the sper- matozoa. The metabolism of sperm cells is characterized by appreciable respiratory activity. Glycerol when added to semen protects spermatozoa during the freezing pro- cess but is not readily oxidized by the cells. Of the amino acids in seminal fluid, glycine has been shown to im- prove sperm cell survival. Glycerylphosphorylcholine is present in high levels in epididymal secretions. By means of a compartmental analysis model in bulls, the mean volume contributions to the ejaculate were 32 to 38 per- cent (1.5 to 2.0 ml.) from the vesicular glands, 31 to 36774 VETERINARY OBSTETRICS percent (1.7 ml.) from the epididymides, and 31 to 32 percent (1.5 to 1.7 ml.) from the prostate and bulboure- thral glands.29 Inositol from the vesicular glands occurs in a high concentration in boar semen where it may act as an os- motic pressure regulator. Ergothionine, a sulphydryl- containing compound from the vesicular glands, occurs in appreciable amounts in boar and stallion semen. An antiagglutinin that prevents the head to head agglutina- tion of spermatozoa is also found in the seminal plasma. Dog semen contained 7 times as much copper and 20 times as much zinc as corresponding blood samples.7 Catalase has been found at low levels in bull and ram semen, 0.3 to 1.1 units per ml., and its addition to bull semen prolonged sperm cell survival by preventing the formation of hydrogen peroxide.13 The sticky, gelatinous, tapioca-like material secreted from the bulbourethral glands in the boar make up about 20 to 30 percent of the total porcine ejaculate,32 and may act to help seal the cervix to prevent a backflow of se- men during or after ejaculation. In stallions this heavy, glairy, gelatinous substance is uncommon in light Thor- oughbred horses but may be present in certain individ- uals or certain ejaculates in amounts of 30 to 50 percent or more of the total ejaculate. Most male animals have a low level, below 100 ng/ ml. of prostaglandins in the seminal plasma. While the ram, buck and man have higher levels. Their function, if any, has not been determined. Possibly their effect on the smooth muscle of the female reproductive tract may aid the transport of spermatozoa.-’8,25 Ram and bull semen which have a high concentration of spermatozoa are opaque white in color with a creamy consistency. The boar, stallion and dog semen which have a much lower concentration of sperm cells have a pearly white to grey translucent color with a more watery con- sistency. The difference between species in the volume of semen is largely due to the amount of secretion from the accessory glands. Coitus and ejaculation are long in the boar and dog, moderately long in the horse, and very short in the bull, ram and buck. In the boar and the dog most of the “sperm- rich” fraction of the semen is ejaculated the first 3 to 6 minutes of coitus. In boars there may be several episodes during the long ejaculation characterized by the passage of “sperm-rich” fluid in between the longer periods in which gelatinous and “sperm-poor” fractions are emit- ted. The ejaculate of all domestic animals can be divided roughly into 3 portions. The first is a sperm-free, clear, watery secretion probably from the diffuse portion of the prostate or possibly the bulbourethral glands or vesicular glands that may often be observed in some animals in the precopulatory period of sexual arousal. This is fol- lowed by the relatively short period of the emptying of the ampullae of the ducti deferentes and the urethra by the sperm-rich fraction. The third phase or portion of ejaculation is much longer and composed mainly of sperm- poor seminal plasma from the accessory glands. This lat- ter portion in the boar and stallion contains the gelati- nous material. In the stallion the last part of this third portion of the ejaculate is spoken of as the “tail end” or “dismount” sample. It is not representative of the entire ejaculate in the horse or in other species. This last phase of ejaculation comprises about 40 to 60 percent or more of the entire volume of the ejaculate. In the bull the pre- sperm fraction is low in fructose and the sperm-rich and post-sperm fractions have a high fructose content indi- cating admixture with the secretions of the vesicular glands.12 Frequency of Service—Since spermatozoan produc- tion is a continuous process not affected by frequency of ejaculation, theoretically there should be no limit to the number of services. There are, however, limitations in all males to the number of services possible within a given time. (See Table 24.) As noted previously, frequent re- peated ejaculations over a relatively short period of time tend to cause a reduction in sexual desire, semen vol- ume, and number of spermatozoa per ejaculate. Young or immature males should be used conservatively inas- much as the decline in semen quality is probably more easily produced and undesirable behavior associated with decreased sexual desire might develop. Each male should be handled, observed, and bred as an individual. In young males a certain degree of size must be attained before coitus can be performed with physical safety. Establishing proper breeding habits in male animals and not permitting these habits to develop in a haphazard fashion is highly important.24 The frus- tration of small, immature males following unsuccessful attempts to copulate with females that are too large, are improperly restrained, or in an unsuitable location, con- ditions which may result in slipping and falling, or in head injuries because of a low ceiling, may produce both physical and psychological injury. Both may have a pro- longed effect on a sire’s attitude toward service. Some males develop sexual desire slowly. Proper development of breeding habits in a male is just as important as train- ing a heifer to milk or a horse to ride. Patience, under- standing and avoiding overuse or harmful experiences are necessary for the young male. In male animals offered frequent opportunities for copulation, libido usually declines before the quality of the ejaculate is lowered to a degree that would affect fertility. In 16 bulls and 8 rams under natural matingINFERTILITY IN MALE ANIMALS 775 Table 24. Approximate Guide to the Frequency of Service and the Number of Females Allotted to Male Domestic Animals* Immature Males Mature Males Hand Breeding Hand Breeding No. of Females No. of Females Species No. of Services/week per Season (year) No. of Services/week per Season (year) Stallion 2-5 15-40 3-12 30-120 Bull 2-4 20-60 4-12 80-120 Boar 2-4 10-40 4-10 30-60 Dog 1-2 (20-40) 2-6 30-80 Ram (Buck) 6-12 (30-40) 6-24 40-80 Pasture Breeding Pasture Breeding (No. of Females) per season (year) (No. of Females) per season (year) Bull 10-15 10-25** Boar 10-20 20-40 Ram (Buck) 20-30 40-80*** *This guide will vary greatly for individual males according to their fertility, sperm producing capacity, degree of libido, age and physical condition. It will also be influenced by systems of management, size of pasture or range and nutrition of the sire and dam. Frequent short periods of sexual rest are desirable. **This figure is for range cattle with a limited breeding season. For dairy cattle on improved pasture with a year-long breeding season this figure could be increased 3 or 4 times. *** Vigorous yearling to adult rams may breed up to 30 to 40 ewes per month; 3 to 8 percent of goat flocks should be bucks. conditions, the bulls bred each estrous female an average of 1.73 times with the greatest number of services in a day being 10; in rams these respective figures were 4.03 and 29.31 In several matings with one female, libido de- clined in bulls and rams but finding another female in estrus rapidly restored their sexual drive. Collecting ejaculates 6 X weekly from 1 to 7 years of age greatly increased sperm harvest in AI bulls without harming the bulls’ growth, reproductive capacity or fertility.3 The average optimum weekly frequency of semen col- lection to maintain libido and to secure the greatest num- ber of spermatozoa were as follows: for the bull 4 ejac- ulations and 30 billion spermatozoa, for the stallion 3 to 4 and 30 billion, for the ram 20 and 25 billion, for the boar 3 and 110 billion, and for the dog 3 ejaculations and 2 billion spermatozoa, respectively.14 In mature bulls properly stimulated, two ejaculates collected twice per week (4 ejaculates/week) produced over 15 to 18 billion spermatozoa and was a practical procedure in AI studs. Coital Injuries in Male Animals Balanitis and posthitis of a severe nature frequently leading to adhesions and inability to protrude or retract the penis are occasionally observed in bulls, especially young bulls with great sexual desire the first few weeks on pasture with cows or heifers. Trauma and infection incurred by frequent service and contamination of the sheath or by exposure to the IBR-IPV virus in the cows’ genital tract may result in severe necrotic and pyogenic infections of the penis and prepuce. Young rams may be similarly affected. This type of infection involving the penis and prepuce will be discussed later in this Chapter. Injury or Trauma to the Penis—In rare instances in the stallion this may be due to the mare kicking at the stallion and striking the erect penis at the time of service. This may cause a hematoma, paraphimosis, laceration, or rupture of the penis. It is easily avoided by the proper supervision of breeding and by being certain that the mare is definitely in estrum. If necessary breeding hobbles or artificial insemination should be used in nervous, excit- able mares. In the bull, occasionally the penis catches on the vulvar lips, in a hymenal remnant, beneath the vulva, or when the bull thrusts and the penis is bent sharply at right angles by the cow suddenly collapsing, a rupture of corpus cavemosum and tunica albuginea or vessels, usually on the dorsal surface of the penis occurs opposite the attachment of the retractor penis muscle. A hema- toma is thus produced. This is often spoken of as a “frac- tured,” “ruptured,” or “broken” penis. This condition is rare in handbred dairy bulls but is not uncommon in beef bulls on pasture. The diagnosis and treatment of these penile injuries and lesions will be discussed later in this Chapter. Hemorrhage from the Prepuce and Penis following service may be due to tumors of the penis or to lacera- tions of the penis or prepuce. In rare instances bleeding776 VETERINARY OBSTETRICS from the urethra may be observed in stallions and bulls. It is usually of unknown origin. Lacerations of distal portion of the boar’s penis is not uncommon. It is usu- ally due to bite wounds inflicted by other boars or sows during breeding. Some of these injuries may require lo- cal wound therapy but most injuries recover without treatment.3b Several affected boars have had a small vas- cular outgrowth or polyp in the urethra, that caused blood to be mixed with semen at ejaculation.1 In several bulls observed by the author irregular-shaped calculi have lodged in the urethra and caused bleeding at the time of service but for a while only slight or moderate symptoms of difficult urination were observed. In young bulls there may occasionally be a small fistula in the glans penis extending into the corpus spongiosium cavemosum. On erection a fine stream of blood comes through the fistula. Some veterinarians have described the presence on the glans penis of blue-red raised areas or ulcers that rupture and bleed. In artificial breeding, rubber bands from the artificial vagina may slip over the penis at the time the bull thrusts. These usually cause deep lacerations or even amputation of all or part of the glans penis if they are not removed promptly. Such an occurrence may be pre- vented by not using rubber bands on the artificial vagina, or by tying them with cord so they cannot slip off. Oc- casionally persons trimming preputial hairs on bulls will snip off the tip of the penis if care is not taken to hold the penis caudal to the preputial orifice. Bleeding from the urethra in dogs is frequently a symptom of fracture of the os penis.2 Tumors should be removed. Sexual rest should be given most animals with hemorrhage from the prepuce and penis. In cases of urinary calculi the prognosis is often hopeless for future breeding. When bleeding occurs from the corpus through a fine fistula, sexual rest or surgery to close the defect are indicated. In young bulls observed by the author which bled from a fine fistula or ulcer on the glans penis the fertility of the bulls when bred nat- urally did not appear affected. Successful incision of the urethra of a few boars and removal of the vascular tissue causing the bleeding has been reported.1 Miscellaneous injuries at the time of coitus in the stallion may include kick injuries resulting in a ventral hernia, fracture of the hind limbs, or severe orchitis. Breeding hobbles, tying up a front leg and a twitch ap- plied to the mare may be indicated to prevent kicking. Application of heavily padded boots to the mares rear hooves has been used. In all breeds of animals especially the larger ones, the footing of the male should be good and the female restrained properly to prevent the male’s slipping and falling, possibly causing gonitis, seen most commonly in the bull; dislocation of the hip; fractures of the limb or pelvis; fractures of the spine; muscle or tendon strains or ruptures; as well as the harmful psy- chological effect on the male from falling or injuring himself during coitus. Large females should not be bred naturally to small males unless restrained with their rear limbs or all four limbs in a hole or pit. Occasionally inguinal hernia with strangulation of the intestine may follow service in stallions and cause severe colic within 1 to 3 hours. The author has observed 2 improperly-han- dled young bulls that fractured the humerus by dis- mounting from a cow sideways, with the affected front leg caught across the cow’s back. Hemospermia in male animals may be caused by pe- nile lesions or fistulas, urethritis, urethral strictures, and vascular lesions in the mucosa, secondary to infections or injury including stallion rings, lacerations or habro- nemiasis of the urethral process, strongyle larvae or in- fectious processes in the accessory glands and urinary calculi.1,6ab After a diagnosis has been reached, follow- ing a careful, complete examination utilizing visual, en- doscopic, cultural, radiographic examinations of the uro- genital organs, adequate, conservative, possibly surgical treatment, along with sexual rest is indicated. Blood cells in the ejaculate is often associated with low fertility.6 Vices of Male Animals Vices are much more common in male animals, es- pecially in the larger species, than in female animals be- cause many males are improperly handled or abused, closely housed or confined in dark, poor quarters, lack exercise, sunlight, normal surroundings, and associa- tions provided female or other castrated animals. Intact mature males are more aggressive than castrated males or females. Behavioral disorders in male animals are often related to or affect the sex act and may reduce copulatory efficiency. Androgens acting during the early period of differentiation organize neural tissue which mediates later sexual behavior in the male. The time this period occurs in the larger animals is not known but in rats it occurs within 5 or 6 days after birth. Masturbation or Onanism is observed in male ani- mals of all species. There is little or no evidence that it has any significant effect on fertility or even on libido or desire to copulate. If males are being used regularly and frequently for service the frequency of masturbation declines. In stallions being raced it is considered to have a det- rimental effect on training. Some persons consider ac- cumulations of smegma in the sheath cause irritation and masturbation in stallions and therefore advise regular cleansing of the sheath with soap and water. Regular ex-INFERTILITY IN MALE ANIMALS 111 ercise under harness or saddle, in a large outside pad- dock away from nonpregnant females or by providing “company” in the form of pregnant mares will help con- trol masturbation. Owners or veterinarians may also use a stallion (Man-of-War) shield or wire brush suspended just in front of the preputial opening, a metal (“bird- cage”) device over the glans or a plastic or adhesive tape ring applied just behind the glans penis to prevent erec- tion and masturbation. These latter ring-like appliances must be removed and penis cleaned once a week and before service or irritation may occur. It is the author’s observation that erection is common in the confined stal- lion but masturbation with ejaculation of spermatozoa is uncommon. He agrees with other authors7 that stallion rings are cruel and of questionable value in preventing the loss of spermatozoa. They may be the cause of ure- thral hemorrhoids and hemospermia. Masturbation as a cause of loss of libido is rare. In other animals regular exercise in a large outside paddock helps greatly to avoid masturbation. In bulls, rams, bucks or dogs a suture of stainless steel wire tied loosely through and across the preputial orifice may be of value. In the pet dog not used for breeding, castration can be performed. Boars may masturbate by inserting their penis into the preputial diverticulum and ejaculat- ing there, resulting in a condition called “balling up.” Once this vice has developed it can only be corrected by the surgical removal of the diverticulum.1 Young boars in artificial insemination studs should be kept isolated in separate pens to prevent pederasty or rectal “copula- tion” which is common in this species.5 It may occur occasionally in young bulls or rams running together. Viciousness in Males is often a result of confinement and ill treatment. Dairy bulls are usually confined and are much more apt to be dangerous than are beef bulls, that have freedom to run with the herd. Proper, intelli- gent handling of male animals from a young age, to- gether with regular daily handling, firm training, and ex- ercise makes most males fairly tractable and easily controlled. Since the larger intact male animals are usu- ally closely confined and caretakers are often afraid of them they are very apt to be teased, irritated and handled indecisively which tends to encourage viciousness. Once a male of a large animal species has become vicious and difficult to manage and this vice is well-developed it is a very difficult, dangerous, and often an impossible task to correct these habits without elaborate facilities and in- telligent, trained help. Not infrequently following cas- tration a formerly vicious stallion will retain his same disposition unless he is retrained. In this respect the vi- cious stallion is similar to the vicious “nymphomaniac” mare. Slowness in Breeding is often an acquired vice in male domestic animals that is favored by improper training, rough or ill treatment or painful accidents that have oc- curred at the time of copulation. This is discussed much more fully later in the section on impotency under forms of infertility in the male. Many male animals develop idiosyncrasies exhibited at the time of mating that usu- ally have their origin in various restraint practices em- ployed by owners prior to permitting service by the male. Other vices seen commonly in stallions as a result of close, unnatural confinement are stall-walking, weaving, cribbing and self-biting or mutilation. Stall walking may possibly be controlled by regular exercise, closing the stall tightly, hobbling, or tying the animal, by placing bales of straw around the stall or by putting the stallion in a large outside paddock or pasture. Cribbing should be controlled by a cribbing strap or by radical surgery. Weaving is difficult to correct, but proper exercise, a large and well-lighted box stall, or an outside paddock may be helpful. Using a cradle, a pole between the halter and a surcingle, or a muzzle may be indicated in self- biting stallions if proper exercise and management can’t control the vice. References Physiology of Male Reproduction—General and Hormones L Asdell, S. A. (1964) Patterns of Mammalian Reproduction, 2nd Ed. Comstock Publishing Co., Ithaca, N.Y. 2. Amann, R. P. (1981) A Review of Anatomy and Physiology of the Stallion, Eq. Vet. Sci., 1, 3, 83. 3. Ashdown, R. R. and Hancock, J. L. (1980) Functional Anat- omy of Male Reproduction, in Reproduction in Farm Animals, 4th Ed., edit, by E. S. E. Hafez, Lea and Febiger, Philadelphia. 4a. Bemis, H. E. and Emmerson, M. A. (1926) Observations on the Various Methods of Surgical Sterilization of Swine, Vet- erinary Pract. Bull. Iowa State Coll. 8, 1, 258. 4b. Cox, J. E., Williams, J. H., Rowe, P. H. and Smith, J. A. (1973) Testosterone in Normal, Cryptorchid and Castrated Male Horses, Eq. Vet. J. 5, 2, 85. 5a. Dutt, R. H., Simpson, E. C., Christian, J. C. and Barnhart, C. E. (1959) Identification of the Preputial Glands as the Site of Production of Sexual Odor in the Boar, J. An. Sci. 18, 4, 1557. 5b. Dykeman, D. A., Katz, L. S. and Foote, R. H. (1982) Behav- ioral Characteristics of Beef Steers Administered Estradiol, Tes- tosterone and Dihydrotestosterone, J. An. Sci., 55, 6, 1303. 6a. Erickson, R. J. and Dutt, R. H. (1963) Progesterone and 6 Methyl- 17 Acetoxy -Progesterone as Inhibitors of Spermiogenesis in the Ram, J. An. Sci., 22, 3, 856. 6b. Ford, R. S. (1968) Buck Deodorizing Possible Now with New Researched Method, Dairy Goat Jour., Nov., 3. 7. Habel, R. E. and Biberstein, E. (1952) Fundamentals of the Histology of Domestic Animals, edit, by Troutmann and Fe- biger (English Translation) Comstock Publ. Co., Ithaca, N.Y. p 356.778 VETERINARY OBSTETRICS 8. Hafez, E. S. E. (1980) Reproduction in Farm Animals, 4th Ed., Lea and Febiger, Philadelphia. 9a. Hughes, P. E. and Varley M. A. (1980) Reproduction in the Pig, Butterworth, Boston, London. 9b. Johnston, S. D., Larsen, R. E. and Olson, P. S. (1982) Canine Theriogenology, XI, Jour. Sci. for Theriog., 51. 9c. Larsen, R. E. (1980) Infertility in the Male Dog, in Current Therapy in Theriogenology, edit, by D. A. Morrow, W. B. Saunders, Co., Philadelphia, 646. 10. Macleod, J., Pazianos, A., and Ray, B. (1966). The Restoration of Human Spermatogenesis and the Reproductive Tract and Uri- nary Gonadotropins Following Hypophysectomy, Fert. and Steril. 17, 1,7. 11. Matsuyama, S., Richkind, M. and Cupps, P. T. (1967) Effects of High Levels of Exogenous Testosterone Propionate on Bo- vine Semen, J. Dairy Sci. 50, 3, 378. 12a. McDonald, L. E. (1975) Veterinary Endocrinology and Repro- duction, 2nd Ed., Lea and Febiger, Philadelphia. 12b. Mickelsen, W. D., Paisley, L. G. and Dahmen, J. J. (1982) Seasonal Variations in Scrotal Circumference, Sperm Quality and Sexual Ability in Rams, JAVMA, 181, 4, 376. L3. Meineke, C. F. and McDonald, L. E. (1961) The Effects of Exogenous Testosterone on Spermiogenesis of Bulls, Amer. J. Vet. Res. 22, 87, 209. 14. Pickett, B. W., Voss, J. L., Squires, E. L. and Amann, R. P. (1981) Management of the Stallion for Maximum Reproductive Efficiency, Colo. State Univ., Ft. Collins, Colo., 80523, 1-84. (Brochure) 15a. Rosenkrantz, H. and Ilievski, V. (1964) Estimated Testosterone Requirement of the Castrated Male Dog, Amer. J. Vet. Res. 25, 104, 47. 15b. Savard, K., Mason, N. R., Ingram, J. T. and Gassher, R. X. (1961) The Androgens of Bovine Spermatic Venous Blood, En- docrin. 69, 2, 324. 16. Schanbacher, B. D., and Lunstra, D. P. (1976) Seasonal Changes in Sexual Activity and Serum Levels of LH and Testosterone in Finnish Landrace and Suffolk Rams, J. An. Sci., 43, 3, 644. 17. Setchell, B. P. (1978) The Mammalian Testis, Cornell Univ. Press, Ithaca, N.Y. 18a. Shenoy, E. V. B., Daniel, M. J. and Box, P. G. (1982) The ‘Boar Taint’ Steroid 5a-androst-16-en-3-one (Androstenone A): an Immunization Trial, Acta Endocrin. (Kbh) 100, 131. 18b. Smith, P. W. and Parks, O. W. (1982) Characterization of Male Goat Odors I 6—transnonenal, Abstr. J. Dairy, Sci. 65, Suppl. 1, 48. 19. Steinberger, E. and Duckett, G. E. (1967) Hormonal Control of Spermatogenesis, Reprod. and Fertil, Suppl 2, 75. 20. Swenson, M. J. (1977) Duke’s Physiology of Domestic Ani- mals, 9th Ed., Cornell Univ. Press, Ithaca, N.Y. 21. Taylor, D. O. N., Thomas, J. W., Marburger, R. G. (1964) Abnormal Antler Growth Associated with Hypogonadism in White-tailed Deer in Texas, Amer. J. Vet. Res. 25, 104, 179. 22. Tepperman, J. (1962) Metabolic and Endocrine Physiology, Yearbook Medical Publishers, Chicago. 23. Turner, C. D. (1961) General Endocrinology, 3rd Ed., W. B. Saunders Co., Philadelphia. 24. Weibe, E. and Roberts, S. J. (1969) Unpublished studies. Puberty 1. Abdel-Raouf, M. (1960) The Postnatal Development of the Re- productive Organs in Bulls with Special Reference to Puberty, Acta Endocrin, 34, Suppl. 49. 2. Abdel-Raouf, M. (1965) Sexual Behavior and Semen Picture of Bulls of The Swedish Red and White Breed Between the Ages of 9 and 15 Months, Nord. Vet. Med. 17, 318. 3. Almquist, J. O. and Cunningham, D. C. (1967) Reproductive Capacity of Beef Bulls I. Postpuberal Changes in Semen Pro- duction at Different Ejaculation Frequencies, J. of An. Sci. 26, 1, 174. 4. Altman, P. L. and Dittmer, D. S. (1962) Growth Including Re- production and Morphological Development, Biological Hand- book, Federation of Amer. Soc. Exper. Biol., Washington, D. C. p 188. 5. Ashdown, R. R. (1962) Adherence Between Penis and Sheath in Beef Calves at the Time of Castration, J. Agric. Sci. 58, 71. 6. Bellows, R. A., Riley, T. M., Kieffer, N. M., Urick, J. J., Brinks, J. S. and Clark, R. T. (1964) Preliminary Studies of Sperm Production and Breeding Ability in Young, Straight and Crossbred Bulls, J. An. Sci. 23, 2, 593. 7. Bichan, P. E. and Hunter, W. K. (1961) A Study of the Sexual Development of a Stud of Performance-Tested Bulls, Proc. of IV Intern, Cong, on An. Reprod. (Hague), IV, 793. 8. Christian, R. E. and Wolf, F. R. (1963) Electroejaculation in the Young Beef Bull, J. of An. Sci. 22, 3, 855. 9. Coulter, G. H. and Foote, R. H. (1979) Bovine Testicular Mea- surements as Indicators of Reproductive Performance and their Relationship to Productive Traits in Cattle: A Review, Theriog., 11, 4, 297. 10. Hauer, E. P., Kellgren, H. C., McCraine, S. E. and Vincent, C. K. (1970) Puberal Characteristics of Quarter Horse Stallions, J. An. Sci. 30, 2, 321. 11a. Jochle, W. (1981) Review: Puberty and Reproductive Aging II, Animal Reprod., Rept., An. Health Newsletter, 4, 22, 48. (100 Old Boonton Road, Denville, N.J. 07834.) lib. Johnston, S. D., Larsen, R. E. and Olson, P. S. (1982) Canine Theriogenology, XI, Jour. Soc. for Theriog., 51. 12. Lagerlof, N. and Carlquist, H. (1961) The Semen of Boars of the Yorkshire Breed Between the Ages of Five and Nine Months, Proc. IV Intern. Cong, on An. Reprod. (Hague) IV, 818. 13. Lunstra, D. D. (1982) Testicular Development and Onset of Pu- berty in Beef Bulls, Progress Rept. #1, U.S. Meat Research Center, Clay Center, Nebr. 14. Lunstra, D. D. and Echtemkamp, S. E. (1982) Puberty in Beef Bulls: Acrosome Morphology and Semen Quality in Bulls of Different Breeds, J. An. Sci. 55, 3, 638. 15. Lunstra, D. D., Ford, J. J. and Echtemkamp, S. E. (1978) Pu- berty in Beef Bulls: Hormone Concentrations, Growth, Testic- ular Development, Sperm Production and Sexual Aggressive- ness in Bulls of Different Breeds, J. An. Sci. 46, 4, 1054. 16. Mather, E. C. (1980) Puberty in the Bull, in Current Therapy in Theriogenology, edit, by Morrow, D. A., W. B. Saunders Co., Philadelphia 339. 17. McCarthy, M. S.. Hafs, H. D. and Convey, E. M. (1979) Serum Hormone Patterns Associated with Growth and Sexual Devel- opment in Bulls, J. An. Sci. 49, 4, 1012. 18. McMillan, K. L. and Hafs, H. D. (1968) Pituitary and Hypo- thalamic Endocrine Changes Associated with Reproductive De- velopment of Holstein Bulls, J. An. Sci. 27, 6, 1614. 19. McMillan, K. L. and Hafs, H. D. (1969) Reproductive Tract of Holstein Bulls from Birth Through Puberty, J. An. Sci. 28, 2, 233. 20. Niwa, T., Mizuko, A. and Ito, S. (1959) Studies on the Age of Sexual Maturity in the Boar, Biol., Abstr. 35, 9, 1959.INFERTILITY IN MALE ANIMALS 779 21. Swierstra, E. E. (1977) Puberty and Spermatogenesis in the Boar, Proc. Ann. Mtg. Soc. for Theriog. St. Paul. Minn. 7. Scrotum and Heat Regulation of the Testes 1. Ferguson, M. B., Miller, O. C. and Graves, C. N. (1967) Internal Scrotal Temperatures of Dairy Bulls, J. An. Sci. 26, 6, 1498. 2. Phillips, R. W. and McKenzie, F. F. (1934) The Thermoregula- tory Function and Mechanism of the Scrotum, Missouri Exp. Stat. Bull, 217. 3. Waites, G. M. H. and Moule, G. R. (1961) Relation of Vascular Heat Exchange to Temperature Regulation in the Testis of the Ram, J. Reprod. and Fertil., 2, 213. The Testes, Spermatogenesis and Spermiogenesis la. Almquist, J. O. and Amann, R. P. (1961) Reproductive Ca- pacity of Dairy Bulls, II. Gonadal and Extragonadal Sperm Re- serves as Determined by Direct Counts and Depletion Trials: Dimensions and Weight of Genitalia, J. of Dairy Sci. 44, 9, 1968. lb. Barnes, M. A., Longnecker, J. V., Charter, R. C., Riesen, J. W. and Wordy, C. U. (1980) Influence of Unilateral Castration and Increased Plane of Nutrition on Sexual Development of Hol- stein Bulls, Theriog. 14, 1, 49. 2. Bloom, G. and Nicander, L. (1962) Electron Microscopical Study of the Protoplasmic Droplet of Mammalian Spermatozoa, In- temat. J. of Fert. 7, 4, 355. 3. Chenoweth, P. J. and Ball, L. (1980) Breeding Soundness Eval- uation in Bulls, in Current Therapy in Theriogenology, edit, by D. A. Morrow, W. B. 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D., Larsen, R. E. and Olson, P. S. (1982) Canine Theriogenology XI, Jour. Soc. for Theriog., 51. 10. Kennelly, J. J. and Foote, R. H. (1964) Sampling Boar Testes to Study Spermatogenesis Quantitatively and to Predict Sperm Production, J. An. Sci., 23, 1, 160. 11. Knudsen, D. and Bryne, N. (1960) The Spermyocytogenesis of the Bull, Acta. Vet. Scand., 1, 140. 12. Langman, J. (1963) Medical Embryology, Williams and Wil- kins Co., Baltimore. 13. Leblonde, C. P., Steinburger, E. and Roosen-Runge, E. C. (1963) Spermatogenesis, in Mechanisms Concerned with Conception, C. G. Hartman, Ed., Pergamon Press, McMillan Co., N.Y. City. 14. Mickelsen, W. D., Paisley, L. G. and Dahman, J. J. (1982) Seasonal Variations in Scrotal Circumference, Sperm Quality and Sexual Ability in Rams, JAVMA, 181, 4, 376. 15. Orbegin, M. C. (1961) Experimental Determination of the Rate of Transit of Spermatozoa in the Bull, Proc. IV Intemat. Congr. on An. Reprod. Hague, Vol. II, 232. 16a. Ortavant, R., Courot, M. and Hochereau, M. T. (1969) Sper- matogenesis and Morphology of the Spermatazoon, in Repro- duction in Domestic Animals, by H. H. Cole and P. T. Cupps. Academic Press, N.Y.C. and London, 2nd ed. 16b. Ott, R. S. and Memon, A. A. (1980) Sheep and Goat Manual, Vol. X, Soc. for Theriog. Hastings, Nebr. 68901, 48. 17. Swierstra, E. E. (1947) Duration of Spermatogenesis in the Boar, J. of An. Sci. 26, 4, 952. 18. Voglmayr, J. K. and Mattner, P. E. (1968) Compensatory Hy- pertrophy in the Remaining Testis Following Unilateral Orchi- dectomy in the Adult Ram, J. Reprod. and Fertil., 17, 179. 19. Woods, G. L., Garcia, M. C. and Kenney, R. M. (1980) Vari- ation in Testicular Size of Standardbred Stallions, Proc., 26th Ann. Conv. AAEP, Anaheim, Cal., 117. Morphology of Spermatozoa 1. Altman, P. L. and Dittmer, D. S. (1962) Growth Including Re- production and Morphological Development, Federation of Amer. Soc. Exper. Biol. Biological Handbook, Washington, D.C. 2. Baker, M., Cragle, R. G., Salisbury, G. W. and Van Demark, N. L., (1957) Spermatozoan Velocities in Vitro, Fert. and Steril., 8, 2, 149. 3. Bishop, D. W., (1962) Spermatozoan Motility, Amer. Assoc, for the Adv. of Science, Washington, D.C. 322. 4. Blom, E. and Birch-Andersen, A. (1960) The Ultrastructure of Bull Sperm, II. The Sperm Head, Nord. Vet. Med. 17, 193. 5. Blom, E. and Birch-Andersen, A. (1965) The Ultrastructure of Bull Sperm, II. The Middle Piece, Nord. Vet. Med. 12, 261. 6. Foote, R. H. (1966) Bovine Male Anatomy and Spermatogene- sis, Proc. 1st Tech. Confer. Nat. Assoc. Art. Breeders. 7. Hadek, R. (1969) Mammalian Fertilization, Academic Press, N.Y.C. 8. Hancock, J. L. (1966) The Ultrastructure of Mammalian Sper- matozoa, In Advances in Reproductive Physiology, A. McLaren, Ed., Vol. I. Academic Press, N.Y.C. 9. Janick, J. and MacLeod, J. (1970) Measurement of Human Sper- matozoan Motility, Fert. and Steril, 21, 2, 140. 10. Kojima, J. (1966) Electron Microscopic Study of the Bull Sper- matozoon, Jap. Jour. Vet. Res. 14, 1 and 2. 11. Lustig, G. and Lindahl, P. E. (1970) Activation of Motility in Bull and Rabbit Spermatozoa by Ultrasonic Treatment Recorded by a Photographic Method, Intemat. J. of Fert. 15, 3, 135. 12. Moeller, A. N. and Van Demark, N. L. (1955) In vitro Speed of Bovine Spermatozoa, Fert. and Steril. 6, 6, 506. 13. White, I. G. (1968) Mammalian Semen, Reproduction in Farm Animals, E. S. E. Hafez, Ed. 2nd Ed., Lea and Febiger, Phil- adelphia, 39. 14. Wu, A. S. H. and Newstad, J. D. (1966) Electron Microscope Study of Bovine Epididymal Spermatozoa, J. An. Sci. 25, 4, 1186. Sperm Transport, Maturation and Storage, and Accessory Gland Secretion 1. Almquist, J. O., Amann, R. P. and O’Dell, W. T. (1958) Sperm Reserves of Dairy Bulls as Determined by Depletion Trials and780 VETERINARY OBSTETRICS Post Slaughter Sperm Counts, J. Dairy Sci. 41, 5, 733. 2. Almquist, J. O. and Amann, R. P. (1961) Reproductive Capacity of Dairy Bulls II Gonadal and Extragonadal Sperm Reserves as Determined by Direct Counts and Depletion Trials: Dimensions and Weight of Genitalia, J. Dairy Sci. 44, 9, 1668. 3. Almquist, J. O. and Amann, R. P. (1962) Reproductive Capacity of Dairy Bulls VI. Effect of Unilateral Vasectomy and Ejacula- tion Frequency on Sperm Reserves; Aspects of Epididymal Phys- iology, Jour. Reprod. and Fertil. 3, 260. 4. Amann, R. P. and Almquist, J. O. (1962) Reproductive Capacity of Dairy Bulls VII Morphology of Epididymal Sperm, J. Dairy Sci. 45, 2, 1516. 5. Asdell, S. A. (1964) Patterns of Mammalian Reproduction, 2nd Ed., Comstock Publishing Associates, Ithaca, N.Y. 6. Berliner, V. (1963) Equine Medicine and Surgery, Amer. Vet. Publ. Inc., Wheaton, 111., p 635. 7. Bialy, G. and Smith, V. R. (1959) Cold Shock of Bovine Epi- didymal Sperm, J. Dairy Sci. 42, 12, 2002. 8. Blandau, R. J. and Rumery, R. E. (1964) The Relationship of Swimming Movements of Epididymal Spermatozoa to their Fer- tilizing Capacity, Fert. and Steril. 15, 6, 571. 9. Blom, E. (1968) Reproduction in Farm Animals, 2nd Ed., Edit, by E. S. E. Hafez, Lea and Febiger, Philadelphia, Pa. 10. Crabo, B. (1965) Studies on the Composition of Epididymal Con- tent in Bulls and Boars, Acta Vet. Scand. 6, Suppl. 5. 11. Day, F. T. (1940) The Stallion and Fertility, Vet. Rec. 52, 34, 597. 12. Faulkner, L. C., Hopwood, M. L. and Wiltbank, J. N. (1968) Seminal Vesiculectomy in Bulls, J. Reprod. and Fertil. 16, 2, 179. 13. Goyal, H. O. (1982) Light Microscopic and Ultrastructural Evi- dence of Epithelial Phagocytosis of Sperm in the Rete Testis and Ductuli Efferentes in the Bull, Amer. J. Vet. Res. 43, 5, 785. 14. Gustafsson, B. (1966) Luminal Contents of the Bovine Epididy- mis Under Conditions of Reduced Spermatogenesis, Luminal Blockage and Certain Sperm Abnormalities, Thesis, Dept, of Obst. & Gynec., Royal Vet. Col. Stockholm, Sweden. 15. Hart, R. G. (1968) The Mechaniams of Action of Cowper’s Se- cretion in Coagulating Rat Semen, J. Reprod. and Fertil. 17, 223. 16. Igboeli, G. and Foote, R. H. (1968) Maturation Changes in Bull Epididymal Spermatozoa, J. Dairy Sci. 51, 10, 1703. 17. Igboeli, G. and Foote, R. H. (1969) Maturation and Aging Changes in Rabbit Spermatozoa Isolated by Ligatures at Different Levels of the Epididymis, Fert. and Steril. 20, 3, 506. 18. Igboeli, G. and Rakha, A. M. (1970) Bull Testicular and Epi- didymal Functions after Long Term Vasectomy, J. An. Sci. 31, 1, 72. 19. King, G. J. and Macpherson, J. W. (1969) Influence of Seminal Vesiculectomy on Bovine Semen, J. Dairy Sci. 52, 11, 1837. 20. Lambiase, J. T. Jr. and Amann, R. P. (1969) The Male Rabbit V Changes in the Sperm Reserves and Resorbtion Rate Induced by Ejaculation and Sexual Rest, J. of An. Sci. 28, 4, 542. 21. Lino, B. F., Braden, A. W. and Turnbull, K. E. (1967) Fate of Unejaculated Spermatozoa, Nature, 213, 5076, 594. 22. Mann, T. (1964) The Biochemistry of Semen, John Wiley and Sons, N.Y.C. 23. Nalbandov, A. V. (1964) Reproductive Physiology, 2nd Ed., W. H. Freeman and Co., San Francisco, and London. 24. Paufler, S. K. and Foote, R. H. (1968) Morphology, Motility and Fertility of Spermatozoa Recovered from Different Areas of Ligated Rabbit Epididymides, J. Reprod. and Fert. 17, 125. 25. Phadke, A. M. (1964) Fate of Spermatozoa in Cases of Obstruc- tive Azoospermia and After Ligation of Vas Deferens in Man, J. Reprod and Fertil, 7, 1. 26. Pineda, M. H., Reimers, T. J. and Faulkner, L. C. (1976) Dis- appearance of Spermatozoa from Ejaculates of Vasectomized Dogs, JAVMA, 168, 6, 502. 27. Rao, A. R., Bane, A. and Gustafsson, B. K. (1980) Changes in the Morphology of Spermatozoa During their Passage through the Genital Tract in Dairy Bulls with Normal and Impaired Sper- matogenesis, Theriog., 14, 1, 1. 28. Ripley, P. L. (1963) Physiology of the Male Accessory Organs, in Mechanisms Concerned with Conception, C. G. Hartman, Ed- itor, Pergamon Press, McMillan Co, N.Y.C. 29. Roussel, J. D., Stallcup, O. T. and Austin, C. R. (1967) Selec- tive Phagocytosis of Spermatozoa in the Epididymis of Bulls, Rabbits and Monkeys, J. of Fert. and Steril., 18, 4, 509. 30. Shideler, R. K., Squires, E. L. and Voss, J. L. (1981) Equine Castration-Disappearance of Spermatozoa, Eq. Pract., 3, 2, 31. 31. Ventura, W. P., Freund, M. and Knapp, F. (1968) Motility of the Vagina, Uterine Body and Homs of the Guinea Pig. Effects of Semen and Male Accessory Gland Secretions, Fert. and Steril. 19, 3, 462. 32. Voglmayr, J. K. and Mattner, P. E. (1968) See The Testicles and Spermatogenesis. 33. White, D. G. and Lincoln, G. J. (1958) Riboflavin in Yellow Semen, Nature, 182, 667. Erection and Ejaculation 1. Beckett, S. B., Purohit, R. C. and Reynolds, T. B. (1975) Cor- pus Spongiosum Penis Pressure and External Penile Muscle Ac- tivity in the Goat During Coitus, Biol. Reprod. 12, 289. 2. Beckett, S. D., Reynolds, T. M., Walker, D. F., Hudson, R. S. and Purohit, R. C. (1974) Experimentally Induced Rupture of the Corpus Cavemosum Penis in the Bull, Amer. J. Vet. Res. 35, 6, 765. 3. Beckett, S. D., Walker, D. F., Hudson, R. S., Reynolds, T. A. and Purohit, R. C. (1975) Corpus Spongiosum Penis Pressure and Penile Muscle Activity in the Stallion During Coitus, Amer. J. Vet. Res. 36, 4, 431. 4. Beckett, S. D., Walker, D. F., Hudson, R. S., Reynolds, T. M. and Vachon, R. I. (1974) Corpus Cavemosum Penis Pressure and Penile Muscle Activity in the Bull During Coitus, Amer. J. Vet. Res. 35, 6, 761. 5. Evans, H. E. and Christensen, G. C. (1979) Millers’ Anatomy of the Dog, W. B. Saunders, Philadelphia. 6. Fellstrom, D., Kihlstrom, J. E. and Melin, P. (1968) The Effect of Synthetic Oxytocin upon Seminal Characteristics and Sexual Behavior in Male Rabbits, J. Reprod. and Fert. 17, 207. 7a. Grandage, J. (1972) The Erect Dog Penis: A Paradox of Flexible Rigidity, Vet. Rec. 91, 141. 7b. Hammond, J. (1955) Progress in the Physiology of Farm Ani- mals, Vol 2, Butterworth, London. 8. Lewis, J. E., Walker, D. F., Beckett, S. D. and Vachon, R. I. (1968) Blood Pressure Within the Corpus Cavemosum of the Bo- vine Penis, Jour. Reprod. and Fert. 17, 155. 9. Masson, Jorge. (1961) Personal Communication, Unpublished data. 10. Seidel, G. E. Jr. and Foote, R. H. (1967) Motion Picture Anal- ysis of Bovine Ejaculation, J. Dairy Sci. 50, 6, 970. 11. Seidel, G. E. Jr. and Foote, R. H. (1969) Motion Picture Anal- ysis of Ejaculation in the Bull, J. of Reprod. and Fert. 20, 313. 12. Watson, J. W. (1964) Mechanism of Erection and Ejaculation in the Bull and Ram, Nature, 204, 95.INFERTILITY IN MALE ANIMALS 781 Semen and the Ejaculate: Frequency of Service 1. Adams, Wm. (1970) Personal Communication. 2. Aitken, R. N. C. (1960) A Histochemical Study of the Acces- sory Genital Glands of the Boar, J. Anat. 94, (1) 130. 3. Almquist, J. O. (1982) Effect of Long Term Ejaculation at High Frequency on Output of Sperm, Sexual Behavior and Fertility of Holstein Bulls, J. Dairy Sci., 65, 814. 4. Almquist, J. O., Amann, R. P. and O’Dell, W. T. (1958) Sperm Reserves of Dairy Bulls as Determined by Depletion Trials and Post Slaughter Sperm Counts, J. Dairy Sci. 41, 5, 733. 5. Almquist, J. O. and Hale, E. B. (1956) An Approach to the Measurement of Sexual Behavior and Semen Production of Dairy Bulls, III Intemat. Congr. on An. Reprod., Cambridge. 6. Altman, P. L. and Dittmer, D. S. (1962) Growth Including Re- production and Morphological Development, Federation of Amer. Soc. Exper. Biol. Biological Handbook, Washington, D C. 7. Bartlett, D. J. (1962) Studies on Dog Semen, I and II. J. Re- prod. and Fertil. 3, 173 and 190. 8a. Bielanski, W., Rzasa, J. and Okolski, A. (1982) Prostaglandins in Stallion Semen, Theriog, 17, 2, 167. 8b. Bielanski, W. and Wierzbowski, S. (1961) Depletion Test in Stallions Proc. IV Intemt. Cong, on An. Reprod. The Hague, Vol. II. 279. 9. Boucher, J. H., Foote, R. H. and Kirk, R. W. (1958) The Eval- uation of Semen Quality in the Dog and the Effect of Frequent Ejaculation on Semen Quality, Libido and Depletion of Sperm Reserves in the Dog, Cor. Vet. 48, 1, 67. 10. Elliot, I. (1969) Symposium on the Management of Beef Cattle for Reproductive Efficiency, Ft. Collins, Colo. 11a. Fasten, J., Almquist, J. O. and Martig, R. C. (1970) Repro- ductive Capacity of Beef Bulls, IV Changes in Sexual Behavior and Semen Characteristics among Successive Ejaculations, J. An. Sci. 30, 2, 245. lib. Everett, R. W. and Bean, B. (1982) Environmental Influences on Semen Output (Bulls), J. Dairy Sci. 65, 1303. 12. Faulkner, L. C., Masken, J. F. and Hopwood, M. L. (1964) Fractionation of the Bovine Ejaculate, J. Dairy Sci. 47, 7, 832. 13. Foote, R. H., Voigt, V. J. and Schales, N. (1960) Catalase Content of Rabbit, Ram and Bull Semen, J. An. Sci. 19, 4, 1218. 14. Foote, R. H. (1969) Physiological Aspects of Artificial Insem- ination, in Reproduction in Domestic Animals by Cole and Cupps, 2nd Ed., Academic Press, N.Y.C. 15a. Gerritus, R. J., Graham, E. F. and Cole, C. L. (1962) Effect of Collection Interval on the Characteristics of the Ejaculate of the Boar, J. An. Sci. 21, 4, 1022. 15b. Hale, E. B. and Almquist, J. O. (1960) Relation of Sexual Be- havior to Germ Cell Output in Farm Animals, J. Dairy Sci., Suppl. 43, 145. 16. Hafs, H. D., Hoyt, R. S. and Bratton, R. W. (1958) Effects on Daily Ejaculation on Sperm Output, Fertility and Libido of Dairy Bulls, J. Dairy Sci. 41, 5, 734. 17. Hafs, H. D., Hoyt, R. S. and Bratton, R. W. (1959) Sperm Characteristics, Sperm Output, Fertility and Libido of Dairy Bulls, Ejaculated Daily or Weekly for Thirty-Two Weeks, J. Dairy Sci., 42, 4, 626. 18. McLeod, J. and McGee, W. R. (1950) The Semen of the Thor- oughbred, Cor. Vet. 40, 3, 233. 19. Mann, T., Minotakis, C. S. and Polge, C. (1962) Semen Com- position and Metabolism in the Stallion and Jackass, J. Reprod. and Fertil. 5, 109. 20. Mann, T. (1964) The Biochemistry of Semen and the Male Re- productive Tract, 2nd Ed., John Wiley and Sons, Inc., N.Y.C. 21. Maule, J. P. (1962) The Semen of Animals and Artificial In- semination, Technical Communication No. 15, Commonwealth Agricultural Bureau, Famham Royal, Bucks, England. 22. Nalbandov, A. V. (1964) Reproductive Physiology, 2nd Ed., W. H. Freeman and Co., San Francisco, and London. 23a. Pickett, B. W., Faulkner, L. C., Seidel, G. E. Jr., Bemdston, W. E. and Voss, J. L. (1976) Reproductive Physiology of the Stallion, VI Seminal and Behavioral Characteristics, J. An. Sci. 43, 3, 617. 23b. Pickett, B. W., Squires, E. L. and Voss, J. L. (1981) Normal and Abnormal Sexual Behavior of the Equine Male, An. Re- prod. Lab., Colo. State Univ. Ft. Collins, Colo. 80523. (Bro- chure) 24. Rice, V. A. and Andrews, F. N. (1951) Breeding and Improve- ment of Farm Animals, 4th Ed., McGraw Hill Book Comp. Inc., N.Y.C. 25. Rodger, J. C. (1975) Seminal Plasma, An Unnecessary Evil?, Theriog., 3, 6, 237. 26. Roberts, S. J. (1971) Veterinary Obstetrics and Genital Dis- eases, 2nd Ed., Woodstock Vt. 05091. 27. Rosenkrantz, H., Langille J. and Mason, M. M. (1961) The Chemical Analysis of Normal Canine Prostatic Fluid, Amer. J. Vet. Res. 22, 91, 1057. 28. Sack, W. (1968) Personal Communication. 29. Seidel, G. E. Jr. and Foote, R. H. (1970) Compartmental Anal- ysis of Sources of the Bovine Ejaculate, Biol, of Reprod. 2, 189. 30. Sojka, N. J., Jennings, L. L. and Hamner, C. E. (1970) Arti- ficial Insemination in the Cat (Felis Catus L.), Lab. An. Care, 20, 2, 198. 31. Sumner, S. L., Ancalmo, R. and Warnick, A. C. (1968) Be- havior of Bulls and Rams During the Breeding Season, J. An. Sci. 27, 4, 1197. 32. Swierstra, E. E. and Rahnefeld, G. W. (1967) Semen and Testis Characteristics in Young Yorkshire and Lacombe Boars, J. An. Sci, 26, 1, 149. 33. Thompson D. L. Jr., Pickett, B. W., Bemdtson, W. E., Voss, T. L. and Nett, T. M. (1977) Reproductive Physiology of the Stallion VIII, Artificial Photoperiod Collection Interval and Seminal Characteristics, Sexual Behavior and Concentrations of LH and Testosterone in Serum, J. An. Sci. 44, 4, 656. 34. Van Demark, N. L. and Mauger, R. E. (1958) Factors Affecting Replenishment of Sperm Numbers in Bulls Frequently Ejacu- lated, J. An. Sci. 17, 4, 1215. 35. White, I. G. and Macleod, J. (1963) Composition and Physi- ology of Semen, in Mechanisms Concerned with Conception, C. G. Hartman, Editor, Pergamon Press, McMillan, Co., N.Y.C. 36. White, I. G. (1968) Mammalian Semen in Reproduction in Farm Animals, E. S. E. Hafez, Editor, 2nd Ed., Lea and Febiger, Philadelphia. Coital Injuries and Vices of Male Animals 1. Adams, W. (1967) Personal Communication. 2. Bloom, F. (1954) Pathology of the Dog and Cat, Amer. Vet. Public. Inc. Evanston, 111. 3a. Fraser, A. F. (1968) Abnormal Behavior in Animals, Edit, by M. W. Fox, W. B. Saunders, Co., Phila., 179. 3b. Hurtgen, J. P. (1982) Reproductive Diseases of Swine, Vet. Clin.782 VETERINARY OBSTETRICS of N. Amer., Lg. An. Pract. 4, 2, 292-293. 4. Marvin, C. (1968) Abnormal Behavior in Animals, Edit, by M. W. Fox, W. B. Saunders Co., Phila., 208. 5. Turkheimer, A. R., Young, D. C. and Foote, R. H. (1958) Tech- nique for Semen Collection; Semen Production in Young Boars, Cor. Bet. 48, 3, 291. 6a. Voss, J. L. (1976) Etiology, Diagnosis, Treatment and Effect on Fertility of Hemospermia in the Stallion Proc. Ann. Mtg. Soc. for Theriog., Lexington, Ky 93. 6b. Voss, J. L. (1981) Hemospermia in the Stallion, in Management of the Stallion for Maximum Reproductive Efficiency by Pickett et al., Colo. State Univ. Ft. Collins, Colo., 80523, pp 79-84. 7. Voss, J. L. and Pickett, B. W. (1981) Stallion Masturbation, Eq. Vet. Data, 2, 5, 54. 8. Williams, W. L. (1943) Diseases of the Genital Organs of Do- mestic Animals, 3rd Ed. Louella Williams, Upland Road, Ithaca, N.Y. Nutrition and Infertility in the Male The nutritional requirements of males are similar to those of nonpregnant females. On the basis of our pres- ent knowledge, the qualitative and quantitative require- ments for reproduction in the male do not exceed those for the growth of young animals or for the maintenance of mature animals in a state of good health. In bulls, rams, and boars rations that are satisfactory for normal growth to 3 years of age are normal for reproduction.11 The requirements for pregnant, and especially lactating, animals are higher than for the male. In large animals the ration should include good quality roughage. The value of good pasture cannot be over-emphasized. The ration should be properly balanced in carbohydrates, protein, and minerals and supply the vitamins known to be es- sential for good reproduction. Although numerous at- tempts have been made to formulate rations that will in- crease spermatozoan production and semen quality, it still appears that there are no specific nutrients concerned only with fertility.12 In few fields are there more opinions with less supporting evidence than in the field of infertility.11 A definite deficiency of any single nutrient is seldom found. Natural-occurring deficiencies are usually mul- tiple. The breeding male should be kept in good physical condition and should not be permitted to become over- weight. A severe deficiency in nutrients affects the testes in a manner similar to ischemia, hypoxia and hypogly- cemia and results in a chronic degeneration of the sem- iniferous tubules.13b A low plane of nutrition is frequently encountered in practice. As physical deterioration progresses into in- anition in the male there occurs an atrophy of the testes, a decrease in the number of spermatozoa per ejaculate, and a progressive loss of sexual desire. Delayed puberty will occur when there is a low plane of nutrition in the young male animal.2,4 Underfeeding during the growth period had a limiting effect on sperm cell production at maturity in bulls.15 Thus a low plane of nutrition may adversely affect reproductive functions in the male but severe effects on reproduction are not observed unless emaciation and inanition are marked. A high plane of nutrition is frequently cited as a cause of infertility, especially in fat, overfed, obese, show an- imals. There is no experimental evidence that a high level of feeding and body condition has any effect on semen production. Fertile rams fitted for show continued to be fertile even though in a very high state of nutrition.8 Obesity did not increase rectal or scrotal temperatures or cause any degenerative changes in the testes. Some au- thors have suggested that certain male animals develop excessive fatness because of an endocrine disturbance such as hypothyroidism, that predisposes the male to in- fertility. This is possible but it has not been proven. Phlegmatic, lazy bulls tend to put on excessive weight. Rearing intensity did not affect a bull’s mating behav- ior.1 High body condition may result in slowness, difficulty or inability to copulate because of paunchiness, laziness, weaknesses in legs and feet and a lack of sexual desire in some males but this is not associated with defective spermatogenesis.4 Excessively fat bulls may possibly have enough fat around the testes in the scrotum, especially the dorsal part, to insulate the testes and affect sper- matogenesis but this has not been proven. Some very fat beef bulls are highly fertile. In some bulls excessive fat in and above the scrotum may be confused with an in- guinal hernia. When the obesity in these males is cor- rected by limited feeding and increased exercise the in- guinal fat is slow to disappear. Therefore high energy intakes are not desirable for bulls past the stage of rapid growth but moderately heavy early feeding may promote early semen production by hastening the onset of pu- berty. Feed Constituents. Under the usual conditions of management the possibility of deficiency in either the quality or quantitity of protein fed to males seems re- mote. When the protein in the ration was below 2 per- cent, low feed intakes, loss of weight, weakness and re- duced libido and sperm cell production occurred in rams and bulls.9,16 Urea was satisfactory as source of protein in ruminant male animals. Although some veterinarians have recommended feeding animal protein such as skim milk, fish meal, turkey mash, or other high-quality pro- tein pellets, there is no evidence that it is necessary, pro- viding adequate grain and good roughage are available.INFERTILITY IN MALE ANIMALS 783 Vitamin deficiencies are seldom observed as a cause of infertility in the larger male domestic animals if the roughage in the ration is near normal in quality or quan- tity. Vitamin A deficiency, if severe and characterized by night blindness and stiffness, may cause cessation of spermatogenesis and atrophy of the seminiferous epithe- lium and a decline in semen quality as well as a decrease in sexual desire. In young bulls vitamin A deficiency may result in cystic pituitary glands.3,5’13b Thirty-five to 100 micrograms of vitamin A per kilogram of body weight daily is ample for reproduction in bulls.11 There is little evidence that deficiencies of vitamins B, C, D, or E are even occasional causes of infertility. Although vitamin E is essential for reproduction in the rat there is no proof or indication that it is necessary for reproduction in do- mestic animals.I3b Mineral deficiencies affecting reproduction in male animals are rare. Deficiencies of calcium, manganese, zinc, iodine, potassium and selenium have not been proven to be causes of male infertility.I0 I3b Deficiencies of co- balt, iron, zinc and copper may cause anemia, lack of appetite and loss of weight, and thus have an adverse influence on male reproduction. These trace minerals, especially zinc which is high in concentration in ejacu- lates of animals, are essential constituents of enzymes.13b A lack of phosphorus, often associated with a lack of protein and low levels of vitamin A under natural con- ditions may cause reduced appetite, a loss in condition and reduced reproductive function. Osteopetrosis with accompanying spondylitis and arthritis in the bull may result from ultimobranchial body hyperplasia or neopla- sia caused by excessive dietary calcium.6 7 Arthritis and spondylitis may cause hesitancy or refusal to copulate. High dietary calcium levels may be caused by feeding alfalfa or clover hay and dairy grain rations fortified with minerals needed by lactating cows but not by bulls. Most reproductive disturbances related to nutrition are caused by underfeeding. If the males is fed a normal balanced ration that will produce normal growth or maintain normal health, reproduction will not suffer be- cause of nutritional deficiencies. In some areas owners feed special fortified rations to breeding males. These special fortified rations have added amounts of various types of protein, vitamins, especially vitamin A and beta- carotene, manganese, cobalt, phosphorus and other min- erals that when fed amply supply their supposed needs for a high level of reproduction. The necessity or value of these feeds is highly questionable. Along with proper nutrition and adequate water and salt, factors such as exercise, sunlight, pasture, and other environmental influences, including parasite control and routine vaccinations, play an important role in maintain- ing the health and activity of the breeding male and in prolonging his usefulness. References 1. Bane, A. (1954) Sexual Functions of Bulls in Relation to He- redity, Rearing Intensity and Somatic Conditions, Acta Agric. Scand. 4, 2, 97. 2. Bratton, R. W., Musgrave, S. D., Dunn, H. O., Foote, R. H. and Henderson, C. R. (1956) Semen Production and Fertility of Young Bulls Raised on Three Different Levels of Feed Intake, J. An. Sci. 15, 4, 1296. 3. Erb, R. E., Andrews, F. N., Hauge, S. M. and Ling, W. A. (1947) Observations on Vitamin A Deficiency in Young Dairy Bulls, J. Dairy Sci. 30, 9, 687. 4. Flipse, R. J. and Almquist, J. O. (1961) Effect of Total Di- gestable Nutrient Intake from Birth to Four Years of Age on Growth and Reproductive Development and Performance of Dairy Bulls, J. Dairy Sci. 44, 5, 905. 5. Ghannam, S., Alaliley, H. and Deeb, S. (1966) The Effect of Different Levels of Vitamin A on the Reproductive Organs of Young Bulls, Intemat. Jour, of Fertil. 11, 3, 306. 6. Krook, L., Lutwak, L. and McEntee, K. (1969) Dietary Cal- cium, Ultimobranchial Tumors and Osteopetrosis in the Bull; Syndrome of Calcitonin Excess, Amer. J. of Clin. Nutr. 22, 2, 115. 7. Krook, L., Lutwak, L., McEntee, K., Henrikson, P. A., Braun, K. , and Roberts, S. J. (1971) Nutritional Hypercalcitonism in Bulls, Cor. Vet. 61, 4, 625. 8. McKenzie, F. F. and Berlinger, V. R. (1937) The Reproductive Capacity of Rams, Mo. Agr. Exp. Stat. Res. Bull. 265. 9. Meacham, T. N., Cunha, T. J., Wamick, A. C., Hentges, J. F., Jr. and Hargrave, D. D. (1963) Influence of Low Protein Rations on Growth and Semen Characteristics of Young Beef Bulls, J. An. Sci. 22, 1, 115. 10. Neatherly, M. W., Miller, W. J., Blackman, D. M., Pate, F. M. and Gentry, R. P. (1972) Effects of Long Term Zinc De- ficiency on Feed Utilization, Reproduction Characteristics, and Hair Growth in the Sexually Mature Male Goat, J. Dairy Sci. 56, 1, 98. 11. Reid, J. T. (1949) Relationship of Nutrition to Fertility in An- imals, JAVMA, 114, 864 and 865, 158 and 242. 12. Rice, V. A. and Andrews, F. N. (1951) Breeding and Improve- ment of Farm Animals, 4th Ed., McGraw Hill Book Co., Inc. N. Y.C. 13a. Salisbury, G. W. (1944) A Controlled Experiment in Feeding Wheat Germ Oil as a Supplement to the Normal Ration of Bulls Used for Artificial Insemination, J. Dairy Sci. 27, 551. 13b. Setchell, B. P. (1978) The Mammalian Testis, Cornell Univ. Press, Ithaca, N.Y., 14850, 359-432. 14. Stevermer, E. J., Kovacs, M. F., Jr., Hoekstra, W. G. and Self, H. L. (1961) Effect of Feed Intake on Semen Characteristics and Reproductive Performance of Mature Boars, J. An. Sci. 20, 4, 858. 15. Van Denmark, N. L. and Mauger, R. E. (1964) Effect of En- ergy Intake on Reproductive Performance of Dairy Bulls, J. Dairy Sci. 47, 7, 798. 16. Wamick, A. C., Meacham, T. N., Cunha, T. J., Roggins, P. E., Hentges, J. R., Jr. and Shirley, R. L. (1961) Effect of Source and Level of Nitrogen on Semen Production and Libido in Rams, Proc. IV. Intemat. Congr. on An. Reprod., Hague, Vol. II, 202.784 VETERINARY OBSTETRICS Hormonal Causes of Infertility and Related Syndromes in Males In male animals there is no infertility condition due to a hormonal cause that uniformly responds to endocrine therapy. Therefore hormonal treatments for lowered fer- tility or impotency are usually disappointing and of ques- tionable value. A lack of sexual desire or libido and reduced sper- matogenesis with testicular atrophy may be caused by a failure of ICSH, LH and FSH to be released from the anterior pituitary gland by factors originating in the hy- pothalamus. There are many “stress” factors, the most important one being inanition due to a low plane of nu- trition, that may cause this failure. In rare cases, espe- cially in dogs, tumors in the pituitary area may cause atrophy of the pituitary gland and failure of gonadotropin production. More satisfactory response to treatment will follow a correct diagnosis of the cause or causes of a lack of libido or reduced spermatogenesis than the use of gonadotropic hormones in an empirical manner. Be- cause of their protein constitution animals become re- fractory to repeated doses of gonadotropic hormones. Successful results following their use is usually fortu- itous and can usually be explained by other therapeutic or management practices. If the pituitary gland is functioning normally and re- leasing ICSH, failure of libido is seldom caused by a lack of testosterone produced in the interstitial cells of the testes. Occasionally in young males, testosterone in- jections may hasten sexual maturity and improve sex drive. Even abdominal cryptorchid testes produce normal amounts of testosterone. Rarely Sertoli cell tumors in dogs and other males may produce sufficient estrogen to suppress the release of ICSH and cause impotency. Tes- tosterone has been used empirically in bulls with abnor- malities of spermiogenesis or evidence of an abnormal environment in the storage of sperm cells in the epididy- mis. As with gonadotropins; testosterone is seldom suc- cessful in the treatment of a lack of sex drive in adult intact males. Thyroidectomy in bulls and stallions re- sulted in lethargy and mild signs of impotency.8,9 Hy- pothyroidism may be present in some obese, lethargic males. Hypothyroidism in male animals has not been proven but a few fat males fed iodinated casein or in- jected with thyroid hormone have lost weight and be- come more alert with an improvement in libido. Thy- roxine therapy has little or no effect on spermatogenesis and is not uniformly or highly successful in males lack- ing sexual desire. Some bulls with low fertility have fasicular cortical nodules in the adrenal that apparently convert proges- terone into large amounts of cortisol.3 This results in a high concentration of spermatozoa and a low fructose concentration in the semen. Cryptorchidism is considered to be an inherited defect resulting in a failure of the fetal or neonatal testes to descend into the scrotum. The male is usually castrated or slaughtered. In humans cryptorchidism has been treated before puberty by gonadotropins or testosterone with very limited success. Most attempts to use hormones to in- duce descent of the testis have failed.1 As discussed previously in this Chapter, testosterone is released from the interstitial cells of the testis in a pulsatile or episodic manner about 7 or 8 times a day under the stimulation of LH (ICSH) released from the anterior pitiutary gland by GnRH from the hypothala- mus. For this reason the plasma concentrations of tes- tosterone vary in stallions during the day from 65 to 1600 pg/ml.2 Geldings have a level basal concentration of plasma testosterone of about 12 to 20 pg/ml. The in- jection of HCG, 10,000 IU, into a gelding has only very slight effect on plasma testosterone concentration. If HCG is injected into a stallion or cryptorchid (“rig”) or a male that has one or both testes retained in the inguinal canal or abdominal cavity, the plasma testosterone concentra- tion rises within one-half hour to 290 to 3750 pg/ml., average 1450 pg/ml.2 This dramatic prompt rise in plasma testosterone concentration in the true “rig” or cryptor- chid horse either one-half to one hour after the injection of HCG, demonstrated by pre- and post injection blood samples, is an excellent diagnostic procedure to conduct on horses that have no observable testes yet have strong male behavior. This test may also be supplemented by determining the plasma concentration of estrogen which is elevated in the stallion and equine cryptorchid due to the presence of sertoli cells that secrete estrogen. HCG injection however has little effect on the plasma estrogen concentration. Estradiol concentration in the plasma of stallions and geldings was 30 to 60 and 5 to 10 pg/ml, respectively.16 Treatment of stallions with 200 mg of testosterone proprionate IM every other day for 88 days or with an- abolic steroids, boldenone undecylinate, 1.1 to 4.4 mg/ kg or nandrolone decanoate, 1.1 mg/kg IM every three weeks for 15 weeks caused a decrease in spermatozoal concentration and motility, a decrease in total sperm per ejaculate and a reduction in scrotal width and testicular size as well as a depression in the plasma LH concen- tration.13,14’15 These treatments had no effect on sexual behavior, libido, or seminal volume or character. Even though these adverse effects were reversible and normal reproductive parameters returned by 90 days after ces- sation of treatment, testosterone or anabolic steroid ther-INFERTILITY IN MALE ANIMALS 785 apy is contraindicated in stallions.13'1415 Libido and abil- ity to ejaculate were gradually lost after castration of stallions. Testosterone restored both these aspects of sexual behavior. Estradiol at a high dosage restored libido how- ever the ability to ejaculate was impaired in geldings.16 Prostatic hyperplasia in old male dogs is due to excess testosterone produced by the testes and can be alleviated to some extent by injections of estrogens. A more sat- isfactory method is castration, which removes the source of testosterone in the body. Prostatectomy is difficult and only seldom performed in dogs. Estrogenic therapy is often temporarily successful because it inhibits secretion of the gonadotopic hormone FSH and LH, from the pi- tuitary gland necessary for androgen production from the interstitial cells in the testes resulting in atrophy of the prostate gland. No function has been ascribed to oxy- tocin in the male but it is most likely concerned with sperm transport and ejaculation. The oxytocin levels in the plasma of men and women are similar.12 Zearalenone, an estrogenic mycotoxin, from moldy com, besides producing effects in the female pig pre- viously discussed, caused reduced libido and depressed plasma testosterone and LH concentrations in young pre- pubertal and pubertal boars.1 At the level of zearalenone fed to the treated boars no adverse effects on body or testis size or sperm production was noted even though sexual behavior was delayed.1 Castration of male animals greatly reduces intermale aggression, and male sexual behavior including mount- ing, and in dogs and toms reduces urine marking or spraying, and objectionable roaming. In bucks and boars castration eliminates the male sex pheromone odor which is testosterone dependent. Progesterone therapy will fre- quently improve patterns of problem behavior in cas- trated or intact males and spayed females. Long-term therapy in males and females, especially the latter should be avoided because of possible side-effects such as mammary tumors or metritis.4 The doses recommended for dogs and cats are 2.2 to 11 mg/kg of medroxypro- gesterone acetate (Depo-Provera) IM or SC or 0.5 to 1.0 mg/kg of megestrol acetate (Ovaban) orally. About 50 percent of behavioral problems improve significantly with drug therapy. Like castration results of therapy de- pend on species, environmental background and individ- ual genetic differences.4 The author has used megestrol acetate and repositol progesterone, 500 mg., or proges- terone in oil 200 to 300 mg. IM every 24 to 48 hours to reduce undesirable sexual behavior in stallions prior to transport, showing or other activities. A recent study has demonstrated that active immu- nization or ram, lambs and bull calves, against Gn RH (LH-RH) can be produced by an adjuvanted product injected subcutaneously at 4 to 6 week intervals. This resulted in reduction in size or atrophy of the testes with low plasma gonadotropin and testosterone concentra- tions after 13 to 15 weeks.7 Further studies are necessary to develop this procedure to the point it may replace cas- tration. Many recent studies have been undertaken to produce immunoneutralization with active or passive im- munization with antibodies to steroid and gonadotropic hormones. Thes studies which have been reviewed76 show promise of producing significant future advances in re- production control in animals. The bulling syndrome in feedlot steers is a major problem for feedlot operators. Of 55,000 steers in one study, 1907 or 2.9 percent became bullers and resulted in an annual loss of about $325,000 due to injury and the need to isolate affected individuals.” The use of hor- mone implants to stimulate the growth rate was shown to be related to the incidence of bulling with a higher incidence with a combined progesterone and estradiol product.” However this syndrome is observed in feed- lots not using hormonal growth stimulants. It is not re- lated to hormonal levels or elevated estrogens in affected animals.6 The “buller” syndrome is apparently the result of management factors together with the inherited nor- mal bovine male sexual behavior that usually is sup- pressed and not exhibited in more isolated steers. Under feedlot conditions the addition of outside, strange ani- mals, irrespective of pen space available, causes an in- crease in the occurrence of bulling. Since a major stim- ulus to bovine male sexual activity and libido is to observe another male mount an animal, other steers become aroused and often wait their turn in line to ride the sub- missive or “chosen” steer.6 This latter animal very likely is a passive non-aggressive steer at the lower end of the “peck order.” Endocrine therapy for infertility in males is seldom indicated. It is usually used as a secondary or supportive line of therapy. It is improper and illogical to administer only hormones such as testosterone, thyroid products, or gonadotropic hormones in impotency, or gonadotropic hormones or thyroid products in cases of low fertility, and expect satisfactory results. A good history and care- ful clinical evaluation of the male should be made to determine, if possible; the etiology of the impotency or infertility, so that intelligent recommendations and treat- ments can be made. If hormones are used for therapy in male animals their limitations should be recognized. References 1. Berger, T., Esbenshade, K. L., Diekman, M. A., Hoagland, T. and Tuite, J. (1981) Influence of Prepubertal Consumption of786 VETERINARY OBSTETRICS Zearalenone on Sexual Development of Boars, J. An. Sci. 53, 6, 1559. 2. Cox, J. E., Williams, J. H., Rowe, P. H. and Smith, J. A. (1973) Testosterone in Normal, Cryptorchid and Castrated Male Horses, Eq. Vet. Jour. 5, 2, 85. 3. Cupps, P. T., Briggs, J. R., Garm, O. and Onstad, O. (1964) Metabolism of Progesterone by Adrenal Gland Homogenates from Bulls, J. of Dairy Sci. 47, 7, 803. 4. Hart, B. L. (1979) Problems with Objectionable Sociosexual Be- havior of Dogs and Cats: Therapeutic Use of Castration and Pro- gestins, Comp. Cont. Educ. 1, 461. 5. Hurxthal, L. M. and Musulin, N. (1953) Clinical Endocrinology, Vol. II, J. B. Lippincott Co., Philadelphia, Pa. 6. Irwin, M. R., Melendy, D. R., Amoss, M. S. and Hutcheson, D. P. (1979) Roles of Predisposing Factors and Gonadal Hor- mones in the Buller Syndrome of Feedlot Steers, JAVMA, 174, 367. 7a. Jeffcoate, I. A., Lucas, J. M. S. and Crighton, D. V. (1982) Effects of Active Immunization of Ram Lambs and Bull Calves, against Synthetic Luteinizing Hormone Releasing Hormone (LHRH), Theriog. 18, 1, 65. 7b. Jochle, W. (1982) Review: Immunological Aspect of the Control of Reproduction and Reprod. Rept. On Health Newsletter, 5, 29, (Sept. Oct.)—10 Old Boonton Road, Denville, N.J. 07834. 8. Kallfelz, F. A. (1982) The Thyroid Gland, In Equine Medicine and Surgery 3rd Ed. Edit, by Mansmann, R. A. and McAllister, C. S., Amer. Vet. Publ., Santa Barbara, Cal., 891. 9. Peterson, W. E., Spielman, A., Pomeroy, B. S. and Boyd, W. L. ,(1941) Effect of Throidectomy Upon the Sexual Behavior of the Male Bovine, Proc. of the Soc. Exper. Biol, and Med. 46, 16. 10. Pickett, B. W., Squires, E. L. and Voss, J. L. (1981) Normal and Abnormal Sexual Behavior of the Equine Male, Colo. State Exp. Stat., General Series 1004, St. Collins, Colo. 11. Pierson, R. E., Jensen, R., Brady, P. M., Horton, D. P. and Christie, R. M. (1976) Bulling among Yearling Feedlot Steers, JAVMA, 169, 5, 521. 12. Rorie, D. K. and Newton, M. (1964) Oxytoxic Factors in the Plasma of the Human Male, Fert. and Steril. 15, 2, 135. 13. Squires, E. L., Bemdtson, W. E., Hoyer, J. H., Pickett, B. W. and Wallach, S. J. R. (1981) Restoration of Reproductive Ca- pacity of Stallions after Suppression with Exogenous Testoster- one, J. and Sci. 53, 5, 1351. 14. Squires, E. L., Todter, G. E., Bemdtson, W. E. and Pickett, B. W. (1982) Effect of Anabolic Steroids on Reproductive Function of Young Stallions, J. An. Sci. 54, 3, 576. 15. Squires, E. L., Todter, G. E. and Pickett, B. W. (1979) The Effect of Androgenic Compounds on Reproductive Performance of Stallions. Proc. 25th. Ann. Conv. AAEP, Miami Beach, 421. 16. Thompson, D. L., Jr., Pickett, B. W., Squires, E. L. and Nett, T. M. (1980) Sexual Behavior, Seminal PH and Accessory Gland Weights in Geldings Administered Testosterone and (or) Estra- diol, J. An. Sci. 51, 6, 1358. Forms of Infertility in the Male According to Lagerlof these forms may be divided into three general categories: I. Reduced to Complete Lack of Sexual Desire and In- ability to Copulate (Impotentia coeundi). II. Inability or Reduced Ability to Fertilize due to Pa- thology of the Testes, Mesonephric Duct and the Accessory Glands (Impotentia generandi). III. Miscellaneous Diseases Affecting the Reproductive Organs. These conditions are present in males of all species. The degree of each condition present in males varies considerably between species, breeds, families, and in- dividuals. Variations also occur due to age, season, nu- trition, management and other factors. There are many degrees, from mild to severe, in each category of the various forms of infertility; a fact which demonstrates strikingly that in males there is a wide range of repro- ductive ability. Sometimes reduced sexual desire and ability to copulate may be associated with reduced fer- tility and poor quality semen but in most cases of infer- tility in males the two conditions are not related. In male animals semen collection is usually possible so that di- rect measurements of sperm quality and other tests may be applied. In examining males for infertility or sterility, accurate breeding and health records on the male and the herd should be obtained and examined. Secondly, there should be a careful, painstaking physical examination of the male including the observation of his mating behav- ior. Thirdly, one or more thorough semen examinations by a trained veterinarian or qualified laboratory are nec- essary. To evaluate the nature of a male’s infertility and sterility so that proper recommendations for therapy, treatment, or rest or disposal of the animal may be made, all three of the above examinations are essential. The prognosis in nearly all forms of infertility or sterility in male animals should be guarded. Reduced To Complete Lack of Sexual Desire and Inability to Copulate (Impotentia Coeundi) Potency is the physical capability of the entire body to coordinate and perform the male’s normal role at co- itus including erection, mounting, intromission and ejac- ulation. A lack of potency is observed in certain males in all species and is characterized by symptoms ranging from a complete lack of sexual interest and inability to copulate to a slight slowness or delay in exhibition of libido, mounting and copulating. Mating and copulatory behavior of males has been reviewed in various spe- cies:12'18 in bulls,5A14'19'20’27 in stallions,36'37'39'4546 in rams,9'23-26'40'41 in dogs,29 in bucks,423 in toms42b and in boars9 28 (see Chapter 12). In the female animal repro-INFERTILITY IN MALE ANIMALS 787 ductive behavior is relatively simple requiring only a willingness to stand to be mounted, or an attitude of im- mobility and acceptance. This attitude is primarily under the control or influence of estrogen which may be en- hanced by progesterone. In the male animal reproductive behavior is more complex requiring identification, seek- ing out, teasing and then the performance of the com- plicated act of copulation. This is under the control or influence of testosterone and other central nervous sys- tem mechanisms. There is little relationship between blood testosterone concentrations, libido and semen quality or quantity.7,9'11 The components of the act of copulation consist of sexual excitment, courtship, erection, mounting, intro- mission, ejaculation, dismounting and refractoriness. There is great variation in the duration of these com- ponents between species and individual males within a species. Mating behavior depends to varying degrees on visual, olfactory, auditory, and tactile cues. In all spe- cies visual and tactile cues are most important in the ac- tual act of copulation. In the dog olfactory clues are highly important in locating females in estrus. In sheep and swine and to a lesser degree dogs and horses the estrous female actively seeks the male. (See Coitus in Chapter 12.) Even blind males may copulate if experienced. Height, width, and color of the female, attitudes of acceptance, such as her stance as the male approaches, reaction of the female to pressure of the bull’s head on her rump or back, pressure of the shoulder on the mare’s rump or biting of the skin of the mare’s rear parts by the stallion and by the boar’s snout lifting the sow’s rear quarters, possibly odor of the rear parts and urine in horses and cattle and sheep utilizing the flehmen reaction, which is characterized by the lifted head, outstretched neck and curling of the upper lips that facilitate the introduction of odors or pheromones from the urine or genitals into the vomemasal organ, and vocalization by the stallion, boar, ram and buck are all significant factors in the pre- copulatory and copulatory acts of domestic male ani- mals. Sex drive, libido, sexual desire or potency of the male is largely determined genetically but environmental in- fluences play an important role in modifying it.2-9-22-23-41'44-47 It is well known that males differ widely in their ability to copulate frequently. In male guinea pigs, rams and bulls it was demonstrated that those with strong sex drive before castration returned to a strong sex drive when treated with increasing amounts of testosterone after cas- tration whereas animals with a weak sex drive returned to a weak sex drive.6,7,9,11,15 It was postulated that the differences between animals were due to the reactivy of their tissues, such as the brain, rather than to the dif- ferences in the amount of hormone secreted or present in the body. Thus variations in endocrine function may be linked with changed reactivity in the target organs and receptors especially the central nervous system, as well as in the hormone-producing organ. Many of the complex components of copulatory be- havior are determined by hormone action during various stages of development and may persist after castra- tion.7,1522 Studies on identical twin bulls showed many similarities in copulatory behavior between brothers but large differences between pairs.2 A significant relation- ship between the degree of libido in father and son groups of Swedish Red and White bulls was reported.27 Sex drive also varies between different lines of bulls within a breed.9 Herefords, Shorthorns, Guernsey and North Devons are genetically slow breeders.9,47 It is extremely difficult to evaluate the libido and mounting ability of Brahman, Zebu or Santa Gertrudis bulls since these breeds copulate mainly at night and rapidly so the copulatory act can only rarely be observed.9,35 Low libido in Zebu bulls was not as- sociated with a deficiency of LH or testosterone.9 It may be necessary in these breeds to place a bull with non- pregnant cycling cattle and then check them for preg- nancy in 40 to 80 days or to use the chin-ball mating device (Frank Paviour Ltd. Hamilton, New Zealand) to determine if the bull in question mounted cows in estrus. This latter device marks a cow’s back as the bull’s chin rubs over it during copulation. But European breeds, es- pecially the dairy breeds, will actively mount confined bulls, steers, and cows in any stage of the estrous cycle. Excessive ambient temperatures may have an adverse ef- fect on sexual activity in boars and bulls.9,14,28 Innate virility is reflected in the number and frequency of copulations that occur in a period of time and these vary widely between males. One study reported on two bulls one of which ejaculated over 40 times in 4 hours and another bull under similar conditions that ejaculated only 10 times.1 With a new stimulus animal or mount the first bull produced over 30 more ejaculates within the next hour. Some virile rams copulated an average of 20 times a day over a 7-day period whereas rams with low libido averaged only 4 copulations per day.23"26 When bulls with high and medium libido, 9 to 10 ser- vices vs 2 to 3 services within a daily 7-1/2 hour pasture mating period, were pasture bred at a ratio of 3 bulls to 114 cycling heifers for 3 weeks, the conception rate on first service was 77.5 vs 59 percent respectively for the high and medium libido bulls. By six weeks the differ- ence in conception for the two groups was only 2.3 per- cent. Thus bulls with high libido when exposed to large numbers of fertile heifers produced earlier conception.6 When only 10 to 12 ewes were single-sire mated to rams788 VETERINARY OBSTETRICS with either high or low libido there was no difference in conception rates.34 Depending on the degree of injury, the age of occur- rence and the degree of socialization permitted,22,24 le- sions of the medial preoptic area of the brain can impair male copulatory behavior in animals. Although libido is genetically influenced, mating ability has a learning component essential for its full expression. Sexual in- hibition of males is seen in all species of animals where rearing or management systems have prevented or re- duced socialization, especially in the young male, by isolation either singly, as may occur in valuable show animals, or in bachelor or all-male groups.9 29,33,41 In these all-male groups homosexual behavior is common. Fur- thermore in all-male groups the dominant males intim- idate the weaker more submissive males. Thus the latter lose their male aggressiveness, become sexually “inhib- ited” and may in the future be an undesirable or “prob- lem” male requiring careful reconditioning, training or culling. In pasture-bred herds or flocks, social ranking or dom- inance in males occurs. This is largely controlled by age, seniority and size, not by testosterone concentrations in the plasma or degree of libido.5,9,40 These dominant bulls or rams if infertile or lacking in libido could markedly decrease the conception rate since they prevent the less dominant or subordinate males from breeding and spend more time in this activity than in breeding cows. If bulls of different ages are used for natural breeding on pasture or range, the owner should consider dividing the females into smaller single-sire groups to obtain the highest fer- tility and to avoid injuries to males.5,9 This is favored by the observation that most pasture-breeding bulls rarely serve the same heifer twice. Also new females coming into estrus were more attractive to males and could promptly restore libido in bulls and rams apparently sa- tiated by formerly-bred females that might still be in es- trus. A study of the effects of the male to female ratio and single- vs multiple-sire groups on efficiency of bulls in natural service revealed that although a few bulls were unable to adequately service large numbers of cows, most bulls with acceptable semen quality, libido and mating ability would achieve good pregnancy rates at a ratio of 1:44 or 1:60 females.8,403 A bull to female ratio of 1:25 was inefficient in realizing a bull’s breeding potential. In multiple-sire groups social ranking affected the num- ber of females mated by each bull with subordinate bulls mating fewer females. It was difficult to identify bulls with acceptable libido and mating ability before the pas- ture breeding season. In over 2000 rams the incidence of sexually-inhibited rams reared separate from ewes when they were first placed with ewes was about 30 percent. Within a few days 80 percent of this inhibited group of rams devel- oped normal libido and sex drive. In about 2000 stallions examined each year for 3 years a low incidence of 0.34 to 1.07 percent of stallions with a lack of sexual desire or libido was reported.4,37,39,45 Impotency is not uncom- mon in stallions and is occasionally characterized by normal intromission and failure of ejaculation or abnor- malities of ejaculation. About 16.7 percent of 625 beef sires of English breeds selected by artificial insemination studs were disposed of because of problems in the collection of semen, mainly refusal to serve an artificial vagina.38 Very few Brahman or Zebu bulls will mount and ejaculate into an artificial vagina. Selection of bulls for their femininity, docility and gentleness tended to favor the selection of bulls with reduced desire.32 However in one study with Santa Ger- trudis bulls there was no relationship between masculin- ity and libido scores.8,9 Although sex drive, mating behavior or libido is largely genetic in nature it is subject to great modification by many environmental or physical factors. Males with a strong sex drive require more severe and prolonged en- vironmental and physical insults to significantly affect their mating behavior than do males with a weak sex drive. Environmental Factors Affecting Sex Desire and Copulatory Ability: Nutrition—Thin, emaciated, semi- starved males or those suffering from deficiencies of TDN., vitamin A, protein, and certain minerals such as phosphorus, zinc and cobalt may have a reduced sex drive. It inanition is severe enough, a complete lack of libido results. As indicated previously a low level of energy intake in growing males retards puberty and the onset of libido. Overfed males tend to become obese and lazy and often suffer from joint and foot troubles related to their over- weight condition. Excessive roughage fed to older bulls and rams may cause great enlargement of the rumen and abdomen interfering with normal, easy copulation and contributing to a lack of sexual desire. Male animals should be fed a properly balanced nu- tritive ration in adequate amounts to maintain a fair to good body condition. Exercise is important in maintain- ing active, healthy male animals. Systemic diseases—Any chronic or acute, severe, de- bilitating disease resulting in rapid or prolonged marked loss of weight, or in anorexia, depression, and weakness will cause a varying degree of loss of sexual desire. These diseases may include: pneumonia, enteritis, tuberculo- sis, paratuberculosis, severe mange and pediculosis, ac- tinomycosis, lymphocytoma, progressive fat necrosis,INFERTILITY IN MALE ANIMALS 789 severe internal parasitisms, advanced metastic tumors, alveolar periostitis, traumatic gastritis, severe chronic peritonitis, anaplasmosis and others. In anaplasmosis the loss of libido was associated with anemia and low hemo- globin and packed-cell volume. All bulls, especially in an AI stud, should be given magnets orally at about one year of age to prevent traumatic gastritis or pericarditis.10 Routine vaccinations of males vs the common infectious diseases of each species is indicated. Early and prompt diagnosis and treatment of all diseases of male animals is imperative to prevent possible loss of reproductive ability. Age—Very young males or old males frequently ex- hibit a reduced-to-complete lack of sexual desire. In older animals this may be due to a possible decline in testos- terone levels, to senility, to a loss of condition, to over- use or to arthritis. In experiments with identical twins it was shown that the time of onset of the lack of sexual desire in older bulls seemed to be largely determined ge- netically.2 There is a great deal of variation in young bulls in the onset of sexual desire and puberty. That this may be modified significantly by the nutritive level has been well- demonstrated. High feeding levels hasten the onset of puberty and sexual desire whereas low or subnormal feeding levels greatly retard the time at which the young male shows sexual desire and will mount and copulate with females. Management practices—Libido will vary within an- imals depending upon their inherent sex drive and the way they are trained, handled and managed. Young males which are isolated apart from others of their species are frequently frightened by the presence and activity of fe- males and other males and are slow to mount and cop- ulate because of their inexperience and timidity. This is not uncommon especially in bulls, rams, stallions and dogs. Young males should be carefully patiently and quietly trained and handled, especially if they are to have their semen collected in an artificial vagina. If a male associates “sex” with pain or punishment, he may decide to give up “sex”! Males with a lack of libido or naturally “slow breeders” can be easily discouraged and made slower by the insertion of a nose ring in a bull, harsh or abusive handling of the male by attendants, improper re- straint of the mount animal, improper footing, mount an- imals that are not in estrum or are too tall or wide, use of an artificial vagina that is too cold or hot, improper preparation of the male for mounting, breeding large males in a confined area with a low ceiling, unskilled persons using an artificial vagina, and excessive use of a male. Males lacking libido if continually used on the same fe- male for semen collection frequently develop sexual in- difference or satiation. Frequent changing of the stim- ulus or mount animals and the breeding site are indicated in bulls inclined to show a lack of libido. The presence of other males near the mount animal or in sight of the breeding male provides further stimulus.20,21 Proper sex- ual preparation of dairy bulls by prolonging the period of sexual stimulation beyond that adequate for mounting and ejaculation will produce higher quality semen with 36 to 250 percent more spermatozoa in the ejaculate.20,21 This is accomplished by a longer period of restraint be- fore permitting copulation, frequent changing of the mount animals, allowing several “false” mounts where copu- lation is not permitted, and moving the male to several different sites for “teasing” or “stewing.” Olfactory stimulation has not been demonstrated to play an im- portant role in the sexual behavior in bulls.19 Some stal- lions and jacks with low desire will fail to copulate with mares that are well-scrubbed and their tails bandaged. Others will so vigorously bite the withers and neck of the mare after mounting that erection is lost. Muzzling of these males or placing a heavy pad or blanket over the neck and withers of the mare is indicated. Other stal- lions will perform intromission and make thrusting movements but fail to ejaculate. This is common in stal- lions with reduced libido that are being used too fre- quently for their reproductive capacity.36,39,45 This failure to ejaculate can be noted by careful observation of the male at copulation by the absence of the usual “flag- ging” of the tail, which can be misleading, the absence of “pulsations” of the penile urethra felt by manual pal- pation during coitus, the failure of the stallion on dis- mounting to be “content” and “relaxed,” and also the lack of spermatozoa in the “tail-end” sample of the ejac- ulate collected from the penis as the stallion dismounts. Psychic factors interfering with normal coition and resulting in impotency have been observed in males of all species, especially stallions.36 Males with a geneti- cally lower sexual desire are much more apt to develop psychic refusal to breed. Usually there is no obvious clinical reason for this failure but if a good history is available it often reveals a traumatic, painful experience or several of them at the last few attempts at copula- tion.30 36 Some bulls and stallions with apparent psychic impotency may actually be afflicted with lesions of the spinal column as described in the next section.13,36 These bulls would apparently have good sexual desire, mount rapidly, have lordosis in the lumbar region and the penis would be directed at the escutcheon well below the vulva. Rapid pelvic thrusts and “seeking” motions would occur but penile exposure was greatly reduced. A prolonged period of sexual rest, a change in the site of copulation and careful preparation may be necessary to encourage790 VETERINARY OBSTETRICS the male to again start to breed. Shy or slow breeding boars may also be observed.9 Males should be properly handled and exercised to maintain optimum physical condition. They should be observed and managed so as to prevent their being bred excessively and losing their sexual desire. The frequency of breeding or the individual capacity of each male should be determined. If the male is bred repeatedly over a short period, this should be followed by a period of sexual rest. These above management factors should encourage the timid, slow breeding male, and control and conserve the vigorous active male. A reduced libido or sex drive in stallions is usually an important cause of concern for the owner(s) because of the value of the animal and the mares presented to him and the loss accrued from failure to impregnate most of “booked” mares within a breeding season. Furthermore in the stallion electro-ejaculation is presently not possi- ble and artificial insemination is limited to certain breeds. The lack of libido in the stallion not only encompasses his reluctance to tease, mount and obtain intromission but many “inhibited” stallions will fail to ejaculate even though a visually normal copulation occurs. The third associated condition in the stallion that is not reported in other male domestic animals is the occurrence of a functional disturbance of the neural mechanism control- ling ejaculation. This may result in a normal ejaculation of seminal fluid from the accessory glands without the ejaculation of spermatozoa from the tail of the epididy- mis and ductus deferens, azoospermia, or the release of urine into the ejaculate usually after the second or third jet of normal semen. No lesions have been found to ex- plain these functional or possibly psychic causes of re- duced libido and failure of ejaculation in the stal- lion.363745 It has been noted that “belling” or “flowering” of the glans penis of the stallion following erection is necessary for ejaculation. However if a normal erection does not occur, ejaculation can often be obtained by us- ing an artificial vagina3 without “belling” or “flowering” of the glans. Psychogenic impotence is common in stallions be- cause they are often reared in isolation, given little free- dom for socialization with other males and females dur- ing puberty, vigorously trained and disciplined firmly for exhibiting normal male sexual behavior during puberty and their early formative years and are expected to per- form instinctively and repeatedly the complete sex act promptly on being retired to stud duty. The most com- mon causes for impotency or lack of libido are overuse as a young stallion, injury during service from being kicked by the mare, and excessive discipline or chas- tisement during the sexual act. Overuse in older horses may cause reduced libido but they respond to sexual rest, while too often effects of overuse of a young stallion may be permanent.36 Impotency in a stallion may be manifested by indifference or excessive aggression to- ward the mare or the handler. The latter aggression is apparently caused by definite signs of frustration on being unable to ejaculate. The author observed this in one older stallion that was aggressive toward the mare, obtained intromission repeatedly, sweating profusely, and emitted a definite “squeal” of frustration on each withdrawal and dismount. Tests for the Measurement of Libido Since libido or potency is a highly significant com- ponent of the fertility of male animals but is difficult to assess easily and accurately, a number of test procedures have been developed and used.6,9 These include: 1) the percentage of times that copulation and ejacula- tion occurred when a male is exposed to a suitable “stimulus” on different occasions, (either by nat- ural service or collection with an artificial vagina) 2) the comparative number of completed or uncom- pleted copulations in a given time period with a “stimulus” female 3) observation of the time elapsed between exposure of a male to a “stimulus” animal and the first cop- ulation (This is called the “reaction” time) 4) assessment of the ability of a male (bull) (ram) to mount a restrained nonestrous female and ejaculate into an artificial vagina 3 times within a limited time (10 minutes) 5) assess the degree of sexual behavior or libido in beef or range-type bulls placed in a small enclosure with a stimulus or ovariectomized, estrogenized heifer (Up to 11 categories of behavior are listed) 6) using a “serving capacity test” by utilizing re- strained nonestrous cows at a ratio of 5 beef or dairy bulls to 2 to 3 cows and noting the number of services by each bull within a forty-minute time period. To be of diagnostic value these tests should be con- ducted under controlled conditions by experienced ob- servers. Some of these tests are not adaptable for use in individual or small herds. Hypothyroidism, hypogonadism, or a pituitary de- ficiency causing a diminished secretion of thyroxine, testosterone, or gonadotropin has not been described or proven by radioimmunoassays in normal intact male an- imals as a cause for a lack of sexual desire. It is possible that moderate deficiencies of these hormones might exist without clinical symptoms other than reduced sexual de- sire. It is the opinion of the author, based on results of hormone therapy, that a hormone deficiency is not aINFERTILITY IN MALE ANIMALS 791 common cause for a lack of sexual desire in male ani- mals. The prognosis in reduced sexual desire or impotency is guarded to poor depending upon the cause and the degree of the inherited or acquired lack of libido. The environmental factors causing or promoting the lack of sex drive can be overcome or moderated so that libido and breeding ability can reach their maximum expres- sion for the individual male. For males affected with a lack of libido it often requires 3 to 6 months or more of proper handling for sexual desire to noticeably improve after adverse influences have been corrected. Treatment should only be instituted after a careful study of the male’s breeding history, after a thorough physical examination of the male, and after careful and repeated observations of the male during coitus. Proper balanced and restricted amounts of good quality grain and rough- age should be provided to reduce obesity, if present, or to increase body condition if the male is too thin. Suf- ficient exercise should be provided. Chronic disease states, especially parasitisms in young males, should be cor- rected or alleviated if possible. The virility and service potential of the male should be assessed and the fre- quency of service should be reduced, if necessary, to the male’s inherent capacity. Often a period of several months of sexual rest is desirable in males that have been ex- cessively overused. If necessary, changes should be made in the location where service occurs to assure good foot- ing and adequate room. Proper restraint of the female, and care, consideration and patience in the handling of the “slow breeding” male may improve his sexual be- havior. If the male is collected with the artificial vagina then a skilled operator should be used. The artificial va- gina should be neither too warm nor too cold and ade- quate pressure should be applied to the penis. Some bulls prefer a coarse, heavy rubber liner to a light, smooth, thin one. A bull that is a “slow breeder” at an artificial insemination stud may benefit from a long period of sex- ual rest or transferring to another stud with a different group of handlers and different practices. Frequent changes of mounts and a longer period of “teasing” or stimula- tion is often helpful. In some instances libido may be restored by allowing the male to run loose with one or more quiet non-pregnant females in a pasture or enclo- sure. As a last resort when the condition fails to respond, bulls, rams and boars may be collected by electroejacu- lation and dogs may be collected by manual manipula- tion. Treatment of impotency in male animals, especially stallions, requires a careful complete history, a complete physical examination and careful repeated observations of the male before and during the sex act under a number of environmental and management situations and most importantly patience and understanding. This often re- quires a long period of sexual rest as horses have a long memory. Retraining should only take place during the regular breeding season in photoperiodic animals. Keep- ing discipline to a minimum during the sex act and pro- moting all factors that will make the sex act a pleasur- able experience is essential for the “inhibited” male. The “stimulus” or mount animal should be highly attractive or desirable to the male, be quiet, the right size and strongly in estrus so it will remain immobile during the sex act.36,37,39,45 The use of an artificial vagina by a skilled operator has proven helpful in many impotent stal- lions.30'36 In some timid, shy, arthritic, lame or overly aggressive stallions, training them to mount a phantom or mannikin and collection with an artificial vagina has been successful,31 especially if an estrous mare is posi- tioned next to the phantom. In other stallions it was nec- essary to permit unrestrained coitus with highly recep- tive mares in a paddock or pasture environment. This increases the possible risk of injury. In many instances following the recovery of the impotent stallion or male, careful, supervised and understanding breeding practices together with the use of the artificial vagina resulted in the male returning to satisfactory service. Some cases of impotency may be incurable. Pickett and co-workers36 and Rasbech37 have cited a number of impotent stallions where urination occurred during about 30 percent of the ejaculations. Using a spe- cial funnel device and shortened artificial vagina the ejaculates of these stallions were fractionated and the contaminated portions were discarded.36 Testicular biop- sies and/or aspiration sample of the contents of the tail of the epididymis may be necessary to diagnose whether azoospermia is due to a functional, organic or degen- erative condition. The latter two would occasion a very poor prognosis. Drug and hormone treatments are of questionable value in most males lacking sex desire. Testosterone in oil or in the “Repositol” form may be used in intramuscular doses of 100 to 500 mg. in bulls and stallions, 50 to 100 mg. in boars and rams and 10 to 50 mg. in dogs and repeated every 2 to 10 days for several injections. Pro- longed high level androgen therapy should be avoided because of the possibility of producing testicular degen- eration and atrophy caused by the suppression of the gonadotropic hormones. One or more injections of cho- rionic gonadotropin at 4 to 7-day intervals in doses of 5000 to 10,000 IU for large animals and 100 to 500 IU for dogs may help stimulate testosterone production by the interstitial cells. Other forms of ICSH or LH may also be used. Males that are obese or lazy, possibly due792 VETERINARY OBSTETRICS to a hypothyroid condition, may benefit from feeding iodinated casein with a 3 percent thyroxine potency at a rate of 1 gm. per 100 lbs. of body weight daily. Thy- roxine may also be used. This helps increase the meta- bolic rate, hastens the loss of weight and occasionally improves the libido. Benzidrine and other stimulants as well as the glucocorticoids and tranquilizers have been used with very questionable success one-half to 24 hours before breeding the impotent male. Injections of vita- mins and feeding of trace minerals, protein and iodine have little value in most slow breeding males. In lame, arthritic stallions or those with laminitis, butazolidin or a similar drug may reduce pain and encourage copula- tion. Two stallions with failure of ejaculation apparently responded to pilocarpine and ephedrine.37 Other factors such as structural lesions of the limbs and diseases of the penis and sheath may cause a re- duction in libido in some males but in others can actually interfere with or prevent normal copulation. Initially males that develop an inability to mount and ejaculate may ex- hibit good libido, but with repeated failures, or due to painful lesions, sexual desire may become greatly re- duced or lost. Joint, Muscle, Nerve, Bone and Tendon Injuries and Pathology. Lesions affecting these structures par- ticularly if they involve the rear quarters may cause a reduction or even cessation of mating behavior and cop- ulation especially in males with genetically reduced vi- rility or sex drive. Coxitis is seen most commonly in dogs as hip dysplasia and in boars, and less frequently in bulls, rams, bucks, and stallions. It is characterized by a short stride and adduction of the limb. Rupture of the round ligament may be observed in bulls with de- generative coxitis. Occasionally bulls or other males may have one or both hips dislocated resulting in inability to copulate. (See Figure 174.) Gonitis is common in bulls and is characterized by a short, stiff gait and distention and enlargement of the capsule of the stifle joint. Rup- ture of the anterior cruciate ligament of the stifle occurs rarely in bulls but is common in the smaller breeds of dogs. This condition in the adult bull usually prohibits mounting. Excessively straight rear limbs, resembling the Elso-heel condition described in cattle8 predispose bulls and stallions to injury of the stifle joint and tarsus. Gonitis, tarsitis or degenerative joint lesions (osteochon- drosis) in the fetlock or phalangeal joints, or ringbone, may result in pain and reluctance or refusal to mount and copulate. Other conditions causing similar signs of reduced li- bido include over-grown claws or hooves, suppurative pododermatitis, quittors or interdigital granulomas, es- pecially in beef cattle, foot rot or interdigital necrosis, tendonitis, suppurative arthritis of the coffin joint, lam- initis or founder,7 traumatic injury to the peroneal nerve resulting in a “dropped” hock and “cocked” fetlock joints, myositis or muscle rupture especially involving the gas- trocnemius or large gluteal or croup muscles and other traumatic lesions of the lower portions of the rear limbs. A progressive lameness resembling laminitis eventually resulting in refusal to stand, was described in related Hereford bulls and was probably caused by a recessive character.4 Polyarthritis may occur in swine due to ery- sipelas, streptococci, mycoplasma or other organisms. Occasionally polyarthritis may occur in bulls secondary to a primary site of infection. Fractures of the pelvis are rare in males. In bulls, dogs and occasionally other males symptoms of impotency may be related to spinal disease and char- acterized by stiffness and soreness in gait, spinal rigid- ity, and pain over the vertebrae. If the spinal cord is compressed then a slight to marked paresis may be pres- ent with a swaying, unsteady gait a slightly flaccid tail and dragging of the rear limbs. Vertebral osteophytes were very common in dairy and beef bulls over six years of age with the possible exception of Brown Swiss bulls and resulted in ankylosis and spondylosis of the thoracic and lumbar vertebrae with occasionally a secondary frac- ture of the spine.2 6 9 A later study indicated that verte- bral body osteophytis were similar in bulls bred once or 6 times a week for 4 to 8 years. The influence of these osteophytes on libido in bulls were minor with only a slight increase in reaction time in bulls, with the larger lesions.1 Synostosis of the sacroiliac joint begins at 2 to 4 years of age in the bull and is complete at 6 to 10 years of age. This is physiologic and no inflammatory signs are observed. Bulls with spondylarthroses espe- cially of the lumbosacral joint, would mount too far cau- dally on the cow, exhibited lordosis and the penis was extended only a short distance and directed too far ven- trally but sexual desire was good.2 Bulls with spondy- losis, often involving most intervertebral spaces and discs, exhibited kyphosis, a stiff back, short stiff hind leg movements or “goose stepping,” and loss of liveliness and mobility. In some bulls mounting was aided by the jaw and neck of the bull pressing on the back of the cow. Spondylarthrosis affected bulls at an average age of 5 years and spondylosis was most common in older bulls, about 10 years of age. Although common dysplastic le- sions in bulls might be genetically conditioned2 the pos- sibility that these conditions and arthritis might be nu- tritional due to excessive calcium intake was demonstrated.6 In dogs, especially those of the brachycephalic breeds, such as the Dachshund, prolapse of the intervertebral discsINFERTILITY IN MALE ANIMALS 793 causing compression of the spinal cord results in similar symptoms associated with an inability to copulate. Rarely tumors, such as lymphocytoma may invade the spinal canal producing compression of the spinal cord and chronic progressive paresis. Depending on the severity of the spinal cord compression, stallions with the “wob- bler syndrome” may or may not be able to mount and copulate. Swedish Landrace boars, especially certain sire lines, had difficulty in copulating due to bone and joint lesions or arthrosis deformans.5 In spastic syndrome, crampiness or “stretches” in bulls, severe acute attacks may interfere with or prevent cop- ulation due to the prolonged spasm of the skeletal mus- cles of the rear limbs and back. (See Figure 175.) Spas- tic syndrome has been observed in all breeds of cattle but most commonly in the Holstein Friesian and Guern- sey breeds. It is probably inherited as a single recessive factor with incomplete penetrance.3 8 It is seen most often in bulls over 3 years of age and is often associated with arthritis or painful lesions of the rear limbs. Spastic signs are not observed when the bull is lying down but become evident on standing. In most bulls the signs are mild and persist for the lifetime of the bull with occasional periods of exacerbation. The prognosis for future breeding in males with joint, muscle, tendon, bone, or nerve lesions depends upon the nature and severity of the condition and the species, age and value of the animal. The treatment in most cases will consist of sexual rest and restriction of activity enforced by confinement in a box stall or small paddock with good footing. In fractures of the spine, dislocation of the hips and compression of the spinal cord due to arthritic lesions and tumors in large animals, the prognosis is poor to hopeless. In arthritic lesions, the prognosis is also poor but often two to eight months or more of rest may permit limited use of the male. Improved or recovered males should be handbred where the footing is good and where the rear parts or the entire female animal are placed in a pit so the male can easily copulate, or breed an arti- ficial vagina. In bulls or rams judicious use of an elec- troejaculator might permit the collection of semen from males that are unable to copulate or that might further injure themselves if allowed to mount naturally. Some males can be trained to ejaculate into an artificial vagina with all four feet on the ground. In dogs with disc lesions surgery may be indicated. In suppurative arthritis of the coffin joint prolonged conservative therapy, not ampu- tation of the claw, is indicated so ankylosis of the joint will occur. Even if the joint is left deformed it will help the remaining normal claw support the animal’s weight. Quittors or interdigital granulomas should be removed surgically followed by stall rest and possibly wiring the toes together. In bulls with acute attacks of spastic syn- drome where treatment is neccesary, “Tolserol” (Squibb) or “Mephinesin” (Abbott) in 8 to 10 gm doses orally three times a day (24 to 30 gms daily) for 2 to 3 days may be administered. Tranquilizers will also help these affected bulls but the bulls should then be observed closely for the duration of the treatment to prevent injury to themselves upon rising. Glucocorticoids or butazolidin or other nonsteroidal prostaglandin antagonists for sev- eral days may also be of supportive value for the alle- viation of arthritic signs. Regular hoof trimming is de- sirable for all large male animals. Lesser infectious or traumatic lesions should receive appropriate and prompt treatment. Diseases of the penis and prepuce are common causes for inability or difficulty in copulating and frequently re- sult in a marked reduction in sexual desire. Inability to normally protrude the penis (phimosis) may be due to: (1) a congenital anomaly in the devel- opment of the penis and prepuce, with or without hy- pospadias, or male pseudohermaphroditism. This may be observed in all species but is seen most commonly in Boston Terriers in which the penis is very short and opens through a defective prepuce just anterior to the scrotum.5 Copulation is not possible. The author has observed one case of a double penis, diphallus, in a bull that prevented normal copulation because of its forked configuration. The urethra was present in only one of the two glans of the penis. (See Figure 164.) A congenital urethral open- ing ventral to the anus associated with two separate scro- tums each containing a testis has been described in a ram.13 (2) A congenitally short penis has been described in bulls, bucks, boars and horses. The author and others4 suspect this condition may be hereditary since the latter observed it in 20 sons of a Hereford bull and the former observed it in two closely-related Guernsey bulls. The retractor penis muscle in these bulls was normal. No adhesions or lesions were present in the prepuce or around the penis preventing normal extension of the penis. As young bulls these affected males may breed heifers nat- urally even though only 6 to 15 cm. of the erect penis protrudes from the sheath. As the bulls get older, their abdomen gets deeper and they become less agile, cop- ulation is impossible as the penis cannot reach the vulva of the cow. In one Guernsey bull the penis was 22 cm. shorter from the tip of the glans to the ischial arch than a penis from a similar-sized bull of the same age. These males can still be collected by an artificial vagina but their use as sires should be discouraged. The author has observed one 12-year-old stallion with a short penis the794 VETERINARY OBSTETRICS Figure 164. Diphallus in a Bull. glans of which failed to “bell” when copulation oc- curred. This stallion had a normal breeding history from 5 to 10 years of age but then an inability to ejaculate on intromission developed. In bulls with a short penis the sigmoid flexure does not form a sharp S-curve in the resting state. A similar defect was described in bucks,15 and in boars.1,10 In the latter the pendulous, infantile, incompletely erect penis would only extend 2 to 5 cm. beyond the preputial orifice. (3) A congenital short retractor penis muscle was de- scribed as a probable recessive character in Friesians in Holland and symptoms were similar to those exhibited by bulls with a short penis.6 Myectomy of this paired muscle midway between the anus and the base of the scrotum, or removing a 4 cm. section of muscle, re- sulted in improvement in the ability to protrude the penis at erection in some of the affected young bulls. This op- eration was forbidden in the Netherlands because of the hereditary nature of this defect.16 It is possible that some of the affected young bulls failing to respond to the op- eration had a short penis. Ten of 38 affected bulls mated normally as young bulls and the other 28 cases were di- agnosed at a young age. Of interest in regard to the above condition is the observation12 that old bulls may have the retractor penis muscle nearly completely calcified yet copulation may be normal with a fully extended penis.10 If myectomy of the retractor muscle is performed it should be done just below the ischial arch to prevent adhesions which occurred if the operation is performed just above the sigmoid flexure of the penis.9 Passive stretching of the retractor penis muscle was of value in some cases. (4) Other conditions that cause an inability to normally protrude the penis are psychic impotency,7'11 injury or lesions of the lumbar or sacral region,2,8 phimosis due to adhesions in the sigmoid flexure area of the penis or of the prepuce, stenosis of the preputial opening from congenital, traumatic or infectious causes, and tumors of the penis and sheath. Rare instances of eunuchoidism have been described317 in bulls and dogs characterized by a complete lack of sexual desire and marked hypo- plasia of the genital organs and penis. This might be a congenital condition in young males or due to Sertoli cell, pituitary, or hypothalamic tumors. In three psychic infertility cases, the affected adult bulls would protrude their penis normally but then on mounting the cow the penis would be retracted before coitus.11 Sexual rest and the use of an artificial vagina on one bull and resection of the retractor muscle on the other two bulls restored their ability for natural service.2,11 The inability of a bull and boar to obtain and maintain an erection and protrude the penis may be due to vascular shunts or anomalous venous drainage of the corpus cavemosus penis. (See Miscellaneous Causes for Inability to Copulate.) If a bull is unable to protrude his penis normally a careful physical examination of the penis and prepuce should be made. The use of tranquilizers, pudendal nerve blocks or an electroejaculator may be helpful in arriving at an accurate diagnosis. A good history and careful ob- servation at several attempts at natural service are veryINFERTILITY IN MALE ANIMALS 795 informative. The penis should be withdrawn from the prepuce and the penis, the retractor penis muscle and the prepuce should be carefully examined. Occasionally young poorly-grown males may be slow to reach puberty and the inability to protrude the penis may be due to the nor- mal prepuberal adhesions between the prepuce and the penis. Bulls with a short penis should be slaughtered and not used for breeding purposes because of the possible hereditary nature of the defect. Deviation of the penis or phallocampsis is a common cause for difficulty or inability to copulate and a loss of libido. These deviations, of persistent penile frenulum, spiral or “corkscrew” glans penis, S curve or “rainbow” curve of the penis are observed most commonly in the polled, English beef breeds including the Angus, Short- horn and Hereford7'8 9'14'20,21 and are seldom observed in the Charolais, Brahman and dairy breeds that have a larger thicker penis. Deviations of the penis may also be due to congenital persistence of the penile frenulum in many breeds of bulls, especially Angus, and uncommonly in dogs and boars.13'1011 It was observed in six of 18 closely related, inbred, subfertile Angus bulls.8 The incidence of persistent penile frenulum in Angus bulls was about 1 percent with some herds having an incidence of 4 to 5 percent.7 The use of these bulls after treatment is ques- tionable for genetic reasons. Two Cocker Spaniels had persistent penile frenulums.616 A persistent frenulum is a band of tissue that extends from near the ventral tip of the glans penis to the pre- puce. It is seen occasionally as a cause for a sharp ven- tral bending or deviation of the glans penis in bulls.16 It has been reported in dogs where it caused discomfort and pain at puberty,12’13 and also in boars.13 At birth the ep- ithelial surfaces of bovine porcine and canine penis and sheath are fused and ventrally the penis and prepuce are united by a band of connective tissue called the frenu- lum. Epithelial separation and rupture of the frenulum occurs normally at puberty. When a persistence of the frenulum occurs there is usually a blood vessel present in the center of the tissue band comprising the frenulum. Cutting of the connective tissue band, without ligation, is a simple procedure and is uniformly successful for the correction of a persistent frenulum. Congenital curvature of the penile bone in the dog is rare.10 The spiral or “corkscrew” type of deviation of the penis is most commonly seen in young bulls, 2-1/2 to 5 years of age. (See Figure 165.) Many affected bulls have successfully bred cows for a year or more before the deviation is noted as a cause of infertility.3 7’20’21 There is evidence to indicate that this condition may be inher- ited as cases have been noted in sons or closely related descendants of an affected bull, especially in the polled Figure 165. A Spiral or Corkscrew Deviation of the Penis of an An- gus Bull. beef breeds.3 In most cases of a spiral deviation, the cor- pus cavernosum appears longer than the supporting structures of the penis including the fibrous tunics. The anatomical basis for the spiraling of the bovine penis is well-described.2-5 When complete erection occurs the corpus cavernosum in the free end of the penis rolls in- side the fibrous tunic and the penis slips and pushes lat- erally under the dorsal apical ligament through the less dense portion of the fibrous tunic and the glans spirals counterclockwise, ventrally and to the right around the line of the penile raphe. This may be favored by the early maturation of the supporting structures of the penis and the later maturation and growth of the penis under the continued influence of testosterone especially in the English beef breeds that have a narrow, thin penis. “Corkscrewing” of the penis occurs at the peak of erec- tion when the integument covering the free end of the penis is stretched. If erection is only partial it does not occur. This may account for the fact that some bulls will only be observed to “cork-screw” occasionally. The au- thor observed an affected Angus bull that was collected several times in rapid succession in an artificial vagina. On the fourth collection “corkscrewing” of the penis did not occur until after the penis entered the artificial va- gina. Thus the report of Seidel and Foote1819 who pho- tographed the penis through a transparent artificial va- gina at the moment of ejaculation and noted a transient twisting of the penis during more than half of the ejac- ulations in normal Holstein bulls is significant. Up to 30 percent of Hereford bulls have a normal straight penis on intromission but have a curled or twisted penis on dismounting.2,5,17 Spiralling of the penis after intromis- sion in normal bulls may increase the tactile stimulus and promote ejaculation.5 In affected bulls premature full796 VETERINARY OBSTETRICS erection occurs prior to intromission resulting in “cork- screwing” that prevents the completion of coitus. Con- traction of the retractor muscles of the sheath during erection might be an additional causative factor in spiral- ling of the penis.2 Spiralling of the glans penis is also observed in bulls being collected by the electroejacula- tor. Some bulls that show a spiral deviation during elec- troejaculation, especially if the penis is manually ma- nipulated, may breed cows naturally without a deviation being evident. Other less common types of deviations of the penis are the ventral or “rainbow” and the mild S-shaped cur- vatures which are also caused by an insufficiency of the apical ligament of the penis.2,6,21 The latter is of little importance and some affected bulls breed successfully. The former definitely prevents normal copulation as the more erect the penis becomes the greater the ventral cur- vature. A persistence of the frenulum or a short retractor penis muscle are not present. Rarely trauma and scarring of the penis and/or prepuce may cause a penile devia- tion. Treatment of the spiral deviation, the ventral or “rain- bow” and the S-shaped deviation usually requires a sur- gical operation in which either a portion of the fascia lata is implanted between the apical ligament and the tunica albuginea or the apical ligament is firmly fastened to the penile tunica albuginea.20 21 Various synthetic prosthetic implants have been used unsuccessfully to re- pair spiral or ventral deviations of the penis. Carbon fi- ber implants show some promise of being of value in producing a strong adhesion between the apical ligament and the tunica albuginea.15 These surgical techniques to correct a spiral or “corkscrew” curvature assist in pre- venting the rotation of the corpus cavernosa within the Figure 166. Ventral or “Rainbow” Deviation of the penis of a Here- ford Bull. Figure 167. A Persistent Frenulum, a Cause of Deviation of the Bo- vine Penis. fibrous tunic by producing adhesions between the two structures. Hematomas, Adhesions of the Penis and Prepuce, Tumors, Phimosis and Paraphimosis—Decreased li- bido and inability to copulate may be associated with phimosis of the penis due to adhesions of the sigmoid flexure of the penis or the deeper portions of the pre- puce, tumors of the penis and prepuce, stenosis of the preputial orifice, paraphimosis or paralysis of the penis or a stenosed preputial ring. 1. Adhesions of the penis in the region of the sig- moid flexure in bulls and rams may be due to trauma from hom injuries or in bulls from injections of local anesthetics to block the dorsal nerve of the penis as was earlier performed to produce anesthesia of the penis to aid withdrawal from the sheath. These connective tissue adhesions prevent obliteration of the S-curve and penile protrusion at the time of erection. Treatment to relieveINFERTILITY IN MALE ANIMALS 797 these adhesions often results in more severe adhesions. Adhesions of the deeper or caudal portions of the freely- moveable prepuce to the abdominal wall or to the skin in the region of the fornix produces a more severe phi- mosis than adhesions of the cranial portion of the pre- puce. These adhesions may be secondary to lacerations of the prepuce especially in young bulls where the pre- puce has not yet completely separated from the glans, or in older vigorous bulls, especially those used in artificial breeding studs and collected with artificial vagina, in which a vigorous thrust may tear the prepuce away from its attachment to the glans for one-third to the entire cir- cumference of the penis. Infection that follows this in- jury may produce abscesses and/or adhesions to the sur- rounding structures preventing the free movement of the prepuce and penis at erection. (See Figures 168 and 169.) Prompt antibiotic therapy both locally in an oily base and parenterally for 7 to 14 days is recommended together with sexual rest for 6 to 12 weeks. Suturing of the pre- puce to the mucous membrane of the glans and the un- derlying connective tissue appears indicated but permit- ting healing by second intention without suturing has proven more satisfactory for the author. A ruptured, “fractured,” or “broken” penis with a secondary hematoma is usually observed in the bull but in rare instances may occur in the stallion due to the mare’s kicking the erect penis as the stallion mounts. In the dog, fracture of the penile bone may be caused by a traumatic injury and may require amputation of the penis or resection or removal of the penile bone.12 Similar traumatic injuries in the other species are uncommon. In the bull, the condition of a “fractured,” “broken,” or ruptured penis occurs most commonly in active bulls Figure 168. Tearing of the Prepuce from its Attachment to the Glans Penis in a Bull. Figure 169. A Chronic Abscess Causing a Severe Phimosis in a Bull. (This abscess was probably secondary to a laceration of the prepuce or a small hematoma or “fracture” of the penis.) with a strong sex drive breeding cows on pasture. It is rarely observed in dairy bulls that are hand bred. The injury apparently occurs at coitus either when the cow or heifer suddenly goes down under the weight of the bull, or due to a sudden ventral bending of the erect penis against the escutcheon of the cow at the moment the bull thrusts, causing a dorsal rupture of the tunica albuginea usually near the distal portion of the sigmoid flexure and opposite the initial attachment of the retractor penis mus- cle. Penile hematomas are apparently due to a sudden angulation or bending of the erect penis at service. They are not only due to a high blood pressure in the corpus cavernosum. Pressures of more than 10,000 mm. of Hg may occur in the corpus cavernosum penis at coitus.2,8,25 Rupture of the penis usually occurs in 2- to 4-year- old bulls and is seen most commonly in Herefords. The symptoms of the injury include a shortening of the stride, stiffness, pain and a slight arching of the back that are generally mild and may not immediately prevent sub- sequent copulations which produce a larger hematoma. A swelling rapidly develops just cranial to the scrotum that varies in size depending upon the amount of hem- orrhage from the ruptured penis and the tissues in- volved.16,17 Hemorrhage is profuse and in a “hand gre- nade” effect because of the very high blood pressure present in the erect corpus cavernosum penis. Prolapse of the prepuce may occur secondary to the edema that often develops. There is usually no difficulty in urina- tion. At first the swelling is soft and fluctuating; later it becomes firm as the hematoma clots and organizes. Pain may be evident but heat is slight. Systemic symptoms I are usually lacking. The bull shows definite reluctance and inability to copulate. If treatment is not undertaken798 VETERINARY OBSTETRICS the clot organizes. The hematoma may become infected producing an abscess. (See Figure 169.) Adhesions may occur between the prepuce, penis, abdominal wall and skin rendering the bull useless for future service. A dif- ferential diagnosis from other conditions such as tumors, chronic fibrous adhesions, lacerations of the penis and prepuce and rupture of the urethra should be considered. The prognosis in these cases should be guarded even when an operation is performed. If an aseptic surgical operation cannot be performed an operation should not be attempted. In this latter situation the bull should be given large doses of parenteral antibiotics for one to two weeks to prevent abscessation. About 50 percent of bulls may recover spontaneously with 3 months of sexual rest. Due to the high rate of recurrence and other complica- tions, surgery is usually recommended for valuable bulls.25 Hematomas that become infected seldom respond to treatment and surgery. The size of the lesion rather than its location was of greatest importance in the prog- nosis.24 25 Some affected bulls damage the dorsal nerve of the penis at the time of the “rupture” so they lose sensation in the glans. Therefore upon recovery these bulls can’t find the vulva and achieve intromission and ejaculation. Before surgery the penis should be with- drawn from the sheath. If the penis can be extended completely or up to 6 to 8 inches and sensation is present in the glans the prognosis is good and surgery may not be necessary.1617 If the penis can only be extended 2 to 4 inches the prognosis is guarded and if the penis can’t be withdrawn from the prepuce and/or the glans lacks sensory innervation, the prognosis is poor.1617 Nearly 50 percent of the hematomas not operated upon and un- treated become infected by the second week after the injury.20'25 If abscesses are present, they should be drained and allowed to heal before surgery is performed. Con- ditions requiring surgery to remove extensive adhesions, abscesses, and scar tissue have a poor prognosis. The operation commonly undertaken to correct this condition of a ruptured penis and hematoma should not be performed until after the blood in the hematoma has clotted firmly and before organization of the clot occurs. This is usually between the fourth and seventh days after the rupture has occurred. Surgery may be attempted after the third week following the injury but is contraindicated between 10 and 21 days.25 From the time of the occur- rence of the hematoma until the time of the operation the bull should be given parenteral antibiotics. Prior to surgery the electroejaculator may be used to determine if normal engorgement of the penis occurs and if sen- sation is present in the glans penis.24’25 If normal en- gorgement of the penis does not occur, an intrapenile hematoma preventing normal distention of the distal por- tions of the corpus cavernosum is probably present. If either of these two conditions is present the prognosis is poor. To perform this operation the bull should be restrained in lateral recumbency after the administration of a pre- anesthetic tranquilizer and gas anesthesia or chloral hydrate17 25 or after a large dose of epidural anesthesia (40 to 60 cc of a 2-percent procaine or xylocaine solu- tion) together with a narcotic dose of chloral hydrate, if necessary. This latter method of anesthesia is supple- mented by local anesthesia under the skin at the opera- tive site. The operation should be under favorable con- ditions with as close an approach to an approach to aseptic surgery as possible, since second-intention healing pro- duces many adhesions. After shaving and disinfecting the operative site, an oblique incision 6 to 10 inches long is made through the skin over the swelling.25 All bleed- ing must be controlled. The clotted blood in the hema- toma is carefully removed and the penis brought to the incision. The fibrin is removed. The break in the tunica albuginea is thoroughly exposed, using great care not to injure the dorsal nerve of the penis, coagulated blood in the corpus cavernosum is expressed, and the rent in the tunica albuginea which is usually 2 to 4 cm. long, spiral, oblique, or longitudinal in direction, is sutured with No. 2 chromic catgut with a shoelace stitch. Most ruptures are in the dorsal or dorso-lateral portion of the penis just cranial to the terminal curve of the sigmoid flexure and opposite the attachment of the retractor penis muscle. Following complete control of hemorrhage, the cavity may be flushed with an antibiotic or saline solution. The elastic layer of fascia containing the vessels and nerves is carefully replaced and sutured. The subcutaneous tis- sues are approximated with catgut and the skin closed with nylon sutures. The wound should heal by primary intention. Following the operation, parenteral antibiotic therapy is continued. Suturing the tunica albuginea is necessary to prevent a possible venous shunt between the corpus cavernosum penis and the dorsal veins of the penis.25 Copulation should not be permitted for at least 2 weeks and preferably longer, 4 to 8 weeks.5’15'16'17'25'26 Success in preventing the development of firm adhesions around the penis was reported by keeping the bull sexually stim- ulated. Housing it next to a heifer or cow in estrum or teasing the bull daily was recommended. Extending the penis several times a week under tranquilization was rec- ommended.16 Using the electroejaculator was not recommended17 until healing had taken place. Daily massage of the affected area for 10 to 20 minutes to break down adhesions and prevent new ones was also rec- ommended.11 This should be continued for 2 to 3 months.INFERTILITY IN MALE ANIMALS 799 Conservative treatment resulted in recovery in 37 of 47 cases.11 Complications of penile rupture include abscess formation, adhesions preventing protrusion, analgesia of the penis due to injury to the dorsal nerves, a recurrence of the hematoma or a shunt between the corpus caver- nosum penis and the dorsal vessels of the penis or the corpus spongiosum on erection.25 Chronic abscesses secondary to hematomas or perfo- rating injuries to the prepuce should be drained into the prepuce if possible to prevent adhesions between the pre- puce and skin that occur when abscesses are drained through skin incisions. (See Figure 169.) If the abscess heals but adhesions preventing normal function of the penis and prepuce remain, then the bull may be operated on as described above to separate the adhesions of the prepuce and the penis from the skin or abdominal wall. The prognosis is guarded to poor. 2. Tumors of the penis and prepuce in bulls, stal- lions, boars and dogs may cause phimosis or paraphi- mosis or prevent normal intromission. In bulls the only significant tumor is the transmissible fibropapil- loma.914 (See Figure 170.) There is definite evidence that this tumor and cutaneous papillomas, or warts (ver- ruca vulgaris) in cattle are similar and caused by the same agent. It is probably infectious in nature and the etiologic agent is considered to be a virus. The fibropapillomas are similar to those observed on the vulva of heifers. They are single or multiple, firm, cauliflower-like growths. Young, susceptible bulls, 9 to 18 months of age, are most commonly affected with papillomas. Young bulls housed together frequently mount each other and may injure the prepuce, affording an invasion site for the tumor virus. Injury to the penis is also predisposed by breeding the young bull before the prepuce and glans Figure 170. Transmissible Fibropapilloma of the Penis in a Young Bull. (Courtesy K. McEntee.) penis are fully separated. For these reasons young beef bulls are most commonly affected. Hemorrhage from the sheath after service and hesitancy or refusal to copulate are frequently noted in bulls with penile tumors. In boars a virus-induced papilloma of the penis which is venereal- ly transmitted has been described.914 In stallions tumors of the penis are uncommon and when present are usually squamous cell carcinomas of low malignancy. (See Figure 171.) Benign squamous papillomas, angiomas and melanomas may occur in or on the sheath and penis of horses.6'9 Carcinomas often ulcerate and usually bleed at the time of service and pro- duce a fetid preputial discharge. They should be differ- entiated from granulomas caused by Habronema larvae. Squamous cell carcinomas may be favored in the stal- lion, bull and dog by the smegma in the sheath.9 The transmissible venereal tumor is the most com- mon one seen in the penis and prepuce of dogs. It is usually spread by coitus. In rare instances the disease may be spread by licking of the vulvar or preputial dis- charges of affected dogs. Intact cells must be trans- planted to transmit the tumor; it is not transmissible by filtrates. The incubation period is from 5 to 6 weeks. All breeds of dogs are susceptible. It is characterized by a discharge of a bloody, fetid exudate from the vagina of the female and from the prepuce of the male. When the penis is exposed, greyish-red nodular growths are ob- served on the penis and the prepuce. The tumor masses are friable and bleed when handled. In advanced cases the tumor may also be observed involving the inguinal lymph glands. The tumor ulcerates easily. It may be found in other cutaneous sites but internal or metastatic in- volvement is uncommon.91014 The transmissible venere- al tumor has been reported widespread throughout the Figure 171. Squamous Cell Carcinoma of the Penis and Sheath in a Stallion.800 VETERINARY OBSTETRICS world but most commonly in tropical countries. The dis- ease may be common in an area and then in the next decade or two disappear or be rarely observed. Papil- lomas, squamous cell carcinomas, sarcomas, and other tumors may occur in the sheath or on the penis of dogs.3 Recent reports have indicated that removal of the canine venereal tumors by electrocautery or surgery followed by chemotherapy with vincristine13 or by vincristine alone, 0.025 mg/kg. IV, once weekly for about 4 weeks4 ap- pear promising. However spontaneous regression of tu- mors is frequent and may occur within 2 months.9 Tu- mors of the sheath and penis of rams, bucks and toms are rare. In the treatment of penile tumors in the bull it should be noted that spontaneous recovery from infectious fi- bropapillomas usually occurred in an average time of less than 4 months, range 1 to 15 months.11419 The nearer the bull was to 2 years of age the better the prognosis.7 If the tumors are multiple on the penis, treatment may be difficult and some veterinarians have empirically rec- ommended the use of wart vaccine. The tissue vaccine was more effective in producing an immunity than was the egg-yolk vaccine.1 Formalin-killed vaccine given in- tradermally to calves at 2 weeks to 6 months of age pro- vided good protection.19 The vaccine was of question- able value in affected bulls. They recommended that semen from affected bulls not be used or frozen because of the danger of transmitting the virus to cows. Disap- pearance of penile tumors in 4 out of 5 young bulls was reported after the administration of an autogenous vac- cine.21 However, others 19 found the vaccine induced no appreciable regression in experimentally induced warts. The value of wart vaccine in the treatment of cutaneous papillomatosis is questionable on the basis of their work, which indicated fairly rapid spontaneous recoveries. Fi- bropapillomas have been removed by the author and others23 from the penis of bulls when they had a narrow base or were pedunculated, by grasping and pulling them off as the bull mounts a cow. Some bleeding occurred, but it was not excessive. By means of a pudendal block or tranquilizers and local anesthesia the penis can be withdrawn from the sheath and the tumors removed with scissors or by cautery and the mucous membrane of the penis or prepuce sutured with fine catgut. The prognosis is good whatever treatment is used. In the stallion the occasional squamous cell carcinoma can be removed by a liberal incision or if necessary by amputation of the penis. Castration should be performed prior to amputation of the penis, since both operations performed simultaneously might cause excessive tissue reaction and swelling. The operation for amputation of the penis is a standard one described by Williams and modified by other authors,22’25,27 to prevent a future stric- ture of the urethral orifice. After restraining the animal in lateral recumbency and giving general or local anes- thesia, the penis is withdrawn and thoroughly washed and prepared for surgery. A catheter is introduced into the urethra. To control hemorrhage, an elastic ligature is placed tightly around the proximal end of the extended penis. In the prolapsed equine penis the operative site is just distal to the internal preputial ring. A triangular in- cision is made over the urethra with the base of the tri- angle cranial and under the amputation site. The urethra is opened and sutured to the edges of this triangular in- cision. The penis is cut off at the base of the triangle. By using strong nylon sutures, the urethral wall, the ven- tral and dorsal portions of the tunica albuginea, and the dorsal skin of the penis, or the prepuce, but not the cor- pus cavernosa are drawn firmly together with many in- terrupted sutures, to control hemorrhage. In the dog, surgery may be indicated for the removal of the transmissible venereal tumor. The earlier surgery is undertaken, the better the likelihood of a successful operation. Liberal excision of the involved tissue is de- sirable. Complete removal of the penis and prepuce is questionable as even in advanced cases the tumor may regress spontaneously. Dogs which recovered were im- mune.3 Whole-blood transfusions from an immune dog resulted in a cure or regression of the tumor in affected dogs. In severe cases where it is difficult or impossible to remove all of the involved tissue, radiation therapy may prove of value. Claims for cures of this disease in dogs should be considered with caution because of the high incidence of spontaneous regression usually occur- ring in less than six months.3 Spaying of females and elimination of stray dogs is very helpful in controlling the disease.10 3. Phimosis or stenosis of the preputial orifice, chronic prolapse of the prepuce, and paraphimosis preventing normal protrusion of the penis is a cause of inability to copulate. It may occasionally be congenital in young dogs, toms and stallions. Stenosis of the pre- putial orifice is usually acquired due to injuries, wounds and infections. In cattle with pendulous sheaths, the pre- putial orifice may be stepped on causing severe contu- sion and swelling. In beef bulls chronic prolapse of the prepuce is a very common cause of posthitis and phi- mosis (See Figure 172.) Congenital stenosis of the external preputial orifice in dogs may be successfully corrected by a dorsal incision of the orifice. Incising a stenotic internal preputial ring in a stallion to permit normal erection and protrusion of the penis was described.4 Removal of the preputial ring in a young cat with dysuria and paraphimosis was re-INFERTILITY IN MALE ANIMALS 801 Figure 172. Chronic Prolapse and Stenosis of the Preputial Orifice of a Santa Gertrudis Bull. ported.6 In the bull, dog or ram the usual procedure to correct a simple stenosis of the preputial orifice caused by cicatricial tissue is to remove from the ventral of the sheath a triangular portion of skin. The base of the tri- angle is at the preputial orifice. After the skin is removed an incision is made through the midline of the prepuce to the apex of the triangle and after careful hemostasis the preputial membrane is sutured to the skin by inter- rupted catgut sutures. Chronic prolapse of the prepuce is most common in Bos indicus cattle such as: Santa Gertrudis, Brahman or Zebu, or their crosses, in Bos taurus cattle it is less common but is seen in the polled beef breeds such as: Angus and Polled Hereford cattle. It is occasionally seen in other beef breeds and is rare in dairy cattle. It prob- ably is an inherited trait. (See Figure 172.) In Polled English breeds prolapse of the prepuce may be due to a genetic absence of the retractor muscles of the prepuce." In these breeds the circumference of the preputial orifice and the length of the prepuce was similar to the normal breeds. In the affected breeds the prepuce commonly prolapses 7 to 20 cm. and depending on the nature of the grazing area, especially the height and type of brush or herbage, and time of year, the prolapsed sheath be- comes dry, traumatized, lacerated, frost-bitten, edema- tous, swollen and fibrotic. Screw worm infestation may also occur resulting in phimosis and rarely paraphimosis. In mild cases diagnosed early the affected bull may be confined in a well-bedded stall. The prolapsed organ should be carefully washed, cleansed and dried. Oily an- tibiotic or bland antiseptic preparations are applied and the prolapse replaced and held in place by a purse-string suture around the preputial orifice. Repeated treatments two to three times a week for three to four weeks before allowing breeding are indicated. In more severe cases where replacement is not possible, circumcision or even amputation of the affected portion of the prepuce may be necessary. Before surgery in severe cases the sheath and penis should be cleaned with hydrogen peroxide and furacin solution, and oily antiseptics or antibiotics and lanolin be applied for about a week to the prolapsed structures under a stockinette held in place by a rubber band.818 The pendulous sheath and prolapsed membranes should be supported for this period to possibly control or reduce the swelling and edema. Hydrotherapy consisting of spraying the prolapsed sheath with warm water at fre- quent periods daily may be helpful. Systemic adminis- tration of antibiotics and diuretics may be indicated. Other authors suggested that immediate circumcision was more practical and economical.2,5 In any surgical procedure as much of the prepuce should be conserved as possible. Removal of large portions of the prepuce may result in inability to protrude the penis the necessary length for natural service. In all severe preputial lesions requiring surgery or extensive treatment, a long recovery period of 30 to 90 days is required for complete healing before service should be permitted. Depending on the type and degree of prolapse of the prepuce, the breed and value of the bull and the operator’s experience one of three (3) general operative procedures may be employed.18 a) circumcision may be employed to correct chronic pro- lapse of the prepuce.10,13'16,17,18 In Brahman bulls the pre- puce is usually long enough to permit a removal of a portion of it by circumcision without causing limitations on penile extension during erection. In the English breeds the operator must conserve as much preputial membrane as possible so the reefing or resection8,15,18 operation is preferred. Following tranquilization and restraint in lat- eral recumbency the prolapsed tissues are washed, cleansed and anesthetized.8,18 General anesthesia may be used. An inverted triangular incision, 5 to 7 cm., 2 to 3 inches, on a side is made on the ventral, posterior as- pect of the sheath through the skin only. The base of the triangle is at the preputial orifice. After removal of the skin an incision is made through the ventral caudal mid- line of the prepuce to the apex of the triangle. Careful hemostasis is highly essential before placing interrupted nonabsorbable nylon sutures to secure the internal pre- putial membrane to the skin. This later prevents the pos- sibility of scarring and stenosis of the preputial orifice. Then the diseased prolapsed portion of the prepuce is removed after placing interrupted nylon sutures around its circumference firmly securing the internal preputial membrane to the external at the preputial orifice. These802 VETERINARY OBSTETRICS sutures are usually about 4 cm. apart on the outside and 1.5 cm. apart on the inside. They should be drawn tightly and overlap to completely control hemorrhage then the prolapsed portion of the prepuce is removed about 1 cm. distal to the suture line. Following the operation the sheath should be supported against the body wall for two weeks. The sutures can be removed in about 6 to 8 days. Paren- teral antibiotics should be given for 7 to 10 days, b) “reefing” type of operation involving resection and anastomosis is superior to other procedures, particularly when the midportion of the prepuce is involved, or when as much prepuce as possible must be conserved.815,18 An incision is made at the skin line of the preputial orifice and at the distal end of the prolapse where the “inner” preputial membrane is normal. A longitudinal incision is made between these two initial transverse incisions and the diseased “outer” preputial membrane and underlying edematous, fibrous or abscessed tissue is removed. Hemorrhage must be carefully controlled. Electrocau- tery, maybe a useful adjunct to ligatures. The normal preputial membrane and underlying tissue is sutured carefully by many interrupted catgut sutures to the skin and subcutaneous tissue at the preputial orifice.2,5'8'15’1718 Antibiotics should be administered locally and systemi- cally for the next 7 to 10 days. A large Penrose drain fastened into the sheath and around the penis to prevent irritation of the suture line by urine and a purse-string suture in the skin at the orifice to invert the suture line was recommended.15-18 This purse-string suture is re- moved after one week. If following this treatment con- striction of the preputial orifice occurs then a second op- eration consisting of a triangular-shaped incision on the ventral-caudal aspect of the preputial orifice is per- formed as previously described. As a preventive mea- sure in bulls affected with chronic prolapse of the pre- puce, removing a large-V-shaped wedge of skin from the suspensory skin flap of the sheath to reduce its pendu- lous attachment has been suggested.13 Where the prepuce is more extensively involved some veterinarians18 use an c) easier amputation technique where the entire prolapsed part is removed by through and through overlapping sutures over a perforated plastic ring securely fastened by interlocking sutures into the pre- putial orifice. This may result in too great a loss of nor- mal preputial membrane. Bulls with a lack of libido and sex drive may fail to breed satisfactorily after these treatments because of pain associated with erection and coitus. Chronic prolapse of the prepuce may be prevented or controlled by the se- lection of bulls with smaller preputial orifices and with less tendency to prolapse their preputial membrane. It is questionable and probably undesirable to operate on af- fected bulls since this condition is genetically predis- posed. These bulls should be culled to decrease the fre- quency of this trait in the population. Males should be selected for lighter, less pendulous sheaths with smaller preputial orifices and stronger retractor penis mus- cles.7,14 Surgical procedures for prolapse of the penis and prepuce in boars and dogs has been described.Ia,c Paraphimosis, the inability to withdraw the penis into the prepuce, results in edema, swelling, and balanopos- thitis. It may occur following erection of the penis through a stenotic preputial ring or orifice caused by a congenital or acquired stricture or by tumors as noted above under phimosis. Paralysis of the penis and paraphimosis may be due to spinal disease or trauma. Paralysis of the penis is seen in bulls with rabies and in horses in the late stages of dourine. It is possible that the posterior paresis re- ported in a few cases of rhinopneumonitis, due to equine herpesvirus I, might be the cause of occasional unex- plained cases of penile paralysis in stallions. Resection of the retractor penis muscle in bulls with pendulant sheaths may cause paraphimosis. It is not observed in the dairy breeds with a sheath that is closely attached to the abdominal wall. The author has observed and had reported to him at least 15 cases of paralysis of the penis with paraphimosis in geldings and stallions following the use of phenothiazine-derived tranquilizers. The product most commonly associated with prolonged or permanent paraphimosis has been withdrawn from the commercial market. The prognosis in paraphimosis in males is guarded and depends upon the promptness of treatment and the de- gree of trauma or necrosis present. Support of the pro- lapsed penis and sheath is essential to minimize gravi- tational edema.1318 Cases of paraphimosis in horses following castration and the use of tranquilizers should have the penis supported or held within the sheath within an hour or two of its occurrence to prevent a chronic prolapse of the organ often necessitating amputation. Cold packs and pressure may reduce the swollen penis and allow replacement. In some cases in dogs and occasion- ally in bulls, enlargement of the preputial opening is nec- essary in order to replace the penis and prevent a re- currence of the condition. For necrosis of the penis secondary to acute paraphimosis and for chronic paral- ysis and prolapse of the penis in dogs and cats is am- putation is recommended. To correct chronic protrusion of the tip of the canine penis due to a “short” prepuce, a “long” penis or inefficient cranial preputial muscles surgically shortening these muscles or removing an ellip- tical portion of skin cranial to the prepuce to draw the prepuce over the penile tip is recommended.3 6a b 9 In bulls cleaning of the penis, removal of necrotic tis-INFERTILITY IN MALE ANIMALS 803 sue, and the liberal application of ointment was rec- ommended.17 Gauze should be wrapped around the penis to protect it. The penis with its gauze dressing should be placed inside the sheath as soon as possible. Petro- leum jelly should be packed into the sheath to prevent adhesions. Frequent withdrawal of the penis and appli- cations of ointment are indicated. Balanoposthitis due to infectious or noninfectious causes may produce a stenosis of the preputial orifice, adhesions of the penis and prepuce to each other or to the surrounding tissues or produce sufficient pain and discomfort that copulation is impossible or not at- tempted. Balanitis is an inflammation of the glans penis, and posthitis is an inflammation of the prepuce. They are often both involved in an inflammatory reaction be- cause of their close apposition. Balanoposthitis is com- mon in the bull, ram and dog and uncommon in the boar and cat. It is observed occasionally in the stallion. The preputial cavity in the bull may normally contain a wide variety of bacteria, molds, protozoa and viruses including: Campylobacter fetus venerealis E. coli, streptococci, staphylococci, B. pyocyaneus, Pseudo- monas aeruginosa, C. pyogenes, Proteus, Actino- mycetes necrophorus, actinobacilli, molds (Aspergil- lus, Mucor, Absidia), mycoplasmas, ureaplasmas, Klebsiella, Hemophilus, Trichomonas fetus, IBR-IPV virus, and other pathogenic and saprophytic organisms. Other male animals have a similar variety of infectious agents as inhabitants of the prepuce. It is often difficult to recover specific slow-growing pathogens from the prepuce of bulls and other males because rapid-growing contaminants overgrow the cultures. Granular venereal “disease” lesions or hypertrophy of lymphoid nodules on the penis and prepuce of bulls and dogs are common, but are not associated with any specific organism and have little significance. (See Figure 173.) Sexual rest and protective antibiotic solutions in oil infused into the sheath usually alleviate acute signs of granular venereal disease or mild balanoposthitis. No obvious balanoposthitis gen- erally accompanies the presence of the above organisms in the preputial cavity with the possible exception of M. tuberculosis and the acute form of IBR-IPV virus in- fections. Tuberculosis of the sheath, penis, prepuce, and penile lymph glands of bulls has been described.37 This avenue of invasion in the bull is invited by tuberculosis of the female genital tract. Tuberculosis of the sheath and penis may be characterized by enlarged, granulomatous bleed- ing lesions of the glans penis, adhesions of the penis, prepuce, and sigmoid flexure with secondary phimosis. The penile lymph glands are enlarged and are likely to be abscessed. In suspicious cases either culture of the Figure 173. Chronic Granular Venereal Disease Lesions of the Bo- vine Penis and Sheath. lesions or a tuberculin test will probably establish the diagnosis. This type of tuberculosis has not been re- ported in recent years in the United States. Several rare cases of actinomycosis affecting the sheath and glans penis of bulls have been reported.37 The lesions resembled those of tuberculosis. Trauma, abrasions, lacerations of the prepuce or glans penis usually result in the introduction of the above wound- infection organisms into the deeper tissues with resulting swelling, inflammation, pain and preputial discharge. This is observed most commonly in young bulls especially those in which the glans penis is not completely sepa- rated from the sheath. In artificial insemination studs in- juries from the artificial vagina may occur including the loss of a rubber band from the vagina onto the glans penis. This may cause a deep laceration or amputation of the glans. Young bulls running together in the early spring months may, by their homosexual behavior and frequent mounting, draw hair into their prepuce where it forms a stenotic ring at the base of the glans with an associated balanoposthitis. In rare cases this ring of hair may result in the sloughing or amputation of the glans penis. Mild balanitis and posthitis have been observed in virgin bulls or in young bulls after they have bred older cows. C. pyogenes, E. coli, and other organisms present in the prepuce of certain bulls may cause a tem- porary vulvovaginitis in females after coitus.3 Although many miscellaneous organisms may be introduced into the prepuce, recovery is usually spontaneous with no clinical lesions. The herpesvirus of cattle, IBR-IPV, can produce an804 VETERINARY OBSTETRICS Figure 174. Dislocated Hip in a Jersey Bull. acute inflammation and ulceration of the penis and pre- puce (infectious pustular balanoposthitis (IPBP)) accom- panied by a short period of elevated body temperature when introduced into the preputial cavity of susceptible bulls.7'26,34 This disease was formerly called vesicular venereal disease in the U.S. or Blaschennausschlag in Germany. The initial area of involvement is the epithe- lium over the lymphoid follicles that becomes necrotic and sloughs. The ulcers on the glans and prepuce caused by the virus are secondarily infected by the bacterial flora of the sheath resulting in a severe pustular balanopos- thitis. Abrasions of the penis and sheath that occur at copulation make the lesions in the acute stage more se- vere. The virus can usually be recovered from the acutely affected bull’s prepuce and penis for about 10 to 14 days. Bulls may spread this disease during this period to cows by copulation producing pustular vulvo-vaginitis. Some cases of balanoposthitis may be so mild that infection may go undetected. The recovery of this virus from the prepuce of bulls for a period of up to 361 days has been reported.29 These are often refractory or immune ani- mals. Serum antibodies are developed but the titers are low 1:10 to 1:100 on the serum neutralization test.25 On histologic section of affected tissues eosinophilic nuclear inclusion bodies may be found in many cells. Epizootic outbreaks of balanoposthitis in young range bulls might be due to this agent." Lymphoid follicular hyperplasia was noted in the prepuce and penis following outbreaks of infectious pustular balanoposthitis (IBR-IPV) in bulls.196 A few outbreaks have been reported in artificial breeding studs where there is a great danger of this virus being disseminated in liquid or frozen semen since antibiotics commonly placed in semen extenders have no effect on this virus.25 Coital exanthema due to the IPV virus was common in dairy herds and was occasionally seen in AI centers in Germany.32 It was demonstrated by electro- phoresis that the IPV virus differed from the IBR virus even though by serological methods they were similar.33 A highly attenuated vaccine was prepared that would protect the cows and bulls if instilled intranasally and intravaginally or into the prepuce of bulls yet would not produce signs of the disease even if semen from recently vaccinated bulls was used for artificial insemination. The field strain of IPV virus if present in the semen would reduce conception rates by about 7 percent and produce signs of the disease. This highly attenuated vaccine was administered as noted above twice at 6-week intervals and then once yearly thereafter. No abortions were pro- duced by the vaccine given to pregnant cows and chal- lenged cattle showed no evidence of disease. The local immunity produced by this vaccine was better than the immunity produced by an intramuscular injection of a vaccine. Bulls in one large AI stud in the U.S. are rou- Figure 175. Spastic Syndrome or Stretches in an 8-year-old Holstein Bull.INFERTILITY IN MALE ANIMALS 805 finely vaccinated with an IBR vaccine intranasally twice or three times a year. There is no evidence that bulls vaccinated with this vaccine have transmitted the IBR- IPV virus in the semen. This has been determined by routine cultures of over 70,000 ejaculates.15'26 In severe cases acute swelling, pain and later local scarring may cause difficulty or slowness in copulation. True adhesions were not observed.7 34 In range bulls with great libido repeated abrasion of infected and inflamed tissues might occasionally produce adhesions. For treat- ment sexual rest is recommended together with local an- tibiotic therapy of the sheath. Most bulls recover within one to two weeks but it may take up to a month before normal copulation will occur. Because of the infections nature of this disease bulls should not be used for service until 6 to 8 weeks after the onset of the attack. Since herpes viruses tend to persist in the body, recurrent dis- semination of virus may occasionally be possible.25 29 Balanoposthitis in rams, “pizzle rot” or ‘‘sheath rot,” may be infectious or noninfectious. The most common infectious form of balanoposthitis is due to the virus that causes ulcerative dermatosis (lip and leg ul- ceration or necrotic venereal disease). This disease has been described in the U.S., England, France and Ger- many.17’20 The lesions on the preputial orifice, prepuce and glans penis are ulcerative and covered by a scab. Removal of the scab reveals a shallow, raw, bleeding crater containing a creamy odorless pus. The preputial lesions may cause phimosis or paraphimosis, and an ex- tensive penile lesion may render the ram useless as a breeder. Lesions may also be present on the lip, nostril, feet, or vulva. The disease should be distinguished from contagious ecthyma and common non-specific lesions occasionally seen on the preputial orifice of rams. Ul- cerative dermatosis is spread by venereal contact and other means. The disease in rams may persist for weeks or months. Affected rams should not be used for breeding. There is no vaccine available nor is there any specific treatment for the lesions. Noninfectious balanoposthitis has been described in the U.S. and Australia. Two types of lesions are rec- ognized, an ulceration of the prepuce near the preputial orifice and a stenosis of the orifice with a secondary chronic ulceration of the deeper portions of the prepuce accompanied by an accumulation of pus and necrotic material. This occurs mainly in wethers, sheep and goats, or occasionally rams 2 to 4 years of age. It is often as- sociated with a wet spring and pasturing sheep on lush fertilized grass, rye, clover or lucerne pastures that are high in protein and the presence of a urea-hydrolyzing C. renale in the wether’s sheath. The urine degradation products are more irritating to sheath tissue than normal urine.22 28 The preputial orifice and prepuce may be ul- cerated and scarred so urination is difficult. Changing of the diet to dry feed with a lower protein intake, or fast- ing, results in an improvement of the balanoposthitis. Young rams housed together may develop similar le- sions possibly due to trauma and contamination. In se- vere cases the sheath may have to be surgically opened ventrally to permit urination to save the life of the ani- mal. Extending the preputial incision too far caudally may render a ram useless for service. Superficial exter- nal lesions may be treated by proper local therapy. A clinically similar type of posthitis was observed in many young beef bulls, but not steers, in South America and Australia. A high incidence occurred in bulls on high planes of nutrition possibly due to the presence of C. renale in the sheath that hydrolized urea to ammonia that caused the lesions. The clinical history and histologic examination indicated the condition was not due to the IBR-IPV virus. Further studies are indicated.24 Balanoposthitis in the horse may occur in geldings or stallions. A thick, fibrous, fatty or edematous sheath is often diagnosed erroneously as due to a balanoposthitis when no inflammatory lesions are present. Balanopos- thitis due to bacterial agents are uncommon in stallions even though various infectious agents may be carried from mare to mare on the penis and prepuce. Early symptoms of dourine, a reportable venereal disease of horses trans- mitted by coitus, are swelling, edema and reddening of the penis and prepuce. This disease, not seen in the U.S., is caused by Trypanosoma equiperdum. Later in the disease process depigmentation of the skin of the genital organs may occur.8 An equine venereal balanitis and vulvitis, formerly called genital horse pox or coital exanthema, caused by a herpesvirus has been described.913 (See Figure 147.) After an incubation period of 6 to 8 days circular, con- fluent, poxlike lesions occur on the skin of the penis. These lesions heal in 10 to 14 days if secondary infec- tions do not occur. Depigmentation of affected areas is common. There is no effect on fertility but affected stal- lions may refuse or hesitate to copulate. With-holding affected stallions from service to prevent the spread of infection to susceptible mares and local conservative treatment of the lesions is indicated. One attack does not confer a permanent immunity.18 This virus is not the rhinopneumonitis virus. The disease is occasionally seen in the U.S. especially on breeding farms where it may spread rapidly by coitus or grooming. Cutaneous habronemiasis, summer sores or genital bursatti may affect the equine penis and prepuce. The Habronema larvae may produce fungoid granulomatous growths 1 to 3 cm. in diameter that may contain firm806 VETERINARY OBSTETRICS necrotic, irregular-shaped masses or “kunkurs.” These lesions bleed readily on manipulation.18'31 The lesions are not seen on the genitals of mares. These lesions may produce intense pruritus. In some cases their presence near the urethral process results in difficult frequent uri- nation with spraying similar to that produced when the urethral diverticulum is distended with smegma causing compression of the urethra. In the colder northern states these lesions subside and usually disappear during the winter months. These granulomas may be treated by top- ical organophosphates, amputation of the penis or the urethral process depending on its size and location.14'31 Local treatment with camphophenique in scarlet oil or an organophosphate preparation daily and a systemic or- ganic phosphate insectide (“Ronnel”) at a dose of 90 mg/ kg by stomach tube repeated in two weeks was recom- mended.36 In countries where the screw worm or Coch- liomyia fly is present, severe infestations of the sheath and glans penis of geldings or stallions may occur re- sulting in pain, bleeding and swelling. Good restraint, often requiring general anesthesia, is necessary to get adequate exposure for local treatment of lesions with Smear 62 or camphophenique. Further infestation should be prevented by confining the animal in a bam and treat- ing the external preputial opening with fly repellant. Multiple, small ulcerous lesions on the penis and pre- puce of a horse associated with spirochetes was re- ported.23 The lesions healed in about three weeks and the spirochetes disappeared. In some horses excessive accumulations of smegma within the prepuce may be as- sociated with a keratin-like coating of the penis and pre- puce. Manual cleansing of the equine sheath with soap or oily antiseptic solutions is accomplished by restraint and the liberal use of cotton swabs. Wearing plastic or rubber gloves is advisable because of the odor of the smegma. Occasionally a heavy growth of pseudomonas and/or Proteus organisms are present in the equine sheath causing an objectionable odor and excessive smegma. Regular cleaning of the sheath with mild soap and water and occasional application of neomycin, or a similar an- tibiotic, in a vegetable oil vehicle may be indicated. Balanoposthitis seldom occurs in the boar. The pre- putial diverticulum in the boar often fills with foul- smelling urine and smegma and externally may resemble an umbilical hernia. (See Figure 160.) This can readily be differentiated from a hernia on clinical examination by squeezing the enlarged diverticulum and expressing its odoriferous contents. In boars concretions and pre- putial calculi and diversion of the penis into the preputial diverticulum occasionally were present, causing difficult urination and inability to protrude the penis.19 Extirpa- tion of the preputial diverticulum of boars will markedly reduce the bacteria in semen collected for artificial in- semination and also greatly reduce the boar odor.1'19 The boar’s sheath may become infested with screwworms. In pigs with hog cholera ulcers of the prepuce as a result of infarction have been reported.12 Ulcerations of the porcine penis due to other causes may be observed. These conditions in boars are usually easily diagnosed and treated. Surgical procedures for prolapse of the penis and extirpation of the porcine preputial diverticulum have been described.6'19 In the dog, balanoposthitis is occasionally observed but seldom if ever, is a cause of failure of copulation. It is characterized by a discharge of pus from the prepuce and it usually responds well to mild antiseptic douches followed by bland antibiotic ointments or solutions. Bal- anoposthitis in the dog should be differentiated from the prostatitis as both are characterized by pus appearing at the preputial opening. Suppurative, ulcerative and fol- licular balanoposthitis or preputial catarrh is common in the dog.5 It is interesting to note that follicular lesions occur in the prepuce of the dog and are similar in nature to the enlarged lymph follicles or to the granular vener- eal disease lesions seen in the prepuce of the bull. (See Figure 173.) As noted under IBR-IPV infection of the prepuce and penis in bulls isolation of a herpesvirus from the sheath of dogs has been reported.10 Balanoposthitis in the dog, as in other animals, is due to mixed infec- tions, trauma, foreign bodies, other general diseases, and debility. The malicious or ill-considered placement of a rubber band around a dog’s penis causes great discom- fort, severe balanoposthitis and even necrosis of the penis. In the dog acquired phimosis is less frequent than is con- genital phimosis.5 The prognosis in balanoposthitis depends upon the se- verity of the trauma or the infection. In mild cases the prognosis is good. In severe chronic cases with adhe- sions between the penis and prepuce or between the pre- puce and adjacent tissues, the prognosis is guarded to poor. Some males may be slow to regain their libido following a painful balanoposthitis. Treatment of mild cases of balanoposthitis may con- sist of douching the prepuce with aqueous or oily anti- septics or antibiotic preparations such as saline, 50 to 200 ppm. of chlorine solution, 1:2,000 acriflavine or very dilute potassium permanganate solutions, 1 percent hy- drogen peroxide solutions, one ounce of bismuth formic iodide in a 500 ml. of mineral oil, 1 gm. iodine in one gallon of mineral oil, infusions of aqueous furacin and other antibiotics in oil in about 25 to 100 ml. volumes. Caustic or irritating antiseptics should be avoided. Treat- ments may be repeated at daily to weekly intervals. In cases of severe balanoposthitis with extensive necrosisINFERTILITY IN MALE ANIMALS 807 of the prepuce and penis adhesions may result if frequent oily antiseptics or antibiotic ointments and systemic an- tibiotics are not employed. Regular gentle protrusion of the penis may be desirable to prevent possible adhesions. Tranquilizers, anesthetics, pudendal nerve block, elec- troejaculator, and adequate restraint are helpful in ap- plying treatment for balanoposthitis. Sexual rest is es- sential during and for sometime after the treatment of acute balanoposthitis to promote recovery and to prevent a loss of libido associated with the painful condition. Miscellaneous Causes for Loss of Libido or Inabil- ity to Copulate include: 1) hernias 2) premature erection 3) short penile bone (dog) 4) loss of sensory innervation of the glans penis 5) vascular shunts causing failure of erection 6) urinary calculi and 7) other causes. 1) Umbilical and ventral hernias as well as a deep pendulous abdomen may interfere or prevent normal copulation by affecting the entry of the penis into the vagina at a natural mating. Umbilical and small ventral hernias may respond to surgery but since umbilical her- nias may be hereditary the affected male should not be used as a sire. About 1 percent of Santa Gertrudis bulls and Holsteins in Australia have umbilical hernias.14 These affected animals should be culled and not operated upon. Extensive unilateral hernias or a deep “paunchy” ab- domen usually observed in older bulls or rams may in- terfere with normal intromission and thrusting especially if arthritic lesions are also present. Marked reduction of roughage and bulky feeds is indicated in these males but the prognosis is usually guarded to poor. 2) Premature erection may occur in the dog, stallion and certain bulls and interfere with normal intromission. Premature erection in the dog as an obstacle to coitus and a cause of impotency has been described.11 Com- plete erection normally does not take place until the ca- nine penis is in the vagina. Artificial insemination was recommended as the quickest and easiest solution for this problem.11 In stallions the glans penis occasionally be- comes too large by “flowering” or “belling” to readily enter the mare’s vulva. This cause of inability to copu- late can usually be overcome by helping to direct the penis into the vulva before it becomes fully erect or by lubricating the vulva. As described previously certain beef bulls with a strong sex drive and with a narrow penis develop a “corkscrewing” or coiling of the free end of the penis at premature full erection that prevents intro- mission. (See Figure 165) 3) Occasionally a dog will have a short penile bone with a long flaccid cranial portion of the penis that is difficult to direct into the vulva at coitus.9 4) Loss of sensory innervation of the glans penis pre- vents natural intromission and the “thrust” reflex nec- essary for ejaculation and leads to a pronounced decline in sex drive. Lack of sensation of the glans penis may be caused by injury to the dorsal nerve of the penis sec- ondary to rupture and hemorrhage of the corpus caver- nosum penis, by the improper technique of injecting lo- cal anesthesia on the dorsal nerve of the sigmoid flexure of the penis, occasionally by an operation to correct the spiralling of the bovine penis or by a rubber band from an artificial vagina or other source that is placed around the penis and not removed for several days. Lack of sen- sation of the glans penis may also be due to necrosis of the mucosa of the glans secondary to severe balanitis of an infectious etiology or due to trauma resulting in se- vere scarring. Amputation of the glans penis by a rubber band or following extensive surgery for a tumor pro- duces the same local “anesthetic” effect. Males that have had experience breeding before the loss of sensation in the glans penis remain sexually active but suffer from a definite loss of libido. Immature males with a similar loss seldom show much sexual desire as demonstrated by mounting and actively seeking the vulva with their penis. In bulls topical anesthesia of the glans penis caused intromission to be difficult and delayed but copulation occurred. Topical anesthesia of the glans as well as the free portion of the penis blocked the ability to copulate. Infiltration of the glans penis with a local anesthetic pre- vented ejaculation. Bulls with unilateral dorsal penile nerve neurectomy were able to copulate but time to ejac- ulation was prolonged. Bulls with bilateral neurectomy were unable to copulate.4 Thus it is possible the bulls may recover from a hematoma or penile surgery and in a few weeks or months develop signs of decreased abil- ity or inability to copulate due to adhesions around the penile nerves with secondary degeneration due to sub- sequent injury or stretching. An experimental study of the results of desensitization of the glans penis in the cat was reported.1 Damage to the nerve supply of the is- chiocavernosus muscle may cause its atrophy and result in the inability of the penis to become erect. 5) Vascular shunts causing failure of erection. In bulls exhibiting a flaccid penis or only a partial erection that was lost rapidly during attempts at natural service or on stimulation with an electroejaculator before in- tromission or full erection was accomplished often were shown to have shunts between the corpus cavemosum penis and the extrocarporeal circulation of the penis.25 Some of these shunts were acquired after rupture of the tunica albuginea of the penis and hematoma formation with spontaneous healing, deep lacerations of the penis and surgical operations to correct penile deviations. In other bulls multiple shunts of a congenital nature were observed in the distal portion (glans) of the penis. Serial808 VETERINARY OBSTETRICS contrast radiography confirmed the suspected diagno- sis,22,25 and surgical correction was described for valu- able bulls with only one or a few shunts. Using a wedge resection of the tunica albuginea, surgery was successful in 4 of 8 bulls.25 English workers described 6 bulls in 3 breeds with good libido but 5 were unable to erect the flaccid penis to protrude it from the sheath. This was caused by major venous drainage of the corpus caver- nosum penis by the dorsal venous system.3 A similar impotence was reported in five boars with inability to obtain or sustain penile erection and copulate. This con- dition was developmental in origin with abnormalities of the dorsal venous system allowing blood to drain from the corpus cavemosum penis.2 6) Urinary calculi lodging in the urethra may occa- sionally be a cause of acute pain, obstruction and rupture of the urethra in male domestic animals and cause re- luctance to copulate and inability to ejaculate. Urinary calculi were described in a bull with inability to copulate and exhibiting impotentia coeundi.21 The author has ob- served several bulls with urethral calculi, that refused to copulate and one that copulated and bled from the ure- thra. In cases of urinary or urethral calculi the prognosis for the future breeding life of the male is grave. Al- though an operation can be performed and the calculi removed, suturing of the urethra often results in a stric- ture. When the urethral and skin incisions in the bull are left open to heal by second intention, in order to save the animal for future breeding an urethral fistula or stric- tures often form. Other calculi may lodge in the same area; or adhesions form in the region of the sigmoid flex- ure and the ability to protrude the penis is lost. Leaving the skin and urethra open to heal by second intention is however occasionally successful in the dog and has been reported in the bull. Depending on the location of the urethral fistula the male may be unable to properly place the semen in the vagina. A urethral calculi retriever (Haver-Lockhart Lab., Shawnee, Ks.) modified after a human retriever for urethral calculi has been described.15 This has proven successful in cases where tranquilizers and muscle relaxants when administered early failed to result in the passage of the calculi from the usual site of lodgement at the sigmoid flexure. The bull is placed in lateral recumbency under tranquilization. Pudendal nerve block may also be used. The penis is fully extended and the retriever with proper lubrication is passed beyond the calculi and then withdrawn removing the obstruction. Stricture formation was reported not to be a serious prob- lem. In the ram calculi may lodge in the sigmoid flexure area as in bulls but are more commonly found in the urethral process. Amputation of the urethral process just proximal to the calculi is usually performed. If most of the urethral process is removed conception rates might be markedly reduced due to poor distribution of semen in the vagina at the time of ejaculation.13 Calculi are common in the male cat16 and uncommon in the dog.6 In order to preserve the breeding potential of these animals conservative therapy such as massage and flushing in the removal of the urethral calculi and in the aftercare is indicated, surgery should be used only as a last resort. The use of a loop of no. 26 twisted steel wire to remove urethral calculi and mucous plugs in the anesthetized cat has been described.5 Up to 1 percent of male cats may develop calculi and recurrence is com- mon.1617 Using a 3" nasal lacrimal duct needle rather than a tom cat catheter and small amounts of 50 percent vinegar in water to remove urethral calculi from anes- thetized cats was recommended.1617 There was experi- mental evidence that several infectious viral agents were important etiologic factors along with other environmen- tal and nutritional factors.16'18 Antibiotics such as Chlo- romycetin, reduction of minerals in the diet, lowering the pH of the urine and increasing the water intake and other conservative therapeutic measures16 may be helpful in controlling urolithiasis in these animals. In the dog calculi tend to lodge at the caudal end of the os penis since the urethra passes along the ventral groove in the penile bone.10 23 Urinary calculi ruptured urethras and bladders, greatly enlarged bulbourethral glands and ve- sicular glands in feetlot lambs or wethers given 12 to 15 mg. implants of stilbestrol or 2 to 5 mg. of stilbestrol daily in the feed was reported.12,20 This occurred as early as 10 to 14 days after the administration of the stilbes- trol. 6) Pain caused by infection of the genital organs or peritoneum may be a cause of impotency or refusal to copulate. A stallion with infection of the ampullae and seminal vesicles refused to copulate.24 The author has observed several bulls with severe acute semino-vesicu- litis that were slow or refused to mount. Two boars with brucellar orchitis refused to copulate and two more had a markedly reduced libido.8 Acute prostatitis in dogs might similarly affect copulation. Necrobacillosis of the liver and traumatic gastritis with acute peritonitis may be as- sociated with failure or refusal to copulate in bulls. Se- vere congenital or acquired cardiac diseases often result in dyspnea and inability to perform coitus by male ani- mals. Reduced to Complete Lack of Sexual Desire and Inability to Copulate 1. Almquist, J. O. and Hale, E. B. (1956) An Approach to the Measurement of Sexual Behavior and Semen Production of DairyINFERTILITY IN MALE ANIMALS 809 Bulls, Proc. Ill Intemat. Congress on An. Reprod., Cambridge. 2. Bane, A. (1954) Studies on Monozygous Cattle Twins XV Sex- ual Functions of Bulls in Relation to Heredity, Rearing Intensity and Somatic Conditions, Acta Agric. Scand. 4, 95. 3. Barton, A. (1960) Instinct and Sexuality in the Dog, Vet. Med. 55, 5, 49. 4. Bielanski, W., Wierzbowski, S. and Zakrzewska, G. (1957) The Results of Mass-wise Evaluations of the Semen and Sexual Re- flexes of Stallions, Zesz. Nauk. Wyxs. Roln. W. Krakowie, Zootechnica 21, 4, 97. 5. Blockey, M. A. deB. (1976) Sexual Behavior of Bulls at Pas- ture: A Review, Theriog. 6, 4, 387. 6. Blockey, M. A. deB. (1978) The Influence of Serving Capacity of Bulls on Herd Fertility, J. An. Sci. 46, 589. 7. Blockey, M. A. deB. and Galloway, D. B. (1978) Hormonal Control of Serving Capacity of Bulls, Theriog., 9, 2, 143. 8. Chenoweth, P. J. (1978) Concepts in Bull Evaluation and Man- agement, Proc. 11th Ann. Conv. AABP, Baltimore, 104. 9. Chenoweth, P. J. (1981) Libido and Mating Behavior in Bulls, Boars and Rams: A Review, Theriog., 16, 2, 155-177. 10. Dunn, H. O., Roberts, S. J., McEntee, K. and Wagner, W. C. (1965) Prevention of Traumatic Gastritis in Bulls by Use of Magnets, Cor. Vet. 55, 2, 204. 11. Foote, R. H., Munkenbeck, N. and Greene, W. A. (1976) Tes- tosterone and Libido in Holstein Bulls of Various Ages, J. Dairy Sci., 59, 11, 2011. 12. Fox, M. W. (1968) Abnormal Behavior in Animals, W. B. Saunders, Co., Philadelphia. 13. Fraser, A. F. (1957) Intromission Phobia in the Bull, Vet. Rec. 69, 621. 14. Fraser, A. F. (1968) Reproductive Behavior in Ungulates, Ac- ademic Press, N.Y.C. 15. Goy, R. W. (1966) Role of Androgens in the Establishment and Regulation of Behavioral Sex Differences in Mammals, J. An. Sci. (suppl) 25, 21. 16. Hafez, E. S. E. (1960) Analysis of the Ejaculatory Reflexes and Sex Drive in the Bull, Cor. Vet. 50, 4, 384. 17. Hafez, E. S. E. (1968) Reproduction in Farm Animals, 2nd Ed. Lea and Febiger, Philadelphia. 18. Hafez, E. S. E. (1969) The Behavior of Domestic Animals, Williams and Wilkins Comp., Baltimore Md. 19. Hale, E. B. (1966) Visual Stimuli and Reproductive Behavior in Bulls, J. An. Sci. 25, Suppl. 36. 20. Hale, E. B. and Almquist, J. O. (1960) Relation of Sexual Be- havior to Sperm Cell Output in Farm Animals, J. Dairy Sci., 43, 145. 21. Hafs, H. D., Knisely, R. C. and Desjardins, C. (1962) Sperm Output of Dairy Bulls with Varying Degrees of Sexual Prepa- ration, J. Dairy Sci., 45, 6, 788. 22. Hart, B. L. and Ladeiog, J. (1980) Accelerated and Enhanced Testosterone Secretion in Juvenile Male Dogs Following Medial Preoptic-Anterior Hypothalamic Lesions, Neuroendocrin. 30, 20. 23. Hulet, C. V. (1966) Behavioral, Social and Psychological Fac- tors Affecting Mating Time and Breeding Efficiency in Sheep, J. An. Sci. Suppl, 25, 5. 24. Hulet, C. V., Blackwell, R. L. and Ercanbrack, S. K. (1964) Observations on Sexually Inhibited Rams, J. An. Sci., 23, 4, 1095. 25. Hulet, C. V., Ercanbrack, S. K., Blackwell, R. L., Price, D. A. and Willson, L. O. (1962) Mating Behavior of the Ram in the One-Sire Pen, J. An. Sci. 21, 4, 857. 26. Hulet, C. V., Ercanbrack, S. K., Blackwell, R. L., Price, D. A. and Wilson, L. O. (1962) Mating Behavior of the Ram in the Multi-Sire Pen, J. An. Sci., 21, 4, 865. 27. Hultnas, C. A. (1959) Studies on Variation in Mating Behavior and Semen Picture in Young Bulls of Swedish Red and White Breed and on Causes of this Variation, Acta. 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For Theriog., Omaha, 20. 42a. Smith, M. C. (1980) Caprine Reproduction, in Current Therapy in Theriogenology, Edit, by D. A. Morrow, W. B. Saunders, Comp., Philadelphia. 42b. Stein, B. S. (1975) The Genital System, in Feline Medicine and Surgery, 2nd Ed., E. F. Catcott, Ed., Amer. Vet. Publication, Santa Barbara, Cal. 43. Swift, B. L., Reeves, J. D. Ill and Thomas, G. M. (1979) Tes- ticular Degeneration and Libido Loss in Beef Bulls Experimen- tally Inoculated with Anaplasma marginale, Theriog., 11, 4, 277. 44. Twiggs, D. G., Popolow, H. B. and Gerall, A. A. (1978) Me- dial Preoptic Lesions and Male Sexual Behavior, Age and En- vironmental Reactions, Science 200, 1414. 45. Vandeplassche, M. (1955) Ejakulationsstorungen beim Hengst, Fortpfl. Zuchthyg. and Haustier 5, 11, 134. 46. Wierzbowski, S. and Hafez, E. S. E. (1961) Analysis of Cop- ulatory Reflexes in the Stallion, Proc. of IVth Intemat. Congr.810 VETERINARY OBSTETRICS on An. Reprod., The Hague. 47. Young, G. B. (1953) Genetic Aspects of Fertility and Infertility in Cattle, Vet. Rec. 65, 271. Joint, Muscle, Nerve, Bone and Tendon Injuries and Pathology 1. Almquist, J. O. and Thomson, R. G. (1973) Relation of Sexual Behavior and Ejaculation Frequency to Severity of Vertebral Body Osteophytes in Dairy and Beef Bulls, JAVMA, 163, 2, 163. 2. Bane, A. and Hansen, H. J. (1962) Spinal Changes in Bulls and Their Significance in Serving Ability, Cor. Vet. 52, 362. 3. Becker, R. B., Wilcox, C. J. and Pritchard, W. R. (1966) “Crampy" Progressive Posterior Paralysis in Mature Cattle, Bull 639. Univ. of Florida, Agr. Exp. Stat. Gainesville, Fla. 4. Brown, C. J., Roussel, J. D. and Stallcup, O. T. (1967) Genetic and Other Aspects of a Hoof Anomaly of Hereford Bulls, J. Dairy Sci., 26, 1, 201. 5. Einarsson, S. (1968) Fertility and Serving Ability of Swedish Lan- drace and Swedish Yorkshire Boars, Nord. Vet. Med. 20, 616. 6. Krook, L., Lutwak, L. and McEntee, K. (1969) Dietary Calcium, Ultimobranchial Tumors and Osteopetrosis in the Bull, Amer. J. Clin. Nutr., 22, 2, 115. 7. Pickett, B. W., Squires, E. L. and Voss, J. L. (1981) Normal and Abnormal Sexual Behavior of the Equine Male, An. Reprod. Lab., Colo. State Univ., Ft. Collins, Colo. 80523. 8. Roberts, S. J. (1965) Hereditary Spastic Diseases Affecting Cattle in New York State, Cor. Vet. 55, 4, 637. 9. Thompson, R. G. (1965) A Study of Vertebral Body Osteophytes in Bulls, Thesis, Cornell Univ., Ithaca, New York. Diseases of the Penis and Prepuce 1. Adams, W. M. (1970) Hormonal and Anatomical Causes of In- fertility, Colloquium on Effect of Diseases and Stress on Repro- ductive Efficiency in Swine, Iowa State Univ., Ames, Iowa. 2. Bane, A. and Hansen, H. J. (1962) Spinal Changes in Bulls and Their Significance in Serving Ability, Cor. Vet. 52, 362. 3. Bloom, F. (1953) Endocrine Glands, Canine Medicine, Amer. Vet. Public. Inc. Evanston 111. 4. Carroll, E. J. (1967) Personal Communication. 5. Crowshaw, E. J. and Brodey, R. S. (1960) Failure of Preputial Closure in a Dog, JAVMA, 136, 9, 450. 6. DeGroot, T. and Numans, S. R. (1946) Over de Erfelijkheid der Impotentia Coeundi bij Stieren, Tijd. v. Diergeneesk 71, 372. 7. Fraser, A. F. (1957) Intromission Phobia in the Bull, Vet. Rec. 69, 621. 8. Haq, I. (1949) Causes of Sterility in Bulls in Southern England, Brit. Vet. Jour. 105, 71, 114, 200. 9. Hofmeyr, C. F. B. (1967) Surgery of Impotentia Coeundi, J. So. Afr. Vet. Med. Assoc. 38, 3 & 4, 275, 395, 399. 10. Holst, S. J. (1949) The Semen of Sterile Boars, Proc. 14th In- temat. Vet. Congr. Vol. III. Sect 4(c), 118. 11. Kendrick, J. W. (1954) Psychic Impotence in Bulls, Cor. Vet. 44, 3, 289. 12. McEntee, K. (1970) Pathology of Domestic Animals, 2nd Ed. Vol I by Jubb, K. V. and Kennedy, P. C., Academic Press, N.Y.C., London. 13. Noice, F. and Schipper, I. A. (1958) Abnormal Urogenital Tract of a Ram, JAVMA, 132, 2, 75. 14. Pickett, B. W., Squires, E. L. and Voss, J. L. (1981) Normal and Abnormal Sexual Behavior of the Equine Male, An. Reprod. Lab. Colo. State Univ., Ft. Collins, Colo., 80523. 15. Richter, J. (1919) Die Unfruchtbarkeit den Ziegenbocke, R. Schoetz, Berlin. 16. VanderSluis, L. (1953) Experiences with the Examination into Herd Infertility, Proc. 1st World Congr. on Fert. and Steril. II, XXV, 703. 17. Williams, W. L. (1943) Diseases of the Genital Organs of Do- mestic Animals, 3rd Ed., Ithaca, N.Y. Deviations of the Penis la. Adams, W. M. (1970) Hormonal and Anatomical Causes of In- fertility, Colloq. on Effect of Diseases and Stress on Reproduc- tion Efficiency in Swine, Iowa State Univ., Ames, Iowa. lb. Ashdown, R. R. (1962) Persistence of the Penile Frenulum in Young Bulls, Vet. Rec. 74, 50, 1464. 2. Ashdown, R. R. and Combs, M. A. (1967) Spiral Deviation of the Bovine Penis, Vet. Rec. 80, 738. 3. Ashdown, R. R. and Pearson, H. (1973) Studies in “Corkscrew Penis” in the Bull, Vet. Rec. 93, 30. 4. Ashdown, R. R., Ricketts, S. W. and Wardley, R. C. (1968) The Fibrous Architecture of the Integumentary Coverings of the Bovine Penis, J. of Anat., 103, 3, 567. 5. Ashdown, R. R. and Smith, J. A. (1969) The Anatomy of the Corpus Cavemosum Penis of the Bull and Its Relationship to Spi- ral Deviation of the Penis, J. Anat. 104, 1, 153. 6. Balke, J. (1981) Persistent Penile Frenulum in a Cocker Spaniel, Vet. Med./Sm. An. Clin., 76, 7, 988. 7. Carroll, E. J., Aanes, W. A. and Ball, L. (1964) Persistent Penile Frenulum in Bulls, JAVMA, 144, 7, 747. 8. Elmore, R. G. (1981) Surgical Repair of Bovine Persistent Penile Frenulum, Vet. Med./Sm. An. Clin., 76, 5, 701 (A Review). 9. Herrick, J. (1958) Personal Communication. 10. Johnston, D. E. (1965) Repairing Lesions of the Canine Penis and Prepuce, Mod. Vet. Pract., 46, 1, 39. 11. Johnston, S. D., Larsen, R. E., Olson, P. S. (1982) Canine Ther- iogenology Vol. XI, J. Soc. forTheriog., Hastings, Nebr., 68901. 12. Joshua, J. O. (1962) Persistence of the Penile Frenulum in a Dog, Vet. Rec. 74, 52, 1550. 13. McEntee, K. (1969) Pathology of Domestic Animals, Vol. I, 2nd Ed., Jubb, K. V. and Kennedy, P. C., Academic Press, N.Y.C. 14. Milne, F. J. (1954) Penile and Preputial Problems in the Bull, JAVMA, 129, 922, 6. 15. Mobini, S., Walker, D. F. and Crawley, R. R. (1982) An Ex- perimental Evaluation of the Response of the Bull Penis to Car- bon Fiber Implants, Cor. Vet. 72, 350. 16. Ryer, K. A. (1979) Persistent Penile Frenulum in a Cocker Span- iel, Vet. Med./Sm. An. Clin., 74, 5, 688. 17. Scott, J. A. (1962) Personal Communication. 18. Seidel, G. E., Jr., and Foote, R. H. (1967) Motion Picture Anal- ysis of Bovine Ejaculation, J. Dairy Sci. 50, 6, 970. 19. Seidel, G. E., Jr., and Foote, R. H. (1969) Motion Picture Anal- ysis of Ejaculation in the Bull, J. of Reprod. and Fert. 20, 313. 20. Walker, D. F. (1964) Deviations of the Bovine Penis, JAVMA, 145, 7, 677. 21. Walker, D. F. and Vaughan, J. T. (1980) Bovine and Equine Urogenital Surgery, Lea and Febiger, Philadelphia.INFERTILITY IN MALE ANIMALS 811 Hematomas, Adhesions and Tumors of the Penis and Prepuce 1. Bagdonas, V. and Olson, C., Jr. (1953) Observations on the Ep- izootiology of Cutaneous Papillomatosis (Warts) of Cattle, JAVMA, 122, 914, 393. 2. Beckett, S. D., Reynolds, T. M., Walker, D. F., Hudson, R. S. and Purohit, R. C. (1974) Experimentally Induced Rupture of the Corpus Cavemosum Penis in the Bull, Amer. J. Vet. Res. 35, 6, 765. 3. Bloom, F. (1954) Pathology of the Dog and Cat, Amer. Vet. Public, Inc. Evanston, 111. 4. Brown, N. O., MacEwen, E. G. and Clavert, C. (1980) Follow- up on Chemotherapy of Venereal Tumors, JAVMA, 177, 8, 676. (Letter). 5. Farquharson, J. (1952) Fracture of the Penis in the Bull, Vet. Med. 47, 5, 175. 6. Feldman, W. H. (1932) Neoplasms of Domestic Animals, W. B. Saunders, Co., Philadelphia, Pa. 7. Formston, C. (1953) Fibropapillomatosis in Cattle with Special Reference to the External Genitalia of the Bull, Brit. Vet. Jour. 109, 244. 8. Goldston, R. T. (1969) The Bovine Penile Hematoma, Proc. of Conference on Reprod. Problems in Animals, Univ. of Georgia, Nov., p. 63. 9. Hall, W. C., Nielsen, S. W. and McEntee, K. (1976) Tumors of the Prostate and Penis, Bull. World Health Org., 53, 3435. 10. Higgins, D. A. (1966) Observations on the Canine Transmissible Venereal Tumor as Seen in the Bahamas, Vet. Rec. 79, 3, 67. 11. Hofmeyr, C. F. B. (1967) Surgery of Impotentia Coeundi, J. So. Afr. Vet. Med. Assoc., 38, 3 and 4, 275, 395, 399. 12. Johnston, D. E. (1965) Repairing Lesions of the Canine Penis and Prepuce, Mod. Vet. Pract., 46, 1, 39. 13. McAfee, L. T. and McAfee, J. T. (1977) Transmissible Venereal Tumor: Surgery and Chemotherapy, Vet. Med./Sm. An. Clin , 72, 199. 14. McEntee, K. (1969) Pathology of Domestic Animals, 2nd Ed., Vol. I. Jubb, K. V. and Kennedy, P. C. Academic Press, N.Y., London. 15. Milne, F. J. (1954) Penile and Preputial Problems in the Bull JAVMA, 124, 922, 6. 16. Noordsy, T. L. (1970) Personal Communication. 17. Noordsy, J. L. (1981) Hematoma of the Bovine Penis: A Tech- nique for Predicting Successful Surgical Correction, Vet. Med./ Sm. An. Clin. 76, 11, 1581. 18. Olson, C., Robl, M. G. and Larson, L. L. (1968) Cutaneous and Penile Fibropapillomatosis and its Control, JAVMA, 153, 9, 1189. 19. Olson, C., Jr., Segre, D. and Skidmore, L. V. (1960) Further Observations on Immunity to Bovine Cutaneous Papillomatosis, Am. J. Vet. Res. 21, 81, 233. 20. Pattridge, P. D. (1953) Surgical Repair of the Fractured Penis in the Bull, Southwest Vet. 7, 1, 31. 21. Pearson, J. K. L., Kerr, W. R., McCartney, W. D. J. and Steele, T. H. J. (1959) Tissue Vaccines in the Treatment of Bovine Pap- illomas, Vet. Rec. 70, 48, 971. 22. Scott, E. A. (1976) A Technique for Amputation of the Equine Penis, JAVMA, 168, 11, 1047. 23. VanderSluis, L. 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(1980) The Reefing Operation in Large Animals, Vet. Med./Sm. An. Clin., 75, 1, 112. 16. Romane, Wm. M. (1960) Circumcision of the Bull, Personal Communication. 17. Walker, D. F. (1967) Diseases of the Penis and Prepuce of the Bull Requiring Surgery, JAVMA, 118, 890, 295. 18. Walker, D. F. and Vaughan, J. T. (1980) Bovine and Equine Urogenital Surgery, Lea and Febiger, Philadelphia. Balanoposthitis 1. Aamdal, J., Hogset, I. and Filseth, O. (1958) Extirpation of the Preputial Diverticulum of Boars Used for Artificial Insemina- tion, JAVMA, 132, 522. 2. Bakos, K., Bane, A. and Thai. E. (1962) Mycoplasma (PPLO) in Relation to Fertility in the Bull, Zentralbl. f. Veterinar. Med 9, 4, 397. 3. Bane, A. (1964) Fertility and Reproductive Disorders in Swed- ish Cattle, Brit. Vet. Jour. 120, 431. 4. Beveridge, W. I. B. and Johnstone, I. L. (1953) Sheath Rot, Non-contagious Posthitis or Chronic Ulceration of the Prepuce of Sheep, Austral. Vet. Jour., 29, and 30, 326 and 1. 5. Bloom, F. (1954) Pathology of the Dog and Cat, Amer. Vet. Publicat. Inc., Wheaton, Illinois. 6. Bollwahn, W. (1981) Surgical Procedures in Boars and Sows, in Diseases of Swine, 5th Ed., Edit, by A. D. Leman, Iowa State Univ. Press, Ames, Iowa, 787.812 VETERINARY OBSTETRICS 7. Bouters, R., Vandeplassche, M., Florent, A. and Devos, A. (1960) Ulcerative Balanoposthitis in Bulls, Vlaams Dierge- neesk, Tijdschr., 29, 171. 8. Bruner, D. W. and Gillespie, J. H. (1973) Hagan’s Infectious Diseases of Domestic Animals, 6th Ed., Comstock Publishing Assoc., Cornell Univ. Press, Ithaca, New York. 9. Bryans, J. T. (1968) The Herpesviruses in Disease of the Horse, Proc. of 14th Annual Meeting AAEP, Philadelphia, 119. 10. Carmichael, L. E. (1970) Personal Communication. 11. Delahanty, D. D. (1955) Personal Communication. 12. Dunne, H. W. (1961) The Pathogenesis and Pathologic Anat- omy of Hog Cholera, Proc. Symp. on Hog Cholera, Univ. of Minn., St. Paul, Minn., 45. 13. Girard, A., Greig, A. S. and Mitchell, D. (1968) A Virus As- sociated with Vulvitis and Balanitis in the Horse—A Prelimi- nary Report, Canad. J. of Comp. Med. 32, 603. 14. Hackett, R. P., Vaughan, J. T. and Tennant, B. C. (1982) Ha- bronema Granulomas in Equine Medicine and Surgery, 3rd Ed., R. A. Mansmann, and E. S. McAllister, Edit. Amer. Vet. Pub- lic., Santa Barbara, Cal. 15. Hillman, R. B. (1982) Personal Communication. 16. Hutchings, L. M. (1948) Sterility in Swine, JAVMA 112, 851, 114. 17. Jensen, R. and Swift, B. L. (1982) Diseases of Sheep, 2nd Ed., Lea and Febiger, Philadelphia. 18. Krai, F. and Schwartzman, R. M. (1964) Veterinary Compar- ative Dermatology, J. B. Lippincott Co., Philadelphia, Pa. 19a. Kross, S. B., Ames, N. K. and Gibson, C. (1982) Extirpation of the Preputial Diverticulum in a Boar. 19b. Larson, L. L., Bartlett, D. E. and Parkes, W. G. (1972) Disease Incidence in Bulls, Proc. 7th Intemat. Congr. on Animal Re- prod. and Art. Insem., 1473. 20. Marsh, H. (1965) Newsom’s Sheep Diseases, 3rd Ed., Williams and Wilkins Co., Baltimore, Md. 21. McEntee, K. (1969) Pathology of Domestic Animals, 2nd Ed., by Jubb, K. V. and Kennedy, P. C., Academic Press, N.Y.C. 22. McMillan, K. R. and Southcott, W. H. (1973) Aetiological Fac- tors in Ovine Posthitis, Austral. Vet. J. 49, 405. 23. Osborne, V. E. and Bain, R. V. S. (1961) Genital Infection of a Horse with Spirochetes, Austral. Vet. Jour., 37, 190. 24. Rubino, M. C. (1979) Ulcerative Posthitis in Bulls in Uruguay, Cor. Vet. 69, 33. 25. Saxegaard, F. (1968) Serological Investigations of Bulls Sub- clinically Infected with Infectious Pustular Vulvovaginitis, Nord. Vet. Med., 20, 28. 26. Schultz, R. D., and Sheffy, B. E. (1980) Current Status of Viral Infections of the Bovine Genital Tract, in Current Therapy in Theriog., Edit, by D. A. Morrow, W. B. Saunders, Co., Phil- adelphia. 27. Scott, J. A. (1962) Personal Communication. 28. Shelton, M. and Livingston, C. W., Jr. (1975) Posthitis in An- gora Wethers, JAVMA, 167, 2, 154. 29. Snowden, W. A. (1965) The IBR-IPV Virus Reaction to Infec- tion and Intermittent Recovery of Virus from Experimentally Infected Cattle, Austral. Vet. Jour. 41, 135. 30. Southcott, W. H. (1962) The Etiology of Ovine Posthitis: Trans- mission of the Disease, Austral. Vet. Jour., 38, 441. 31. Stick, J. A. (1979) Amputation of the Equine Urethral Process Affected with Habronemiasis, Vet. Med./Sm. An. Clin. 74, 10, 1453. 32. Straub, O. C. (1970) Personal Communication. 33. Straub, O. C. (1970) Vaccination Against Coital Exanthema (IPV) Intemat. Conf. on Cattle Diseases, Philadelphia. 34. Studdert, M. H., Barker, C. A. V. and Savan, M. (1964) In- fectious Pustular Vulvovaginitis (IPV) Virus Infection of Bulls, Am. J. Vet. Res. 25, 105, 303. 35. Watson, R. H. and Mumame, D. (1958) Noncontagious Ovine Posthitis (Sheath Rot): Some Aspects of its Course and Etiol- ogy, Austral. Vet. Jour., 34, 125. 36. Wheat, J. D. (1961) Habronemiasis of the Equine Prepuce, Vet. Med., 56, 11, 477. 37. Williams, W. L. (1943) Diseases of the Genital Organs of Do- mestic Animals, 3rd Ed., Ithaca, New York. Miscellaneous Causes in Loss of Libido and Inability to Copulate 1. Aronson, L. R. and Cooper, M. L. (1966) Seasonal Variation in Mating Behavior in Cats after Desensitization of the Gians Penis, Science, 152, 226. 2. Ashdown, R. R., Barnett, S. W. and Ardalani, G. (1982) Im- potence in the Boar, 2: Clinical and Anatomical Studies, Vet. Rec. 110, 15, 349. 3. Ashdown, R. R. and David, J. S. E. (1979) Impotence in the Bull: Abnormal Venous Drainage of the Corpus Cavemosum Penis, Vet. Rec. 104, 423. 4. Beckett, S. D., Hudson, R. S., Walker, D. F. and Purohit, R. C. (1978) Effect of Local Anesthesia of the Penis and Dorsal Penile Neurectomy on the Mating Ability of Bulls, JAVMA, 173, 7, 838. 5. Crago, W. H. (1969) A Simple Method for Removing Urethral Calculi in Male Cats, JAVMA, 154, 11, 1386. 6. Dibartola, S. P. and Chen, D. J. (1981) Canine Urolithiasis, Compend. on Cont. Educ., 3, 3, 226. (A Review.) 7. Fabricant, C. G., Rich, L. J. and Gillespie, J. H. (1969) Feline Vimses XI Isolation of a Vims Similar to a Myxovirus from Cats in Which Urolithiasis was Experimentally Induced, Cor. Vet., 59, 4, 667. 8. Hutchings, L. M. and Andrews, F. N. (1946) Studies on Bru- cellosis in Swine: Brucella Infection in the Boar, Amer. J. Vet. Res., 7, 25, 379, 385, 388. 9. Johnston, S. D., Larsen, R. E. and Olson, P. S. (1982) Canine Theriogenology, Vol. XI, J. of the Soc. for Theriog., Hastings, Nebr., 68901. 10. Kirk, R. W., McEntee, K. and Bentinck-Smith, J. (1968) Canine Medicine, Edit, by E. J. Catcott, Amer. Vet. Public., Inc., Wheaton Illinois. 11. Leonard, E. P., Rickard, C. G. and McEntee, K. (1953) Im- potence, Canine Medicine, Amer. Vet. Public., Inc., Evanston, Illinois, 165. 12. Marsh, H. (1961) Urethral Occlusion in Lambs on Feed Con- taining Stilbestrol, JAVMA, 139, 9, 1019. 13. Masson, J. (1963) Personal Communication. 14. Murray, G. R. (1970) Personal Communication. 15. Oehme, F. W. (1968) A Urinary Calculi Retriever for Nonsurgi- cal Treatment of Urolithiasis in Bulls, Vet. Med. 63, 1, 53. 16. Osborne, C. A. and Lee, G. E. (1978) Feline Cystitis, Urethritis, Urethral Obstruction Syndrome, Mod. Vet. Pract. 59, 173, 349, 513. 17. Rich, L. J. (1969) Feline Urethral Obstruction, Etiologic Factors and Pathogenesis, Thesis, N.Y.S. Veterinary College, Cornell University. 18. Rich, L. J. and Fabricant, C. G. (1969) Urethral Obstruction in Male Cats. Transmission Studies, Canad. J. Comp. Med. 33, 2, 164.INFERTILITY IN MALE ANIMALS 813 19. Stein, B. S. (1975) The Genital System, in Feline Medicine and Surgery, 2nd Ed., E. J. Catcott, Ed., Amer. Vet. Public., Santa Barbara, Cal., 303. 20. Udall, R. H. and Jensen, R. (1958) Studies on Urolithiasis II, The Occurrence in Feedlot Lambs Following Implantations of Diesthylstilbestrol, JAVMA, 133, 10, 514. 21. VanderSluis, L. (1953) Experiences with Examination into Herd Infertility, Proc. First World Congr. on Fert. and Steril., Vol. II, 25, 703. 22. Walker, D. F. and Vaughan, J. T. (1980) Bovine and Equine Urogenital Surgery, Lea and Febiger, Philadelphia. 23. Whitehead, J. E. (1964) Feline Medicine and Surgery, Edit, by E. J. Catcott, Amer. Vet. Public., Inc., Wheaton, Illinois. 24. Williams, W. L. (1943) Diseases of the Genital Organs of Do- mestic Animals, 3rd Ed., Ithaca, New York. 25. Young, S. L., Hudson, R. S. and Walker, D. F. (1977) Impo- tence in Bulls Due to Vascular Shunts from the Corpus Caver- nosum Penis, JAVMA, 171, 7, 643. Incapacity or Reduced Capacity to Fertilize in Males, Including Hereditary Disorders: (Impotentia Generandi) Fertility is the normal functioning of the testes, ac- cessory glands and ducts to deliver sperm of normal quantity and quality. Fertility and potency are not cor- related or related and may be divergent in the same male animal. Infertility or sterility in males is usually char- acterized by normal sexual desire and the ability to cop- ulate and ejaculate, but a complete or abnormally high percentage of failure of fertilization or conception, or delayed returns to estrum indicating early embryonic death in the females. Although most of the causes of incapacity or reduced capacity to fertilize in males is due to acquired diseases or pathological lesions, a significant number of causes are congenital or hereditary and should be recognized to avoid their perpetuation or increase in future genera- tions. Some of these hereditary conditions causing a mild or moderate problem in young males, such as hypoplasia of the testes, can predispose the male to testicular de- generation and more severe infertility or sterility. Ex- cellent reviews of the inherited disorders of cattle related to infertility and fertility have been published.12,25 The incapacity or reduced capacity to fertilize may be characterized by either of two findings following a com- plete semen examination. In one the semen is essentially normal on examination, and in the other the semen is abnormal in morphology, concentration, motility or other qualities. The former condition is often difficult to ex- plain satisfactorily with our present knowledge; how- ever, recent findings in cytogenetics and electronmi- croscopy have indicated several promising leads. Impotentia Generandi Associated with Apparently Normal Semen Production in cattle has been reviewed in Chapter XIII in the discussion of herd infertility, “re- peat breeders,” or failure of conception in females fol- lowing service by bulls infected with brucellosis, vibrio- sis, trichomoniasis, and possibly IBR-IPV virus, my- coplasma, ureaplasma or other organisms. Active brucel- losis in a herd of cattle is associated with symptoms of infertility; and the intrauterine insemination of brucella- infected semen usually results in infertility. Boars in- fected with Br. suis may carry and transmit the organ- isms to the female at coitus resulting in early embryonic death and signs of infertility as well as abortions. After examining 828 bulls for infertility in 1953 it was deter- mined that 374, or 45.2 percent were affected with vibri- osis or trichomoniasis.22 In this series of cases, however, only 15 of the 374 bulls had trichomoniasis. Sixty per- cent of 105 herds in all parts of Sweden in 1955 were or had been infected with vibriosis.7 The incidence of vibriosis in naturally-bred herds, especially beef herds, in the United States is possibly equally high. A number of herds with infertility resembling vibriosis were investigated but without finding the cause.10 An- other study reported on herd infertility problems arising in 47 herds in which no diagnosis could be made because no pathological conditions were found in the bulls or cows to explain the sterility.22 Errors or deficiencies in man- agement, as discussed in Chapter XIII may also be the cause of widespread infertility in some herds. Infertile, disease-free male animals with an apparently normal se- men picture in regards to motility, concentration and morphology are uncommon if their reproductive man- agement is good. Abnormal acrosomes, knobbed spermatozoa, related to defective spermiogenesis involving the Golgi appa- ratus has been described in bulls, boars and dogs as a cause of infertility in semen with normal motility and concentration of spermatozoa. Certain of the stains or techniques used for preparing spermatozoa for morpho- logical examination do not reveal this defect; while oth- ers such as nigrosin eosin, India ink or Giemsa show a refractile unstained or lightly stained area in the anterior pole or acrosome of the head of the spermatozoa. An eosin B. and fast green stain of the acrosome of sper- matozoa permits examination by a light microscope.23,24 Certain sterile Swedish Landrace boars had as many as 80 to 90 percent of their spermatozoa with an acrosomal, knobbed defect.3 Males with about 50 percent of their spermatozoa with acrosomal defects had low fertility. Phase contrast microscopy revealed these defective ac- rosomes. Sometimes the anterior border of the sperma- tozoa was flattened due to a protrusion and bending over of the acrosome.3 Nearly all of the spermatozoa in some bulls were affected. The defective acrosome apparently814 VETERINARY OBSTETRICS rendered the sperm cell incapable of penetrating and fer- tilizing the ovum.8 The nature of this defect in bulls as seen under the electronmicroscope has been illus- trated. 3,6,8,19,20 This defect in spermiogenesis is appar- ently due to an autosomal recessive sex-linked defect in Friesian cattle.9 This defect has been reported in a sterile Boxer dog and in Charolais and Holstein bulls in the U.S.18 (See Figure 178.) This defect was described in two subfertile bulls, a Holstein and a Jersey.20 They had nonreturn rates from AI of 40 and 59 percent, respec- tively. Three of four sons of the Holstein bull were sim- ilarly affected. In the latter Holstein bull 0.3 to 6.2 per- cent of the spermatozoa had knobbed acrosomes, 1.7 to 9.1 percent had ruffled acrosomes and 2.1 to 21.9 per- cent had an incomplete or missing portion of the acro- some. This was a defect in spermiogenesis and could be seen in the spermatids.19,20 Aging of spermatozoa also produce acrosomal changes and infertility.21 Two nearly sterile bulls had semen with normal mo- tility and concentration of spermatozoa. After staining with opal blue and examining the stained cells with a phase-contrast microscope, eversion of the galea capitis and cratershaped depressions in the nucleus were found.1 Apparently similar invaginations of the nuclear envelope in the bull and the boar were described that were asso- ciated with a severe disturbance of spermiogenesis with many other abnormalities of the sperm cell.5 Feulgen stain and phase-contrast microscopy revealed these invagina- tions to be located near the anterior border of the post- nuclear cap in the equatorial segment of the sperm head. These crater-shaped depressions in the nucleus have been the subject of further studies in which depending on the type of staining and microscopy have been called “dia- dem sperm,” “pouch formations,” nuclear lesions and vacuolar defects.86,186 The percentage of affected sper- matozoa in ejaculates is variable. When over 20 to 30 percent of sperm cells are affected, fertility is moder- ately to severely reduced even though the motility and numbers of spermatozoa were normal. This defect ap- parently is not hereditary, but the cause is not known. Special staining and examination procedures are neces- sary to observe these nuclear lesions. A sterile Ayrshire bull produced sperm cells with nor- mal motility and concentration but with up to 20 percent abaxial tails and 17 percent swollen midpieces.2 Even though the concentration and motility of sperm cells in the ejaculate is normal, special staining and examination of cells from infertile males is indicated. Studies in cytogenetics have shown that gene or chro- mosome defects may occur at the time of meiosis and result in infertility. An apparently normal semen picture may accompany these defects. Certain bulls with excel- lent appearing semen in which genital infections were excluded had a low fertility due to intrachromosomal ab- berrations.15,16 The spermiogenic epithelium showed a cytologic picture indicative of structural changes in the chromosomes including translocations and inversions. Although affected spermatozoa may fertilize the ovum, the zygote will often lack a balanced gene complement and death often results at an early stage of gestation or this defective chromosome complement may be carried into the next generation where usually about 50 percent of the male individuals are affected with infertility. Some offspring from affected bulls may be completely normal. Generally the greater the number of genes involved in translocation or inversion the greater the degree of in- fertility. In affected bulls diagnosis at present can only be made with an electronmicroscopic study of the ger- minal epithelium. By this technique acquired disturb- ances in spermatogenesis can be distinguished from the congenital or constitutional disturbances. These forms of sterility represented only a small number of all those that actually occurred.16 Gustavsson13 reported on a translo- cation defect of the chromosomes in the Swedish Red and White breed of cattle. About 14 percent of the cattle were heterozygotes and 0.34 percent were homozygotes for the translocation. Daughters of translocation sires ex- hibited a greater infertility rate, apparently due to early embryonic deaths, than daughters of normal sires. The metaphase and anaphase figures from the meiotic divisions of the spermatocytes in the seminiferous epi- thelium in 4 boars and 7 bulls with normal semen pic- tures that were relatively or completely sterile were ana- lyzed.14 Two boars had acrosomal defects of their spermatozoa. This study concluded that even though some chromosome changes were apparent, the primary or principal cause of defective spermatozoa was to be found in the nonchromosomal structures, namely the divisional apparatus. The relationship of spermatozoal DNA and male in- fertility has been reviewed.11 The conclusions are pres- ently equivocal. A group of stallions with impaired fer- tility with semen of normal quality were studied.17 The infertility might have been caused by an inherent enzy- matic disturbance that resulted in the early death of the sperm cell in the female genital tract. These above preliminary studies on infertile males with essentially normal semen and spermatozoa have indi- cated that defects in genes and chromosomes especially during meiosis, and developmental defects of the sperm cell during spermiogenesis may occur. Future studies in the fields of cytogenetics, cellular biology and electron- microscopy will undoubtedly further elucidate the mech- anisms of male infertility occasionally associated with anINFERTILITY IN MALE ANIMALS 815 apparently normal or nearly normal semen picture. Impotentia generandi associated with abnormal se- men production is much more commonly observed and is due to pathology of the testes, the epididymis, the ductus deferens, the accessory glands and the urethra whereby sufficient numbers of healthy fertile sperm cells are not deposited properly at the time of coitus to cause the fer- tilization of the ovum and the normal development of the embryo. Abnormal semen may be due to congenital, hereditary or acquired causes. The latter are the most common. The former is highly important in the selection of sires because of the genetic implications. Occasion- ally both groups of causes are involved in an infertile male. Pathology of the Testes with Abnormal Semen Production, Hypoplasia Prior to the work of Lagerlof in 193412 studies on the pathology of the testis were incomplete and generally limited to the more obvious and severe clinical lesions such as orchitis and fibrosis. Since then a great amount of work has been done on correlating semen abnormal- ities with testicular pathology. The two are closely re- lated and semen examinations reflect fairly accurately the conditions present in the seminiferous tubules of the testes. However, it is necessary to consider that it re- quires about 60 days from the first stages of spermato- genesis to the ejaculation of spermatozoa. Lagerlof12 divided the pathological conditions affect- ing the testis proper into testicular hypoplasia, testicular degeneration, testicular fibrosis, and testicular inflam- mation. The author believes that since testicular fibrosis usually follows testicular degeneration and testicular in- flammation, and since testicular inflammation usually produces an acute, severe testicular degeneration, testic- ular fibrosis and testicular inflammation should be con- sidered under testicular degeneration. If this classifica- tion is accepted then the two most common changes occurring in the testes causing disturbed spermatogenesis are hypoplasia, which is congenital or hereditary, and degeneration of the seminiferous tubules, which is usu- ally acquired but may be predisposed by genetic defects, weaknesses, or inherent constitution. Testicular pathology due to congenital or heredi- tary causes includes hypoplasia, certain defects in the seminiferous tubules and sperm cells including cytoge- netic and chromosomal defects, cryptorchidism and in- guinal hernias. The latter two conditions interfere with the normal thermal regulation of the testes which results in sterility or infertility. Hypoplasia of the testes is observed occasionally as a unilateral or bilateral condition at the time of puberty, or later, in all domestic animals. It is noted most com- monly in bulls, rams, boars and stallions. Testicular hy- poplasia was a cause of 23 percent of the testicular pa- thology in Swedish bulls; this did not include the cases of inherited testicular hypoplasia of the Swedish High- land breed.13 This is a slightly higher incidence than the 12 to 17 percent given by other workers. 1,9'14b’20 The he- reditary type of hypoplasia affected as many as 25 to 30 percent of the male and female animals of the Swedish Highland breed, a polled breed.13 Gonadal hypoplasia in this breed was largely limited to those cattle that were 90 percent or more, white.17 Cattle with black ears were not affected. In these white cattle hypoplasia of the left testis occurred in about 25 percent of all the bulls, in the right testis in 1 percent, and in both testes in 4 to 5 per- cent. This condition is due to a single recessive auto- somal gene with incomplete penetrance.7 A similar widespread condition affecting the gonads of both males and females of a breed has not been described outside of Sweden. Most workers agree that testicular hypoplasia is con- genital and possibly hereditary in origin and is caused by a marked lack of, or reduction in, spermatogonia in the gonads during fetal life. Hypoplasia may be partial or total due to a failure of germinal cells to develop in the yolk sac, failure to migrate to the gonad, failure to multiply in the gonad or that undergo extensive degen- eration after they have entered the gonad. Unilateral or bilateral hypoplasia in bulls of both beef and dairy breeds and in other species have been observed occasionally in the United States but the incidence is generally low and the condition is sporadic. (See Ligure 176 and 177.) In a few instances a familial trend was noted. It has been reported that dwarfs or beef cattle with a dwarf tendency are likely to show evidence of testicular hypoplasia. Some valuable beef bulls with unilateral testicular hypoplasia have been used as breeders and may produce as many as 20 percent of offspring with hypoplasia and poor qual- ity semen.3 Marked hypoplasia of the testes, 10 percent by weight of normal testes, may occur in bulls, boars, rams, dogs and tom cats with the rare XXY karyotypic syndrome or human Klinefelter’s syndrome.6 The symptoms of testicular hypoplasia in bulls vary greatly. In most cases sexual desire is excellent and co- itus is prompt. Because of this the owners may not sus- pect the sterility for some time. The degree of either uni- lateral or bilateral testicular hypoplasia varies from nearly complete hypoplasia and sterility to only slight and often unsuspected hypoplasia. Lowered conception rates are often evident in the latter bilaterally affected males.816 VETERINARY OBSTETRICS Figure 176. Bilateral Testicular Hypoplasia in a Fat 3-Year-Old An- gus Bull. Severe testicular hypoplasia is usually observed in young bulls one to two years of age. In sterile bulls with bilateral hypoplastic testes the semen is usually clear and watery with few or no spermatozoa. If the ejaculate is centrifuged and the sediment stained, giant cells and oftentimes medusa cells or ciliated cells from the effer- ent tubules may be observed. Giant cells or multinuclear cells with 6 to 8 nuclei apparently result from incomplete maturation divisions of the primary spermatocytes. The nuclei divide but the cytoplasmic divisions are not com- pleted.5 These cells are seen in testicular hypoplasia and severe degeneration. The sexual organs develop nor- Figure 177. Bilateral Testicular Hypoplasia in a 2-year-old Holstein Bull. Figure 178. Abnormal Acrosomes or Knobbed Spermatozoa in a Sterile Bull. (Courtesy K. McEntee.) mally except for the affected testes. Histologically the seminiferous tubules are very underdeveloped, with usu- ally only the basal layer of cells being present. Males which are severely affected with testicular hy- poplasia are nearly sterile, but an occasional conception may occur in females bred to them. The semen picture shows a low concentration of spermatozoa, and the pos- sible presence of a few giant cells. If azoospermia is present in repeated ejaculates complete sterility is as- sured. The affected testes are one-third to two-thirds nor- mal size, but are usually firmer, or occasionally softer, than normal. (See Figure 177.) Histologic section re- veals that one-half to two-thirds of the seminiferous tub- ules are undeveloped. Varying degrees of spermatoge- nesis may be present from spermatogonia, spermiocytes, Figure 179. Lack of Intact Sperm Cells and Coiled Tails in a Sterile Guernsey Bull. (Spermatozoan motility was nearly absent.)INFERTILITY IN MALE ANIMALS 817 spermatids, to abnormal and normal mature spermato- zoa. Three types of testicular hypoplasia in 3 inbred lines of Hereford cattle were studied.3 The first type was char- acterized by seminiferous tubules lined only with Sertoli cells. These bulls were sterile and the line became ex- tinct. In the second line of bulls about 30 to 40 percent of the tubules were normal but only a few tubules were stage 8 with sperm cells lining the lumen. Reduced sper- matogenesis was present. In the third line the bulls had reduced spermatogenesis, conglutination of spermatids and many giant cells. In another line of cattle the bulls had large firm testes but reduced sperm cell output due to blockage of the tubules before they entered the rete resulting in sperm stasis and atrophy of the seminiferous epithelium. In some bulls with a moderate to slight amount of tes- ticular hypoplasia the conception rate is low, about 20 to 40 percent. The testicles may appear nearly normal in size and consistency. The spermatozoan concentration is from 100,000 to 500,000 per cmm, the motility is usu- ally low, and the number of pathological or abnormal spermatozoa is high, 30 percent or greater. Depending upon the degree of hypoplasia, affected bulls will have a small firm epididymis especially in the tail region indicating reduced spermatogenesis and low go- nadal sperm reserves. This will also be revealed by rap- idly decreasing concentrations of spermatozoa in suc- cessive ejaculates.9 Slight or mild cases of hypoplasia with reduced spermatozoan concentration and motility predispose the bull to testicular degeneration. In some bulls sterility due to mild testicular hypoplasia may not be observed or become apparent until the bulls reach 3 to 4 years of age. The spermatic cords of hypoplastic testicles are shorter as the testes are less heavy and the scrotum smaller than in normal males. Postpubertal bulls that have a scrotal circumference of less than 32 cm. should be suspected of having testicular hypoplasia or testicular degeneration with atrophy. In obese bulls with much fat in the in- guinal region the thermal insulation so provided these hypoplastic testes might contribute to the infertility. (See Figure 176.) Testicular hypoplasia may be erroneously diagnosed in young immature males that are underdeveloped or are retarded in growth at the generally accepted time of pu- berty for the species. The fertility and the percentage of normal spermatozoa produced increased from puberty to two years of age in beef bulls.15 The diagnosis of tes- ticular hypoplasia should not be made before two years of age in the bull and horse or before one year of age in the boar, ram, dog or tom, unless the hypoplasia is marked and the male is well-grown. Testicular hypoplasia and atrophy were observed in about 3.4 percent of 9,000 rams examined in Australia.8 The condition was usually unilateral and of a permanent nature. The spermatic cord was usually short and the af- fected testis was drawn up toward the inguinal canal. The consistency of the testis was either soft and flabby, or hard, indurated and fibrotic. The testes were de- creased in size. The semen was always abnormal, with an increased number of abnormal spermatozoa and small, round, non-nucleated, germinal epithelial cells. An as- sociation between this type of testicular hypoplasia and unilateral cryptorchidism was suggested. The fibrotic small testes in some of the rams described above might have been due to trauma or other causes, producing second- ary, degeneration and atrophy. Sterility in boars is relatively uncommon.10 In 30 boars with testicular pathology, 8 or 26.6 percent had hypo- plasia. These were young boars that were sterile or of very low fertility. A genetic or hereditary factor was probably present in hypoplasia in boars.10 Young boars may only ejaculate 2 to 3 billion spermatozoa when they are bred 2 to 3 times a week. If they are bred more often, the number of spermatozoa ejaculated may drop below 2 billion and infertility result. At 10 to 12 months of age most boars have matured sufficiently so that large num- bers of spermatozoa are produced and infertility due to oligospermia is not a problem.1318 In cases in which se- men examination was possible, spermatozoa were either absent or present in low concentrations of 20,000 to 70,000 per cmm. The number of pathologic spermatozoa was not high but there was a large percentage of im- mature sperm cells with a protoplasmic droplet on the middle piece. The motility was usually poor. The av- erage weight of the hypoplastic testes was 226 to 240 gm., while normal testes weighed 594 to 632 gm. His- tologic examination showed hypoplasia varying from only a single layer of germinal cells to widespread changes in the seminal epithelium. Eunuchoidism or complete lack of sexual desire, may rarely occur in dogs, men and bulls with testes in the normal position or in unilateral or bilateral cryptorchid- ism.217a‘' The testes are small and atrophic. The inter- stitial cells are hypoplastic or fail to secrete androgen. In man eunuchoidism is characterized by low plasma con- centrations of FSH and LH.17a Testosterone given par- enterally will produce secondary sex characteristics but the male relapses to the eunuchoid state if injections are discontinued. This condition may have been due to the XXY or Klinefelter’s syndrome in animals or to tes- ticular feminization due to a defect in the androgen re- ceptors and characterized by a feminine appearance, re- tained testes, a normal vulva and vestibule, rudimentary818 VETERINARY OBSTETRICS accessory reproductive organs and an XY karyo- type. 16b'17a Hypoplasia associated with a decrease in interstitial cell activity and a failure of normal antler growth in white- tailed deer in southwestern U.S. was reported.19 Testic- ular hypoplasia in the dog and cat is seldom described. Gonadal hypoplasia in a strain of grey collies that also had abnormalities of the blood, eyes and digestive tract was described.4 In the diagnosis of testicular hypoplasia, especially where it may be associated with a lack of sexual drive, the stage of development of the male and whether or not puberty has occurred must be considered. Testicular hy- poplasia may be diagnosed erroneously in young, poorly- fed, slow-maturing males, especially of Bos indicus breeding. The prognosis in testicular hypoplasia is poor. Af- fected animals should not be used for breeding because the condition may be hereditary. Severely affected ani- mals are sterile or highly infertile. Mildly or moderately affected animals may have only a lowered fertility but are more prone to early testicular degeneration. Libido is usually normal or excellent. The numbers of motile normal spermatozoa per ejaculate or insemination largely determine the fertility of the animal in question not the percentages of the dead, poorly viable, immotile and ab- normal spermatozoa. The treatment of testicular hypoplasia is animals has been unsuccessful. The germinal epithelium of these af- fected animals apparently cannot respond to gonado- tropic therapy because spermatogonia are lacking or re- duced in numbers. Hereditary or Congenital Sperm Cell Defects, Male Intersexes and Cryptorchidism Sperm cell defects, possibly heritable, have been de- scribed in male domestic animals in which a large per- centage of spermatozoa produced by a male are similarly affected. Returned tails and narrow heads were reported to be hereditary in certain bovine families of the Jersey breed exhibiting much sterility.2 Another study12 also reported on infertile Jersey bulls with coiled or returned tails with a lowered motility rate. With repeated frequent ejacu- lations the numbers of abnormal sperm cells was greatly reduced. The defect in these bulls was apparently ge- netic. These defects may be similar to the Dag-effect. Dag defect—Danish workers have described 15 re- lated bulls, tracing back to a common ancestor bom in 1934, in the Danish Jersey breed that had a low initial spermatozoan motility of 10 to 15 percent and very poor fertility. These bulls had about 40 to 50 percent of their spermatozoa with strongly coiled, folded or split tails, the Dag defect.9 The fibers in the axial filament were normal in the testis but abnormal when the cells reached the cauda epididymis. This defect was shown to be due to an autosomal recessive factor. The defect developed in the distal part of the head of the epididymis.9 An in- fertile Holstein bull with a normal volume and concen- tration of semen but only 10 to 20 percent motility was studied.llb About 25 percent of the spermatozoa had tail abnormalities somewhat resembling the Dag defect with an aberrant, defective arrangement of the fibrils. There was no evident abnormality of the seminiferous epithe- lium. A Canadian worker reported on three unrelated Hereford bulls with this Dag defect.13 The “tail stump” defect of spermatozoa originally described in Holstein Friesian bulls in Canada,6 and then in bulls in Denmark5 and India and recently in rabbits, a stallion and a dog.lc is caused by deranged spermio- genesis that results in a severe infertility or sterility. The head of the affected spermatozoa is normal but the mid- dle piece and tail are markedly defective with a stub or stump appearance at the base of the head. This defect is caused by an abnormality on the centriollar apparatus that blocks normal formation of the midpiece and tail.56 Spermatozoan numbers in the ejaculate are normal but motility is very poor depending on the percentage of “tail stump” spermatozoa which may vary from 20 to over 90 percent. Other sperm cell abnormalities may also be present such as loose or separate heads. There may be a cytoplasmic droplet around the “stump.” This condi- tion is possibly due to a recessive gene.lc 5b Corkscrew sperm defect—A nongenetic defect seen in the Red Danish, Jersey, Friesian and Abderdeen Angus breeds due to an irregular distribution of the mitochon- drial sheath together with a high incidence of persistent proximal droplets in affected sperm cells was described.3 Pseudo-droplet defect—A “pseudo-droplet defect” seen in 5 related Friesian bulls was reported.4 From 7 to 26 percent of spermatozoa in affected bulls had rounded or elongated, thickened areas on the midpiece. Reduced motility and infertility increased as the bulls became older. Lack of intact sperm cells was described in Guernsey bulls with a history of complete sterility.7 8 The ejacu- lates of these bulls contained practically no intact sper- matozoa, but only free heads and tails. Motility was low. Intact spermatozoa were fewer than 5 percent of the to- tal. All heads showed a deep indentation marking the point of separation from the tails. The middle piece was thickened and varying degrees of coiling of the middle piece and tail occurred. This disintegration or separationINFERTILITY IN MALE ANIMALS 819 of the heads and tails of spermatozoa in the sterile Guernsey bulls was associated with the migration of the protoplasmic droplet from the proximal to the distal end of the middle piece which occurred in the head of the epididymis.7 While there was no conclusive evidence that the defect was inherited, the evidence was very sugges- tive. Eight Hereford bulls with low fertility had a high percentage of tailless heads in their ejaculate.14 Acrosomal defects or knobbed spermatozoa have been described in bulls, boars and dogs. This defect has been reported as due to an autosomal recessive gene in Holstein Friesian bulls.lla As described previously in this Chapter, certain stains and techniques are very helpful in diagnosing this defect in what often appears to be a normal semen sample associated with complete sterility or infertility. Deficiency in tail development and lack of motility was reported in stallions of one Thoroughbred blood line in which the condition might have been genetic in na- ture.10 The author has studied two stallions with con- genitally lowered fertility with 50 to 75 percent of their spermatozoa having a single abnormality; in one stal- lion, a Standardbred, a grossly defective midpiece and the other, a Thoroughbred, an abaxial attachment of the midpiece to the head in over 60 percent of the sperma- tozoa. In stallions abaxial attachment of the midpiece to the head of the spermatozoa is commonly observed and this usually is not associated with infertility in the stal- lion and boar as it often is in the other species of ani- mals. (See Semen Evaluation.) A sterile Ayrshire bull with up to 20 percent abaxial tails and 17 percent swol- len midpieces was described.111 Sperm cell concentration and motility was normal. Ciliary diseases in man and animals have been re- viewed.13 Many of these are congenital or hereditary dis- eases affecting all body cilia in the respiratory and gen- ital tracts resulting in chronic upper respiratory infections and infertility or sterility. These ciliary diseases usually result in the immotile-cilia syndromes.13 One of these in humans is called Kartagener’s syndrome that is usually characterized by sterility associated with immotile sperm cells and other cilia in the body and in many cases situs inversus13 83 The normal concentration of live sperma- tozoa is present. Two similar cases have been described in dogs.13 This defect of the tail and midpiece resembles several other defects in animals characterized by living sperm cells grossly lacking in motility. Inbreeding, Chromosomal Aberrations and Intersexes Inbreeding generally results in reduced fertility ac- companied by an increase in the number of abnormal seminiferous tubules, lowered semen quality and hypo- plasia.4,5,19 Inbreeding in dogs resulted in lower concep- tion rates, lower numbers of pups whelped alive and in reduced ejaculate quality of studs by lower sperm counts compared to outbred dogs.24 There were wide differ- ences in fertility between inbred lines of cattle from a few with excellent fertility to those in which the line died out because of infertility. The response to inbreeding with respect to fertility is variable with each line or family. Inbred lines usually undergo a period of infertility or ste- rility and if the line does not become lost due to dele- terious genes, the fertility of the remaining animals in the line is often fairly satisfactory.173 Five inbred, related bulls showed a low sperm cell concentration and a large number of pathological spermatozoa with a reduced mo- tility.13 The infertility in these bulls was considered to be due to an autosomal recessive gene. In identical twin bulls great similarity of the semen and spermatozoa, du- ration of motility, and frequency of abnormal sperm heads has been noted.13 The great difference between identical twin pairs of bulls and the similarity of each bull of a twin pair indicated that the differences between the twin pairs as well as the similarities within the pairs, were genetic, since all were reared under similar conditions. Hereford, Angus, Holstein and Shorthorn bulls had the best conception rate in England.25 In the United States and Canada Guernsey bulls generally have a lower con- ception rate than other breeds.2 Nine of 19 Guernsey bulls used for artificial insemination had lower than average non-return rates, below 64% at 60-90 days. Two of these 19 bulls had 1/29 centric fusion with 59 chromosomes and 3 others had achromatic gaps and chromatid breaks.2 In 743 young bulls examined cytologically in the U.S. no translocations were found.10 Other cytogenetic stud- ies on bulls, horses and swine were reported.20 Aneu- ploid cell lines in two related boars were associated with reduced litter size in their offspring as well as some of their daughters.23 Cytogenetic disturbances in spermatogenesis caused two abnormalities in the primary spermatocytes includ- ing (1) “stickiness” of chromosomes in which they failed to separate at anaphase, and (2) a pyknotic nucleus and multiple spindle formation due to a dysfunction of the mechanism of cell division due to extra centrosome di- visions resulting in the formation of giant cells with a number of nuclei.16 In both conditions the semen was thin and watery. In the former the semen centrifugate was made up almost entirely of pyknotic nuclei and was characteristic for this condition seen most often in the Swedish Lowland Holstein Friesian breed in which in- tensive inbreeding had occurred. The latter condition oc- curred in only a few bulls. The semen centrifugate was820 VETERINARY OBSTETRICS composed of giant cells and pyknotic nuclei and these affected bulls belonged to the same family so a reces- sive gene might have been involved. As mentioned pre- viously, the Gustavsson anomaly or a Robertsonian 1/ 29 chromosomal translocation occurred in Swedish cat- tle that resulted in a degree of infertility characterized by early embryonic deaths.14 A translocation anomaly in a boar was associated with reduced litter size.20 Probably other primary cytogenetic disturbances of spermatoge- nesis occur and will be described in the future. The male tortoise-shell, black and orange stripes or including white, tricolored or calico tom cats are un- common because the genes for yellow or orange color are carried on the female, X, chromosome. However, rare male tortoise-shell cats have an abnormal sex chro- mosome constitution of XXY resembling Klinefelter’s syndrome in man. This condition in cats has been well- described.1118'22 These male cats have very small testes and are sterile due to failure of the seminiferous tubules to develop. One affected cat had no spermatogonia in the seminiferous epithelium. The possible incidence of male to female tricolored cats was 1:200 to 1:3000.11 18 Other types of chromosome combinations in tricolored male cats: XXY, XX/XY, XX/XX/XXY, XX/XXY, XY/XXY, and XX/XXY have been reported.1118'22 A recent study and review of male tortoiseshell and tricolored cats17b indicated that those with the 39XXY karyotype were all sterile with very small testes, no ger- minal epithelium, no libido and no secondary sex char- acteristics. Those with a 38XY/38XX and 38XY/39XXY karyotypes had a variable fertility with libido and sec- ondary sex characteristics. While those with 38XX/38XY karyotypes were fertile normal males. It was suggested that because of their coat color these cats were examined cytogenetically but other cats with a different color might also show chromosomal abnormalities. A polled Hereford bull with good libido had very small, one-tenth normal-sized testes, azoospermia and a 61,XXY karyotype.7 This XXY or Klinefelter’s syndrome seen in about 1 in 500 live-bom human males has also been re- ported in rams, boars and dogs.7 Undoubtedly cytoge- netic defects occur in stallions as have been described in mares but defects of the reproductive organs are much more obvious in stallions and seldom would these ani- mals be selected for service. Infertility in hybrids usually occurs when there are major differences in the chromosomes of the parents. Minor gene differences may be overcome so fertility is possible. The failure of gametogenesis in some hybrids is apparently due to asynapsis during the first meiotic division of the primary spermatocyte. Sterility is more common in the male hybrids. Even in some intraspecies crosses where the chromosomes are nearly similar, hy- brid fertility, particularly of males, may not result.lc A common example of the above hybrid infertility in do- mestic animals is the horse and ass cross producing the hybrid mule, with chromosome numbers of 64, 62 and 63, respectively. Hybridization attempts in goats and sheep obtained conception but all the embryos died.15 In the bison x domestic cattle cross, as well as the yak X domestic cattle, and yak X zebu crosses, the bulls are likely to be sterile.6'12 This was believed due to the inheritance of the small, thick scrotum from the bison or yak causing an elevated scrotal temperature that ad- versely affected the large testes inherited by these hy- brids from the domestic cattle or zebu that required a lower testicular temperature for the normal functioning of the seminiferous tubules. Recent cytogenetic studies indicate that chromosomal incompatabilities are more likely a cause for the infertility of these hybrid males. In bovine twins of unlike sex the female twin or free- martin is sterile due to the vascular anastomosis with the male twin which is usually considered to be normal. (See Chapter IV.) Most bulls bom cotwin with freemartins are chimeric with from 5 to 95 percent of their blood lymphocytes being XX cells. Of 12 chimeric bulls stud- ied in an AI stud, 58 percent were culled for poor semen quality and infertility associated with testicular degen- eration and hypoplasia.3'8 One of the infertile bulls had a skewed sex ratio of 29 males to 71 females suggestive of germ cell chimerism.8 Further study on bulls cotwin to freemartins is indicated. Male intersexes are invariably sterile. Intersexuality may arise from aberrations of genetic or chromosomal origin, aberrations of gonadogenesis, and reversal of sex involving the accessory or external genital structures.lb Male pseudohermaphroditism is found in the caprine, porcine and occasionally the bovine, equine and other species. True hermaphroditism is uncommon. In both horses and cattle this latter condition was characterized by ovotestes, no scrotum, an underdeveloped penis, uterine tissue and vesicular glands and chromosomal chi- merism.9 True hermaphroditism is also seen in the other domestic animals including the goat, dog, pig and cat.9'22 In the Saanen and Toggenburg breeds of goats the in- cidence of intersexes varies from 5.8 to 14.9 percent. They have a wide range of abnormality from phenotyp- ically nearly normal males to nearly normal females. This condition in goats is caused by a single recessive sex- linked gene linked to the dominant gene for polledness. (See Chapter III.) No case of a homed pseudohermaph- rodite has been described. Most affected goats have testes, often intra-abdominal, and external genitalia of an in- termediate type. They are genetic females (XX) withINFERTILITY IN MALE ANIMALS 821 positive sex chromatin. A high incidence of infertility in polled Saanen goats was described in which the reces- sive character caused pseudohermaphroditism in female goats and hypoplasia, sperm granulomas of the epidid- ymis and a high percentage of sperm cell abnormalities in some male goats.21 The infertility problem in Saanen goats could be largely avoided by raising for breeding purposes only those goats with a homed parent. Intersexes in pigs are common but not as common as in goats. They also are of the male pseudohermaphrodite type. The condition is probably caused by a recessive gene. The affected animals are genetic females, the testes are invariably intra-abdominal and externally a charac- teristic “fish hook” vulva with a prominent “clitoris” or phallus is present.1911 Male pseudohermaphrodites are also occasionally observed in cattle, horses, sheep and dogs.21a Three affected sons of a Brown Swiss bull have been reported.12 Cryptorchidism in animals, if bilateral, results in ste- rility. In horses cryptorchids may be spoken of as “ridg- lings,” “rigs” or “originals.” Unilateral cryptorchidism is more common and usually results in near normal fer- tility because of normal sperm production from the testis located in the scrotum. The term “monorchidism” is in- correct and should not be used. Cryptorchidism or in- complete descent of the testis or retention of the testis occurs in all domestic species but is seen most com- monly in stallions, boars, dogs, less commonly in rams and bucks, uncommonly in bulls, and rarely in tom cats. (See Chapter III.) The undescended testis may be located anywhere from just caudal to the kidney to within the inguinal canal. Many abdominal testes are located close to the internal inguinal ring. Often the loosely attached epididymis in the horse may have descended into the in- guinal canal. Occasionally testes not in the abdominal cavity, in- guinal canal or scrotum may be located ectopically under the skin of the ventral caudal abdomen, especially in bulls, alongside the penis, or rarely in the femoral canal or in the perineal region. This is more commonly the case in male pseudohermaphrodites where no scrotum is pres- ent. In some animals in which the testis is retained in the inguinal canal it will descend spontaneously into the scrotum in a few months to a year after birth. In a few cases in colts, testes may have descended into the scro- tum at birth and later became cryptorchid and located in the inguinal canal. Although a noted veterinarian1811 has reported that the testes of newborn colts can invariably be palpated in or just above the scrotum, further study, confirmed by castration, should be undertaken since the gubemaculum is large in newborn foals. By 30 days after birth the gubemaculum is greatly reduced in size and the testes can be readily palpated in most foals. It would seem very unlikely the descended testes at birth could, with time, assume the internal relationships found in ab- dominal cryptorchidism. All retained or cryptorchid testes are small, soft and flaccid weighing in the horse 25 to 131 gms.; normal descended testes usually weigh 170 to 325 gm.4 No spermatozoa are produced by the re- tained testis but well-developed or degenerate seminif- erous tubules may be present. Spermatogenesis is com- pletely inhibited by the elevation of the temperature of the affected testis. The interstitial or Leydig cells are not affected so sexual activity is normal or even exaggerated in some cryptorchids. Cryptorchid animals should not be used for breeding. The Technical Development Committee20 in England reported that cryptorchidism in the horse is inherited in a dominant manner while in the other species it is a re- cessive trait. Unilateral cryptorchidism more often af- fects the right testis especially in dogs, possibly because the right testis develops in the embryo a greater distance from the scrotum.5 In 4 studies,4,8b,u,19b from university clinics it was reported that in over 1000 cryptorchid horses about 90 percent of the inguinal or abdominal testes were unilateral and of the abdominal testes about 70 to 75 per- cent were left-sided. These reports indicted that in about 60 percent of the presented cases the cryptorchid testis was intraabdominal. Based on his field experience the author strongly suspects this latter figure is biased. Many of these latter cases of cryptorchidism were probably re- ferred to the clinics for specialized surgery. Most prac- ticing veterinarians can detect inguinal testes by palpa- tion assisted by heavy tranquilization and remove these retained testes by a slightly modified routine castration. Three of the cryptorchid testes contained teratomas or cysts, two of these were abdominal.4 Removal of cryp- torchid equine testes has been well-described.1,2,11 The latter described a paramedian laparotomy approach for the removal of the abdominal testes. In dogs cryptorchidism is seen most commonly in the brachycephalic breeds including: Boxers, Pomeranians, Dachshunds, Sealyhams, Cairn Terriers, and also in Whippets, Chows, Cocker Spaniels, Poodles, and oth- ers. The incidence of cryptorchid testes in dogs in En- gland was reported to be between .05 to 0.1 percent.20 In most dogs the testes are in the inguinal canal at birth and descend into the scrotum during the first week after birth. In some dogs the testes don’t descend till near puberty.3 Possibly because dogs are maintained intact for many years, retained testes are predisposed to neo- plasms. Sertoli cell tumors and seminomas in unde- scended testes tend to be more malignant.5,6,13,18 A highly822 VETERINARY OBSTETRICS significant association of cryptorchidism and testicular tumors was reported with 58 or 53 percent of 108 Ser- toli-cell tumors and 23 or 33.8 percent of 68 seminomas occurring in retained testes.18 These tumors affected the retained or abdominal right testes more frequently than the retained left testes. Dogs with scrotal testicular tu- mors were older than dogs developing cryptorchid tes- ticular tumors.18 Signs of feminization were present in 16.7 percent, 50 percent, and 70 percent of the dogs with Sertoli cell tumors in the scrotum, inguinal canal and abdominal cavity, respectively. This may be due to the earlier detection and removal of affected testes in the external sites. Cryptorchidism and cryptorchidectomy in the dog and tom cat has been recently reviewed.25 Tu- mors of undescended testes in man occurred 50 times more often than tumors of scrotal testes.8 Early removal of undescended testes is recommended. Cryptorchidism in swine is a monogenic sex-limited recessive.15 To eliminate this condition in swine or other species, all parents of cryptorchid animals should be dis- carded as breeders. The incidence in swine may reach 1 to 2 percent in some herds. If affected pigs are fattened rapidly and sold at or before six months of age very little or no boar odor will develop in the carcass. In sheep cryptorchidism is seen in all breeds especially in inbred families, as it probably is due to an autosomal recessive or a dominant gene with incomplete penetrance. The in- cidence in sheep is 0.5 percent with 90 percent of uni- lateral abdominal cases involving the right testis.103 The rapid progress possible in the elimination of cryp- torchidism, probably due to a recessive defect with in- complete penetrance, in flocks of Angora goats by rigid culling of parents and even close relatives of affected animals was described.19,23 An excellent bibliography on cryptorchidism in dogs and other animals has been com- piled.12 A few cases of left-sided cryptorchidism in Hereford cattle have been reported in which the condi- tion appeared to be due to a dominant gene with variable expressivity.24 Cryptorchidism is common in male fetal monsters and other defective individuals. Treatment of cryptorchid animals, especially those where breeding is to be considered, should be discour- aged. In humans where treatment is more frequently un- dertaken only those testes that would ultimately descend spontaneously would descend after gonadotropin ther- apy.8 Orchiopexy has proven to be a failure in producing satisfactory spermatogenesis. Torsion or rotation of the descended testis is ob- served occasionally in the stallion17b and rarely the dog.17c,d It may be associated with an excessively long mesor- chium, caudal ligament of the epididymis and the proper ligament of the testis. Torsion must be greater than 180° to produce circulatory disturbances in the testis with strangulation and pain associated with a unilateral scrotal swelling and a stiff, “hiking” abduction of the rear leg in the affected side. It develops most frequently in the Standardbred but the author has observed the condition several Thoroughbreds. Apparently some horses at their racing gait are unable to draw the testis out of the scro- tum. Suspensories have been tried on horses but are of limited value. Unilateral or bilateral castration is indi- cated. Torsion or rotation of the retained or cryptorchid testes with strangulation of the spermatic cord is most com- monly seen in the dog in association with testicular tu- mors, especially the Sertoli-cell tumor.17c Symptoms may be acute or chronic with signs of abdominal pain and/ or obstruction. Diagnosis is suspected by a retained or cryptorchid testis in an older dog and is confirmed by laparotomy. Torsion of a retained testis has been ob- served very rarely in the pig. Manual torsion or “twisting” of ram lambs is an old castration technique of shepherds. The tail of the epi- didymis or ventral portion of the testis is manually ro- tated dorsally and then after several rotations of the testis around the tensed spermatic cord, the entire structure is pushed into the inguinal canal where it is retained and undergoes degeneration and atrophy due to the interrup- tion of circulation. Imperfect descent of the testes in cattle not associ- ated with cryptorchidism has resulted in testes located horizontally and fairly high in the scrotum. This may be due to the attachment of the cremaster muscle to the cau- dal aspect of the testis, fixation of the distal end of the scrotum to the perineal region,26 or lower than normal attachment of the gubemaculum. (See Figure 180.) This imperfect descent of the testes may result in impaired fertility with degeneration and atrophy due to difficulty of the thermoregulatory mechanism of the testes to op- erate properly. This condition might be genetic.7 Stal- lions that carry the testes high in the external inguinal ring may have low fertility for the same reason. Multiple heterotopic nodules of testicular tissue scat- tered over the peritoneum have been described in a few pigs.21 These may be confused with a malignant neo- plasm. Scrotal or inguinal hernias, if large, may seriously depress fertility by markedly interfering with the normal thermoregulatory function of the scrotum and testes re- sulting in testicular degeneration. (See Testicular De- generation.) If the inguinal ring and hernia is small there is a greater chance for strangulation of the intestine. In- guinal hernia is considered a common hereditary defect in horses and pigs; it is less common in bulls, dogs andINFERTILITY IN MALE ANIMALS 823 'v / Figure 180. Abnormal Attachment of the Cremaster Muscle to the Left Testis Causing a Nearly Horizontal Position of the Testis High in the Scrotum (The right testis of the bull was normal). rams, and rare in the tom cat. The incidence in swine was greatly increased from 7.5 to 43.2 percent in two generations by selective inbreeding.22 It was most com- mon in the left side of the scrotum. Hernias usually ap- peared from birth to 30 days of age. It was considered to be a double recessive character. In cattle leftsided scrotal hernias were most common especially in the Hereford or Polled Hereford breeds.10,1617 (See Figure 181.) In an inbred strain of Basenjii about 75 percent of the pups had inguinal hernias.9 Animals with inguinal hernias should be castrated and not used for breeding. Reduction of the hernia and closure of the hernial ring can be per- formed through the inguinal canal, through an incision in the abdominal wall just cranial and medial to the ring or by a flank incision above the ring. Figure 181. Left Inguinal Hernia in a Hereford Bull. References Impotential Generandi, Hereditary Disorders and Failure to Fertilize with Apparently Normal Semen 1. Aamdal, J. (1951) Changes in the Chromatin Substance of the Sperm and Galea Capitis as a Cause of Sterility in Bulls, Nord. Vet. Med. 3, 102. 2. Aughey. E. and Renton, J. P. (1968) Abnormal Spermatozoa in An Ayrshire Bull, Vet. Rec. 82, 129. 3. Bane, A. (1961) Acrosomal Abnormality Associated with Sterility in Boars, Proc. IV Intemat. Congr. on An. Reprod. (Hague) Vol. IV, 810. 4. Bane, A. (1968) Personal Communication. 5. Bane, A. and Nicander, L. (1965) Pouch Formations by In- vaginations of the Nuclear Envelope of Bovine and Porcine Sperm as a Sign of Disturbed Spermiogenesis, Nord. Vet. Med. 17, 149. 6. Blom, E. and Birch-Andersen, A. (1965) The Ultrastructure of the Bull Sperm II The Sperm Head, Nord. Vet. Med. 17, 4, 193. 7. Boyd, H. (1955) Bovine Genital Vibriosis, Thesis, Royal Vet. Coll., Stockholm, Sweden. 8a. Buttle, H. R. L. and Hancock, J. L. (1965) Sterile Boars with Knobbed Spermatozoa, J. Agric. Sci. 65, 255. 8b. Coulter, G. H., Oko, R. J. and Costerton, J. W. (1978) Inci- dence and Ultrastructure of “Crater” Defect of Bovine Sper- matozoa, Theriog., 9, 2, 165. 9. Donald, H. P. and Hancock, J. L. (1953) Evidence of a Gene- Controlled Sterility in Bulls, J. Agric. Sci. 43, 178. 10. Frank, A. H. and Bryner, J. H. (1958) Observations on Vi- briosis of Cattle in Relation to Impaired Fertility, Proc. U.S. Livestock Sanit., Assoc. 57th Meeting, 165. 11. Gledhill, B. L. (1970) Enigma of Spermatozoal Deoxyribonu- cleic Acid and Male Infertility: A Review, Amer. J. Vet. Res. 31, 3, 39. 12. Gledhill, B. L. (1973) Inherited Disorders Causing Infertility in the Bull, JAVMA, 162, 11, 979. 13. Gustavsson, I. (1969) Cytogenetics, Distribution and Pheno- typic Effects of a Translocation in Swedish Cattle, Hereditas 63, 68. 14a. Henricson, B. and Backstrom, L. (1964) A Systematic Study of Meiotic Divisions in Normal and Subfertile or Sterile Boars and Bulls, Jour. Reprod. Fertil., 7, 53. 14b. Holst, S. J. (1949) Sterility in Boars, Nord. Vet. Med., 1, 87. 15. Knudsen, O. (1954) Cytomorphological Investigations into the Spermiocytogenesis of Bulls with Normal Fertility and Bulls with Acquired Disturbances in Spermiogenesis, Acta, Path, et Mi- crobiol. Scand. Suppl. Cl. 16. Knudson, O. (1958) Studies on Spermiocytogenesis in the Bull, Intemat. Jour, of Fert. 3, 389. 17. MacLeod, J. (1951) Fertility in Thoroughbred Stallions, Lec- ture, 1st Annual Stud Managers Course, College of Agr., Univ. of Kentucky, Lexington, Ky., 102. 18a. McEntee, K. (1954) (1968) Personal Communication. 18b. Miller, D. M., Hrudka, F., Cates, W. F. and Mapletoft, R. J. (1982) Infertility in a Bull with a Nuclear Sperm Defect: A Case Report, Theriog., 17, 6, 611. 19. Saacke, R. G. and Amann, R. P. (1966) Inherited Abnormal Acrosomal Caps of Bull Spermatozoa, J. An. Sci. 25, 3, 929. 20a. Saacke, R. G., Amann, R. P. and Marshall, C. E. (1968) Ac- rosomal Cap Abnormalities of Sperm from Subfertile Bulls, J. An. Sci. 27, 5, 1391.824 VETERINARY OBSTETRICS 20b. Sager, F. (1965) Personal Communication. 21. Salisbury, G. W. and Flerchinger, F. H. (1967) Aging Phenom- ena in Spermatozoa, I, II, III, J. Dairy Sci. 59, 10, 1675, 1679, 1683. 22. VanderSluis, L. (1953) Experiences with the Examination into Herd Infertility, Proc. First World Congr. On Fert. and Steril. II, 25, 703. 23. Wells, M. E. and Awa, O. A. (1970) New Technique for As- sessing Acrosomal Characteristics of Spermatozoa, J. Dairy Sci. 53, 2, 227. 24. Wells, M. E. and Awa, O. A. (1970) Distribution of Acrosomal Abnormalities Among Types of Spermatozoa, J. Dairy Sci. 53, 3, 382. (Abstr.) 25. Young, G. B. (1953) Genetic Aspects of Fertility and Infertility in Cattle, Vet. Rec. 65, 271. Abnormal Semen Production, Hypoplasia la. Adams, W. M. (1970) Hormonal and Anatomical Causes of In- fertility, Colloquium on Effect of Diseases and Stress of Re- productive Efficiency in Swine, Iowa State Univ., Ames, Iowa. lb. Blom, E. and Christensen, N. O. (1951) Congenital Absence of the Epididymis, Ductus Deferens, or Glandual Vesicularis (Aplasia Segmentalis Ductus Wolfii) in the Bull, Yearbook Royal Vet and Agr. Coll, Copenhagen Denmark 1. 2. Bloom, F. (1954) Pathology of the Dog and Cat, Amer. Vet. Public. Inc., Evanston, 111. 3. Carroll, E. J. and Ball, L. E. (1969) See Inbreeding. 4. Cheville, N. F. (1968) The Gray Collie Syndrome, JAVMA, 152, 6, (Part 1), 620. 5. Cupps, P. T. and Laben, R. C. (1960) Spermatogenesis in Re- lation to Spermatozoa Concentration in Bovine Semen, J. Dairy Sci. 43, 6, 782. 6. Dunn, H. O., Lein, D. H. and McEntee, K. (1980) Testicular Hypoplasia in a Hereford Bull with 61XXY Karyotype: The Bo- vine Counterpart of Human Klinefelter’s Syndrome, Cor. Vet. 70, 137. 7. Eriksson, K. (1950) Hereditability of Reproductive Disturb- ances in Bulls of Swedish Red and White Cattle, Nord. Vet. Med. 2, 943. 8. Gunn, R. M. C., Sanders, R. N. and Granger, W. (1942) Stud- ies in Fertility in Sheep, Commonwealth of Austral., Council for Sci. and Ind. Res. Bull 148. 9. Haq, I. (1949) Causes of Sterility in Bulls in Southern Brit., Vet. Jour. 105, 3, 4, 5 and 6; 71, 114, 143, 200. 10. Holst, S. J. (1949) Sterility in Boars, Nord. Vet. Med. 1, 2, 87. 11. Johansson, I. (1961) Genetic Aspects of Dairy Cattle Breeding, Univ. of 111., Press, Urbana, 111. 12. Lagerlof, N. (1934) Morphologische Unteruschungen uber Ver- anderungen in Spermabild und in den Hoden bei Bullen mit Ver- minderter oder aufgehebener Fertilitat, Acta Path, et Microbiol. Scand. Suppl. XIX. 13. Lagerlof, N. (1938) Infertility in Male Domestic Animals, Proc. 13th Intern. Vet. Congr. 1, 214. 14. MacLeod, J. (1951) Fertility in Thoroughbred Stallions, 1st An- nual Stud Managers Course, College of Agr. Univ. of Ken., Lexington, Ky., 102. 15. Martig, R. C. and Almquist, J. O. (1969) Reproductive Ca- pacity of Beef Bulls III, J- An. Sci., 28, 3, 375. 16a. McEntee, J. (1969) Pathology of Domestic Animals, 2nd Ed., Vol. 1, edited by Jubb, K. V. and Kennedy, P. C., Academic Press, N.Y.C. and London. 16b. McEntee, K. (1979) Pathology of the Testis of the Bull and Stallion, Proc. Soc. for Theriog., Mobile, Alab., 80. 17a. Setchell, B. P. (1978) The Mammalian Testis, Cornell Univ. Press, Ithaca, N.Y. 14850, 359-432. 17b. Settergren, I. (1961) The Relationship Between Body and Ear Colour and Ovarian Development in Females of the Swedish Highland Breed, Proc. 4th Intemat. Congr. on Animal Reprod. (The Hague) 752. 18. Swierstra, E. E. (1970) Personal Communication. 19. Taylor, D. O. N., Thomas, J. W. and Marburger, R. G. (1964) Abnormal Antler Growth Associated with Hypogonadism in White-Tailed Deer in Texas, Amer. J. Vet. Res., 25, 104, 179. 20. VanderSluis, L. (1953) Experiences with the Examination into Herd Infertility, Proc. 1st World Congr. On Fert. and Steril. H, 25, 703. 21. Williams, W. L. (1943) Diseases of the Genital Organs of Do- mestic Animals, 3rd Ed., Ithaca, N.Y. Sperm Cell Defects la. Afzelius, B. A. (1979) The Immotile-Cilia Syndrome and Other Ciliary Diseases, Intemat. Rev. of Exp. Path., 19, 1 (Academic Press, N.Y.C.) lb. Aughey, E. and Renton, J. P. (1968) Abnormal Spermatozoa in an Ayrshire Bull, Vet. Rec. 82, 129. lc. Barker, C. A. V. (1979) Two Cases of “Tail Stump” Sperm Defect, Proc. for Soc. for Theriog., Mobile, Alab., 27. 2. Blake, T. A. (1945) Inheritance of Morphological Characters in the Sperms of Cattle, Nature, 155, 631. 3. Blom, E. (1959) A Rare Sperm Abnormality “Corkscrew- sperms,” Associated with Sterility in Bulls, Nature, 183, 1280. 4. Blom, E. (1968) A New Sperm Defect “Pseudo droplets” in the Middle Piece of the Bull Sperm, Nord. Vet. Med. 20, 279. 5a. Blom, E. and Birch-Andersen, A. (1966) The Ultrastructure of a Sterilizing Tail Defect (the “Dag Defect”) in the Bull Sperm, State Veterinary Lab., Copenhagen, Denmark. 5b. Blom, E. and Birch-Andersen, A. (1978) Ultrastructure of the “Tail Stump” Sperm Defect in the Bull, Proc. 13th Nord. Vet. Congr. (Finland), 305. 6. Coubrough, R. I. and Barker, C. A. V. (1964) Spermatozoa: An Unusual Midpiece Abnormality Associated with Sterility in Bulls, Proc. 5th Intemat. Congr. on An. Reprod., Trento, Vol. 5, 219. 7. Hancock, J. L. and Rollinson, D. H. L. (1949) A Seminal De- fect Associated with Sterility in Guernsey Bulls, Vet. Rec. 61, 742. 8a. Johnson, S. D., Larsen, R. E. and Olson, P. S. (1982) Canine Theriogenology, Soc. for Theriog. Jour. Vol. XI, 62—93. 8b. Jones, W. A. (1962) Abnormal Morphology of the Spermatozoa in Guernsey Bulls, Brit. Vet. Jour., 118, 257. 9. Koefoed-Johnson, H. H., Andersen, J. B., Andersen, E., Blom, E. and Phillepsen, H. (1980) The Dag Defect of the Tail of the Bull Sperm, Studies on the Inheritance and Pathogenesis, Ther- iog., 14, 6, 471. 10. MacLeod, J. and McGee, W. R. (1950) The Semen of the Thor- oughbred, Cor. Vet. 40, 3, 233. 11a. Saacke, R. G., Amann, R. P. and Marshall, C. E. (1968) Ac- rosomal Cap Abnormalities of Sperm from Subfertile Bulls, J. An. Sci., 27, 5, 1391.INFERTILITY IN MALE ANIMALS 825 lib. Settergren, I. (1970) Unpublished data and personal commu- nication. 12. Swanson, E. W. and Boyd, L. J. (1972) Factors Affecting Coiled Tail Spermatozoa in the Bull, Amer. J. Vet. Res. 23, 93, 300. 13. Wenkoff, M. S. (1978) A Sperm Mid-Piece Defect of Epidid- ymal Origin in Two Hereford Brills, Theriog., 10, 4, 275. 14. Williams, G. (1965) An Abnormality of the Spermatozoa of Some Hereford Bulls, Vet. Rec. 77, 41, 1204. Inbreeding, Hybrids, Chromosome Aberrations, and Intersexes (Hermaphrodites) la. Bane, A. (1954) Studies on Monozygous Cattle Twins XV Sex- ual Functions of Bulls in Relation to Heredity, Rearing Intensity and Somatic Conditions, Acta. Agric. Scand. 4, 95. lb. Biggers, J. D. and McFeely, R. A. (1966) Intersexuality in Do- mestic Mammals, in Advances in Reprod. Physiol. Acad. Press, N.Y.C. lc. Benirschke, K. (1967) Sterility and Fertility of Interspecific Mammalian Hybrids, in Comparative Aspects of Reproductive Failure, Springer-Verlag, New York Inc. p. 218. 2. Bongso, A. and Basrur, P. K. (1976) Chromosome Anomalies in Canadian Guernsey Bulls, Cor. Vet. 66, 476. 3. Bongso, T. A., Jainudeen, M. R. and Lee, J. Y. S. (1981) Testicular Hypoplasia in a Bull with XX/XY Chimerism, Cor. Vet. 71, 376, (A Review). 4. Carroll, E. J. (1968) Testicular Pathology in Young Beef Bulls with Special Reference to Inbreeding, Thesis, Cornell Univ., Ithaca, N.Y. 5. Carroll, E. J. and Ball, L. E. (1970) Effects of Mating Systems on Reproductive Functions in Beef Bulls, Amer. J. of Vet. Res. 31, 2, 241. 6. Deaken, A. (1943) Field Fertility Tests and Causes of Sterility in Bulls, Dept, of Agr. Central Exper. Farm, Ottawa, Can. 7. Dunn, H. O., Lein, D. H. and McEntee, K. (1980) Testicular Hypoplasia in a Hereford Bull with 61XXY Karyotype: The Bo- vine Counterpart of Human Klinefelter’s Syndrome, Cor. Vet. 70, 137, (A Review). 8. Dunn, H. O., McEntee, K., Hall, C. E., Johnson, R. H., Jr. and Stone, W. H. (1979) Cytogenetic and Reproductive Studies of Bulls Born Cotwin with Freemartins, J. Reprod. Fert., 57, 21. 9. Dunn, H. O., Smiley, D., Duncan, J. R. and McEntee, K. (1981) Two Equine True Hermaphrodites with 64XX/64XY and 63X0/ 64XY Chimerism, Cor. Vet., 71, 123, (A Review). 10. Fecheimer, N. S. (1973) A Cytogenetic Survey of Young Bulls in the U.S.A. Vet. Rec. 93, 535. 11. Foley, C. W., Lasley, J. F. and Osweiler, G. D. (1979) Ab- normalities of Companion Animals, Iowa State Univ. Press, Ames, Iowa, 202. 12. Gilmore, L. O. (1949) The Inheritance of Functional Causes of Reproductive Efficiency, A Review, J. of Dairy Sci. 32, 71. 13. Gregory, P. W., Mead, S. W., Regan, W. M. and Rollins, W. C. (1951) Further Studies Concerning Sex-Limited Genetic In- fertility in Cattle, J. Dairy Sci. 34, 1047. 14. Gustavsson, I. (1969) Cytogenetics, Distribution and Pheno- typic Effects of a Translocation in Swedish Cattle, Hereditas 63, 68. 15. Hancock, J. L. (1964) Attempted Hybridization of Sheep and Goats, 5th Intemat. Congr. on Animal Reprod. and Art. Insem., Trento, Italy 3, 445. 16. Knudson, O. (1958) Studies on Spermiocytogenesis in the Bull, Intemat. J. of Fertil. 3, 3 and 4, 390. 17a. Krehbiel, E. V., Carter, R. C., Bovard, K. P., Gaines, J. A. and Priode, B. M. (1969) Effects of Inbreeding and Environ- ment on Fertility of Beef Cattle Matings, J. An. Sci. 29, 4, 528. 17b. Long, S. E., Gruffydd-Jones, T. and David, M. (1981) Male Tortoiseshell Cats: An Examination of Testicular Histology and Chromosome Complement, Res. Vet. Sci., 30, 274. 18. Loughman, W. D., Frye, F. L. and Congdon, T. B. (1970) XY/XXY Bone Marrow Mosaicism in Three Male Tricolor Cats, Amer. Jour. Vet. Res. 31, 2, 307. 19a. McNitt, J. E., Stonaker, H. H. and Carroll, E. J. (1966) Breed- ing Soundness in Beef Bulls, Proc. Western Sect. Amer. Sco. Animal Science. 17, 25. 19b. Pond, W. C., Roberts, S. J. and Simmons, K. R. (1961) True and Pseudohermaphroditism in a Swine Herd, Cor. Vet. 51, 3, 394. 20. Popescu, C. P. (1981) Cytogenetic Studies in Domestic Animals in Connection with Reproductive Disorders, INRA, CNRZ. France, Abstr., J. An. Sci., Suppl. 1, #97, p. 165. 21a. Setchell, B. P. (1978) The Mammalian Testis, Cornell Univ. Press, Ithaca, N.Y. 14850, 359-432. 21b. Soller, M., Laor, M., Bamea, R., Weiss, Y. and Ayalon, N. (1964) Polledness and Infertility in Male Saanen Goats, J. of Hered. 54, 237. 22. Thuline, H. C. (1964) Personal Communication. 23. Vogt, D. W., Arakaki, D. T. and Brooks, C. C. (1974) Re- duced Litter Size Associated with Aneuploid Cell Lines in a Pair of Full-Brother Duroc Boars, Amer. J. Vet. Res. 35, 8, 1127. 24. Wildt, D. E., Baas, E. J., Chakraborty, P. K., Wolfe, T. L. and Stewart, A. P. (1982) Influence of Inbreeding on Repro- ductive Performance, Ejaculate Quality and Testicular Volume in the Dog, Theriog., 17, 4, 445. 25. Young, B. G. (1953) Genetic Aspects of Fertility and Infertility in Cattle, Vet. Rec. 65, 271. Cryptorchidism, Hernias, Torsions and Miscellaneous Abnormalities 1. Adams, O. R. (1964) An Improved Method of Diagnosis and Castration of Cryptorchid Horses, JAVMA, 145, 5, 439. 2. Arthur, G. H. (1961) The Surgery of the Equine Cryptorchid, Vet. Rec. 73, 16, 385. 3. Ashdown, R. R. (1963) The Diagnosis of Cryptorchidism in Young Dogs: A Review of the Problem, J. Sm. An. Pract. 4, 261. 4. Bishop, M. W. H., David, J. S. E. and Messervy, A. (1966) Cryptorchidism in the Stallion, Proc. Royal Soc. of Med. 59, 769. 5. Brodey, R. S. and Martin, J. E. (1958) Sertoli Cell Neoplasms in the Dog. The Clinicopathological and Endocrinological Find- ings in Thirty-Seven Dogs: JAVMA, 133, 249. 6. Brodey, R. S. and Reif, J. S. (1969) The Relationship Between Canine Testicular Neoplasia and Cryptorchidism (Abstr.) JAVMA, 154, 11, 1385. 7. Carl, J. (1943) An Inherited Defect in Bulls, (Horizontal Testes), Berl. Munch. Tierarztl. Wschr., p. 8. 8a. Chamey, C. W. and Wolgin, W. (1957) Cryptorchidism, Hoe- ber-Harper Inc., N.Y.C. 8b. Coryn, M., DeMoor, A., Bouters, R. and Vandeplassche, M. (1981) Clinical Morphological and Endocrinological Aspects of826 VETERINARY OBSTETRICS Cryptorchidism in the Horse, Theriog, 16, 4, 489. 9. Fox, M. W. (1963) Inherited Inguinal Hernia and Midline De- fects in the Dog. JAVMA, 143, 6, 602. 10a. Jensen, R. and Swift, B. L. (1982) Disorders of Sheep, 2nd Ed., Lea and Febiger, Philadelphia. 10b. Kingrey, B. W. (1961) Personal Communication. 11. Lowe, J. E. and Higginbotham, R. (1969) Castration of Ab- dominal Cryptorchid Horses by a Paramedian Laparotomy Ap- proach, Cor. Vet., 59, 1, 121. 12. Mann, P. H. (1956) A Case of Unilateral Cryptorchidism in a Mongrel Dog, Cor. Vet. 46, 1, 6. 13. McEntee, K. (1969) Pathology of Domestic Animals, 2nd Ed. Edited by Jubb, K. V. and Kennedy, P. C. Academic Press, N.Y.C. and London. 14. McGee, W. R. (1967) Personal Communication. 15. McPhee, H. C. and Buckley, S. S. (1934) Inheritance of Cryp- torchidism in Swine, Jour, of Hered. 25, 295. 16. Milne, F. (1958) Personal Communication. 17a. Noordsy, J. L. (3966) Inguinal Hemioplasty in the Bovine Male, Vet. Med. 61, 2, 147. 17b. Pascoe, J. R., Ellenburg, T. V., Culbertson, M. R., Jr. and Meagher, D. M. (1981) Torsion of the Spermatic Cord in a Horse, JAVMA, 178, 3, 242. 17c. Pearson, H. and Kelly, D. F. (1975) Testicular Torsion in the Dog: A Review of 13 Cases, Vet. Rec. 97, 200. 17d. Peduzzi, R. J. and Carlson, D. J. (1980) Testicular Torsion (Dog) (A Review) Canine Pract. 7, 3, 79. 18a. Reif, J. S. and Brodey, R. S. (1969) The Relationship Between Cryptorchidism and Canine Testicular Neoplasia, JAVMA, 155, 12, 2005. 18b. Sager, F. (1972) Personal Communication. 19a. Shelton, M. (1978) Reproduction and Breeding of Goats, J. Dairy Sci. 61, 994. 19b. Stickle, R. L. and Fessler, J. F. (1978) Retrospective Study of 350 Cases of Equine Cryptorchidism, JAVMA, 172, 343. 20. Technical Development Committee. (1954) Cryptorchidism with Special Reference to the Condition in the Dog, Vet. Rec. 66, 482. 21. Todd, G. C., Nelson, L. W. and Migaki, G. (1968) Multiple Heterotropic Testicular Tissue in the Pig—A Report of 7 Cases, Cor. Vet. 58, 4, 614. 22. Warwick, B. L. (1926) A Study of Hernia in Swine, Wise. Agr. Exper. Stat. Bull. 69. 23. Warwick, B. L. (1961) Selection Against Cryptorchidism in Angora Goats, J. An. Sci. 20, 1, 10. 24. Wheat, J. D. (1961) Cryptorchidism in Hereford Cattle, J. He- red. 52, 244. 25. Wolff, A. (1981) Castration, Cryptorchidism and Cryptorchi- dectomy in Dogs and Cats, Vet. Med./Sm. An. Clin., 76, 12, 1739. 26. VanderSluis, L. (1953) Experiences with Examination into Herd Infertility, Proc. First World Congr. on Fert. and Steril. II, XXV, 703. Acquired Testicular Pathology Testicular Pathology Due to Acquired Causes is much more common than congenital or hereditary causes and includes testicular degeneration, orchitis, fibrosis and calcification. (See Figures 180 through 190.) Lagerlof and others estimated that 75 to 80 percent of testicular pathology is related to testicular degeneration including fibrosis and orchitis. The epithelium of the seminiferous tubules is highly sensitive to any adverse influences with resulting marked effects on spermatogenesis. Testicular degeneration may be mild or severe and is usually bi- lateral as it is most commonly due to generalized disease processes. Unilateral degeneration can occur secondary to local testicular lesions such as tumors. Testicular de- generation may develop very rapidly within a few days or hours; while testicular regeneration proceeds slowly over weeks and months. If the basal layers of the ger- minal epithelium including the spermatogonia and Ser- toli cells are destroyed regeneration of the germinal ep- ithelium is not possible and the animals remain sterile. The pattern and signs of testicular degeneration are about the same despite the species or the etiologic factor(s) in- volved. In all cases degenerative changes in the mech- anism of cell division or centrosomes are present in the primary spermatocytes and are responsible for reduced motility and increased numbers of pathologic sperma- tozoa with an abnormal morphology. Sperm cell num- bers and concentration are decreased depending on the degree of degeneration of the seminiferous tubules. In severe disturbances of spermatogenesis, spermatocytes with restitution nuclei, with double the normal number of chromosomes as well as pyknotic nuclei are present in the ejaculate.17 Testes with degeneration of the seminif- erous tubules are usually atrophic, softer and smaller than normal testes. In chronic cases the testicle may be firm due to fibrosis; even calcium may be deposited espe- cially in the areas just peripheral to the rete testis. His- tologically it may be difficult to distinguish between slight degrees of testicular degeneration and hypoplasia. Hy- poplastic testes have a predisposition to degeneration. Setchell28 has described the natural and induced dis- functions of the testes in man and animals and has pro- vided an extensive bibliography covering the testicular effects of radiation, heat, cold, nutrient supply, chemical and immunological damage, chromo&omal, hormonal, viral, neoplastic and miscellaneous disease factors on the testes.28 Causes of Testicular Degeneration include: Thermal influences associated with elevation of the testicular temperature such as: cryptorchid and ectopic testes; inguinal hernias; (See Figure 180 and 181) scrotal dermatitis due to, irritants, choriopic mange in rams26a and bulls (See Figure 182), myiasis in sheep, and lo-INFERTILITY IN MALE ANIMALS 827 Figure 182. Scrotal Dermatitis and Edema in a Bull Secondary to Chorioptic Mange. (Temporary testicular degeneration and infertility resulted that lasted for 2 to 3 months.) calized skin infections, pox lesions or wounds; contu- sions and hematomas of the scrotum and testes; pro- longed elevated body temperature as in certain infectious diseases and in prolonged high environmental tempera- tures, particularly associated with high humidity. Tes- ticular degeneration is most common in tropical climates and involving breeds originating in the temperate zones.3 “Summer” infertility in bulls in the temperate zone is usually an individual bull problem. As many as 20 to 30 percent of bulls in a midwestern AI stud required air con- ditioning to maintain production of high quality semen during summer months when the ambient temperature and humidity are high. Direct heating of the scrotum may also be involved.22 Bulls were exposed to heat stress for 8 hours a day for 7 days; this resulted in a deleterious effect on semen quality reaching its peak at 2 to 3 weeks after the stress with recovery by 9 weeks.16 Rams main- tained at ambient temperatures of 90° F. or above de- velop a marked drop in semen quality with about 10 per- ent motility and 70 percent abnormal sperm cells within a few weeks.4'83'24 Recovery was not complete until 2 to 3 months after normal temperatures were restored. Shearing rams, especially their scrotums, monthly dur- ing the summer months greatly improved conception rate and embryo survival.12 High ambient temperatures will also cause lowered fertility due to testicular degeneration in boars.29’31 Heat primarily affects the spermatocytes but usually does not affect the spermatogonia, elongated spermatids or epididymal spermatozoa in the bull.27 Heat has no effect on the Leydig cells. Even 10 to 20 hours insulation of the scrotum with a plastic bag that raised the skin temperature to 35° C had a definite depressing effect on semen quality that lasted for 3 to 9 weeks with a return to normal semen quality by 13 weeks.27 Lagerlof19 carried out early classical experiments demonstrating that overheating or insulation of the scrotum of bulls caused rapid testicular degeneration and when normal scrotal temperature was restored, recovery was slow. Males that lie down for long periods of time such as bulls with bo- vine spastic syndrome, or males that are unable to rise, often develop testicular degeneration and atrophy due to the prolonged elevation of testicular temperature from the testes being held close to the body. When the scrotal temperature of bulls was raised to 38.4° C or 0.3° C be- low body temperature, the motility and percent of live spermatozoa in the semen decreased to zero by the sec- ond week.86 After normal scrotal temperature was re- stored 11 weeks elapsed before motile cells were ob- served and 18 weeks were required for the recovery of normal semen quality. Application of an irritating oint- ment to the scrotum of boars resulted in increased heat to the area with testicular degeneration that was char- acterized initially with many immature sperm cells with a protoplasmic droplet followed by an increase in mor- phologically abnormal spermatozoa as the condition ad- vanced.10 Colorado workers6 have reported on the damage to spermatogenic function induced in range beef bulls by low temperature down to -25° F. associated with winds of 60 miles per hour causing frostbite, necrosis of skin, scrotal dermatitis, heat, swelling, testicular degeneration and adhesions. Older bulls with pendulous scrotums were most seriously affected. The severity of the after effects were related to the amount of adhesions produced. Bulls provided proper wind shelter and dry bedding were not affected by such temperatures and wind. Scrotal frostbite resulting in infertility was reported in boars in Minne- sota.2 Scrotal dermatitis in dogs or other males due to any cause may result in testicular degeneration due to the elevation of the temperature of the testes.196 This is favored by mild degrees of testicular hypoplasia. The presence of excessive fat in the inguinal region probably has little effect on the thermoregulatory mechanisms of the scrotum and testes unless short spermatic cords or other defects in the testes are present. The author has observed several bovine cases of mild scrotal hydrocele of unknown etiology where semen quality was not sig- nificantly affected. A severe chronic hydrocele resulting828 VETERINARY OBSTETRICS in poor semen quality in a 3 year old bull was described. The bull responded to unilateral castration with a return to normal fertility 3 months after the operation." A hy- drocele secondary to a tumor of the tunica vaginalis was described in a dog.25 Vascular lesions of the testes—Interference with the circulation and infarction of the testis can be produced by manual torsion of the testis or by the emasculatome used for castration of lambs or calves. Congestion and pain of the scrotal testis due to naturally-occurring tor- sion or contusion has been reported in racing stallions, particularly Standard-bred trotters. With vigorous exer- cise these animals would start to spraddle their rear legs, become lame and then change from a trotting to a pacing gait. Affected Thoroughbred stallions would race nor- mally for nearly one-half mile and develop an altered “hopping” gait. The testes would be swollen, congested and painful for the next 3 to 4 days. Dogs with inguinal or abdominal cryptorchid tests may occasionally develop torsion of the testis with a sudden onset of pain and as- sociated symptoms. The author has observed one case of testicular torsion in a cryptorchid pig. Hemorrhagic infarction of the testis may follow torsion. Tumors of the abdominal testes may also predispose to torsion. Testicular biopsies, particularly in bulls, often result in focal areas of testicular necrosis because of vessel damage when a desirable size of testicular material is obtained.26 For this reason a technique of aspiration bi- opsy in bulls for cytologic but not for histologic studies was recommended.17,18 Testicular biopsies are more eas- ily and safely done in the stallion and other animals.1,14 Testicular biopsies, even with a biopsy needle, may oc- casionally cause a degree or area of testicular degener- ation due to interruption of the blood supply. In one study in dogs in which 28 biopsies were performed, one re- sulted in unilateral testicular degeneration and atrophy.14 Inflammation of the testicular artery in the horse may be caused by strongyle larvae, the equine arteritis virus and other unknown agents. This may produce areas of testicular degeneration.20 Strongyle larvae can pro- duce adhesions between the testis and its tunics. Age- associated vascular lesions such as hyaline degeneration in older bulls, rams and dogs may cause degenerative changes in the seminiferous tubules.20 Suspensories of any type whether solid or mesh should not be used in shipping male animals. They have not proven necessary. The solid type might result in over-heating of the testes and both types might become maladjusted and cause pressure on the spermatic cord and affect testicular cir- culation.7 Varicocele is seen occasionally in the internal sper- matic vein of rams and stallions but not bucks. (See Fig- Figure 183. Varicoceles or Thrombosis of the Spermatic Vein in a Ram. (Courtesy K. McEntee.) ure 183.) As in man the adverse effects on semen qual- ity especially motility are probably slight to moder- ate.5,15,21,28 A severe case of infertility due to bilateral varicoceles in a 4-year-old ram with a high percentage of abnormal acrosomes along with other spermatozoal abnormalities and degeneration of the seminiferous ep- ithelium was reported.23 Varicocele may effect both the circulation of blood and the heat regulatory mechanism of the pampiniform plexus. Varicoceles may be palpated in rams.15 In a recent review156 of varicoceles in rams it was proposed that this condition was caused by exces- sive venous pressure in the internal spermatic vein pos- sibly due to arterio-venous shunts. The condition devel- ops slowly over several years so it is usually seen in older rams. The incidence is low. In severe cases the varicocele may reach a size of 7 to 15 cm. and cause immobility, reduced libido as well as testicular degen- eration, and infertility secondary to hypoxia of the sem- iniferous tubules. In large varicoceles a laminated thrombosis may be present. Affected rams should be culled as no cure is available and the condition might be hereditary.156 Irradiation, as other causes of degeneration of the testes, produces interference with spermatogenesis by injuring spermatogonia, spermatocytes and spermatids. The spermatocytes are most sensitive to irradiation while Leydig and Sertoli cells are quite resistant. The amountINFERTILITY IN MALE ANIMALS 829 of irradiation and length of treatment are highly impor- tant in the degree of effects produced and the rate of recovery. The first change in the semen noted was ab- normal sperm cells about the sixth week after exposure of bulls to 100 to 400 roentgens.12 A decrease in sperm cell numbers occurred by the eighth week and these numbers did not begin to return to a normal level until 15 weeks. All bulls had reached nearly normal levels by 24 weeks after exposure. Bulls given doses totalling 600 to 1100 roentgens, developed aspermia by 16 weeks, re- mained aspermic for 10 weeks and fairly good recovery had occurred by 12 to 24 months.13,14 Hormonal causes—Testicular degeneration and atro- phy of the testes occurs in the dog and rarely in other animals due to tumors of the anterior pituitary gland or hypothalamus interfering with the production of gonad- otropic hormones. This is called dystrophia adiposo- genitalis syndrome in dogs.8b Besides testicular atro- phy, obesity and other signs commonly develop. Excessive estrogenic hormone produced by Sertoli cell tumors and testosterone, and rarely estrogens, produced by Leydig cell tumors my suppress FSH and LH production and cause testicular degeneration. In the past (1950’s) infer- tile men with oligospermia were treated with large doses of testosterone for a prolonged period to completely sup- press spermatogenesis. Following this treatment a “re- bound phenomena” was reported in which higher than normal concentrations and numbers of spermatozoa were produced. In summarizing this data only 7.5 percent of 840 men treated showed any significant improvement.3 Prolonged doses of testosterone, estrogens or anabolic steroids should not be given to male animals.11 (See Hor- monal Causes of Infertility in Males.) Age Effects—McEntee10 stated “Permanent and pro- gressive testicular degeneration occurs fairly frequently in all species without any indication of its pathogenesis. ” Senile'atrophy of the testes is common in dogs over 10 years of age and in cats over 12 years of age.1 A decline in fertility in bulls as they became older has been re- ported.45 Vibriosis might have been present as a factor in the latter report. A decline in fertility of 0.31 to 0.51 percent per year in over 150 bulls used in artificial in- semination as measured by nonreturn rates was re- ported.7 Aged bulls, 7 to 13 years old had a lower sperm cell output per ejaculate than young bulls, 2 to 6 years old, 7 billion and 10 billion, respectively.7 Aged bulls had 10 percent fewer morphologically normal sperma- tozoa and the motility rate was lower. Degeneration of the testes based on semen examinations in aging stallions was similarly described.9 The author has observed that older bulls after they reach 8 to 10 years of age may develop testicular degeneration fairly rapidly at any time. It is an uncommon bull that produces good quality fertile semen up to 15 or more years of age. Many disease, genetic and management factors influence this age ef- fect. Subacute or acute trauma, stress, or disease may cause rapid or progressive testicular degeneration in males. Those that have been associated with reduced fertility and a decline in semen quality are: shipping under ad- verse conditions of heat and cold, severe fatigue, ex- cessive physical work, traumatic gastritis in bulls,6 liver or abdominal abscesses, multiple severe contusions with fractured ribs as would occur in a fight between bulls, severe arthritis, severe myiasis or “fly strikes” in rams, severe screw-worm infestations, moderate to severe foot rot in rams, suppurative arthritis and severe quittors in bulls, acute laminitis in rams, horses and possibly other species, buckshot wounds especially of the scrotum and testes, kick wounds and resulting hematomas of the testes and scrotum in stallions, and extensive infected wounds. Good care and management will do much toward avoid- ing testicular degeneration due to these causes. Although Polish workers8 reported a temporary reduction in fer- tility for about three months after shipping 29 bulls from Holland to Poland, 60 bulls, used for artificial insemi- nation, moved 300 to 2000 miles in the U.S. without a suspensory and no reduction in semen quality was noted in the months following shipment.15 Acute or chronic, localized or systemic infectious diseases are common causes of testicular degeneration with moderately to severely reduced fertility in males. Infections producing orchitis or epididymitis have a di- rect effect on the testes due to the inflammatory reaction causing heat, edema, congestion, circulatory interfer- ence, ischemia and even infarction due to the thick firm tunica albuginea that restricts normal swelling of the tes- ticular parenchyma. In bacterial diseases localizing in the testes, abscessation may occur. (See Figures 184 and 185.) Infectious agents resulting in orchitis are: Brucella abortus, both field strains and Strain 19 in bulls;17 Bru- cella suis in boars; miliary or chronic tubercular infec- tious with Mycobacterium tuberculosis of the testes in bulls and boars; Corynebacterium pyogenes, usually carried to the testes by the blood from primary infectious sites in bulls and rams; Actinomyces bovis in bulls,14 Malleomyces mallei (glanders organism) in horses; Sal- monella abortus equi and “epizootic cellulitis” due to the arteritis and the influenza viruses in horses; Co- rynebacterium ovis and Pasteurella pseudotubercu- losis in rams; lumpy skin disease in cattle; sheep pox virus in rams;19 an enteric virus, possibly IBR-IPV virus, that markedly affected the spermatocytes and caused ar- rested spermatogenesis in bulls has been described in830 VETERINARY OBSTETRICS Figure 184. Acute Orchitis of the Right Testis in a Holstein Bull. Belgium.1,2 These workers1,2,10 reported on a G-UP virus isolated from the genital organs of bulls that caused in- fertility and an abnormal sperm picture, degeneration of the seminiferous epithelium, ulcers in the mouth, stiff gait, anorexia and other lesions highly suggestive of foot and mouth disease. A more chronic virus orchitis of bulls has been reported in Czechoslovakia.21 Other possible related viruses may cause orchitis in bulls.12 The IBR- IPR virus when injected into susceptible bulls may cause a severe and rapid degeneration of the seminiferous ep- ithelium and sterility.26,29 Most bulls recovered and were fertile in about 3 months. During the height of the de- generation only Sertoli cells and spermatogonia lined the seminiferous tubules. A few bulls developed an edema of the scrotum and fibrous adhesions occurred around the testes and spermatic cord. Canine distemper affecting sexually mature dogs may cause a mild orchitis and testicular degeneration as well as an epididymitis.519 Brucella canis in dogs caused scrotal swelling and dermatitis, orchitis, fibrosis, atro- phy and sterility.5,6,73,11,22 After oral inoculation of dogs with Br. canis 20 to 80 percent of the sperm cells were abnormal, including swollen midpieces and distal pro- toplasmic droplets within 3 to 4 weeks after the inocu- lation. By 8 weeks nearly all spermatozoa exhibited marked defects generally attributed to the epididymitis and seminiferous tubule degeneration.11 (See Abortion and Epididymitis due to Brucella canis.) Any acute or subacute epididymitis would reduce fertility both be- cause of the inflammatory reaction and heat produced as well as by obstructive lesions in the epididymal tube. (See Epididymitis due to Brucella ovis.) The probable viral disease of specific bovine venereal epididymitis and vaginitis, “epivag,” also causes an orchitis with testic- ular degeneration and atrophy.3 A mycoplasma was iso- lated from three ovine cases of orchitis,20 and Myco- plasma hyorhinis infection in swine often results in swelling of the scrotum and adhesions between the testes and the tunics.28 Chlamydia psittaci may cause orchitis as well as polyarthritis in rams.23 This organism was re- covered from two other cases of orchitis in rams.8 A seminal vesiculitis syndrome in bulls characterized by seminal vesiculitis, epididymitis and orchitis was de- scribed by Colorado workers27 from which they re- Figure 185. Acute Orchitis and Periorchitis Secondary to a C. pyo- genes Infection. (After unilateral castration and a 6 to 8 month rest period this bull (Figs. 184 and 185) recovered and was fertile for over 3 years.)INFERTILITY IN MALE ANIMALS 831 Figure 186. Longitudinal Section of a Normal Bovine Testis (Note Figure 188. Advanced Testicular Degeneration, Fibrosis and Atro- the bulging an the uniform color and texture of the parenchyma) phy, Especially of the Left Testis. (Courtesy K. McEntee). covered a chlamydial agent. Nocardia farcinica in bulls,3 and Besnoitia besnoiti have been occasionally reported as a cause for orchitis in bulls.7b l6,24 Severe obstructive lesions such as sperm granulomas affecting the efferent ducts may cause a back pressure from the spermatozoa and the testicular secretions resulting in testicular de- generation. (See Figure 189.) The affected testes may be somewhat enlarged.19 Sporadic infections of the testis with Figure 187. Testis with Advanced Testicular Degeneration, Fibrosis and Calcification (Courtesy K. McEntee). Figure 189. Fibrosis and Sperm Granuloma of the Tail of the Epi- didymis of the Left Testis in a Ram due to Br. ovis. (Note the mod- erate atrophy of the left testis compared to the normal right testis.) (Courtesty P C. Kennedy.)832 VETERINARY OBSTETRICS staphylococci, streptococci, E. coli, Proteus and Pseu- domonas organisms have been reported as a cause of or- chitis in dogs and other male domestic animals.25 Erhl- ichiosis of horses resulted in edema of the legs, sheath and scrotum and orchitis with secondary testicular atro- phy.13 During the acute disease inclusion bodies were commonly observed in the leucocytes. This disease should be differentiated from equine infectious anemia, piro- plasmosis and dourine. Infectious diseases of a systemic nature that cause testicular degeneration and lower fertility temporarily due to the accompanying high fever include: pneumonia and shipping fever, possibly IBR-IPV, equine infectious anemia, actinobacillosis, strangles, blue-tongue virus vaccination,9 and tick-borne fever infection in rams.30 (See Figure 190.) Pseudorabies in swine had no effect on semen quality or fertility unless severe clinical signs developed.18 Those infectious diseases causing gradual debilitation, loss of weight and testicular degeneration with atrophy include: foot and mouth disease, actino- mycosis, Johne’s disease, pyelonephritis, chronic peri- tonitis, and lymphomatosis. Nutritional factors related to testicular degeneration are usually those caused by severe underfeeding or star- vation. (See Nutrition and Infertility in Males.) Diets for males sufficient for growth and maintenance are ade- quate for fertility. Chronic disease states associated with Figure 190. Edema of the Scrotum of A Standardbred Stallion, As- sociated with Equine Infectious Anemia. inanition and debility and testicular atrophy may include: severe parasitisms, either external or internal such as: lice, mange, ticks, roundworms, flukes, and etc., senile changes due to worn or diseased teeth, chronic arthritis, tumors, fat necrosis around the large intestine in bulls, severe spastic syndrome and other possible diseases in- terfering with the intake and passage of food through the gut. Malnutrition may complicate these other chronic diseases. Improper care and management of bulls ac- customed to special care and feeding may cause a marked loss in weight resulting in impotency and testicular de- generation and atrophy. This has been observed in sev- eral instances when a young fertile, but timid, bull was introduced into a new herd and permitted to run with the cows in a small, confined area. The cows would drive the bull away from the feeding racks causing the bull to become emaciated and sterile. Severe vitamin A defi- ciency characterized by night blindness, lacrimation and opthalmia usually precedes testicular degeneration and poor semen quality. Under range conditons during drouths vitamin A deficiency usually is accompanied by protein and carbohydrate deficiencies. Malnutrition, debility and cachexia produce degeneration and atrophy of the sem- iniferous epithelium by causing a suppression of the re- lease of gonadotropic hormones from the pituitary. Zinc deficiency may be associated with certain cases of in- fertility in animals.14 A high level of feeding and the accompanying obesity has no effect on semen quality in a normal male, but does effect their libido and willingness to breed. The au- thor has observed a number of highly-conditioned beef show bulls producing semen of excellent quality. How- ever, if obesity accompanies testicular hypoplasia, a short spermatic cord and much fat in the inguinal ring it does not follow that the obesity is the primary cause of the resulting infertility. Poisons or toxins may adversely affect the germinal epithelium. Testicular degeneration in bulls and hyper- keratosis in rams was caused by ingestion of chlorinated napthalenes.12 Dipping of rams in arsenic solutions causes degeneration of the seminiferous tubules in sheep.7 An- timony compounds injected for the treatment of heart- worms in dogs have been reported to cause temporary sterility.1 There is no evidence that copper sulphate or phenothiazine used in worming sheep have harmful ef- fects on the testes. There is no evidence that systemic organic phosphate insecticides affect semen quality in bulls.6 Severe prolonged toxemia and reduced semen quality lasting for 6 to 12 months resulted from using chlorpyrifos (Dursban 44) pour-on for the control of lice in AI bulls.4 This compound, which did not affect steers or cows, probably interacted in some manner with tes-INFERTILITY IN MALE ANIMALS 833 tosterone to produce these effects. Potassium nitrate also had no effect on semen pro- duction. The author has seen no ill effects from the use of sodium iodide for actinomycosis or actinobacillosis in bulls in artificial insemination studs. A number of chem- ical, metals and rare earth salts can produce degeneration of the seminiferous epithelium in a variety of species.11 Setchell14 has cited many references on chemical com- pounds that affect testicular function including cadmium salts, other heavy metals, diesters of methane sulfonic acid, nitrofurans, halogenated compounds, alcohol and actinomycin D in animals and man.1214 Auto-immunization might play a role in a few cases of testicular degeneration. Degeneration has been pro- duced experimentally in rams, bulls and laboratory animals by the subcutaneous injection of autologous testicular material together with Freund’s adjuvant. Degeneration may occur with or without inflammation. No natural cases of testicular degeneration due to au- toimmunization have been reported.2’9'10’12'13 Two re- ports have indicated that anti-LH serum or an anti-LH adjuvant product injected every 3 weeks in bull calves and ram lambs will induce testicular degeneration and sterility. This product immobilizes the male’s own go- nadotropic hormones and testosterone necessary for spermatogenesis. Lymphocytic thyroiditis, a possible genetic autoimmune disease of dogs, especially Cocker Spaniels, Corgis and Beagles, may also be associated with lymphocytic orchitis and infertility.8b Testicular Neoplasms. Testicular tumors are uncom- mon in most domestic animals except the dog and pos- sibly old bulls. Primary testicular tumors are usually of three main types and originate from the interstitial cells, Figure 191. Bilateral Interstitial Cell Tumors of a Testis in an Old Infertile Guernsey Bull. (Courtsey K. McEntee.) Figure 192. Sertoli Cell Tumor of the Testis of a Bull. (Courtesy K. McEntee.) the Sertoli cells and the germinal epithelium. The in- creased incidence in dogs may be due to a genetic pre- disposition in dogs and to the maintainance of intact male dogs until they become senile. The incidence of tumors in cryptorchid or retained testes in high, especially in dogs, for the same reason. In the larger animals rela- tively few uncastrated males are kept until they reach an advanced age. Sperm cell production and fertility of bulls with testicular tumors over 1.0 cm. in diameter were sig- nificantly lower than in unaffected bulls or bulls with small tumors.6 Bulls with large interstitial tumors had 30 percent of their ejaculates discarded as unfit for use for artificial insemination while normal control bulls had only 2 percent of their ejaculates discarded. (See Figure 191.) Thus large tumors result in testicular degeneration prob- ably due to the compressing effect of the tumor on the adjacent seminiferous tubules. The degeneration may also be due to the excess steroids produced by the interstitial, or Sertoli cell tumors.12 (See Figure 192.) Lymphosar- coma of the testis of animals is rare. In bulls testicular tumors are seldom observed except in old animals. Interstitial cell tumors of a benign type are occasionally observed in bulls over 7 to 10 years of age. These may be multiple and in some cases they are large enough to be palpable as small, round, masses, liver-like in consistency, and causing the testes to feel lumpy on palpation. Interstitial cell tumors were found834 VETERINARY OBSTETRICS in 19 percent of 52 Guernsey bulls.6 This was signifi- cantly higher than the 6 percent incidence in 164 bulls of the other breeds. An interstitial cell tumor in a testis of a 3-month-old calf was described.9 This type of tumor usually has a deep ochre or orange-brown color with a homogeneous, glassy consistency resembling a corpus luteum.12 (See Figure 191.) An adenocarcinoma, semi- nomas and several Sertoli cell tumors have been de- scribed in bulls. (See Figure 192.) The benign interstitial cell tumors in old men, dogs and probably bulls may be related to a hormone imbalance.9 Small fibropapillomas or melanomas and varicose dilatations of scrotal veins occur in older bulls and are occasionally seen on the scrotal skin. These small varicose lesions on bulls’ testes may be associated with improper temperature regulation of testes and infertility during the hot summer months. In stallions testicular tumors have been described only occasionally. Uncommon dermoid cysts or teratomas of the testicle of the horse are most often found in crypt- orchid testes.4a,b'13'24,28 They often contain large cystic structures and hair or bone. Forty-nine testicular tumors Figure 193. Testicular Abscesses in a 3-Month-Old Calf. of a total of 142 neoplasms were found in 77,000 slaugh- tered horses.9 Rare seminomas in stallions were de- scribed.91013 26 The latter report described two equine seminomas that metastasized. Only one testicular teratoma was found in 700 horses castrated at the New York State Veterinary College.12 An adenocarcinoma in a retained testicle in a horse with metastasis to the lungs and mediastinum was described.9 Occasional interstitial cell tumors of the equine testis have been reported.12,23 In some of the cases the affected an- imals were extremely aggressive and vicious but after castration became gentle and quiet. Sertoli cell or sus- tentacular cell tumors in horses were rare.13 A melanoma of the scrotum has been observed in a stallion.7 Lipomas on the surface of the equine testis are not uncommon.12 In rams testicular tumors are rare. No large series of testes in old boars, rams, or cats has been examined.9 In boars testicular tumors are very unusual. A malig- nant tumor of an undescended testis in a boar was de- scribed.28 A teratoma was observed in a cryptorchid por- cine testis.4 A seven-year-old boar with a seminoma of a testis that was four times as large as the opposite testis was reported.8 When the boar was bred, about 250 ml. of semen was collected but no spermatozoa were present and on histologic section areas of necrosis were found in the tumor. In cats testicular tumors apparently are rare. Several Sertoli cell tumors in this species have been reported.13'27 In dogs testicular tumors are observed at any age but most commonly in dogs over five years old. There was a higher incidence of testicular tumors in dogs than in humans.9 An incidence of 16 percent of tumors in 580 unselected adult dogs was reported.5 The three principal testicular tumors in dogs are, seminomas, Sertoli cell tu- mors (tubular adenomas), and interstitial cell tumors.13 Their comparative incidence is noted in Table 25. Ter- atomas have not been recorded in canine testes.4 Most canine tumors are usually benign but up to 10 percent of the Sertoli cell tumors and a few seminomas may be malignant in character.5,17 Of 177 tumors in 85 dogs, 55 percent were multiple, 45 percent were bilateral and 35 percent of the dogs had two or more types of tumors.19 Five percent of all tumors developed in cryptorchid testes. There is a signficant correlation of Sertoli cell tumors and seminomas with cryptorchidism in dogs, (See Crypt- orchidism). The age of the affected dogs averaged 10 to 11 years but the range was 3 to 20 years. Dogs with affected cryptorchid testes were younger than dogs with affected scrotal testes. In another survey of 198 dogs with testicular tumors, the numbers of seminomas, Sertoli-cell tumors, intersti- tial cell tumors and combinations of several types of tu-INFERTILITY IN MALE ANIMALS 835 Table 25. Summary of Reports on the Comparative Incidence of Testicular Tumors in Dogs Tumors Innes9 Dow5 Scully & Coffin19 Mulligan15 Totals No. Percent Seminoma 32 45 55 14 146 35.3 Sertoli cell 15 36 33 13 95 23.5 Interstitial cell 14 56 88 12 170 41.1 mors were 47, 46, 67 and 38, respectively. Concom- mitant clinical changes with each type of tumor was reviewed.11 In a large cohort study the incidence of tes- ticular neoplasms in cryptorchid dogs over 6 years of age was 68.1/1000 dog-years at risk. The incidence of Ser- toli cell tumors and seminoma was twice as high in dogs with unilaterally retained inguinal testicles as in abdom- inal cryptorchids.18 Seminomas are noted in old dogs over 7 years of age and arise from the germinal epithelium of the seminif- erous tubules.13 These tumors originate in atrophic sem- iniferous epithelium and the tumor is intratubular before becoming diffuse.19 These tumors grow slowly for months but may develop rapidly at any time. They are rather soft in consistency and hemorrhage or necrosis may be pres- ent. On section they appear dull-white or gray in color. Affected dogs may exhibit lameness and pain by crouch- ing and hunching. Seminomas were frequently bilateral and occasionally metastasized to the regional lymph nodes.11,12,19'22 A seminoma in an abdominally located testis was removed. Nine months later a large metastatic tumor of the abdominal cavity was diagnosed.22 In some cases seminomas and interstitial cell tumors are present together in the testis. Sertoli cell tumors, or tubular adenomas are possibly the least common of the principal tumors of the canine testis. This tumor arises from the Sertoli or nurse cell of the seminiferous tubules and is usually seen in older dogs. The tumor is often characterized by marked feminization of the male by the estrogens secreted by the tumor cells.3 Recent studies indicated that the estrogenic substances produced by the tumor and causing feminization of the male were not the usual estrogens found in animals.21 The dog may attract other males. The penile sheath is swollen. There is a definite loss of hair, especially on the abdomen and lower parts of the body, and a loss of sexual desire. Mammary hypertrophy or gynecomastia, and enlargement of the nipples and in some cases de- velopment of mammary tumors may occur. Atrophy of the testicular tissues and penis develops. Pigmentation of the abdominal skin and scrotum and female distri- bution of body fat are exhibited. The prostate may undergo marked enlargement due to squamous metaplasia and cysts; or it may become markedly involuted due to atro- phy of the epithelial elements and collapse of the acini.19 Bone marow hypoplasia due to endogenous estrogen myelotoxicosis from Sertoli cell tumors were reported in eight dogs, five of which died due to hemorrhage with thrombocytopenia, anemia and infection and fever as- sociated with granulocytopenia.20 These tumors are rather large in size, firm, nodular, and fibrous on palpation. Rarely a large hydrocele may be associated with Sertoli cell tumors, especially those that metastasize. On cross section Sertoli-cell tumors are pale-yellow or grey in color and may contain necrotic, cystic, or hemorrhagic foci. If no metastases have occurred recovery from the above dramatic symptoms takes place promptly after the af- fected testis is removed. Interstitial-cell tumor, adenoma, or Leydig-cell tu- mor is the most common tumor in old dogs. Although this tumor is present in many old dogs, it is of little clin- ical significance. Most of them are found only at au- topsy. They are often overlooked because of their small size; 1 mm. to 2 cm. is their usual size.12 Although 41.1 percent of testicular tumors cited in Table 25 were of the interstitial cell type, this percentage might well have been higher if all the small interstitial cell tumors had been found and recorded. Careful work in one study showed that 50 percent of testicular tumors were of the intersti- tial cell type.19 Nodular hyperplasia of the interstitial cells is seen commonly in older dogs with senile testicular atrophy. Nodular hyperplasia is probably a preneoplastic change but the division between nodular hyperplasia and interstitial cell tumor is arbitrary.12 These tumors prob- ably produce androgens because the prostate in affected dogs is normal or hypertrophied. In uncommon instances these interstitial cell tumors may produce estrogenic compounds resulting in male feminizing syndrome with alopecia, atrophy of the prepuce and gynecomastia.14 The tumors consist of single or multiple well-circumscribed nodules, brownish-orange in color and soft in consist- ency. Large tumors may occasionally be palpated in the testes of old dogs. They are similar in appearance to a corpus luteum and are likely to be bilateral and often contain hemorrhagic and necrotic foci. This condition probably is nodular hyperplasia of the interstitial cells and possibly these nodules should not be called true tu- mors.9 Although two cases in which this tumor metas- tasized have been described, metastasis is rare.9 Melanomas and mast cell tumors are not uncommon in the scrotal skin of the dog. The latter are usually ma- lignant.2 A scrotal hemangioma in a dog resulted in fatal hemorrhage.25 Canine tumors should be carefully differ-836 VETERINARY OBSTETRICS entiated from orchitis or epididymitis, traumatic swell- ings or hydrocele. The latter condition may be either congenital or secondary to orchitis. Canine perianal gland tumors are probably androgen-dependent tumors that can be arrested by castration.16 About 85 percent occur in older male dogs with a definite breed incidence in Cocker Spaniels. Genetic hereditary influence on acquired testicular degeneration have been reported in identical twin bulls.1 Genetic constitution appeared to influence the onset of generalized arthritis, fat necrosis, traumatic gastritis, and associated testicular degeneration in identical twin bulls. The increased predisposition and earlier occurrence of testicular degeneration in bulls with some testicular hy- poplasia was noted.12 Certain bulls may be more resis- tant to testicular degeneration than other bulls when af- fected by similar etiologic agents. Thus the genetic constitution of each male and his seminiferous epithe- lium and their resistance or ability to withstand adverse influences must be considered in the etiology and signs of testicular degeneration. The signs of testicular degeneration are similar in all species of animals despite the etiologic factor(s) in- volved. The signs vary in degree from mild to severe depending upon the cause and duration of the degener- ation. The fertility of the male may range from only slightly reduced conception rates, to moderate to severe infertil- ity, to complete sterility. The age of the male with testicular degeneration may vary from young to old with most cases in the older an- imals. The size of the testes is usually reduced from normal to about one-half to two-thirds normal size depending on the duration and degree of degeneration and atrophy of the seminiferous tubular epithelium. Since 77.1, 72.2 and 49.9 percent of the testicular volume is comprised of seminiferous tubules in 2.5-year-old, adult, and one and one-half-year-old bulls1 the close association of the de- gree of testicular degeneration and testicular size is ap- parent. In acute orchitis, other inflammatory conditions, obstruction of the efferent ducts, or testicular tumors, an increase in testicular size is often noted. The consistency of the testes is soft and flabby in acute, moderate to severe testicular degeneration. This is understandable since about 70 percent of the volume of the testis is composed of seminiferous tubules and their contents. In mild testicular degeneration consistency dif- fers only slightly from an elastic, tonic, slightly tense, fluctuating normal consistency. In these cases comparing the testicular consistency of the bull in question with several normal bulls of the same age may be helpful. The use of a tonometer has proven of value in the ob- jective measurement of testicular consistency.45 In 150 bulls in an AI stud, soft, medium and firm consistencies of the testes were found in 14, 30 and 56 percent, re- spectively. Bulls with soft testes tended to produce fewer sperm cells. The tonometer test correlated closely with other tests of semen quality. Acute orchitis is characterized by a tense swelling and enlargement of the testis accompanied by pain and heat. This should be differentiated from hydrocele or hema- tocele. Chronic degeneration and atrophy of the testes especially in older males whether following severe acute or chronic diseases is characterized by fibrosis of the testes often with calcification. The latter is impossible to pal- pate but about 25 percent of 158 bovine testes from abat- toir material revealed calcification on radiographic ex- amination.2 Fibrotic testes are hard, firm and often lack tonicity or elasticity. Ultrasonics can be of value in the detection of connective tissue in fibrosis of the testes.4 Testes containing tumors may be enlarged and have an irregular shape and consistency on palpation. The libido or sex drive is usually not related or as- sociated with testicular degeneration except in acute or- chitis or other painful testicular diseases or in testicular atrophy associated with severe debility or inanition due to a variety of causes. As indicated previously the Ley- dig-cells are much more resistant to stress factors than the cells of the germinal epithelium. The semen examination is very helpful in diagnosing testicular degeneration. Semen may be collected by the artificial vagina, by electroejaculation or other methods as will be described later. The former method is pre- ferred. Since it requires about 50 to 60 days or more for sperm cells to develop from spermatogonia until they are ejaculated, it may be desirable in diagnosing testicular degeneration to take several samples at weekly or greater intervals. The semen production and qualtiy in young immature bulls continues to improve in motility, con- centration and morphology for months after puberty is reached. So if an initial semen sample is poor, subse- quent samples are indicated. The first semen samples taken after a long period of sexual rest may also be misleading as these are often of poor quality with many dead or aging spermatozoa with acrosomal degeneration. In males in which testicular degeneration is severe, semen quality is usually poor. Sperm cell concentration may be reduced to one-third to one-half of normal values or show severe oligosper- mia or azoospermia. Watery, translucent semen is com- mon in severely affected bulls and rams. Sperm cell motility is reduced one-third to one-half or more due to an increase in abnormal cells, dead cells,INFERTILITY IN MALE ANIMALS 837 (necrospermia), or poorly viable defective cells. The du- ration of motility after ejaculation is shortened. Sperm cell morphology after staining reveals an in- crease in dead spermatozoa and abnormal heads, tails, and middle pieces. The degree of change in the mor- phology of cells may vary from normal semen which usually contains from 5 to 15 percent abnormal cells, to a 15 to 20 percent increase in abnormal cells in mild cases of testicular degeneration, to a 20 to 30 percent increase in moderate testicular degeneration, and to a 35 to 60 percent or greater increase in severe testicular de- generation. The occurrence of large numbers of sper- matozoa with primary abnormalities that arise during spermatocytogenesis or spermatogenesis and early sper- miogenesis are more indicative of a severe testicular de- generation than the presence of secondary abnormalities that occur later in spermiogenesis or during passage and storage of spermatozoa in the epididymis.17 8 (See Se- men Examination.) The appearance of primitive cells such as giant cells and spermatocytes with restitution or pyk- notic nuclei together with a marked reduction in sperm cell concentration and motility are signs of severe de- generation of the testes. Other tests for viability and longevity may be em- ployed but are more difficult to perform and do not add greatly to the information obtained by the previous tests. The volume of the ejaculate is not related to the degree of testicular degeneration since most the ejaculate comes from the secretions of the accessory glands. Testicular biopsies may be of value in certain species such as the dog and stallion, but are impractical for technical rea- sons in the bull.8 Furthermore the above signs and ad- ditional tests of sequential semen samples will accurately reveal the relative degree of progression and regression of testicular degeneration. Prognosis—The prognosis in testicular degeneration is variable depending upon the causative factors, the du- ration and degree of the degeneration, and the age and value of the male. Although testicular degeneration can occur rapidly within a few hours, days or a week or more, recovery is very slow usually requiring 3 to 6 months or more in moderate to severe cases. The prognosis in slight or mild cases of testicular degeneration in young or mid- dle-aged bulls due to transient and correctable causes is fair to good. Controlled breeding during the recovery pe- riod may result in fair to good fertility in some males. The prognosis is guarded to fair in young males with only moderate evidence of testicular degeneration; and in older males suddenly developing infertility due to a transient disease where advanced testicular changes do not occur, such as in; mild cases of trauma to the testes, scrotal inflammations, toxemia or poisonings, mild ex- posure to irradiation, chronic but curable systemic dis- eases causing debility, and inanition due to semistarva- tion. The prognosis is poor in progressive senile testicular degeneration, in acute severe orchitis especially if it is bilateral and associated with abscessation, in advanced fibrosis and atrophy of the testes, in degeneration as- sociated with hypoplasia in young to middle-aged males, and in older males with bilateral tumors of the testes. Once the testes have been severely damaged regen- eration can never be complete. If severe secondary in- fections or lesions occur in the epididymides, accessory glands, or vasa deferentia the prognosis is also guarded to poor. The treatment of testicular degeneration requires the correction or the alleviation of the causative factor(s). Sexual rest is usually advised, since in most cases fer- tility is reduced to a point where the use of the male is questionable. Males with mild degrees of degeneration not severely influencing fertility should be used spar- ingly so as to maintain as large a number as possible of normal, motile spermatozoa in each ejaculate. A bal- anced ration high in vitamin A and a good quality and variety of protein are indicated. Good-quality roughage or pasture is highly desirable. Some exercise especially on pasture is usually recommended for the larger farm animals, although it has been shown that forced exercise has no effcet on the fertility of the bull.9 If excessive heat and humidity is the cause of the temporary infer- tility in bulls, air conditioning or cooling is indicated. Hormones are of no proven value. Testosterone, var- ious FSH products, and thyroxine have been tried but none have any demonstrated effect in the therapy of tes- ticular degeneration or hypoplasia. Plasma concentra- tions of these hormones are usually normal or elevated in affected males. Furthermore the gonadotropic hor- mones to be of any value must be given over a period of a month or more and should be prepared from bio- logic sources from the same species to prevent antihor- mones from developing. Many studies have reported on the uniformly poor results from the hormonal or dietetic therapy of testicular degeneration in men.61012 In acute orchitis, sexual rest is imperative. Physical rest is usually advisable and can be provided by close confinement of the male. In the early acute stages heavy parenteral broad-range antibiotic therapy is indicated. Glucocorticoid or non-steroidal anti-inflammatory agents along with the antibiotics might be helpful in reducing the inflammatory reaction. Ice packs should be applied to the testes by a suitable sling or bag fixed between the legs and tied over the back. This therapy should be con- tinued until the acute, severe symtpoms have subsided.838 VETERINARY OBSTETRICS When the orchitis is unilateral and severe or incurable, removal of the affected testis may hasten recovery or save the breeding life of a valuable male. The testis should be examined carefully and cultured after removal to de- tect the responsible agent so that suitable precautions can then be taken for the future use of the sire if his fertility returns. The Brucella-infected bull or boar should not be used either artificially or naturally in a Brucella-free herd. Heat or a mild counter-irritant ointment to the inflamed testis and swollen scrotum should never be used. The preferred treatment for testicular tumors is prompt cas- tration or removal of the affected testis. If metastases have occurred, symptoms caused by the secondary tu- mors will usually develop within a few months. Crypt- orchid testes should be removed while the affected males are still young to prevent the occurrence of tumors or abdominal complications common in these structures in later life. Acquired Testicular Pathology (Degeneration, Orchitis, Fibrosis) Thermal Effects and Vascular Lesions 1. Clark, T. L. (1969) Equine Testicular Biopsy (abstr.) JAVMA, 154, 11, 1367. 2. Crabo, B. and Hurtgen, J. (1977) Evaluation of Boar Fertility and Artificial Insemination Methods, Proc. of Conf. for Soc. for Theriog., Minneapolis. 3. Donaldson, L. E. (1963) Some Observations on the Semen and Testicular Characteristics of Beef Bulls in Northern Queensland Jour, of Agric. Sci., 20, 2, 203. 4. Dutt, R. H. and Hamm, P. T. (1957) Effect of Exposure to High Environmental Temperature and Shearing on Semen Production of Rams in Winter, J. An. Sci., 16, 2, 328. 5. Dubin, L. and Hotchkiss, R. S. (1969) Testis Biopsy in Subfer- tile Men and Varicocele, Fert. and Steril., 20, 1, 50. 6. Faulkner, L. C., Hopwood, M. L., Masken, J. F., Kingman, H. E. and Stoddard, H. L. (1967) Scrotal Frostbite in Bulls, JAVMA, 152, 5, 602. 7. Fincher, M. G., Olafson, P. and Ferguson, J. (1942) Sterility in Bulls, Cor. Vet., 32, 4, 407. 8a. Gunn, R. M. C., Sanders, R. N. and Granger, W. (1942) Stud- ies in Fertility in Sheep, Commonwealth of Austral. Council for Sci. and Prod. Res. Bull. 148. 8b. Gerona, G. R. and Sikes, J. O. (1970) Effects of Elevated Scro- tum Temperature on Spermatogenesis and Semen Characteris- tics, J. Dairy Sci., 53, 5, 659 (Abstr.). 9. Haq, I. (1949) Causes of Sterility in Bulls in Southern England, Brit. Vet. Jour., 105, 4, 5, 6, 71, 144, 143, 200. 10. Holst, S. J. (1949) Sterility in Boars, Nord. Vet. Med., 1, 87. 11. Hopkins, S. M., Larsen, R. E. and Drost, M. (1981) Unilateral Castration as Treatment for Hydrocele in a Bull, JAVMA, 178, 8, 837. 12. Hulet, C. V., El-Sheikh, A. S., Pope, A. L. and Casida, L. E. (1956) The Effects of Shearing and the Level of Feeding on Fertility in Rams, J. An. Sci., 15, 3, 616. 13. Hurtgen, J. P. (1981) Influence of Housing and Management Factors on Reproductive Efficiency of Swine, JAVMA, 179, 1, 74, (A Review). 14. James, R. W., Heywood, R. and Fowler, D. J. (1979) Serial Percutaneous Testicular Biopsy in the Beagle Dog, J. Sm. Anim. Pract., 20, 219. 15a. Jensen, R., Flint, J. C., Brown, W. W. and Collier, J. R. (1962) Arteriosclerosis and Phlebosclerosis in Testes of Sheep, Amer. J. Vet. Res., 23, 94, 480. 15b. Jensen, R. and Swift, B. L. (1982) Diseases of Sheep, 2nd Ed., Lea and Febiger, Philadelphia. 16. Johnston, J. E., Naelopaa, H. and Frye, J. B., Jr. (1963) Phys- iologic Responses of Holstein, Brown Swiss and Red Sindhi Crossbred Bulls Exposed to High Temperatures and Humidities, J. An. Sci., 22, 2, 432. 17. Knudsen, O. (1958) Studies on Spermatocytogenesis in the Bull, Intemat. Jour, of Fert., 3, 3 and 4, 389. 18. Knudsen, O. (1960) Testicular Biopsy in the Bull, Intemat. Jour, of Fert., 5, 2, 203. 19a. Lagerlof, N. (1934) Morpholigische Untersuchungen uber Ver- anderungen im Spermbild und in den Hoden bie Bullen mit Ves- miderter Oder aufgehabener Fertilitat, Acta, Pathol, et Micro- biol. Scand. Suppl. XIX. 19b. Larsen, R. E. (1980) Infertility in the Male Dog, in Current Therapy in Theriogenology, Edit, by D. A. Morrow, W. B. Saunders Co., Philadelphia, 646. 20. McEntee, K. (1970) Pathology of Domestic Animals, Ed. 2, Vol. I. edited by Jubb, K. V. and Kennedy, P. C. Academic Press, N.Y.C. and London. 21. MacLeod, J. (1969) Further Observations on the Role of Var- icocele in Human Male Fertility, Fert. and Steril., 20, 4, 545. 22. Moule, G. R. and Waites, G. M. H. (1963) Seminal Degen- eration in the Ram and Its Relation to the Temperature of the Scrotum, J. Reprod. and Fertil., 5, 433. 23. Ott, R. S., Heath, E. H. and Bane, A. (1982) Abnormal Sper- matozoa Testicular Degeneration, and Varicocele in a Ram, Amer. J. Vet. Res., 42, 2, 241. 24. Ott, R. S. and Memon, M. A. (1980) Sheep and Goat Manual, Vol. X, Soc. for Theriog., Hastings, Nebr., 68901. 25. Patnaik, A. K. and Lui, S-K. (1975) Leiomyoma of the Tunica Vaginalis in a Dog, Cor. Vet., 65, 228. 26a. Rhodes, A. P. (1976) The Effect of Extensive Chorioptic Mange of the Scrotum on Reproductive Function of the Ram, Austral, Vet. J., 52, 250. 26b. Roberts, S. J. (1971) Veterinary Obstetrics and Genital Dis- eases, 2nd Ed., Edwards Bros, Inc., Woodstock, Vt. 27. Ross, A. D. and Entwistle, K. W. (1979) The Effect of Scrotal Insulation on Spermatozoal Morphology and the Rates of Sper- matogenesis and Epididymal Passage of Spermatozoa in the Bull, Theriog., 11, 2, 111. 28. Setchell, B. P. (1978) The Mammalian Testis, Cornell Univ. Press, Ithaca, N.Y., 14850, 359-432. 29. Stone, B. A. (1981/82) Heat Induced Infertility in Boars, Anim. Repro. Sci., 4, 283. (An Ind. Div., Dept. Agric., Adelaide, Australia.) 30. VanderSluis, L. (1953) Experiences with the Examination into Herd Infertility, Proc. 1st World Congr. on Fert. and Steril., II, XXV, 704. 31. Wettemann, R. P., Wells, M. E. and Johnson, R. K. (1979) Reproductive Characteristics of Boars During and After Expo- sure to Increased Ambient Temperatures, J. An. Sci., 49, 6, 150.INFERTILITY IN MALE ANIMALS 839 Irradiation, Hormone, Age and Traumatic Effects 1. Bloom, F. (1953) Endocrine Glands, Canine Medicine, Amer. Vet. Publ. Inc. Evanston, 111. 2. Casarett, G. W. and Hursh, J. B. (1956) Effects of Daily Low Doses of X-rays on Spermatogenesis in Dogs, Radiation Res., 5, 473. 3. Chamy, C. W. (1959) The Use of Androgens for Human Sper- matogenesis, Fert. and Steril., 10, 6, 557. 4. Collins, W. E., Inskeep, E. K., Dreher, W. H., Tyler, W. J. and Casida, L. E. (1962) Effect of Age on Fertility of Bulls in Artificial Insemination, J. Dairy Sci., 45, 8, 1015. 5. Dawson, J. R. (1938) The Breeding Efficiency of Proven Aged Sires, J. Dairy Sci., 21, 725. 6. Dunn, H. O., Roberts, S. J., McEntee, K. and Wagner, W. C. (1965) Prevention of Traumatic Gastritis in Bulls by the Use of Magnets, Cor. Vet., 55, 204. 7. Hahn, J., Foote, R. H. and Seidel, G. E., Jr. (1969) Quality and Freezability of Semen from Growing and Aged Dairy Bulls, J. of Dairy Sci., 52, 11, 1843. 8a. Jackowski, L., Walkowdki, L. and Korycki, St. (1961) Studies on the Quality of Semen of Imported Bulls During the Accli- matization Period, Proc. 4th Intemat. Congr. on Reprod., Hague, Vol. IV, 801. 8b. Larsen, R. E. (1980) Infertility in the Male Dog, in Current Ther- apy in Theriogenology, edit, by D. A. Morrow, W. B. Saunders Co., Philadephia, 646. 9. MacLeod, J. and McGee, W. R. (1950) The Semen of the Thor- oughbred Cor. Vet., 40, 3, 233. 10. McEntee, K. (1970) Pathology of Domestic Animals, 2nd Ed., Vol. 1, edit, by Jubb, K. V. and Kennedy, P. C., Academic Press, N.Y.C. and London. 11. Meineke, C. F. and McDonald, L. E. (1961) The Effects of Ex- ogenous Testosterone on Spermiogenesis of Bulls, Amer. J. Vet. Res., 22, 87, 209. 12. Murphree, R. L. and Parish, N. R. (1956) Effects of Whole Body Radiation on Semen Characteristics in Bulls, J. An. Sci., 15, 4, 1300. 13. Pace, H. B., Murphree, R. L. and Hupp, E. W. (1959) Effects of Total Body Irradiation on Semen Production of Boars, J. An. Sci., 18, 4, 1554. 14. Welch, P. R. and Murphree, R. L. (1965) Sperm Production in Chronically Irradiated Bulls, J. An. Sci., 24, 4, 1045. 15. Willett, E. L. (1957) Effect of Transportation upon Fertility of Bulls, J. Dairy Sci., 40, 10, 1367. Infectious Causes of Orchitis and Testicular Degeneration 1. Bouters, R. (1963) Experimentale Onderzoekingen over de De- generatieve Invloed van een Entero-virus op het Spermaephiteel van Steeren, Thesis, Veterinary College, Gent, Belgium. 2. Bouters, R. (1964) A Virus with Enterogenic Properties Causing Degeneration of the Germinal Epithelium in Bulls, Nature, 201, 217. 3. Bruner, D. W. and Gillespie, J. H. (1973) Hagans’ Infectious Diseases of Domestic Animals, 6th Ed. Cornell Univ., Press, Ith- aca, N.Y. 4. Bruner, D. W. and Gillespie, J. H. (1973) Hagans’ Infectious Diseases of Domestic Animals, 6th Ed. Cornell Univ., Press, Ith- aca, N.Y. 5. Carmichael, L. E. (1968) Personal Communication—Cornell Veterinary Virus Research Institute, Ithaca, N.Y. 6. Carmichael, L. E. and Bruner, D. W. (1968) Characteristics of a Newly-Recognized Species of Brucella Responsible for Infec- tious Canine Abortion, Cor. Vet., 58, 4, 579. 7a. Carmichael, L. E. and Kenney, R. M. (1968) Canine Abortion caused by Brucella canis, JAVMA, 152, 6, Part 1, 605. 7b. Cheema, A. H. and Toofanian, F. (1979) Besnoitiosis in Wild and Domestic Goats in Iran, Cor. Vet., 69, 159. 8. Crenshaw, G. L. and McGowan, B. (1966) Ram Epididymitis Vaccination, Proc. 70th Ann. Meeting U.S.L.S.A., 476. 9. DeBoom, H. P. A. (1962) Personal Communication. 10. Florent, A. (1963) Viral Infertility, in Infertility in Livestock, FAO, Rome, 36. 11. George, L. W., Duncan, J. R. and Carmichael, L. E. (1979) Semen Examination in Dogs with Canine Brucellosis, Amer. J. Vet. Res., 40, 1589. 12. Gledhill, B. L. (1968) Viral Infertility in Cattle, Cor. Vet., 58, 466. 13. Gribble, D. H. (1969) Equine Ehrlichiosis, JAVMA, 155, 2, 462. 14. Kimball, A., Twiehaus, M. J. and Frank, E. R. (1954) Acti- nomyces Bovis Isolated from Six Cases of Bovine Orchitis, Amer. J. Vet. Res., 15, 57, 551. 15. Kirk, R. W. (1980) Current Veterinary Therapy, 7th Ed., W. B. Saunders, Co., Philadelphia, London and Toronto. 16. Kumi-Diaka, J., Wilson, S., Sanusi, A., Mjohu, C. E. and Osori, D. I. K. (1981) Bovine Besnoitiosis and Its Effect on the Male Reproductive System, Theriog., 16, 5, 523. 17. Lambert, G., Deyoe, B. L. and Painter, G. M. (1964) Postvac- cinal Persistence of Brucella Abortus Strain 19 in Two Bulls, JAVMA, 145, 909. 18. Larsen, R. E., Shope, R. E., Jr., Leman, A. D. and Kurtz, H. J. (1980) Semen Changes in Boars After Experimental Infection with Pseudorabies Virus, Amer. J. Vet. Res., 41, 5, 733. 19. McEntee, K. (1970) Pathology of Domestic Animals, 2nd Ed., Vol. 1 edited by Jubb, K. V. and Kennedy, P. C. Academic Press, N.Y.C. and London. 20. Mcllwain, O. D. and Bolin, R. M. (1967) A Mycoplasma As- sociated with Ovine Orchitis, Amer. Jour. Vet. Res., 28, 124, 885. 21. Mensik, J., Bohac, J. and Setka, R. (1961) The Etiology of In- fectious Orchitis in Bulls in Czechoslovakia, Vet. Bull. 31, 323. 22. Moore, J. A. and Kakuk, T. J. (1969) Male Dogs Naturally In- fected with Brucella canis, JAVMA, 155, 8, 1352. 23. Norton, W. L. and Storz, J. (1967) Polyarthritis of Sheep, (1) Arthritis and Rheumatism, 10, 1, (Abstr. Vet. Med. 63, 2, 1968, 170). 24. Pols, J. W. (1960) Studies on Bovine Besnoitiosis with Special Reference to the Etiology, Onderstepoort, J. Vet. Res., 28, 265. 25. Roberts, S. J. (1971) Veterinary Obstetrics and Genital Diseases, 2nd Ed., Woodstock, Vt. 26. Sheffy, B., Roberts, S. J. and Parsonson, I. (1970) Unpublished data. 27. Stroz, J., Carroll, E. J., Ball, L. and Faulkner, L. C. (1968) Isolation of a Psittacosis Agent (Chlamydia) from Semen and Epididymis of Bulls with Seminal Vesiculitis Syndrome, Amer. J. Vet. Res., 29, 3, 549. 28. Switzer, W. P. (1964) Diseases of Swine, 2nd Ed. Edit, by Dunne, H. W., Iowa Sate Univ. Press, 502. 29. Vandeplassche, M. (1969) Personal Communication. 30. Watson, W. A. (1964) Infertility in the Ram Associated with Tick- borne Fever Infection, Vet. Rec., 76, 41, 1131.840 VETERINARY OBSTETRICS Nutritional, Toxic, and Autoimmunizing Causes 1. Bishop, R. L. (1950) The Effect of Fuadin of the Semen of Dogs, Vet. Med., 45, 9, 384. 2. Busey, W. M. (1965) Immunologically Induced Testicular De- generation in Rams, Dissert. Abstr. 66, 5379. 3. Busey, W. M. (1965) Immunologically Induced Testicular De- generation in Rams, Dissert. Abstr. 66, 5379. 4. Everett, R. W. (1982) Effect of Dursban 44 on Semen Output of Holstein Bulls, J. Dairy Sci., 65, 1781. 5. Faulkner, L. C. (1970) Personal Communication. 6. Faulkner, L. C., Carroll, E. J. and Benjamin, M. (1964) Effect of Coumaphos on Bulls, JAVMA, 145, 5, 456. 7. Gunn, R. M. C., Sanders, R. N. and Granger, W. (1942) Studies in Fertility in Sheep, Commonwealth of Austral. Council for Sci. and Ind. Res. Bull. 148. 8a. Jeffcoate, I. A., Lucas, J. M. S. and Creighton, D. B. (1982) Effects of Active Immunization of Ram Lambs and Bull Calves against Synthetic Luteinizing Hormone Releasing Hormone, (LHRH), Theriog., 18, 1, 65. 8b. Johnston, S. D., Larsen, R. E. and Olson, P. S. (1982) Canine Theriogenology, Jour. Soc. for Theriog., Vol XI, 88. 9. Losos, G. J. (1967) Experimental Induction of Testicular Lesions in Bulls by Auto-immunization, Ph.D. Thesis, Cornell Univ., Ithaca, N.Y. 10. Losos, G. J., Winter, A. J. and McEntee, K. (1968) Induction of Testicular Degeneration in Bulls by Isoimmunization, Amer. J. Vet. Res., 29, 12, 2295. 11. McEntee, K. (1970) Pathology of Domestic Animals, 2nd Ed., Vol. I, edited by Jubb, K. V. and Kennedy, P. C., Academic Press Inc., N.Y.C. and London. 12. McEntee, K. and Olafson, P. (1953) Reproductive Tract Pathol- ogy in Hyperkeratosis of Cattle and Sheep, Fert. and Steril., 4, 2, 128. 13. Menge, A. C. (1965) Effects of Immunizing Bulls with Semen and Testis, J. An. Sci., 24, 3, 926. 14. Setchell, B. P. (1978) The Mammalian Testis, Cornell Univ. Press, Ithaca, N.Y., 14850, 359-432. 15. Sikes, J. D. (1959) Effects of Potassium Nitrate on Bovine Se- men Production and Various Spermatozoan Characteristics, J. Dairy Sci., 42, 5, 930. Testicular Neoplasma, Genetic and Miscellaneous Causes 1. Bane, A. (1954) Sexual Functions of Bulls in Relation to He- redity, Rearing Intensity and Somatic Conditions, Acta. Agric. Scand., 4, 2, 97. 2. Bloom, F. (1954) Pathology of the Dog and Cat, Amer. Vet. Public. Inc. Evanston, 111. 3. Brodey, R. S. and Martin, J. E. (1958) Sertoli Cell Neoplasms in the Dog. The Clinicopathological and Endocrinological Find- ings in Thirty Seven Dogs, JAVMA, 133, 249. 4a. Cotchin, E. (1956) Neoplasms of Domestic Animals; A Review, Commonwealth Bureau of An. Health, #4, Bucks, England. 4b. Cotchin, E. (1977) A General Surgery of Tumours in the Horse, (A Review), Eq. Vet. J., 9, 1, 16. 5. Dow, C. (1962) Testicular Tumors in the Dog, J. Comp. Path, and Therap., 72, 3, 247. 6. Dunn, H. O. and McEntee, K. (1964) Semen Quality and Fer- tility in Dairy Bulls with Testicular Tumors, Intemat. J. of Fert., 9. 4, 613. 7. Feldman, W. H. (1932) Neoplasms of Domestic Animals, Phil- adelphia, Pa. 8. Holst, S. J. (1949) Sterility in Boars, Nord. Vet. Med., 1, 2, 87. 9. Innes, J. R. M. (1942) Neoplastic Diseases of the Testis in An- imals. J. of Path, and Bact., 54, 485. 10. Knudson, O. and Schantz, B. (1963) Seminoma in the Stallion, A Clinical Cytological and Pathologicoanatomical Investigation, Cor. Vet., 53, 3, 395. 11. Lipowitz, A. J., Schwartz, A., Wilson, G. P. and Ebert, J. W. (1973) Testicular Neoplasms and Concomitant Clinical Changes in the Dog, JAVMA, 163, 12, 1364. 12. McEntee, K. (1970) Pathology of Domestic Animals, 2nd Ed., Vol. I edited by Jubb, K. V. and Kennedy, P. C., Academic Press, Inc., N.Y.C. and London. 13. Moulton, J. E. (1961) Tumors of Domestic Animals, Univ. of California Press, Berkeley, Cal. 14. Muller, G. H. and Kirk, R. W. (1969) Small Animal Dermatol- ogy, W. B. Saunders Co., Philadelphia. 15. Mulligan, R. M. (1949) Neoplasms in the Dog, Williams & Wil- kins Co., Baltimore, Md. 16. Nielsen, S. W. and Aftosmis, J. (1964) Canine Perianal Gland Tumors, JAVMA, 144, 2, 127. 17. Reif, J. S. and Brodey, R. S. (1969) The Relationship Between Cryptorchidism and Canine Testicular Neoplasia, JAVMA, 155, 12, 2005. 18. Reif, J. S., Maguire, T. G., Kenney, R. M. and Brodey, R. S. (1979) A Cohort Study of Canine Testicular Neoplasms and Con- comitant Clinical Changes in the Dog, JAVMA, 163, 12, 1364. 19. Scully, R. E. and Coffin, D. L. (1952) Canine Testicular Tu- mors, Cancer, 5, 3, 592. 20. Sherding, R. G., Wilson, G. P., Ill and Kociba, G. J. (1981) Bone Marrow Hypoplasia in Eight Dogs with Sertoli-Cell Tumor, JAVMA, 178, 5, 497. 21. Siegal, E. T., Forchielli, E., Dorfman, R. I., Brodey, R. S. and Prier, J. E. (1967) An Estrogen Study in the Feminized Dog with Testicular Neoplasia, Endocrin., 80, 272. 22. Simon, J. and Rubin, S. B. (1979) Metastatic Seminoma in a Dog, Vet. Med./Sm. An. Clin., 74, 7, 941. 23. Smith, H. A. (1954) Interstitial Cell Tumor of an Equine Testis, JAVMA, 124, 926, 356. 24. Stick, J. A. (1980) Teratoma and Cyst Formation of the Equine Cryptorchid Testicle, JAVMA, 176, 3, 211. 25. Thornburg, L. P. and Breitschwerdt, E. B. (1976) Canine He- mangioma of the Scrotum with Total Bleeding, JAAHA, 12, 797. 26. Vaillancourt, D., Fretz, P. and Orr, J. P. (1979) Seminoma in the Horse: Report of Two Cases., J. Eq. Med. Surg., 3, 213. 27. Whitehead, J. E. (1967) Neoplasia in the Cat, Vet. Med., 62, 1, 44. 28. Williams, W. L. (1943) Diseases of the Genital Organs of Do- mestic Animals, 3rd Ed., Ithaca, N.Y. Signs, Diagnosis, Prognosis and Treatment of Testicular Degeneration 1. Amann, R. P. (1960) Quantitative Testicular Histology and The- oretical Sperm Production of Holstein Bulls, J. Dairy Sci., 43, 6, 883. 2. Barker, C. A. V. (1956) Some Observations on Testicular Cal- cification in Bulls, Canad. J. of Comp. Med. and Vet. Sci., 20, 2. 37.INFERTILITY IN MALE ANIMALS 841 3. Blom, E. (1950) On Methods of Evaluating Bull Semen, Thesis, C. Mortensen, Copenhagen, Denmark. 4. Foote, R. H. and Hahn, G. (1968) Unpublished data, Ithaca, N.Y. 5. Hahn, J., Foote, R. H. and Cranch, E. T. (1969) Tonometer for Measuring Testicular Consistency of Bulls to Predict Semen Quality, J. An. Sci., 29, 3, 483. 6. Howard, R. P., Simmons, F. A. and Sniffen, R. (1951) Differ- ential Diagnosis in the Male Sterility, Fert. and Steril., 2, 2, 95. 7. Lagerlof, N. (1938) Infertility In Male Domestic Animals, Proc. 3rd Intemat. Vet. Congr. Vol. I, 214. 8. Roberts, S. J. (1971) Veterinary Obstetrics and Genital Diseases, 2nd Ed., Edwards Bros. Inc., Woodstock, Vt. 9. Snyder, J. W. and Ralston, N. P. (1955) Effect of Forced Ex- ercise on Bull Fertility, J. Dairy Sci., 38, 2, 125. 10. Swyer, A. I. M. (1956) Therapeutic Agents in Defective Sper- matogenesis, Intemat. J. of Fertil., 4, 360. 11. Weisman, A. I. (1950) End Results of the Treatment of Male Infertility, A Study of 600 Males, Fert. and Steril., 1, 3, 216. Pathological or Functional Disturbances of the Epi- didymis, Ductus Deferens and Accessory Reproduc- tive Glands in the Male Causing Failure of Fertiliz- ation or Conception. Pathology of the Epididymis—Disease of the epi- didymis includes: infection of the epididymal duct and epididymitis, anomalies causing sperm granulomas, tu- mors, and functional or hormonal disturbances. Epididymitis, or inflammation of the epididymis, is occasionally observed as an acquired lesion in all species of animals and is caused by or may be secondary to the same factors causing orchitis. Infectious causes of epi- didymitis most commonly involve the tail of the epididy- mis but may involve the body and head of the epididy- mis. These include: Brucella abortus in bulls, Brucella suis in boars, Brucella ovis and Actinobacillus seminis23 30 in rams, Brucella canis in dogs,12 Strep- tococcus zooepidemicus in the stallion,51 C. pyogenes and other miscellaneous organisms such as streptococci, staphylococci, Proteus, E. coli, C. pseudotuberculosis, Pseudomonas aeruginosa and Mycoplasma bovi- genitalium.43 Infections may be caused by organisms, such as mycoplasma or possibly ureaplasma invading the epididymis through the ductus deferens or by way of the blood or lymph vessels. (See seminovesiculitis.) Trau- matic injuries may also produce an epididymitis.45 Ca- nine distemper virus in sexually mature dogs causes an epididymitis.37 A specific bovine venereal epididymitis and vaginitis or “epivag” has been described in Chapter XIII. This venereal and probably viral disease, found only in East, South, and Central Africa, is usually characterized in the bull by a marked bilateral hardening and swelling of the tail of the epididymis and sterility. Pathological fibrotic changes also occur in the ductus deferens, testes, and vesicular glands.9,32 There is no cure for affected males but artificial insemination has been an effective control measure to prevent the spread of this venereal disease. Other diseases of the testis and epididymis of bulls in South Africa have been described.53 Besnoitiosis due to Besnoitia besnoiti produces elephantiasis of the scrotal skin and cysts in the scrotum, inguinal canal, testes, and epididymis. These cysts may persist and calcify, causing sterility. Chlamydia psittaci has been isolated from the epi- didymis of young bulls with epididymitis, orchitis and seminal vesiculitis, that is a possible agent producing the clinical seminal vesiculitis syndrome.48 Brucella ovis (brucellary epididymitis) is a common venereal disease of sheep causing ram epididymitis and infertility worldwide.23 25 27 In California in 1956 ex- amination of 1882 rams revealed a 27 percent incidence of infection. Of 175 ewe lambs bred to clinically normal rams, 75 percent lambed within a 30-day period while only 47 percent of 171 ewe lambs bred to clinically-in- fected rams lambed during the same period.42 In Idaho in 1970, 1890 rams were examined in 37 large com- mercial flocks. Twenty four percent of the rams were clinically affected and over 97 percent of the flocks were infected. The disease was more common in the black- face breeds and crosses.47 Ewes bred to infected rams had a greatly increased number of services per concep- tion and fewer lambs per ewe than ewes bred to non- infected control rams.40 The infective organism is spread mainly by venereal contact to susceptible rams breeding a ewe recently bred by an infected ram, or by rams penned together mount- ing each other and having rectal copulation, penile con- tact with a contaminated perineal region, or oral infec- tion from infective feed or water.1 23,28 Ewes play a minor role in the spread of the infection and are relatively re- sistant to the infection; but occasional abortions due to Brucella ovis are reported. Young rams raised from in- fected ewes are not infected. Rams are readily infected by the conjunctival, oral, rectal or preputial instillation of the organism. Rams may spread the organism for 3 to 4 years while ewes spread infection for a much shorter period of several days after an occasional abortion. Fol- lowing infection the antibody levels rise by the third to sixth week and persist for up to a year after the end of the bacteremic stage of the disease, which ends in about 60 days. The organisms localize in the epididymis, ve- sicular glands, ampullae, liver, and kidneys. The organ- isms cause perivascular lesions with edema and fibrosis in the epididymis resulting in obstruction of the lumen and stasis of the epididymal contents and finally extra- vasation of semen that, because of its high lipid and my- colic acid content, results in the formation of a spermatic842 VETERINARY OBSTETRICS granuloma resembling tubercular granulomas.2,3,34 (See Figure 189.) Over 90 percent of these lesions affect the tail of the epididymis but occasionally the body and head of the epididymis may be involved. If the lesions are unilateral, fertility is normal or only slightly impaired; if they are bilateral, sterility is usually present.1,23,50 In 29 naturally-infected rams the semen quality, including motility and concentration was inferior in 50 percent of the rams and normal in only 25 percent.40 It takes 1 to 4 months from the onset of infection to the development of the lesions in the tail of the epididymis. The tail, or occasionally other portions, of the epididymis enlarges 3 to 5 times normal size and becomes fibrotic or with an occasional abscess. Some infected rams fail to de- velop gross palpable lesions. Diagnosis is based on clinical palpation of the epididy- mis to detect induration, spermatic granulomas, ab- scesses and enlargements, especially involving the tail of the epididymis. In advanced cases testicular degen- eration, atrophy and later mineralization of the testis may occur. Some affected rams would be difficult to differ- entiate on clinical examination from those with epididy- mitis due to other causes such as C. pseudotuberculosis or Actinobacillus seminis. These latter infections are more sporadic, variable in location and resemble abscesses rather than granulomas. Enlargement of the head of the epididymis is more likely due to granulomas secondary to anomalies of the efferent ducts. The combination of clinical palpation of the testes, culturing the semen and the complement-fixation test on serum was most effec- tive in locating shedders of Brucella ovis. Screening tests were run at 1:10 dilutions.2 Other serologic tests have included the agar gel diffusion test and the ELISA test. Controlling ram epididymitis in a flock is highly im- portant to maintaining good fertility in the flock. Before the breeding season all rams that show clinical or sero- logic evidence of epididymitis should be eliminated. In valuable purebred rams semen examination and culture may be used.40 Various vaccination procedures have been used successfully to protect rams against Brucella ovis. In New Zealand they have used a combination of Br. ovis bacterin and strain 19 Brucella abortus vaccine.10,46 In the U.S. an alum-precipitated commercial Br. ovis bacterin has been developed and approved39,41 that is given subcutaneously in two doses 3 to 6 weeks apart and fol- lowed by a single injection repeated each year. (Cutter Laboratories and Colorado Serum Co.) This vaccine may occasionally cause a granuloma and some soreness and irritation at the site of the subcutaneous injection behind the elbow, but abscessation is rare. Vaccination causes a serum titer to develop that lasts several years after the combined vaccines were given.46 The combination of the vaccine with other control practices was highly effective in infected flocks of sheep. One study in which clinically affected rams were culled, together with a vaccination program starting with ram lambs 4 to 5 months of age, the incidence of culling dropped from 44 percent at the onset to 2 percent after three years of the trial and re- mained low for the next 7 years.39,41 To rapidly reduce or eliminate the Br. ovis infection in a flock, identify and isolate or cull all rams with clinical disease, sero- logically test and cull positive rams every 30 to 60 days until the incidence is below 1 percent. By testing and isolation practices a Br. ovis clean ram flock may be established. A more practical and less expensive pro- cedure is to follow a vaccination program.1,23 Actinobacillus seminis, actinobacillary epididymi- tis or epididymo-orchitis has recently been described as a venereal disease of rams that is similar in many re- spects to the foregoing epididymitis due to Br. ovis. It also is world-wide in distribution; is transmitted in a sim- ilar manner with a similar incubation period and the complement fixation test on serum, clinical palpation of lesions, and culture of semen are used in the diagnosis of the disease. It differs somewhat from the brucellary epididymitis by the frequent development of clinical, unilateral or bilateral orchitis and periorchitis with mod- erate to severe systemic signs including elevation of body temperature to 40 to 42° C and even death in the early stages of the disease. Subclinical infections are not un- common. After the acute stage of the disease chronic adhesions around the testes may develop, degeneration, atrophy and even mineralization of the testis may occur. The epididymis becomes enlarged and indurated due to sperm granulomas or abscesses that may involve the head, body or tail or the entire epididymis. Rarely abscesses may rupture through the scrotum and produce a dis- charging fistula. The diagnosis, prevention and treat- ment of actinobacillary epididymitis is similar to bru- cellary epididymitis except no vaccine is presently available for the former disease.23,49,50 Canine brucellosis due to Brucella canis is apparently widespread in the U.S. among dogs, especially Bea- gles,12 causing abortion in bitches and swelling of the scrotum, firm enlargement of the epididymis, especially in the tail, and degeneration and atrophy of the testis with sterility in males. The disease is spread by direct contact with aborted fetuses, placental tissues and the infective vaginal discharges of bitches for several weeks after abortion. Venereal transmission to females by the semen from chronically-infected males is a common mode of spread. Following exposure a bacteremia develops within one to three weeks with a generalized lymphadenitis. Antibodies develop that can be detected by the agglutin-INFERTILITY IN MALE ANIMALS 843 ation test; 1:100 is considered positive. These antibodies may last indefinitely or as long as a bacteremia persists. The organisms can often be recovered from the lymph glands, spleen, liver, prostate, testes and epididymides. Clinical lesions need not be present. The prognosis is poor in clinically-affected male dogs. Any possible ef- fective antibiotic therapeutic regimen must be heroic and sustained. If the genital organs are seriously damaged or if the lesions are bilateral, recovery is unlikely. Efforts to develop a bacterin have been unsuccessful. Prevention and control of canine brucellosis presently is based on monthly serologic tests of all dogs in the kennel, and those entering, together with segregation and destruction of positive animals. Brucella canis has caused human infections. (See Brucella canis abortion.) The prognosis in severe or moderate epididymitis is poor, as obstructions usually occur preventing the dis- charge of spermatozoa from that testis. There is no prac- tical cure in animals once the epididymis is obstructed. In the occasional case of bilateral epididymitis the prog- nosis is hopeless. In recent years operations have been devised to bipass the obstructed portion of the epididy- mis in humans but the percentage of cures is low. If in a valuable animal the epididymitis is unilateral and the accessory glands and the vas deferens have no lesions or infection caused by the same organisms, uni- lateral castration may be indicated followed by a long recovery period for the normal testis during which re- peated tests and cultures of the semen may be performed to be certain the genital infection has been eliminated. Anomalies of the Epididymis may be either congen- ital or hereditary and consist of: (1) a spermiostasis due to distention of aberrant efferent or epididymal tubules with the secondary formation of spermatic granulomas in the region of the head of the epididymis, (2) seg- mental aplasia of the mesonephric (Wolffian) duct or ductus deferens and (3) mesonephric or paramesonephric duct cysts or remnants near the epididymis or ductus def- erens.22'34-36 Spermiostasis, resulting in spermatoceles and in time, by the same process as described under infec- tions involving the escape of sperm cells into adjacent tissues, spermatic granulomas, resembling tubercular granulomas, may be caused initially by blind-end ing rudimentary mesonephric tubules or ductuli aber- rantes.22'34 36 These tubules most often are defective ef- ferent tubules. They may be attached to the rete or ep- ididymis and therefore produce lesions involving the head region, or caput of the epididymis and only rarely other portions of the epididymis. Spermiostasis was noted in 208 (25 percent) of 836 bulls in one or more of the ef- ferent ducts.36 Sperm granuloma is common in bucks less common in rams, uncommon in bulls and rare in the other domestic animals. The frequency of occurrence of granulomas is not related to the incidence of blind-end- ing or aberrant efferent tubules as found in normal an- imals.2-35 In rams it has been confused with ram epi- didymitis which usually causes spermatic granulomas in the tail of the epididymis. In bucks the condition is usu- ally bilateral resulting in complete sterility. The inci- dence in bucks in Germany was reported to be 20 to 25 percent and therefore the condition was of great eco- nomic importance. In bulls of two Danish breeds the in- cidence was about 3 percent, and more than 90 percent of the cases were unilateral so most bulls remained fer- tile.47 There was considerable evidence that bovine spermiostasis in the mesonephric ducts is genetically de- termined by a recessive hereditary factor. The author has observed two related Brown Swiss bulls with spermios- tasis and granulomas of the left caput epididymidis. Spermiostasis with spermatocele and spermatic granu- lomas develop slowly thus young, even bilaterally af- fected, males may be fertile for a year or more until the fibrous tissue of the granuloma completely obstructs the mesonephric duct. Spermatozoa and fluid are continued to be produced in the seminiferous tubules and absorbed in the efferent ducts and head of the epididymis if the obstruction is located at the distal portion of the head. If the obstruction is located at the proximal portion of the head or in the efferent tubules the pressure may pro- duce testicular degeneration but the size and consistency of the testicle may remain nearly normal due to the ac- cumulation of testicular secretions.34'36 Segmental aplasia of the mesonephric or Wolffian duct, epididymis or ductus deferens may occur con- genitally in all species but has been well-described in bulls.4 7 34 36 The majority of cases are unilateral and the body, tail, entire epididymis, and even a part or all of the vas deferens may be missing. In unilateral cases the bull is fertile. In the latter instance the vesicular gland on the same side may also be hypoplastic or missing. (See Figures 194 and 195.) The incidence of bovine seg- mental aplasia of the mesonephric duct in Denmark was 0.59 to 1.18 percent.4'5 A 5 percent incidence in 828 infertile bulls was recorded in the Netherlands,52 while the incidence in 584 “normal” bulls was 1.7 percent. In 12 of 18 Simmental bulls in Switzerland the epididymal aplasia was bilateral.26 This condition has been described in dogs.14 24 The author has observed a few cases in Hol- stein, Guernsey and Angus bulls in New York State. There was a strong indication that segmental aplasia of the me- sonephric duct was hereditary as in 19 male offspring of a unilaterally affected bull there were 4 sons similarly affected. The missing segment was most often lacking844 VETERINARY OBSTETRICS Figure 194. Segmental Aplasia of the Terminal Portion of the Right Ductus Deferens with a Marked Dilation of the Ampulla with Semen in a Bull. on the right side. In older bulls spermatoceles and/or granulomas may develop just proximal to the missing segment. In unilaterally affected bulls the sperm cell concentra- tion and the total number of spermatozoa per ejaculate may be about one-half normal. Careful clinical palpation of the testes and epididymides, and a rectal examination of the ampullae and vesicular glands in the larger species will usually detect and delineate the extent of the seg- mental aplasia. A small epididymis accompanies severe hypoplasia of the testis. The testis associated with seg- mental aplasia of the epididymis is usually normal in size or may occasionally be atrophied. Palpation of a very small or missing tail of the epididymis is highly indic- ative of segmental aplasia. The head of the epididymis, if present, is often enlarged due to distention with sperm. If the segmental aplasia is located in the ductus deferens, the tail of the epididymis may be enlarged. In rare cases the missing mesonephric segment may be located in the Figure 195. Aplasia of the Right Ampulla and Ductus Deferens and Arrested Development of the Right Vesicular Gland in a Bull. ductus deferens near the urethra causing distention of the ampulla. (See Figures 194 and 195.) There is no treatment for this condition, other than possible surgery to reunite the unaffected portions of the mesonephric duct. Because of the possible hereditary na- ture of this anomaly affected males should be discarded.INFERTILITY IN MALE ANIMALS 845 Mesonephric or Wolffian, or paramesonephric or Mullerian duct cysts or remnants and miscellaneous anomalies may be found in males and are of little con- sequence except in cases where they may be large and are confused with defects or diseases of the epididymis on palpation. Ectopic rests of adrenal cortical tissue may be found in the testis, epididymis or spermatic cord, es- pecially in the horse.34,35 A rare case of a Holstein bull, twin to a freemartin, had an area of testicular rete tissue outside of the testis in the region of the head of the ep- ididymis.13 This is commonly observed in the rat. Par- adidymides, detached segments of mesonephric tubules, were seen on the spermatic cord and epididymis in 25 to 46 percent of calves and are of no significance.5 Oc- casional mesonephric duct cysts may be found in bulls near the head and tail of the epididymis and some may be lined by ciliated cells, “medusa cysts.” Parameso- nephric cysts or uterus masculinus are seen commonly in 24 to 44 percent of bulls on the dorsal surface of the urogenital fold between the ampullae and ductus defer- ens or rarely in or near the epididymis.5,6,24 Primary tumors of the epididymis are rare in all an- imals. Testicular tumors in dogs or other animals may invade the epididymis or spread through the epididymis to the ductus deferens and cord. Occasionally metastatic tumors such as lymphosarcomas and Sertoli cell tumors in the bull,34"36 may develop in the epididymis. Primary tumors of the epididymis are nonexistent in the tom cat and rare in the dog.8 Only 2 cases of fibromas of the epididymis in dogs were described. Miscellaneous Diseases of the Epididymis—Ob- struction and enlargement of the epididymis in bulls re- sulted from a metaplastic process in hyperkeratosis.38 Feeding highly chlorinated napthalenes caused external symptoms of hyperkeratosis and complete sterility. Fer- tility was gradually regained in about 10 months after withdrawal of the toxic agent. Sperm granulomas of the ductus deferens and tail of the epididymis sec- ondary to adenomyosis of the duct wall has been de- scribed.34"36 This condition may be related to chronic es- trogen stimulation. It was observed in 6.2 percent of 695 bulls from an AI center. It has also been observed in dogs with Sertoli cell tumors and in two stallions with secondary sperm granulomas.36 Sperm granulomas may also occur secondary to congenital anomalies, infectious agents, vascular and traumatic lesions and autoimmune reactions. Fifty-three (6.3 percent) of 83 bulls had sperm granulomas of the epididymis.35 There is definite evidence that a change in the en- vironment of spermatozoa, especially in the tail of the epididymis, due to probable changes in the epididymal epithelium may result in a reduction or absence of mo- tility or akinesia or necrospermia associated with bent or looped cells. Testosterone maintains the function of the epididymis. Estrogens injected into adult bulls caused an increase in abnormal bent or looped sperm tails.16 Fre- quent collection of these treated bulls resulted in a de- cline of abnormal sperm cells. Three infertile Jersey bulls with many vacuolated basal epithelial cells of the cauda epididymis and with many secretory granules in the lu- men of the duct were reported.11 Inbred Jersey bulls with impaired fertility characterized by poor quality semen with bent, looped and coiled tails, tailless heads, abnormal heads and thickened midpieces were reported later.17 This genetic condition was caused by a reduced sex steriod production due to the subnormal formation of its pre- cursor, alpha-hydroxyprogesterone.17 Testicular injury and reduced production of sperm cells, hormonal upsets, as excess estrogen, and insulation of the scrotum produces changes in the epididymal plasma resulting in sperm defects especially reduced motility and tail or midpiece defects. These defects develop in the corpus and tail of the epididymis.18"21 Poor sperm cell motility, seen occasionally in stallions, may not be due to an intrinsic defect of the spermatozoa but due to a failure of the epididymis to properly support the cells for their relatively long storage period in that organ.31 One of the first and most striking effects following hypophy- sectomy of young human males was the complete loss of motility in sperm cells already present in the epididy- mis. Exogenous testosterone therapy was suggested. Three bulls with spermakinesia associated with a high per- centage of bent and coiled tails was described.19,21 Ex- haustion trials showed that as the storage time in the ep- ididymis decreased the semen quality improved indicating a disturbed function of the epithelium of the cauda ep- ididymis. The sodium and potassium levels in the sem- inal plasma of the cauda epididymis were very low pos- sibly related to an endocrine imbalance. Since about 95 percent of pet male dogs are not cas- trated and therefore contribute to the problem of over- population of dogs, it has been reported that a simple operation of injecting 1 ml. of an aqueous solution of 4.5 percent chlorhexidine digluconate into the tail of the canine epididymis, after a sedative dose of “Rompun,” produces azoospermia within 4 weeks by causing a scle- rosing obstruction of the epididymis or ductus deferens, chemical vasectomy.44 Further, such studies should be pursued. Pathology of the Ductus Deferens and Ampullitis Infection and inflammation of the ductus deferens is usually associated with an orchitis, epididymitis, or sem-846 VETERINARY OBSTETRICS inal vesiculitis. Infection of the ductus deferens appar- ently occurs less commonly in animals in which the am- pullae or dilated proximal portions of the ductus deferens are absent. In the stallion and bull, infections with or- ganisms such as Br. abortus, streptococci, C. py- ogenes, tubercle bacillus, Ps. aeruginosa, mycoplasma, ureaplasma and others including viruses, have been ob- served. (See infectious causes for orthitis and epididy- mitis.) The infection is usually unilateral but may be bi- lateral. As discussed previously segmental aplasia may oc- casionally be present in the ductus deferens, usually uni- laterally and paramesonephric cysts or a uterus mascu- linus, are common in the urogenital fold between the two ampullae, especially in bulls. Careful rectal examination will usually reveal a thick- ened, firm and possibly painful enlargement when am- pullae are diseased. Semen examination may reveal leu- kocytes and the infective organisms. In some cases the semen contains clots of pus and the motility of the sper- matozoa is poor. If the motility is good immediately after ejaculation, the spermatozoa often lose their motility rapidly on storage. In cases of segmental aplasia where the missing segment is near the urethra, the ampullae may become greatly enlarged and distended with sper- matozoa but no inflammatory reaction is present. Often the vesicular gland on the same side as the missing seg- ment is also hypoplastic or absent. Treatment of infected or diseased ampullae is similar to treatment for seminal vesiculitis. References Diseases and Aplasia of the Epididymis and Ductus Deferens, Infections and Tumors of the Epididymis 1. Beeman, K. B., Hummels, S. and Rahaley, R. (1982) Epididy- mitis in Rams, (A Review), Vet. Med./Sm. An. Clin., 77, 11, 1649. 2. Biberstein, E. L. and McGowan, B. (1958) Epididymitis in Rams— Studies on Laboratory Diagnosis, Cor. Vet., 48, 1, 31. 3. Biberstein, E. L., McGowan, B., Olander, H. and Kennedy, P. C. (1964) Epididymitis in Rams—Studies on the Pathogenesis, Cor. Vet., 54, 1, 27. 4. Blom, E. and Christensen, N. O. (1951) Congenital Absence of the Epididymis, Ductus Deferens or Glandular Vescularis (Apla- sia Segmentalis Ductus Wolffii) in the Bull, Yearbook Royal Vet. and Agr. Col. Copenhagen, Denmark, 1-64. 5. Blom, E. and Christensen, N. O. (1956) Examination of the Gen- itals, of Slaughtered Male Calves as a Means of Elucidating the Frequency of Genital Malformation in the Bovine Male, Proc. 3rd. Intemat. Congr. on Animal Reprod., Cambridge. 6. Blom, E. and Christensen, N. O. (1958) Cysts and Cyst-like For- mations (Inter Alia Spermiostasis) in the Genitals of the Bull, Yearbook of the Royal Vet. and Agr. Col., Copenhagen, Den- mark, 101-133. 7. Blom, E. and Christensen, N. O. (1960) The Etiology of Sper- miostasis in the Bull, Nord. Vet. Med., 12, 453. 8. Bloom, F. (1954) Pathology of the Dog and Cat, Amer. Vet. Publicat. Inc., Evanston, 111. 9. Bruner, D. W. and Gillespie, J. H. (1973) Hagan’s Infectious Diseases of Domestic Animals, 6th Ed., Cornell Univ. Press, Ith- aca, N.Y. 10. Buddie, M. B. (1958) Vaccination in the Control of Br. ovis Infection in Sheep, New Zealand Vet. J., 6, 41. 11. Cappucci, D. T. and Cupps, P. T. (1966) Lesions of the Epi- didymides and Testes from Infertile Bulls, JAVMA, 148, 11, 1391. 12. Carmichael, L. E. and Kenney, R. M. (1968) Canine Abortion Caused by Brucella canis. JAVMA, 152, 6, 605. 13. Carroll, E. J. (1967) Personal Communcation. 14. Copeland, M. D. and Maclachlan, N. J. (1976) Aplasia of the Epididymis and Vas Deferens in the Dog, J. Sm. An. Pract., 17, 443. 15. Crenshaw, G. L. and McGowan, B. (1966) Ram Epididymitis Vaccination, Proc. 70th Ann. Meeting U.S.L.S.A., 476. 16. Cupps, P. T. and Briggs, J. R. (1965) Changes in the Epididymis Associated with Morphological Changes in the Spermatozoa, J. Dairy Sci., 48, 9, 1241. 17. Cupps, P. T., Laben, R. C. and Huff, R. L. (1970) Steroid Me- tabolism in an Inbred Strain of Jersey Cattle, J. of Dairy Sci., 53, 1, 79. 18. Gustavsson, B. (1965) A Case of Akinesia of Bull Sperm As- sociated with a Functional Disturbance of the Epididymis, Nord. Vet. Med., 17, 67. 19. Gustavsson, B. (1966) The Luminal Contents of the Bovine Ep- ididymis Under Conditions of Reduced Spermatogenesis, Lu- minal Blockage and Certain Sperm Abnormalities, Acta. Vet. Scand. Suppl. 17. 20. Gustavsson, B. (1966) Luminal Contents of the Bovine Epididy- mis under Conditions of Reduced Spermatogenesis, Luminal Blockage and Certain Sperm Abnormalities, Thesis, Dept. Ob- stet. and Gynec., Royal Vet. Col., Stockholm. 21. Gustavsson, B., Crabo, B. and Rao, A. R. (1972) Two Cases of Bovine Epididymal Dysfunction, Cor. Vet., 62, 392. 22. Hemeida, N. A., Sack, W. O. and McEntee, K. (1978) Ductuli Efferentes in the Epididymis of Boar, Goat, Ram, Bull and Stal- lion, Amer. J. Vet. Res., 39, 12, 1892. 23. Jensen, R. and Swift, B. L. (1982) Diseases of Sheep, 2nd Ed., Lea and Febiger, Philadelphia. 24. Kanagawa, H., Ishikawa, T., Kowata, K. and Fujimoto, Y. (1960) Some Observations on Remnants of the Mullerian Duct in Slaughtered Bulls in Hokkaido, Jap. Jour. Vet. Res., 8, 4, 323. 25. Keogh, J., Doolette, J. B. and Clapp, K. H. (1958) The Epi- demiology of Ovine Brucellosis in South Australia, Austral. Vet. J., 34, 412. 26. Konig, H., Weber, W. and Kupferschmied, H. (1972) Aplasia of the Epididymis in the Bull, Schweitzer Archiv. f. Tierheilk- unde, 114, 73. 27. Lawrence, W. E. (1961) Ovine Brucellosis: A Review of the Dis- ease in Sheep Manifested by Epididymitis and Abortion, Brit. Vet. J., 117, 435. 28. Laws, L., Simmons, G. C. and Lerdford, C. G. (1972) Experi- mental Brucella ovis Infection in Rams, Austral. Vet. J., 48, 313.INFERTILITY IN MALE ANIMALS 847 29. Leonard, E. P., Richard, C. G. and McEntee, K. (1953) Im- potence, Canine Medicine, Amer. Vet. Publicat. Inc., Evanston, 111., 165. 30. Livingston, C. W., Jr. and Hardy, W. T. (1964) Isolation of Actinobacillus seminis from Ovine Epididymitis, Amer. J. Vet. Res. 25, 106, 660. 31. MacLeod, J. (1964) Personal Communication. 32. Mare, J. and VanRensburg, S. J. (1961) The Isolation of Viruses Associated with Infertility in Cattle, A Preliminary Report, J. S. Afr. Vet. M. A., 32, 201. 33. McEntee, K. (1968) Personal Communication. 34. McEntee, K. (1970) Pathology of Domestic Animals, 2nd Ed., Vol. 1, edit, by Jubb, K. V. and Kennedy, P. C., Academic Press, Inc., N.Y.C. and London. 35. McEntee, K. (1976) Pathology of the Epididymis, Proc. VIII, Congr. on An. Reprod. and AI, Krakow, 1186. 36. McEntee, K. (1979) Pathology of the Epididymis of the Bull and Stallion, Proc. for Soc. for Theriog., Mobile, Alab., 103. 37. McEntee, K. (1980) Current Veterinary Therapy, 7th Ed., Edit, by Kirk, R. W., W. B. Saunders, Co., Philadephia and London. 38. McEntee, K. and Olafson, P. (1953) Reproductive Tract Pathol- ogy in Hyperkeratosis of Cattle and Sheep, Fert. and Steril., 4, 2, 128. 39. McGowan, B. (1979) Epididymitis in Rams: Effect of Vaccina- tion and Culling on the Clinical Incidence of the Disease, Cor. Vet., 69, 67. 40. McGowan, B. and Devine, D. R. (1960) Epididymitis of Rams. The Effect of Naturally Occurring Disease upon Fertility, Cor. Vet., 50, 2, 102. 41. McGowan, B. and Harrold, D. R. (1979) Epididymitis in Rams: Studies on Vaccine Efficacy, Cor. Vet., 69, 73. 42. McGowan, B. and Schultz, G. (1956) Epididymitis in Rams. Clinical Description and Field Aspects, Cor. Vet., 46, 2, 277. 43. Parsonson, I. M., Al-Aubaidi, J. M. and McEntee, K. (1974) Mycoplasma Bovigenitalium: Experimental Induction of Geni- tal Disease in Bulls, Cor. Vet., 64, 240. 44. Pineda, M. H. and Hepler, D. I. (1981) Chemical Vasectomy in Dogs, Long-Term Study, Theriog., 16, 1, 1. 45. Pulsford, M. F., Eastick, B. C., Clapp, K. H. and Roberts, R. (1967) Traumatic Epididymitis of Dorset Horn and Poll Dorset Rams, Austral. Vet. J., 43, 3, 99. 46. Ris, D. R. (1967) The Persistence of Antibodies Against Bru- cella ovis and Brucella Abortus in Rams Following Vaccination: A Field Study, N.Z. Vet. Jour., 15, 94. 47. Simmons, R. E., Brown, G. M., Ranger, C. R. and Pietz, D. E. (1970) A Survey of the Incidence of Ram Epididymitis in Idaho, Caused by Brucella ovis, Proc. 74th Ann. Mtg., USAHA, 157. 48. Storz, J., Carroll, E. J., Ball, L. and Faulkner, L. C. (1968) Isolation of a Psittacosis Agent (Chlamydia) from Semen and Ep- ididymis of Bulls with Seminal Vesiculitis Syndrome, Amer. J. Vet. Res., 29, 3, 549. 49. Swift, B. L., Craddock, F., Hancock, H. A., Jensen, K., Thomas, G. M. and Trueblood, M. S. (1982) Ram Epididymitis: A Clin- ical Report, Theriog., 17, 3, 343. 50. Swift, B. L. and Weyerts, P. R. (1970) Ram Epididymitis: A Study on Infertility, Cor. Vet., 60, 2, 204. 51. Vanderschaaf, A. and Hendrikse, J. (1963) Infection of the In- ternal Genital Organs of a Stallion with Str. zooepidemicus, Tijdschr. v. Diergeneesk. 88, 13, 834. ' 52. VanderSluis, L. (1953) Experiences with the Examination into Herd Infertility Proc. 1st World Congr. on Fert. and Steril II XXV, 704. 53. VanRensburg, S. W. J. (1953) Bovine Sterility Caused by In- fectious Diseases in South Africa, Brit. Vet. J., 109, 226. Diseases of the Accessory Glands Diseases of the Vesicular Gland, (Seminal Vesi- cle)—Although congenital defects, usually unilateral, of the vesicular glands including hypoplasia, cysts and either absence or doubling of the gland has been reported35a b often in association with segmental aplasia of the meso- nephric duct, seminal vesiculitis is the most common condition found affecting the gland of bulls, stallions and boars. It is rare in bucks and rams. Gross inflammatory lesions are found most commonly in the vesicular gland of the accessory reproductive glands and the ampullae. The incidence of seminal vesiculitis in bulls was re- ported as 0.8 percent of 2000 bulls examined in Den- mark,56 4.2 percent of 828 infertile bulls examined in Holland,47 2.5 percent of 7359 bulls examined in Col- orado,1112 and 4.6 percent in 343 bulls studied in New York State.353 A bovine seminal vesiculitis syndrome seen in midwestem United States was described4 that differed from the usual sporadic cases observed elsewhere. Up to 10 percent, or an average of 5 percent, of groups of young beef bulls running together and fed heavily and grown rapidly for sale were affected. While breeding bulls grown more slowly on limited rations had an incidence of only 1.3 percent. In housing arrangements where 10 to 20 young bulls, 10 to 15 months of age, run together, the incidence of seminal vesiculitis may reach 20 to 30 percent of the bulls.32 These young affected bulls usually recover without treatment. Seminal vesiculitis in stal- lions and boars is observed less commonly. Seminal vesiculitis may be caused by a variety of pathogenic organisms. The most common cause in the United States is C. pyogenes, (See Figures 196 and 197.) This organism may localize in the seminal vesicle from other primary, pyogenic, infective foci such as rumen- itis, liver abscess, traumatic gastritis, lung abscess or from a navel infection in a young calf.23,35ab It may possibly enter as an ascending or descending infection from the prepuce and urethra or from an ampullitis, epididymitis or orchitis." Infection may be spread in groups of young bulls by homosexual activities and contact of the penis and prepuce to the rear parts of a bull that another had recently mounted. It is possible that certain organisms as C. pyogenes may invade the seminal vesicle second- ary to a temporary infection with a virus or other agent, possibly a mycoplasma. In countries where brucellosis is still prevalent, Bru- cella abortus is the most common cause for seminal848 VETERINARY OBSTETRICS Figure 196. Seminovesiculitis in a Bull. vesiculitis. In 30 bulls with positive brucella titers of serum and semen plasma, Br. abortus was recovered on cul- ture of guinea pig inoculation of the semen in 15 or 50 percent.5 Twenty six of these bulls were examined and had clinical gross lesions in the genital organs and nine- teen had lesions found on autopsy. Seminal vesiculitis was found in 17 bulls, ampullitis in 5 bulls, orchitis in 5 bulls, and epididymitis in 2 bulls. In some a combi- nation of lesions were found. Brucella suis commonly localizes in the seminal vesi- cles in boars.17 Examination of 9 boars serologically pos- itive for brucellosis revealed Brucella suis in the sem- inal vesicles of 8 boars, in the epididymides of 6, in the prostate of 4 and in the semen of 7. No macroscopic lesions were present.16 In 37 boars infected with Br. suis orchitis was uncommon, occasional macroscopic lesions were observed in the vesicular glands, while nearly all infected boars had microscopic lesions in the epididymi- des and vesicular glands so that 75 percent of the boars periodically secreted organisms in their semen.45 Pus and leucocytes were seldom found in infected semen. Infer- tility in boars is frequently associated with the shedding of Brucella suis organisms in apparently normal ap- pearing semen. The excretion of Br. abortus was re- ported in the semen of a stallion.46 Organisms found in infected vesicular glands included: streptococci and staphylococci in bulls and boars,22 Pseudomonas aeru- ginosa and Actinobacillus actinoides,27 Proteus,35 My- coplasma bovigenitalium1,9,20,21,33,37 38,41 and bovis,30 33 and Mycobacterium tuberculosis. Mycobacterium paratuberculosis was recovered from the feces and se- men from an affected bull used in an AI center.31 On necropsy, M. paratuberculosis was isolated from the vesicular glands and prostate. Ureaplasmas have recently been recovered from bo- vine seminal vesiculitis lesions and reproduced experi- mentally.19,33 Hemophilus somnus has been isolated from the accessory sex glands of bulls but not from the testis or epididymis.26,33 Although a higher incidence of infec- tion was present in young bulls, the pathological signif- icance of H. somnus in the bull awaits further study. Virus infections described under orchitis and epididy- mitis have also been reported to cause seminal vesiculitis including the enteric virus, possibly IBR-IPV,10 and the “epivag” virus.34 Chlamydia psittaci was recovered from the semen or organs of 6 to 10 bulls from two beef herds where the seminal vesiculitis syndrome was commonly observed in young beef bulls.4,33,43 44 The Chlamydia re- covered from one of these bulls was indistinguishable from Chlamydia psittaci in California responsible for epizootic bovine abortion and enzootic abortion of ewes. The seminal vesiculitis syndrome reported in Colorado4,12,44 appeared clinically similar to those de- scribed in Wisconsin and Czechoslovakia.32 36 Naturally occurring cases of seminovesiculitis in bulls due to Mycoplasma bovigenitalium have been de- scribed along with experimental studies.18 33,38,41 In nat- ural cases the semen was stringy and mixed with pus. The vesicular glands especially the cranial portions were firm, swollen and nodular. Postmortem examination and culture of all portions of the male genital tract showed Figure 197. Ejaculates Containing Clots of Pus from a Bull with Seminovesiculitis.INFERTILITY IN MALE ANIMALS 849 the organism had become widely distributed throughout the tract. The organism persisted in the experimental bulls for at least 17 weeks and could be recovered from the semen for 11 weeks. The usual antibiotics used in ex- tended semen had no effect on Mycoplasma bovigeni- talium. This organism caused a necrotizing vasculitis in many bulls and was present in the carpal joint of one bull.41 Earlier studies cited by Parsonson40'41 reported the pathologic lesions produced in the genital tract of cows. This could not be confirmed with M. bovigenitalium.21 However these authors showed the organism was patho- genic for the vesicular glands, udder and joints. Prior to the inoculation of the vesicular glands in the experimen- tal bulls, mycoplasma could be recovered from their pre- putial and nasal cavities.40 41 This could be done also in control bulls but on autopsy no mycoplasma could be recovered from the urethra or internal reproductive or- gans of the control bulls but could be from the experi- mental inoculated bulls. After inoculation the viability of the spermatozoa decreased markedly in bulls with seminovesiculitis, ampullitis and epididymitis caused by mycoplasma. Inoculated vesicular glands became en- larged, swollen and nodular. Many polymorphonuclear leucocytes and eosinophiles were present in the inflamed tissues and exudate. Recent studies have shown that the presence of my- coplasma and possibly ureaplasma, in semen, especially processed frozen semen from normal bulls had an ad- verse effect on motility often requiring the discarding of that ejaculate of semen. Nine of 14 bulls with a post- thawing motility below 30 percent were positive for M, bovigenitalium on culture.24 In a Czechoslovakian study28 12 of 44 semen samples from which mycoplasma were isolated had low motility, while only 2 of 31 samples free of infection had a low, unsatisfactory motility. This lowered motility might be due to the affinity of the sperm cell for mycoplasma or due to epididymal infection re- sulting in epididymal plasma alterations that affect the sperm cells.38 39 All strains of ureaplasmas (T myco- plasmas) when inoculated into bovine oviductal tissue cultures caused a cilia stopping effect (CSE) progressing to collapse and eventual sloughing of the cilia due to the cytotoxin produced by the organism.443 This effect on cilia may possibly explain the decline in motility of sper- matozoa in contact with ureaplasma or mycoplasma since the body and tail of the sperm cell is a modified cilia. It may also explain the infertility in cows when these organisms are introduced into the cervix, uterus and ovi- ducts where cilia perform a necessary function in sperm transport.443 Further studies are needed. Experimental infection of the vesicular glands with Mycoplasma bovis resulted in a persistent infection for at least 8 months during which time the organism was shed continually not intermittently like M. bovigenital- ium. Furthermore there was no tendency for the infec- tion to spread to other genital organs as there was with the latter mycoplasma.30 A local semen agglutination re- sponse developed that produced higher titers to M. bovis in the seminal plasma than in blood serum.14 Seminal vesiculitis affects males of all ages. In bulls it has been reported as early as 10 months to one and one-half years of age. Usually there are no external signs of the disease. Occasionally however some males will show signs of mild peritonitis with an arched back, re- duced appetite, pain on defecation or on rectal exami- nation and hesitation in mounting and thrusting. These occasional signs are observed usually in bulls having ab- scesses of the vesicular glands caused by C. pyogenes infection adjacent to the peritoneum. On rectal exami- nation seminal vesiculitis, especially bovine cases due to the latter infection, are characterized by two general findings, firstly, irregular enlargement of the gland, fi- brosis, peritoneal adhesions, loss of lobulations, fluc- tuation, and abscessation. (See Figures 196 and 197.) In rare cases fistulas occur due to rupture of an abscess into the rectum. In the other more common cases a portion or all of the vesicular gland may become thickened and fibrotic with only slight enlargement and loss of lobu- lations of the gland and with no adhesions. The first type of bovine seminovesiculitis was usually unilateral and due to chronic purulent inflammatory le- sions with chronic interstitial changes and was com- monly caused by C. pyogenes.23 The second type of seminal vesiculitis was usually bilateral and character- ized by degenerative changes in the epithelium and in- flammatory changes were variable.23 Cultures of these latter vesicular glands were frequently negative for bac- teria. Large amounts of Feulgen positive chromatin masses were found in the lumen of affected glands and in the semen of the latter degenerative type of seminal vesiculi- tis, but not in the former. In both types varying numbers of polymorphonuclear leucocytes were usually found in the semen. In the former purulent type of seminal vesic- ulitis large clots or flocculi were commonly observed while in the latter the semen may be viscid or “ropy.” Leu- cocytes in the semen may also come from other portions of the urogenital tract including the prepuce so their presence is not diagnostic of seminal vesiculitis. In some chronic cases few or no leucocytes will be present in the semen of affected bulls. Semen quality will vary be- tween affected bulls, with a lowered motility of the sperm cells, an elevated pH, a high catalase activity, and a low- ered fructose content being commonly found. Although lowered fertility has been associated with seminal vesic-850 VETERINARY OBSTETRICS ulitis many affected bulls breeding cows naturally have a good conception rate. One affected bull with good fer- tility had been used for at least three years in an artificial insemination stud although periodically a number of ejaculates had to be discarded as being unsatisfactory.352 In thirty cows bred to an affected bull, 7 or 23 percent aborted from three months to term.352 In bulls with sem- inal vesiculitis 40.5 percent had satisfactory quality se- men and 50 percent had semen of questionable quality, while normal bulls had 83.7 satisfactory and 11.7 per- cent questionable quality of semen. The use of a bull for artificial insemination with Bru- cella abortus infection of the accessory glands or am- pullae may spread the disease and cause infertility. One infected bull used artificially infected 71 percent of the cows in 41 Brucella-free herds.42 In young beef bulls with the seminal vesiculitis syndrome, 8 of 10 affected bulls had substandard quality of semen and leucocytes were consistently found in the ejaculate.1112 Blom5b reported on 25 bulls with seminal vesiculitis and/or ampullitis of which 10 had malformations of the excretory ducts including: segmental aplasia or hypopla- sia of the Wolffian duct, accessory vesicular glands, per- sistent uterus masculinus and asymmetrical implantation of the ampullae. These anomalies possibly interfered with closing of the duct orifices in the colliculus seminalis predisposing to bacterial infection. The possible genetic transmission of these defects together with the poor prognosis of a cure favors slaughter of the animals. Not infrequently bulls with a seminal vesiculitis will have another focus of infection in the testis, epididymis or ampulla. In the seminal vesiculitis syndrome, espe- cially in groups of young beef bulls, focal or diffuse nonsuppurative interstitial inflammatory lesions were commonly present in the epididymides, testes, ampullae, prostate and less commonly in the bulbourethral glands.4 This widespread infection of the male reproductive tract was also found in mycoplasmosis due to M. bovi- genitalium.1 2 18 33 38 41 The viruses and Chlamydia re- covered from diseased vesicular glands by African34 Czechoslovakian36 Belgian10 and Colorado44 workers also affected a number of the reproductive organs besides the vesicular glands. In the seminal vesiculitis syndrome, however, the principal signs are related to the vesicular glands.4 Diagnosis is based on the clinical signs noted above. Ampullitis and prostatitis may be difficult to diagnose by rectal palpation in the bull and stallion. Culture of the semen is usually an unsatisfactory method for di- agnosing the causative bacterial agent because of the contamination from the sheath. A technique was devel- oped to collect non-contaminated urethral samples from bulls.42 A tranquilizer was administered to quiet the bull and allow withdrawal of the penis. Rectal massage aided the protrusion of the penis from the sheath. The penis was washed with an antiseptic solution and the urethra was irrigated with sterile saline. A 10 inch or 25 cm. sterile silastic tube was inserted up the urethra leaving 1 or 2 inches, about 4 cm. protruding. Rectal massage of the vesicular glands, prostate and ampullae resulted in the collection of their secretion into sterile vials for cul- tural purposes.42 Only 4 of 158 urethral samples were contaminated. The prognosis in seminal vesiculitis is fair to poor depending upon the causative agent, the presence of other foci of infection in the reproductive tract, the duration and severity of the infection and the value of the male. Males with Brucella infections, tuberculosis or possibly mycoplasmosis of the seminal vesicles, or those with secondary lesions of the testes, epididymides, ampullae or prostate should be slaughtered. Many young bulls with the seminal vesiculitis syndrome with catarrhal or de- generative seminal vesiculitis overcome the infection spontaneously in a few months.12-32 During this period their use for breeding purposes is questionable. Bulls with active acute lesions of seminal vesiculitis with a dis- charge of pus in the semen should not be used for arti- ficial insemination as only rarely will the antibiotics used in extended semen destroy the organisms present. Many bulls with seminal vesiculitis caused by organisms other than Brucella or Mycobacterium may be used naturally or even artificially with quite satisfactory conception rates especially if a large amount of mucopurulent material is not present in the ejaculate. Further studies on the pos- sible viral causes of this disease and the duration of the carrier state is definitely needed. Treatment with high levels of broad range antibiot- ics, or antibiotics to which the causative agent is sen- sitive, for two weeks or longer together with mild mas- sage of the vesicular gland to remove its contents may result in recovery or elimination of the infection in some males after 2 to 6 months. In C. pyogenes infection the gland is usually left severely indurated and largely de- stroyed. Acute cases of seminal vesiculitis tend to be- come chronic. Chronic cases, if abscessation does not occur, tend to become fibrotic and indurated similar to the mammary gland following a severe infection. In long- standing chronic cases pus or high leucocyte numbers are seldom observed in the semen. In recent years surgical removal of the affected vesic- ular glands has been recommended for selected bulls in artificial insemination studs or where conservative treat- ment has failed or is not deemed advisable, and where the only detectable lesion of the genital tract is in theINFERTILITY IN MALE ANIMALS 851 seminal vesicle and extensive adhesions are not present. In an aseptic manner and under epidural and local anes- thesia together with tranquilization, an elliptical incision was made in the ischiorectal fossa after suturing the anus tightly closed. 15 29'35a By a combination of blunt and sharp dissection the affected gland was isolated and removed close to the urethra after ligation at that point. Some dif- ficulty was experienced if adhesions were present es- pecially in separating the peritoneum from the cranial portion of the gland. Following surgery heavy prolonged antibiotic therapy was recommended. The results were satisfactory in all cases except in one bull that developed a degree of paralysis in the sphincter of the bladder with cystitis and urinary complications. Regular and frequent examination of the genital tract and semen for a year or more should be followed after treatment to be certain the condition doesn’t recur at an- other site due to a resistant or secondary focus of infec- tion. Disease of the prostate gland is rare in all animals except the dog in which acute or chronic prostatitis and benign prostatic hyperplasia (BPH) are common. Other less common canine prostatic diseases include neo- plasms, retention or congenital cysts and rare calculi.7b-8 The disease conditions affect all breeds of dogs equally. These diseases in the dog resemble those in man.16 About 60 percent of all intact male dogs over 5 years of age have enlarged prostates usually due to BPH. Infection in the prostate gland may be a source of bacteria for re- current cystitis.76'8’11’12 A combination of the above pros- tatic lesions is not uncommon in old dogs. On rectal pal- pation of the prostate, abscesses, retention cysts, and tumors are characterized by asymmetrical enlargement of the gland. The other pathological conditions are usu- ally symmetrical.11,12 Almost all prostatic diseases are usually clinically characterized by either or all lower uri- nary tract signs, systemic signs, especially in acute pros- tatitis, and abnormalities or difficulties in defeca- tion.811'12 Prostatitis in the dog is often associated with hyper- plasia of the gland. It is probably due to an ascending infection through the urethra but may occur secondary to hematogenous infection or even descending infec- tions. A wide variety of organisms have been isolated from infected glands including Brucella canis, E. coli, streptococci, staphylococci, Proteus and rarely blasto- myces.22 Acute prostatitis in the dog is a diffuse or local suppurative inflammatory reaction with a tendency for abscess formation.19 Bacteria, leukocytes, and blood are frequently found in the urine, the latter portion of the ejaculate, or observed at the preputial orifice. This should be differentiated from a balanoposthitis. Acute prostatitis may be painful and characterized by constipation, in arched back, tenesmus, dysuria, elevated temperature and pulse rate, occasionally anorexia and vomiting, and a leucocytosis. Palpation of the infected gland per rectum causes pain and “splinting” of the abdomen. Chronic prostatitis is occasionally observed and may be associ- ated with benign prostatic hyperplasia.6'7b'811'13a'b'14’19 The treatment of prostatitis is frequently successful. Administration of broad range antibiotics are indicated over a prolonged period. If the ordinary antibiotics do not control the infection, cultures of the prostatic secre- tions may be made and the antibiotic sensitivity of the causative organism determined. Laxatives and suppor- tive therapy may be indicated. If prostatitis is due to Brucella canis the prognosis is poor. (See Brucella canis abortion.) Clinical prostatitis in the bull and boar is rare and may be caused by Brucella abortus or suis. Subclinical in- fections may be more common and due to a variety of bacteria and viruses as described under seminal vesicu- litis. Benign prostatic hyperplasia (BPH) is present in about 50 percent of dogs over 5 years of age that have not been castrated.713'8 The condition is probably due to an endo- crine imbalance with an excess of testosterone being se- creted which causes an enlargement and hyperplasia of the gland. Some speak of this condition as prostatic hy- pertrophy but this terminology is not correct. The mod- erate to greatly enlarged gland may be smooth or nodular and may contain small cysts. When cysts are not present the preputial discharge from an infected hyperplastic prostate is usually purulent; when cysts are present the discharge is watery-grey or bloody. This cystic fluid may be voided with the urine producing albuminuria. Usually dogs with marked prostatic hyperplasia are constipated. Rectal impaction and tenesmus and stranguria predispose to rectal dilation and the development of a perineal her- nia. Occasionally cystitis and hydronephrosis may de- velop. Usually little discomfort is shown by the dog with a hyperplastic prostate unless constipation, stranguria, or perineal hernia occurs.1’7b'8’1112 Severe obstruction of the urethra does not occur in dogs as in man because of the bilobed-nature of the gland in the dog in contrast to the trilobed structure of the gland in man. Rarely the bladder may become strangulated in a perineal hernia. Digital examination of the prostate bimanually per rectum and by abdominal palpation may reveal a nodular or smooth, enlarged prostate. It is often helpful to exert pressure through the abdominal wall at the pelvic brim to push the prostate caudally so that it can be palpated rectally. The consistency will vary with the nature of the hyperplasia from firm and fibrous, to soft, or even flue-852 VETERINARY OBSTETRICS tuating if cysts are present. Normal prostate glands are 2.5 to 3 cm. in diameter while hyperplastic glands may be twice as large or even larger if cysts are present. Pros- tatic cysts often occur with benign prostatic hypertrophy or from blocked prostatic ducts or vestiges of the Mul- lerian duct. No signs are observed until these cysts be- come large and press on the bladder or rectum with re- sulting dysuria or tenesmus with constipation.7b'8 Large cysts and abscesses frequently extend into the abdominal cavity. The latter are fatal if they rupture or leak intra- peritoneally. A prostatic cyst in a Great Dane dog con- tained 15 quarts of a sanguineous fluid.14 A number of diagnostic procedures have been used to determine the nature, severity and type of prostatic dis- ease including palpation, per rectum, ejaculation,7,1 pros- tatic massage, aspiration and punch biopsy, radiography and contrast radiography, culture of urine or prostatic secretions, and in acute prostatitis white blood cell counts. These tests must be carefully performed, interpreted and evaluated with skill and experience together with a com- plete history and physical examination,2,4,76,8,11,12,17 be- fore treatment is recommended, particularly in older dogs and in recurrent prostatic problems. Rectal massage of the gland may give temporary relief by reducing the size of the cysts. Estrogenic therapy with oral or injectable estrogens in low doses have been used in prostatic hyperplasia. Antibiotics should be adminis- tered along with estrogenic therapy. During estrogenic therapy it is desirable to monitor the blood picture to diagnose incipient myelotoxicosis. Gradually reducing the dose during the next few weeks may give relief but continued dosing is required. Estrogens act by suppress- ing the pituitary gonadotropins and this causes an atro- phy of the Leydig cells and suppression of testosterone production. The estrogens do not directly antagonize the androgens. The most satisfactory method of reducing the size of the prostate is castration, as this removes the source of the androgen causing the hyperplasia. Within 2 to 3 weeks after castration the prostate gland begins to no- ticeably involute and by 6 to 8 weeks it is relatively small in size and atrophied. However castration does not re- duce the large cysts or abscesses in infected glands or affect calculi that may rarely be present.8,18 In compli- cated cases, prostatectomy or marsupialization of the large cyst or abscess through the abdominal wall may be in- dicated.13,811'12 The urethra is transected and anasto- mosed into the neck of the bladder and the ducti defer- entia are ligated and the proximal portions are removed. When perineal hernias have developed, perineal her- niorraphy may be indicated.15,23 Squamous metaplasia—The effect of prolonged es- trogen stimulation of the prostate gland has been de- scribed.8,10,11,1"19 In dogs with Sertoli cell tumors of the testes, estrogens produced by the tumor cause squamous metaplasia with enlarged cystic prostate glands or atro- phy of the glands. These lesions can be produced ex- perimentally by administering estrogens and this is an- other reason why castration is a more effective therapy than estrogen administration. Furthermore high pro- longed dosing with estrogens may cause anemia, leu- copenia and aplasia of the bone marrow.6 Estrogen-in- duced changes in the prostate are apparently irreversible in the dog. A squamous metaplasia of the uterus mas- culinus may also occur. Similar, but reversible, prostatic lesions to those in the dog, occurred in wethers grazing on certain clovers such as red clover or subterranean clover that contained high levels of estrogens.5 The bulbourethral glands also be- came cystic, dilated with urine and debris and greatly enlarged in castrated sheep. In some cases urinary ob- struction, prolapse of the rectum and even death oc- curred. A similar condition occurred in wethers in feed lots if their ration was supplemented with excessive es- trogens or estrogen implants were given to provide growth stimulation.9 Adenocarcinoma of the prostate in the dog is rare. It is usually seen in dogs over 10 years of age.6,8,10,11,12,16,19 Only 3 cases of carcinoma in over 500 diseased prostate glands were reported.21 Persistent straining at the time of defecation was characteristic of all 3 advanced cases. Pain was a commonly observed symptom. Adenocarci- noma of the prostate results in a nodular asymmetrical enlargement of the gland. The tumor may vary in con- sistency from very hard to soft and is slow to metastasize and therefore signs of disease are seldom observed until the condition is terminal with emaciation and locomotor difficulties.81112 A biopsy may reveal the nature of the tumor and differentiate it from benign prostatic hyper- trophy (BPH) in the early stages.4,17 Castration, estrogen therapy and radiation therapy are of definite value in man in delaying the growth of the tumor even though metas- tasis has occurred.13 Prostatectomy would be indicated if the carcinoma had not metastasized. However the prognosis is poor. Other tumors of the prostate are very rare; these include: leiomyomas, fibromas, sarcomas and hemangiomas.10,11 Two cases of adenocarcinoma of the prostate in the tom cat were reported.11 References Diseases of the Accessory Male Glands A. Diseases of the Seminal Vesicles 1. Al-Aubaidi, J. M. (1970) Bovine Mycoplasma, PhD Thesis, N.Y.S. Vet. Col., Cornell Univ., Ithaca, N.Y.INFERTILITY IN MALE ANIMALS 853 2. Al-Aubaidi, J. M., McEntee, K., Lein, D. H. and Roberts, S. J. (1972) Bovine Seminal Vesiculitis Due to Mycoplasma Bo- vigenitalium, Cor. Vet., 62, 581. 3. Ball, L., Griner, L. Q. and Carroll, E. J. (1964) The Bovine Seminal Vesiculitis Syndrome, Amer. J. Vet. Res., 25, 105, 291. 4. Ball, L., Young, S. and Carroll, E. J. (1968) Seminal Vesiculi- tis Syndrome Lesions in Genital Organs of Young Bulls, Amer. J. Vet. Res., 29, 6, 1173. 5a. Bendixen, H. C. and Blom, E. (1947) Undersogelser over Fo- rekomsten of Brucellose Hos Tyre specielt med Henblik paa Be- tydmigen velden kunstige Insemation, Maanedsskr. for Dyrl., 59, 3, 4, 5, 61. 5b. Blom, E. (1979) Studies on Seminal Vesiculitis in the Bull; Malformation of the Pelvic Organs as a Possible Predisposing Factor in the Pathogenesis, Nord. Vet. Med., 31, 241. 6. Blom, E. and Christensen, N. O. (1947) Studies on the Patho- logical Conditions in the Testis, Epididymis and Accessory Sex Glands in the Bull, Skand. Vet. Tijdskr., 37, 1. 7. Blom, E. and Christensen, N. O. (1965) Seminal Vesiculitis in the Bull, Caused by C. pyogenes, Nord. Vet. Med., 17, 435. 8. Blom, E. and Dam, A. (1964) Escherichia coli in Bull Semen and Their Possible Causal Significance for the Etiology of Ve- siculitis, Proc. Vth Intemat. Congr. on An. Reprod., Trento, V, 253. 9. Blom, E. and Emo, H. (1967) Mycoplasmosis: Infections of the Genital Organs of Bulls, Acta. Vet. Scand., 8, 186. 10. Bouters, R. (1964) A Virus with Enterogenic Properties Causing Degeneration of the Germinal Epithelium in Bulls, Nature, 201, 217. 11. Carroll, E. J., Ball, L. and Scott, J. A. (1963) Breeding Sound- ness in Bulls—A Summary of 10,940 Examinations, JAVMA, 142, 1105. 12. Carroll, E. J., Ball, L. and Young, S. (1968) Seminal Vesiculi- tis in Young Beef Bulls, JAVMA, 152, 12, 1749. 13. Cooper, W. L. (1979) Methods of Determining the Site of Bac- terial Infections in the Stallion Reproductive Tract, Proc. for Soc. forTheriog., Mobile, Alab., 1. 14. Corbeil, L. D., Bier, P. J., Hall, C. E. and Duncan, J. R. (1976) Immune Response to Genital Mycoplasmosis in Bulls, Theriog., 6, 1, 39. 15. Delahanty, D. D. (1963) Seminal Vesiculitis—One Cause of Infertility in The Bull, Farm Research, Cor. Agr. Exp. State, 29, 2, 14. 16. DeKeyser, J., Spincemaille, J. and Brone, E. (1962) Brucella suis in Sperm and Genitals of Naturally Infected Boars, Vlaams Diergeneesk, Tijdschr., 31, 6, 171. 17. Deyoe, B. L. (1967) Pathogenesis of Three Strains of Brucella suis in Swine, Amer. J. Vet. Res., 28, 125, 951. 18. Doig, P. A. (1981) Bovine Genital Mycoplasmosis, Can. Vet. J., 22, 339. 19. Doig, P. A., Ruhnke, H. L., Waelchli-Suter, R. O., Palmer, N. C. and Miller, R. B. (1981) The Role of Ureaplasma, In- fection in Bovine Reproductive Disease, Compend. on Cont. Educ., 3, 9, 324. 20. Emo, H. (1960) Mycoplasmosis: Demonstration of Pathogenici- ty of a Danish Strain of Mycoplasma, Acta. Vet. Scand., 8, 184. 21. Emo, H. and Phillipsen, H. (1969) Mycoplasmosis: Cervical and Uterine Infection of Heifers with a Danish Strain of My- coplasma Bovigenitalium, Acta. Vet. Scand., 10, 108. 22. Fennestad, K. L., Pedersen, P. S. and Muller, T. (1955) Staph- ylococcus aureus as a Cause of Reproductive Failure and so- called Actinomycosis in Swine, Nord. Vet. Med., 7, 11, 929. 23. Galloway, D. B. (1964) A Study of Bulls with the Clinical Signs of Seminal Vesiculitis, Acta. Vet. Scand. 5, Suppl. 2. 24. Hall, C. E. and McEntee, K. (1981) Reduced Post-thawing Sur- vival of Sperm in Bulls with Mycoplasmal Vesiculitis, Cor. Vet., 71, 111. 25. Hoover, T. R. (1979) Bacterial Seminal Vesiculitis in Bulls, Proc. for Soc. for Theriog., Mobile, Alab., 92. 26. Humphrey, J. D., Little, P. B., Stephens, L. R., Bamum, D. A., Doig, P. A. and Thorsen, J. (1982) Prevalence and Distri- bution of Hemophilus somnus in the Male Bovine Reproduc- tive Tract, Amer. J. Vet. Res., 43, 5, 791. 27. Jones, T. H., Barrett, K. J., Greenhorn, L. W., Osborne, A. D. and Ashdown, R. R. (1964) Seminal Vesiculitis in Bulls As- sociated with Infection by Actinobacillus actinoides, Vet. Rec., 76, 24. 28. Jurmanova, K. and Sterbova, J. (1977) Correlation Between Im- paired Spermatozoan Motility and Mycoplasma Findings in Bull Semen, Vet. Rec., 100, 157. 29. King, G. J. and McPherson, J. W. (1969) Influence of Seminal Vesiculectomy on Bovine Semen, J. Dairy Sci., 52, 11, 1837. 30. LaFaunce, N. A. and McEntee, K. (1982) Experimental My- coplasma Bovis Seminal Vesiculitis in the Bull, Cor. Vet., 72, 150. 31. Larsen, A. B., Stalheim, O. H. V., Hughes, D. E., Appell, L. H., Richards, W. D. and Hines, E. M. (1981) Mycobacterium paratuberculosis in the Semen and Genital Organs of a Semen- Donor Bull, JAVMA, 179, 2, 169. 32. Larson, L. L. (1969) Disease Incidence in 1481 Bulls Examined for Use in Artificial Insemination, AVMA, Ann. Meeting, Min- neapolis, Mimeographed Notes. (See Proc. 7th Internat. Congr. on Animal Reprod. and Art. Insem., (1972), 1473. 33. Lein, D. H. (1982) Bovine Reproductive disorders Associated with Ureaplasma, Mycoplasma, Hemophilus somnus and Chla- mydia, Proc. Ann. Conf. Soc. for Theriog. Milwaukee, Wise. 34. Mare, J. and VanRensburg, S. W. J. (1961) The Isolation of Viruses Associated with Infertility in Cattle—A Preliminary Re- port, J. S. Afr. Med. Assoc., 32, 201. 35a. McEntee, K. (1962) Seminal Vesiculitis in the Bull, Proc. USLSA. (66th Ann. Meeting). 160. 35b. McEntee, K. (1970) Pathology of Domestic Animals, 2nd Ed., Vol. 1, Edit, by Jubb, K. V. and Kennedy, P. C., Academic Press Inc., N.Y.C. 36. Mensik, J., Bohac, J. and Setka, R. (1961) The Etiology of Infectious Orchitis in Bulls in Czechoslovakia, Vet. Bull., 31, 323. 37. Onoviran, O., Truscott, R. G., Fish, N. A., Barker, C. A. V. and Ruhnke, H. L. (1975) The Recovery of Mycoplasmas from the Genital Tracts of Bulls in Artificial Breeding Units in On- tario, Can. J. Comp. Med., 39, 474. 38. Panangala, V. S., Hall, C. E., Caveney, N. T., Lein, D. H. and Winter, A. J. (1982) Mycoplasma bovigenitalium in the Upper Genital Tract of Bulls: Spontaneous and Induced Infec- tions, Cor. Vet., 72, 929. 39. Panangala, V. S., Winter, A. J., Wyesinka, A. and Foote, R. H. (1981) Decreased Motility of Bull Spermatozoa Caused by Mycoplasma bovigenitalium, Amer. of J. Vet. Res., 42, 12, 2090. 40. Parsonson, I. M. (1970) Mycoplasma Bovigenitalium. Experi- mental Induction of Genital Disease in Bulls, PhD. Thesis, Cor- nell Univ., Ithaca, N.Y.854 VETERINARY OBSTETRICS 41. Parsonson, I. M., Al-Aubaidi, J. M. and McEntee, K. (1974) Mycoplasma bovigenitalium: Experimental Induction of Gen- ital Disease in Bulls, Cor. Vet., 64, 240. 42. Parsonson, I. M., Hall, C. E. and Settergren, I. (1971) A Method for the Collection of Urethral Samples from Bulls for Micro- biological Examination, JAVMA, 158, 175. 43. Shewen, W. E. (1980) Chlamydial Infections in Animals: A Review, Can. Vet. J., 21, 2. 44a. Stalheim, O. H. V., Proctor, S. J. and Gallagher, J. E. (1976) Growth and Effects of Ureaplasmas (T. Mycoplasmas) in Bo- vine Oviductal Organ Cultures, Infection and Immunity, 13, 3, 915. 44b. Storz, J., Carroll, E. J., Ball, L. and Faulkner, L. C. (1968) Isolation of a Psittacosis Agent. (Chlamydia) from Semen and Epididymis of Bulls with Seminal Vesiculitis Syndrome, Am. I. Vet. Res., 29, 3, 549. 45. Vandeplassche, M. et al. (1969) Brucella suis infection and In- fertility in Swine, (abstr.), IAVMA, 154, 9, 1050. 46. Vanderplassche, M. and Devos, A. (1960) Excretion of Bru- cella Abortus in the Semen of a Stallion, Vlaams Diergeneesk Tijdschr., 29, 199. 47. VanderSluis, L. (1953) Experiences with the Examination into Herd Infertility, Proc. 1st World Congr. on Fert. and Steril., II XXV, 703. B. Diseases of the Prostate and Bulbourethral Glands 1. Archibald, I. (1957) The Surgery and Treatment of the Diseased Canine Prostate Gland, Pfizer Review, #18. 2. Archibald, I. and Bishop, E. J. (1956) Radiographic Visualiz- ation of the Canine Prostate Gland, IAVMA, 128, 7, 337. 3. Archibald, J. and Cawley, A. I. (1956) Canine Prostatectomy, IAVMA, 128, 4, 173. 4. Barsanti, J. A., Shotts, E. B., Jr., Prasse, K. and Crowell, W. (1980) Evaluation of Diagnostic Techniques for Canine Pros- tatic Diseases, JAVMA, 177, 2, 160. 5. Bennetts, H. W. (1947) A Further Note on Metaplasia of the Sex Organs of Castrated Male Sheep on Subterranean Clover, Austral. Vet. J. 23, 10. 6. Bloom, F. (1968) Canine Medicine, Edit, by Catcott, E. J., Amer. Vet. Public. Inc., Wheaton, 111. 7a. Cockerell, G. L. and MacCoy, D. M. (1978) Clinicopathologi- cal Manifestations of Selected Neoplasms, Cor. Vet., 68, Suppl. 7, 133. 7b. Finco, D. R. (1980) Diseases of the Prostate Gland of the Dog, in Current Therapy in Theriogenology, edit, by D. A. Morrow, W. B. Saunders Co., Philadelphia, 654. 8. Greiner, T. P. and Betts, C. W. (1975) Diseases of the Prostate Gland, in Textbook of Veterinary Clinical Medicine, Edit, by S. J. Ettinger, W. B. Saunder, Co., Philadelphia, 1274-1306. 9. Hale, W. H., Homeyer, P. G., Culbertson, C. C. and Bur- roughs, W. (1955) Response of Lambs Fed Varied Levels of Diethylstilbestrol, J. of An. Sci., 14, 4, 909. 10. Hall, W. C., Nielsen, S. W. and McEntee, K. (1976) Tumors of the Prostate and Penis, Bull, World Health Organ., 53, 247. 11. Hombuckle, W. E. and Kleine, L. J. (1980) Current Veterinary Therapy, Vol VII, Edit, by R. W. Kirk, W. B. Saunders Co., Philadelphia, 1146-1150. 13a. Hombuckle, W. E., MacCoy, D. M., Allan, G. S. and Gunther, R. (1978) Prostatic Disease in the Dog, Cor. Vet., 68, Suppl. 7, 284. 13b. Johnston, S. D., Larsen, R. E. and Olson, P. S. (1982) Canine Theriogenology, Soc. for Theriog. Jour. Vol. XI, 1-93. 14. Kirk, R. W., McEntee, K. and Bentinck-Smith, J. (1968) Ca- nine Medicine, Edit, by Catcott, E. J., Amer. Vet. Public., Inc., Wheaton, 111. 15. Larsen, J. S. (1966) Perineal Hemiorrhapy in Dogs, JAVMA, 149, 3, 277. 16. Leav, I. and Ling, G. V. (1968) Adenocarcinoma of the Canine Prostate Gland, Cancer, 22, 1329. 17. Leeds, E. B. and Leav, I. (1969) Perineal Punch Biopsy of the Canine Prostate Gland, JAVMA, 154, 8, 925. 18. Lumb, W. V. (1952) Prostatic Calculi in a Dog, JAVMA, 121, 14. 19. McEntee, K. (1970) Pathology of Domestic Animals, 2nd Ed., Vol. I, edit, by Jubb, K. V. and Kennedy, P. C., Academic Press, Inc., N.Y.C. and London. 20. Mulligan, R. J. (1949) Neoplasms in the Dog, Williams & Wil- kins Co., Baltimore, Md. 21. Schlotthaur, C. F. and Miller, J. A. S. (1941) Carcinoma of the Prostate Gland in Dogs, JAVMA, 99, 239. 22. Shull, R. M., Hayden, D. W. and Johnston, G. R. (1977) Uro- genital Blastomycosis in a Dog, JAVMA, 171, 730. 23. Walker, R. G. (1965) Observations on Perineal Hernia in the Dog, Vet. Rec., 77, 93. Miscellaneous conditions in the male animal in- cluding infection of the external genitalia. Tumors of the penis and prepuce have been described previously in this Chapter. Perianal (circumanal) gland neoplasms are seen only in dogs and usually around the anal ring and tailhead but also may be found elsewhere on the body. The neo- plasms involved are adenomas which are androgen de- pendent and carcinomas which are not androgen depen- dent and which must be differentiated from squamous cell carcinomas and adenocarcinomas arising from the anal sac or skin.4'29 Of 472 dogs with perianal gland neo- plasms about 82 percent were adenomas and 18 percent were carcinomas. About 80 percent occurred in male dogs, 10 to 15 percent in spayed females and about 5 percent in intact females.4'29 Dogs of the Cocker Spaniel, En- glish bulldogs, Samoyed and Beagle breeds were most often affected. The preferred treatment of perianal gland adenomas is castration rather than excision. In ulcerated or recurrent cases excision should be considered. In 123 dogs with adenomas only 7 had a recurrence of the adenoma after castration.29 About 10 to 20 percent of the perianal gland neoplasms (PGN) and nearly all of the carcinomas were malignant. Many metastasized to the iliac lymph nodes as determined by rectal palpation with resulting consti- pation and tenesmus. Most of these cases are inoperable and do not respond to castration. Radiation or chemo-INFERTILITY IN MALE ANIMALS 855 therapy has been tried in these cases with limited suc- cess.29 Infections of the prepuce, penis, terminal urethra and semen with bacteria, molds, protozoa, viruses and fungi occur in all male animals from the external envi- ronment and from infectious diseases of the upper uro- genital tracts. In normal healthy animals the upper uro- genital system is free of infectious organisms. However because of the location and structure of the prepuce and free portion of the penis, similar to the vestibule and caudal vagina in the female animal, these organs harbor a wide variety of saphrophytic and occasionally patho- genic organisms usually without any clinical signs of in- fection (See diseases of the prepuce and penis). Certain organisms present in the prepuce of “carrier” animals are considered to be venereal in nature and transmitted from the male to the female and cause an infectious disease of the reproductive tract. The organisms that are trans- mitted from the male prepuce to the female vagina at coitus are usually considered to be contaminants if no infectious inflammatory process is produced. A local in- fectious inflammatory process is most apt to occur if an older male is bred to a virgin female. A vulvitis, ves- tibulitis or vaginitis may develop with a secondary re- action of lymphoid tissues resulting in granular venereal vulvitis or vaginitis in the cow, ewe or bitch. This is followed in time by a local immunity with a regression of the inflammatory reaction. If organisms from the pre- puce and penis are carried into the uterus at coitus as in the mare, bitch and sow, temporary or prolonged en- dometritis may result depending on the degree of resis- tance or susceptibility of the female animal and the time required for immunity to develop. In artificial insemination in animals even if the col- lection and storage of semen is performed in a manner approaching asepsis many organisms from the penis and prepuce are in the ejaculate. In one study in stallions the mean bacterial population in undiluted semen collected in the above careful manner was 573,000 organisms per ml. Twenty one different species of bacteria were iso- lated many of which were potentially pathogenic.25 Cul- turing the penis and preputial cavity is of questionable value in the diagnosis of infertility because of the large number and variety of organisms recovered. However, it is of value in specific venereal infections to detect a carrier animal and after treatment to determine if he is free of the infection.5 (See culturing of the stallion in CEM and the bull for vibriosis and trichomoniasis.) Schultz and co-workers have described a practical method to test bovine semen samples for specific pathogen-free bovine semen.21,22 A compilation of the infectious organisms recovered from the prepuce, penis and semen of animals follows: in cows- m mares- Organisms resulting in venereal infections and dis- eases: Brucella abortus, Campylobacter fetus venerealis (vibriosis), Tricho- monas fetus, Mycoplasma bovigenitalium6 IBR-IPV virus, epi- vag virus in Africa, ureaplasmas,6 rarely Mycobacterium tuberculosis, Paratuberculosis16 26 27,28 and possi- bly papilloma virus21 and Chlamy- dia.24 Hemophilus equigenitalis, Trypa- nosoma equiperdum (Dourine), and equineherpes virus 3 (equine coital exanthema) [Possible “venereal” dis- eases, depending on the virulence and numbers of organisms introduced and the susceptibility of the mare might also include: Pseudomonas aeruginosa10,12 Klebsiella pneumoniae var genital- ium, Streptococcus genitalium and Actinibacillus equuli (Shigella)] Brucella ovis and melitensis, Acti- nobacillus seminis, and Spheropho- rus (Bacillus) necrophorus (lip and leg ulceration) and Toxoplasma gondii7 Brucella suis and possibly Staphy- lococcus aureus Brucella canis9 and the transmissible venereal tumor Other organisms, often called “opportunists” found in the prepuce that may either contaminate or infect fe- males at coitus or by artificial insemination are numer- ous and varied and include: the ubiquitous Gram nega- tive and Gram positive organisms and fungi and yeasts15,21 the most common of which are: Streptococci spp, Staphylococci spp., E. coli, Corynebacterium pyogenes, C. renale, Alkaligenes, Enterobacter spp., Serratia, Bordatella, Citrobacter spp., Proteus spp., bacillus spp., mi- crococcus spp., Spirochetes, Lepto- spira spp., Actinobacilli, Actino- myces spp., Aspergillus, Absidia, Rhizopus, Madura, Candida (Mo- nilia)15,20 and others. Viruses other than those causing venereal diseases may be transmitted by bovine semen including foot and mouth disease,3,13 21 bovine virus diarrhea-mucosal virus (BVD- MD),13,23 blue tongue8,13,21,22 ephemeral fever, bovine enteroviruses, parapoxvirus, lumpyskin disease virus, and others.13 Schultz stated that it is reasonable to assume in ewes- and does in sows— in dogs-856 VETERINARY OBSTETRICS that bovine adenoviruses, corona viruses, enteroviruses, parvoviruses and rotaviruses which are ubiquitous con- taminants are occasionally present in semen but there is no evidence they play a role in genital disease or infer- tility.21 Swine semen can contain foot and mouth disease virus, swine vesicular disease virus, parvovirus, picor- naviruses, adenoviruses and Japanese encephalitis vi- rus.13,18 Semen should be obtained from bulls in studs free of the vims as determined by repeated serologic tests or semen cultures.13 21,22 Maintaining a high level of im- munity by repeated vaccination with an efficacious in- activated BVD vims vaccine or with an attenuated nasal vaccine for IBR-IPV will probably prevent the elimi- nation of these common viruses in the semen of bulls.22,23 In one study a positive relationship was made between bulls latently infected with blue tongue vims that could be recovered from their semen and the presence of vesic- ulations between the acrosome and nucleus and virus- like particles in the affected spermatozoa.8 These vesicu- lations were different from the vacuoles, “craters” or “pouches” in the nuclear envelope of spermatozoa de- scribed previously in which the defects were hypothe- sized to be caused by a vims. (See spermatozoan ab- normalities.) Currently there is no definite evidence that viruses such as parainfluenza 3 vims13 bovine leukemia virus1,13,14,22,28a or porcine pseudorabies vims17 are spread in the semen. Bovine herpes mammillitis vims has not been reported to have been found in semen.22 Hemophilus somnus ap- parently is part of the resident bovine preputial flora.11 It should be noted that a number of these organisms are also common contaminants or residents of the upper re- spiratory tract. It is impossible to eliminate all organisms from the prepuce and free portion of the penis or the caudal por- tions of the female genital tract. However it is definitely desirable to control the venereal diseases and to prevent heavy contamination of the anterior or deeper portions of the female genital tract with vimlent organisms es- pecially in susceptible females with low resistance. The control and prevention of the venereal diseases have been discussed under the chapters on infertility in the various female domestic animals. To control the severe contamination of the female gen- ital tract with organisms from the males’ prepuce at co- itus various breeding hygiene practices have been fol- lowed with bulls15 and horses. The mares’ external genitalia and perineal region are carefully washed with soap and water and rinsed thoroughly. The tail is ban- daged and the mare is restrained. The stallion’s genitalia are also washed with a bland soap and water and thor- oughly rinsed before copulation. Excessive dust, saw- dust, sand or mud in the breeding shed or area is to be avoided. As mentioned under infertility in mares excess washing and the use of antiseptics on the stallion may irritate the prepuce and penis, may severely alter the “normal” bacterial flora and/or favor the development of strains of bacteria resistant to the antiseptic (chlor- hexidine) and possibly other antibiotics.2,12,193 In the boar surgical removal of the preputial diverticulum may re- duce preputial bacteria. The author has attempted to “douche” bulls’ sheaths prior to collection of semen in a sterile artificial vagina with very limited success in re- ducing bacterial contamination of semen. If artificial insemination is practiced the extension of the semen with extenders containing antibiotics has been a common and successful practice in reducing the num- bers of bacteria introduced into the genital tract of the female and has resulted in an improvement in conception rates (See vibriosis or campylobacteriosis in cattle). The use of lincomycin and spectinomycin semen extenders to control mycoplasms and the further addition of min- ocycline HCL to also control ureaplasma has been re- ported.6 The use of an extender containing penicillin and gentamycin greatly reduced the bacteria in the semen and prolonged the viability of the equine spermatozoa.253 In a study comparing polymyxin B sulfate and gentamycin it was recommended that the preferred antibiotic treat- ment for equine semen to control Klebsiella and Pseu- domonas organisms was 1000 units of the former anti- biotic per ml. of extended semen.25b The semen should be added to the fresh skimmed milk (heated to 95° C for 4 minutes in a double boiler before its use) extender with antibiotics and incubated at 38° C for at least 15 minutes to permit the bacteriocidal effects to occur. Similar re- sults have been obtained with bull and boar semen (See artificial insemination). To help prevent carrying the ubiquitous ureaplasmas, mycoplasmas and other organ- isms from the vulva and caudal vagina into the cervix and uterus on the insemination pipette, a sterile plastic cannula, through which the pipette may be inserted, can be used.6 Further studies on this practice should be con- ducted as a recent report indicated that routine use of a “protected” or “double” sheath was of questionable value.196 References Miscellaneous Diseases of the Male Animal: Perianal Gland Neoplasms and Infections of the Prepuce, Penis, Terminal Urethra and Semen. 1. Bartlett, D. E. (1979) Bovine Leukosis and AI, Bov. Pract., 14, 111.INFERTILITY IN MALE ANIMALS 857 2. Bowen, J. M. (1982) Effects of Washing on the Bacterial Flora of the Stallion’s Penis, Abstr. Eq. Vet. Data, 3, 9, 137. 3. Callis, J. J. and McKercher, P. D. (1980) Dissemination of Foot and Mouth Disease Virus through Animal Products, Bov. Pract., IS, 170. 4. Cockerell, G. L. and MacCoy, D. M. (1978) Clinical Patho- logical Manifestations of Selected Neoplasms, Cor. Vet., 68, (Suppl. 7) 133. 5. Cooper, W. L. (1979) Methods of Determining the Site of Bac- terial Infections in the Stallion Reproductive Tract, Proc. for the Soc. for Theriog., Mobile, Alab. 1. 6. Doig, P. A. (1981) Bovine Genital Mycoplasmosis, Canad. Vet. J., 22, 339. 7. Dubey, J. P. and Sharma, S. P. (1980) Prolonged Excretion of Toxoplasma gondii in Semen of Goats, Amer. J. Vet. Res., 41, 5, 794. 8. Foster, N. M., Alders, M. A., Luedke, A. J. and Walton, T. E. (1980) Abnormalities and Virus-like particles in Spermatozoa from Bulls Latently Infected with Bluetongue Virus, Amer. J. Vet. Res. 41, 7, 1045. 9. George, L. W., Duncan, J. R. and Carmichael, L. E. (1979) Semen Examination in Dogs with Canine Brucellosis, Amer. J. Vet. Res., 40, 11, 1589. 10. Hughes, J. P., Asbury, A. C., Loy, R. G. and Burd, H. E. (1967) the Occurrence of Pseudomonas in the Genital Tract of Stallions and Its Effect on Fertility, Cor. Vet., 57, 1, 53. 11. Humphrey, J. D., Little, P. B., Stephens, L. R., Bamum, D. A., Doig, P. A. and Thorsen, J. (1982) Prevalence and Distri- bution of Hemophilus somnus in the Male Bovine Reproduc- tive Tract, Amer. J. Vet. Res., 43, 791. 12. Johnson, T. L., Kenney, R. M., McGee, W. R. and Polk, H. C., Jr. (1980) Pseudomonas Infection in a Stallion: A Case Re- port, Proc. 26th Ann. Conv. AAEP, Anaheim, Cal., 111. 13. Kahrs, R. F., Gibbs, E. P. J. and Larsen, R. E. (1980) The Search for Viruses in Bovine Semen, A Review, Theriog., 14, 2, 151. 14. Kaja, R. W. and Olson, C. (1982) Non-lnfectivity of Semen from Bulls Infected with Bovine Leukosis Virus, Theriog., 18, I, 107. 15. Kendrick, J. W., Harlan, G. P., Bushnell, R. B. and Kronlund, N. (1975) Microbiologic Contamination of Bovine Semen, Theriog., 4, 4, 125. 16. Larson, A. B., Stalheim, O. H. V., Hughes, D. E., Appell, L. H., Richards, W. D. and Hines, E. M. (1981) Mycobacterium paratuberculosis in the Semen and Genital Organs of a Semen- Donor Bull, JAVMA, 179, 2, 169. 17. Larsen, R. E., Shope, R. E., Jr., Leman, A. D. and Kurtz, H. J. (1980) Semen Changes in Boars after Experimental Infection with Pseudorabies Virus, Amer. J. Vet. Res., 41, 5, 733. 18. Lukert, P. D. (1977) Rapid Techniques for the Detection Pi- comaviruses in Boars’ Semen, JAVMA, 171, 10, 1090 (Ab- stract). 19a. Nakahara, H. and Kozukue, H. (1982) Isolation of Chlorhexi- dine Resistant Pseudomonas aeruginosa from Clinical Lesions, J. Clin. Microbiol., 15, 1, 166. 19b. Newman, S. K. (1983) Do We Need More AI Sanitary Precau- tions, Hoard’s Dairyman, Feb. 10, p. 172. 20. Richard, J. L., Fichtner, R. E. and Pier, A. C. (1976) Yeasts in Bovine Semen, Cor. Vet., 66, 362. 21. Schultz, R. D. (1977) When Can We Achieve Our Goal of Pro- viding Specific Pathogen-Free Bovine Semen? Proc. 81st Ann. Mtg. USAHA, Minneapolis, Minn. 141. 22. Schultz, R. D., Adams, L. S., Letchworth, G., Sheffy, B. E., Manning, T. and Bean, B. (1982) A Method to Test Large Numbers of Bovine Semen Samples for Viral Contamination and Results of a Study Using This Method, Theriog., 17, 2, 115. 23. Sheffy, B. E., Hall, C. E. and Williams, A. J. (1980) Patho- genesis of BVD Virus Infection in Adult Bulls, A Factor in Pro- duction of BVD Virus Free Semen, Proc. 84th Ann. Mtg. USAHA, Louisville, Ky. 24. Shewen, W. E. (1980) Chlamydial Infections in Animals: A Re- view, Canad. Vet. J., 21, 2. 25a. Simpson, R. B., Bums, S. J. and Snell, J. R. (1975) Microflora in Stallion Semen and Their Control with a Semen Extender, Proc. 21st Ann. Conv. AAEP, Boston, Mass., 255, J. Reprod. Fert. Suppl. 23, 139-142, 1975). 25b. Squires, E. L. and McGlothlin, D. G. (1980) Antibiotic Treat- ment of Stallion Semen, Proc. Ann. Mtg. Soc. For Theriog., Omaha, Nebr., 64. 26. Thoen, C. O., Hines, E. M., Stumpff, C. D., Parks, T. W. and Sturkie, H. N. (1977) Isolation of Mycobacterium bo vis from the Prepuce of a Herd Bull, Amer. J. Vet. Res., 38, 6, 877. 27. Thoen, C. O. and Muscoplat, C. C. (1979) Recent Develop- ments in Diagnoses of Paratuberculosis (Johnes Disease), JAVMA, 174, 8, 838. 28a. Thurmond, M. C. and Burridge, M. J. (1982) Application of Research to Control of Bovine Leukemia Virus-Free Cattle and Semen, JAVMA, 181, 12, 1531. 28b. Williams, W. L. (1941) Diseases of the Genital Organs of Do- mestic Animals, Ithaca, N.Y., 319. 29. Wilson, G. P. and Hayes, H. M., Jr. (1979) Castration for Treatment of Perianal Gland Neoplasms in the Dog, JAVMA, 174, 12, 1301. DIAGNOSIS OF STERILITY AND INFERTILITY IN THE MALE AND EVALUATION OF BREEDING SOUNDNESS The examination of a male animal to assess his fer- tility or breeding soundness includes both objective and subjective tests or observations usually during a single examination or over a short time period. This results in a value judgment or opinion on the part of the veteri- narian. Its scientific validity is limited by the number and frequency of tests performed, their objectivity and their repeatability. In referred laboratory tests the ex- pertise of the laboratory personnel in the fields of serolo- gy, microbiology, and pathology are also involved. Most males can be categorized as either a satisfactory potential breeder, a questionable potential breeder or an unsatis- factory potential breeder.9 However, a single breeding soundness examination does not indicate the males’ past soundness nor his ability to cause conception in the fu- ture since too many unknown variables of management, nutrition, and disease in the male and the females to which he was, or will be, bred make retrospective or prognos- ticative specific judgments uncertain. For this reason the veterinarians’ knowledge and experience in the fields of male anatomy, physiology, behavior and pathology are858 VETERINARY OBSTETRICS of paramount importance in arriving at a considered judgement or opinion. The client should be informed that this is an opinion and not an absolute factual determi- nation unless the findings conclusively indicate the male is permanently sterile. As the late noted Nils Lagerlof stated to the author, “Never indicate that a certain male is fertile based on your examination; only indicate that you see no reason why this male should not be fertile.” Since much more basic and applied research over the past 30 years has been conducted on bulls than other male animals, the discussion in this chapter on male in- fertility will emphasize the bovine species. However, the similarities between males of all domestic species are so marked all species are included. The breeding soundness or fertility examination of male animals is usually requested in three situations; a pre- purchase or sale examination for either the buyer or the seller or both; the prebreeding season examination in beef bulls, stallions or rams to assure fertile males are used during the breeding season; and when an infertility prob- lem arises in the females bred to the male to determine if the male was the cause of the problem and if so whether the condition in the male is temporary or permanent. Thus the primary objective of evaluation of breeding sound- ness is to determine which males are infertile so they may be temporarily or permanently eliminated from breed- jjlg I’2,6a,lKBulls)10,19(Stallions)6,12(Rams&Bucks)7,8(Boars)8b(Dogs&Toms)6a,8 Historically breeding soundness evaluations (BSE) in bulls was developed in Colorado by Drs. H. J. Hill, L. C. Faulkner, J. S. Scott, J. A. Scott, E. J. Carroll and L. Ball, following severe winters in the late 40s’ and 50s’ when frostbite of the scrotum of range beef bulls resulted in severe herd infertility in subsequent breeding seasons. These evaluations were made possible by the development of the bovine electroejaculator to obtain se- men samples. The results of a study from 1954 to 1962 of 10,940 beef bulls in Colorado revealed that 79.2 per- cent of the bulls were satisfactory potential breeders, 11.2 percent were questionable potential breeders and 9.5 percent were unsatisfactory bulls to be culled or with- held from breeding.' A similar study of 1,005 bulls in Missouri produced similar results of 83.5, 9.8 and 6.9 percent, respectively.2 Less than 0.5 percent of bulls in both studies were unable to be classified. A similar re- port on 1,846 bulls examined over a period of 19 years for use in artificial insemination has also been pub- lished.6 Both mature and immature bulls were examined and 17 to 19 percent of the bulls were rejected as un- satisfactory. The examination for infertility of any sire should be careful and thorough, following a definite procedure so that no symptom or lesion will be missed. A complete record of this examination should be made as the ex- amination progresses. A careful, complete examination of a male is essential to the assessment of his breeding potential. This examination of the male should consist of three major components (1) history and/or breeding records, (2) physical examination including the assess- ment of libido or sex drive and the various serological, cultural and other diagnostic tests and (3) the examina- tion of the semen. History and Records—Breeding records are very helpful in the diagnosis of fertility. If the male was bred to a sufficient number of normal females, these records accurately indicate the relative fertility of the sire. If pos- sible these records should be reviewed for two time in- tervals of 1 to 2 years and the past 6 months. This review will indicate the number of services per conception over a period of several years as well as the past few months, which is of value in diagnosing whether a venereal dis- ease or a pathologic condition affecting the sire is acute or chronic. If records are not available, pregnancy ex- aminations on females recently bred by the male may be necessary. The records of the females bred to this male should be reviewed to see if there is an increased inci- dence of abnormal genital discharges, delayed estrums or abortions occurring after breeding, indicating possible vibriosis, trichomoniasis, canine brucellosis or the pres- ence of some other disease causing the early or late death of the embryo or fetus. If two or more males are used for natural breeding in the same herd the breeding rec- ords may be necessary to determine if one or more bulls are infertile. The conception rate in a pasture-bred herd may be a good index to the fertility of the bulls in that herd. If possible a number of the daughters of the bull ex- amined should be observed for conformation and the presence of any inherited defects; also, their conception rates should be noted. In multipara the litter size, and viability of the offspring of the sire and his daughters should be noted. The breeding records of the male’s sire and dam should be reviewed if they are available. These animals and/or their relatives should be examined or a record obtained for any evidence of hereditary disease. If the male’s sire and dam are dead the reasons for their death should be checked. Bulls that have been operated upon for umbilical hernia, deviated penis, or other de- fects are not desirable, as they may transmit these de- fects. The health history of the male should be reviewed. Any illnesses, especially those requiring veterinary treat- ment, should be investigated. This review should in- clude diseases suffered as a young animal as well as any recent sickness. The records of any and all preventiveINFERTILITY IN MALE ANIMALS 859 vaccinations of the male should be secured. Information should be obtained on the ration fed the male, the amount and frequency of feeding and whether any signs of nu- tritional deficiency are present. The physical examination of the male consists of noting the following: his age, according to his registra- tion papers and his teeth; his conformation and the con- dition of his hoofs, limbs, and joints; any defects either congenital, hereditary, or acquired, and their severity; his general condition, attitude, temperament and hair coat. Obesity and emaciation are serious concerns in breeding males. The body temperature should be taken and a care- ful clinical examination made of the eyes, circulatory, respiratory, digestive, urinary and lymphatic systems, for evidence of disease that might affect his present or future health. Any unusual symptoms such as coughing, nasal discharge, bloody urine, persistent or intermittent diarrhea, and icterus should be carefully investigated. The teeth, oral cavity, eyes, and face should be examined for actinomycosis, carcinoma, blindness, or other lesions. A rectal examination of the kidney(s) and bladder, acces- sory sex glands and ductus deferens (ampullae) iliac lymph glands, and internal inguinal rings should be performed in large animals. If the conformation of the male is poor or defective, the gait and manner and ease of mounting should be ob- served carefully. Too straight or “postleg” rear limbs, arthritis and spastic syndrome in bulls are frequently as- sociated. Slightly “sickle-hocked” bulls and bulls with a good heel are preferred over the former. It is also de- sirable to discriminate against males with other confor- mational defects including: sickle-hocks, bow-legged or camped behind rear limbs.9 Any signs of posterior weak- ness or paresis as indicated by a limp flaccid tail and ataxia is very undesirable in breeding males. If rear limb lameness is present the joints should be examined for arthritis and the hooves examined for pododermatitis, deformities, laminitis or quittors. Twenty five percent of 600 boars purchased over a two-year period by 71 pro- ducers in Illinois were never used due to lameness or lack of libido.12 The examination of the male in the presence of the female is desirable and necessary in order to observe the degree of sexual desire or libido, which may vary from no interest in the female to extremely eager mounting. Any abnormalities, hesitancy, or evidence of pain on erection, mounting, copulating, and ejaculating should be noted. Tests for libido or sexual desire are often dif- ficult, time consuming and hard to adequately carry out on a large number of males. (See prior discussion in this Chapter.) However in a cited study9 20.6 percent of 548 bulls were culled as poor potential breeders with 55 per- cent of those culled for physical abnormalities, 43 per- cent for poor libido or serving capacity and only 2 per- cent for poor semen quality. At this time the penis and prepuce should be examined for evidence of inflamma- tion, granular venereal disease in bulls, tumors, adhe- sions, congenital short penis, phimosis, and deviation of the penis. Any history or evidence of vices or bad habits should be watched for before and during the physical examination. In some males it may be desirable to ex- amine the penis further, if necessary under tranquiliza- tion, a pudendal nerve block, or general anesthesia. Some owners who sell purebred males take a motion picture of the male copulating with a female before a sale, to prevent having the male returned with the report that it would not copulate normally. At this time the male’s gait and manner of moving, his positioning of himself on the mount, his seeking actions with his penis, his intromis- sion and thrusting action and his dismounting are also noted. Any lameness or abnormal gait should be closely investigated. Spastic syndrome, or “stretches,” in bulls may not be noted in the early or mild cases unless the bull is seen as it rises or is backed. Promptness and vigor of intromission and ejaculation, however, are not a guar- antee of fertility. The rest of the reproductive system should be care- fully examined, clinically.911 (See Stallion,6 ram and buck,7'8 dog- and boar.8) The testes, epididymides, spermatic cord and scrotum may be examined by pal- pation. This should be done bimanually with the large male properly restrained or tranquilized to prevent injury to the examiner. The size and shape of the scrotum and the position of the testes in the scrotum should be ob- served. Any wryness or difference in the appearance of the two sides of the scrotum should be a cause for further careful examination. A “tilted” or “horizontal” testis in a bull is often located dorsally in the scrotum due to a misplaced attachment of the cremaster muscle resulting in testicular degeneration and atrophy. The testes should be palpated for size, shape, consistency, and the pres- ence of adhesions to the scrotum. The scrotum of bulls, rams and possibly stallions should be measured by tape, calipers or ones’ fingers. Any unusual findings should be compared with the other testis or with the testes of a normal male if one is available. The head, body and tail of each epididymis should be carefully palpated for en- largements, missing segments, granulomas and ab- scesses. Any unusual softness, firmness, swelling, atro- phy, heat or pain in the testes, scrotum, or epididymis should be carefully checked. This examination will re- veal the possible presence of scrotal hernias, cryptor- chidism, testicular hypoplasia, segmental aplasia of the mesonephric duct, varicocele, hydrocele, adhesions, tes-860 VETERINARY OBSTETRICS ticular degeneration, fibrosis and mineralization (cal- cium deposition), testicular atrophy, orchitis, possible tumors, and other testicular, epididymal, or scrotal pa- thology. Semen production is closely related to testicular size and consistency. Many workers"’1’17'18'29 have reported a close relationship between scrotal circumference, and the number of spermatozoa produced in exhaustion trials in bulls. There was no relationship between the scrotal size and body size on the numbers of sperm cells in a single ejaculate. The average scrotal circumference in bulls is as follows: A Compilation of Measurements of Scrotal Circum- ference in Centimeters of over 3,000 Bulls indicated the following Classification of Bulls of all Breeds, except Brahmas.11’5,6 Age In Months Classification 12-14 15-20 21-30 30+ Score’ Very good— > 34** >36 >38 >39 40 Good— 30-34 31-36 32-38 33-39 24 Poor— <30 <31 <32 <34 10 [Brahmas (average) —(Pre- 27-29 31-33 35-37] pubertal) *Score designated for analysis of potential breeding ability in bull evaluation procedure for Society for Theriogenology. **Centimeters (Scrotal tapes may be obtained from Lane Manuf. Inc., Denver Colo.) As described previously in this Chapter the scrotal cir- cumference of rams and the testis width and length in stallions is also closely correlated with their output of spermatozoa. The number of spermatozoa produced per gram of normal seminiferous tubules or testes is fairly constant for adult normal bulls since about 75 percent of the testis is composed of seminiferous tubules. For bulls over 6 years of age the scrotal circumference as an in- dicator of sperm cell production may be of limited value because of chronic testicular changes in older bulls. A tonometer was developed that could objectively measure the consistency of the testes.17 This was highly correlated with semen quality tests. Normal testes have a firm “springy” tone. A soft or very firm consistency often was related to poor semen quality, testicular de- generation, fibrosis or atrophy. An examination of the retractor penis muscle, the sig- moid flexure of the penis, and the external palpation of the sheath and penis should follow the examination of the testes and scrotum. Often a short or limited protru- sion of the penis in bulls is associated with paunchiness or excessive obesity, a “dropped loin” on mounting and inability to copulate successfully. Any swelling, fibrous tissue, abscesses, hematomas, growths or adhesions should be noted and their significance evaluated. The Bos in- dicus bulls or their crosses often have a very pendulous and long prepuce. These breeds and the polled breeds usually have a mild to moderate eversion of the prepuce with a predisposition to trauma, infection and frostbite. Rectal examination of the accessory reproductive glands as well as other pelvic and abdominal organs is neces- sary in the physical examination of the male. This can readily be done with the hand and arm in the bull and stallion, and with the finger in the dog. In the boar and ram examination is difficult or impossible. In the large animals the pelvic urethra is noted as a firm round struc- ture on the floor of the caudal portion of the pelvis. The Cowper’s or bulbo-urethral glands are covered with muscle so they cannot be palpated but they are seldom diseased. In the bull and stallion the prostate gland is palpated as a thick transverse fibrous band of tissue around the ur- ethra at the cranial end of the pelvic urethra and just caudal to the neck of the bladder and the ampullae and vesicular glands. These accessory reproductive glands are carefully palpated for their size, and consistency. Any abnormality is carefully recorded especially if a patho- logical process, inflammation, induration or abscess is noted by a thickening of the part, atrophy, or swelling of the organ, and if pain is produced on palpation. In severe inflammations extensive adhesions may be pres- ent. If one or a portion of one of the accessory glands, ampulla, or ductus deferens is missing or dilated a con- genital anomaly is usually present. In the dog the size of the prostate can be noted. If the gland is asymmetrical an abscess, cyst or carcinoma should be suspected and confirmed. On palpation through the abdominal wall large prostatic cysts or a distended colon may be palpated if the prostate is hyperplastic. In rare cases in the dog a perineal hernia may be present associated with a hyper- plastic prostate, and should be differentiated from a di- lation or diverticulum of the rectum. In the bull and stal- lion the kidneys and other pelvic structures may also be examined for evidence of cystitis, nephritis, or possible tumors. Fat necrosis is rarely found in bulls. Other diagnostic tests and examinations should be per- formed on valuable sires especially where herd records indicate that a venereal disease might be present. These tests have been described previously in this chapter, in Chapter 3 on abortion diseases or in chapters on infec- tious, reproductive and systemic diseases transmitted by coitus or by artificial insemination with infective semen. These tests would include the many serologic tests, flu- orescent antibody tests, cultures of preputial mucus or semen or other special tests including tuberculin tests or tests for blood parasites, or autoimmune factors. Isola-INFERTILITY IN MALE ANIMALS 861 tion of all new acquired males for 4 to 8 weeks while tests for infectious, contagious or venereal diseases and the administration of effective vaccines are being con- ducted is a sound practice to prevent the introduction of diseases into a herd or band of females by newly ac- quired males. SEMEN COLLECTION AND EXAMINATION The third part of a careful examination of a male is the semen examination. This is of great diagnostic value in determining the cause, severity and degree of testic- ular or accessory gland pathology present, as well as being of value in estimating the male’s fertility. There is usu- ally a definite correlation between testicular pathology, disease of the reproductive tract and accessory glands and the semen characteristics and fertility. The tech- niques and procedures used in the semen examination of bulls, rams and humans are more accurate than in the other animals because more work, research and detailed observations have been made on these species. More work on the other species of animals is highly desirable and is being undertaken. From the many reports in humans, bulls, and rams and the less numerous reports in boars, stallions, dogs and tom cats, the same general principles are applicable in semen examinations of all species. Se- men characteristics or quality usually remain rather con- stant and within narrow limits for nearly all ejaculates from each male over a period of months and even years. Due to acute, severe, adverse influences, semen quality may decline rather rapidly but improvement is slow and usually requires months for recovery to occur. Since it takes approximately 50 to 70 days for the development of mature sperm cells from spermatogonia until ejacu- lation, it is possible for acute testicular degeneration to be present in the testes yet the semen quality as it ap- pears in the ejaculate to be fairly satisfactory. The dis- eased state or infertility may become evident in 2 to 6 weeks. Testicular biopsies are seldom indicated in do- mestic animals except in aforementioned situations since one or more semen samples usually accurately reflect the condition of the seminiferous tubules of the testes. Males with the highest quality or the lowest quality of semen and fertility on the initial examination usually have the same quality when they are re-examined, of no se- vere systemic disease or stress occurs before times of collection (See Semen Quality, Examination and Fertility5,7'80’81'123). Be slow to condemn a male or give a poor prognosis based on a single semen examination revealing poor quality semen; especially if the male is young and immature, if the male has recently been se- verely stressed or had an acute debilitating disease, if the male is very valuable, if the male has not ejaculated recently, or if his semen has been collected and exam- ined under adverse conditions by untrained persons. The entire ejaculate should be examined and not just a por- tion of it such as the “tail end” sample taken from a stallion or other male as it dismounts. Usually bulls, rams and men with good to fair semen samples have good to excellent fertility; while males with poor to very poor semen samples are invariably infertile or ste- rile. (See Semen Quality Examination and Fer- tility. 54b’60“63’80'81) In stallions, boars and dogs where most of the ejaculate enters the uterus poor to very poor semen samples result in reduced fertility and small litter size in the latter, to occasional sterility. Completely sterile stal- lions are rare. If some motile, normal sperm cells are present in the ejaculate conception is possible in all spe- cies. Occasionally males with apparently normal-ap- pearing, good quality semen samples may be incapable of producing conception. Therefore the examination of semen samples and the physical examination of the males as a means of evaluating fertility should be performed carefully and the result should be interpreted conserva- tively. If one criterion used to evaluate semen is poor, the sample should be graded poor or questionable be- cause usually for satisfactory or good fertility all of the criteria must be satisfactory or good. Occasionally one poor criterion of semen quality maybe compensated for by a good criterion, for example, good motility and low concentration often result in fair conception rates. The Collection of Semen for examination is practical and fairly easy in all species of male domestic animals except possibly the boar and cat, in which certain indi- viduals may require general anesthesia and electroejacu- lation. The Bull may have semen collected in several ways, but only two are of practical value for semen evaluation. The simplest and earliest method of semen collection was from the vagina, by means of a spoon or syringe with a long nozzle following a natural service. A speculum may be helpful in this method. This technique is unsatisfac- tory because the relatively small volume of semen is mixed with a large volume of vaginal mucus so this method was not suitable for the evaluation of semen quality. The massage technique in the bull, first described in 19257 as a means of obtaining semen for examination and artificial insemination, has been further de- scribed.311'23 This method is employed rather seldom be- cause some skill and experience are necessary to mas- sage the ampullae per rectum; some bulls respond poorly to the procedure, and semen collections are usually not as clean and contain many more bacteria than those pro-862 VETERINARY OBSTETRICS duced by other methods because the semen passes through the prepuce and drips from the preputial hairs. For this latter reason it is necessary to carefully wash, rinse, and dry with a brush and cotton pledgets or a clean towel the prepuce and the preputial hairs and the region around the preputial opening with warm physiological saline so- lution or clean warm water. This washing, if combined with stroking of the sheath, may induce urination, which is desirable inasmuch as urine is toxic to spermatozoa and massage of the ampullae is likely to stimulate uri- nation. The prepuce should be carefully douched with 250 to 500 ml. of a physiological saline solution to re- move epithelial cells, smegma, and dirt. Sexual stimu- lation of the bull with a cow or another bull is helpful in obtaining a satisfactory semen sample. The bull should be handled quietly and kept relaxed. The operator, wear- ing a glove and sleeve, gently inserts his lubricated hand and forearm into the bull’s rectum, emptying it of feces. The seminal vesicles are then gently massaged a few times with the fingers by backward and downward strokes to- ward the urethra and a cloudy fluid containing few if any spermatozoa is expelled. An assistant with a funnel and several test tubes collects the seminal fluid and semen as it drips from the preputial opening or penis. The am- pullae are then massaged similarily in a slow, rhythmic manner. With the second finger between the ampullae and the third and fourth fingers on the outside of the ampullae, the ampullae are “stripped” of semen by pres- sure against the floor of the pelvis and then the pelvic urethra may be massaged. Sometimes the ejaculate is re- tained in the sigmoid flexure of the penis or in the prox- imal portion of the prepuce; therefore after massaging the ampullae, the S-curve of the penis should be straight- ened out. About 80 percent successful collections were reported in 100 attempts on 15 bulls.23 Twenty one bulls were massaged 102 times and semen satisfactory for use in artificial insemination was collected with an average volume of 5.9 ml. with a slightly reduced concentra- tion." No injury or bleeding was produced. Fertility was equal to samples collected in the artificial vagina. If massaged regularly by the same operator most bulls usu- ally become accustomed and conditioned to this proce- dure within 3 to 4 weeks and produce a good semen sample promptly at the time of each collection. The in- dications for using the massage technique are the same as in the electroejaculation technique, namely, in bulls that are impotent, unwilling, or are unable to copulate. Another author22 has described a method of gentle man- ual massage of the glans through the sheath wall to pro- duce erection and ejaculation without restraint in gentle, calm bulls in a quiet isolated environment. In practice the massage technique on bulls is seldom used because it required more skill and patience than the other collec- tion procedures. Electroejaculation in bulls has proven to be a prac- tical, easy, rapid and routine technique, especially for range beef bulls.-'-'3-4-51214'17-21-25 This technique was first described and extensively used in rams in 1936.16 Mod- ifications to adapt this technique to bulls has been suc- cessful. The probe is inserted into the rectum after the feces have been removed. The probe is usually available in three sizes about 60, 75 and 95 mm. in diameter with longitudinal electrodes, 3 in number on its ventral sur- face, and these must be kept clean and lightly sanded for good contact.'1 The probe is about 30 to 35 cm. long. For best results the largest probe that can be inserted into the rectum should be used. No portion of the electrodes should contact the anus when the machine is in use.- The older instruments such as the Dzuik, Marden and Ni- cholson electroejaculators, the former with ring instead of longitudinal electrodes, have been improved to avoid excessive stimulation of the motor nerves to the rear limbs that often resulted in damage to muscles.4,5 The use of a modified sine wave instead of the pulse wave for elec- troejaculation of bulls has also improved the ease of electroejaculation of bulls.--'4-5'14 A man should stand behind the bull being ejaculated to prevent the expulsion of the probe. These various types and models of ejacula- tors for bulls, rams and possibly boars may be purchased commercially.* (See footnote.) A technique of electroejaculation using a ring or hand electrodes either slipped over the first and third fingers of a rubber glove, or held by the hand over the region of the base of the penis and prostate gland or the pos- terior portion of the ampullae has been described.—’13-25 This technique was favored over the rectal probe by some veterinarians because the bull reacted more favorably and with less vigorous contractions of the muscles of the rear limbs and back and other undesirable side reactions than with the older 4 electrode probes. The newer 3 electrode probes largely avoid these reactions. Furthermore using the ring electrodes required two men to ejaculate and collect the semen and the man behind the bull applying the electrodes cannot observe the protrusion of the penis and whether ejaculation is occurring.3'4 The use of the finger electrodes has declined in recent years as results were not as uniformly successful as the results with the improved electroejaculators. *3 Electrode probe, Lane Manufacturing Inc., Denver, Colo., and Nicholson Manufacturing Comp., Chicago, 111., Marden Electronics Co., Bryan, Texas, Standard Precision Electronics Co., Denver Colo. (Battery operated) and Production Products Inc., Lyndale, Ave., Min- neapolis, Minn.INFERTILITY IN MALE ANIMALS 863 It is highly desirable to place the bull in a solid stan- chion or chute with a pipe or bar behind their stifles in- asmuch as they tend to push forward. The front of the stanchion should be constructed so that the bull’s shoul- ders push against supports and choking cannot occur. The footing should be good to prevent slipping. Injured bulls may require a squeeze chute or a sling to support the bull during semen collection. All bulls stiffen slightly and arch their back or “hunch,” the anal sphincter con- tracts and clear seminal fluid dribbles from the sheath when the current is applied. Some bulls ejaculated with the rectal probe lean to one side or raise and extend one hind leg or rarely even both hind legs. This may be caused by the probe not being located on the midline and stim- ulating the sciatic or pelvic nerves. It may also be due to using too much power. With the newer improved models of electroejaculators these reactions are minimal. Care should be used to not apply the current until the electrodes are through the anus and in the rectum as this is painful to the bull. Occasionally a broken or exposed wire at the base of the probe will cause abnormal re- actions especially noticeable on inserting the probe and applying the current. Although the actions of the bull may make this technique appear painful, it apparently is not; repeated electroejaculation do not create fear or re- sistance to entering the same stall. The different vari- ations in bulls in response to electroejaculation have been described.-'17'26 The preputial hairs may be clipped and adjacent area washed, rinsed and dried or the ventral abdomen may be brushed. Teasing or sexually-exciting bulls or a rectal examination of the accessory glands prior to electroejac- ulation greatly aids the collection of a good sample. To prevent cold shock to the sperm cells, a rubber cone from an artificial vagina with an attached glass or plastic vial is placed in a plastic bag containing warm water at 90 to 100° F. attached to a metal ring about 7.5 cm. in di- ameter with a long handle.14 The amount and consisten- cy of the ejaculate can thus be observed as it is emitted. An artificial vagina may also be used to collect semen during electroejaculation. Although modifications in technique and procedures may be required in using elec- troejaculation on certain bulls, stimulation should begin at the lowest power settings especially in young bulls. Power or voltage within a power step is controlled by a variable-stimulator knob. This knob should be manipu- lated smoothly and fairly rapidly and full power within that power step should be approached gradually by turn- ing the knob only part way initially until maximum power in that step is reached after 3 to 4 stimuli. Stimuli should be applied for 2 to 3 seconds with a short rest interval, when the knob is returned to zero, of only about one- half to not over 1 second. Usually 5 to 10 stimuli are applied at each power step. Usually 9 to 14 stimuli are necessary to cause erection and protrusion of the penis and 9 to 20 to begin and 18 to 35 stimuli to complete ejaculation.— 5 A definite regular rhythm should be maintained during this procedure. Each bull must be treated as an individual and should be observed as the current is applied to assess his particular response. Only the amount of voltage or power needed to elicit the nec- essary responses and gently build up stimulation should be used in bulls and rams. About 90 percent of the bulls will erect, protrude their penis and ejaculate a repre- sentative semen sample with the rectal probe. As the penis becomes erect and the glans protrudes through the pre- putial orifice, more power or voltage is applied and nearly full erection occurs. With more power the clear seminal secretion becomes milky and opaque indicating ejacu- lation is occurring and the semen should be collected. Electroejaculation usually requires about 3 to 5 minutes to accomplish. If a bull fails to protrude his penis with stimulation, change the position of the rectal probe or exert forward pressure on the sigmoid flexure above the scrotum. Occasionally the tip of the glans will catch in the prepuce near the orifice. There may be a variation in effects of electroejaculation between bulls and from time to time in the same bull. In general young bulls respond better to electroejaculation and produce more normal ejaculates than do old bulls. Too many early stimulations at a subejaculatory level will yield much accessory gland fluid but may make it difficult to obtain an ejaculation. Too rapid an increase may lead to resistance on the part of the bull or a pre- erection ejaculation and to contamination or loss of se- men in the prepuce. Neither general nor local anesthesia nor tranquilization prevented normal electroejacula- tion.28 Tranquilization may aid in protrusion of the penis. In some bulls excessive seminal fluid may be secreted during electroejaculation resulting in semen with a low concentration of sperm cells. Experienced operators of an electroejaculator can routinely produce ejaculates nearly similar in volume and concentration to ejaculates col- lected in the artificial vagina. However the concentration of spermatozoa was consistently higher in semen col- lected with the artificial vagina and volume was con- sistently greater in semen collected by electroejacula- tion.--’2'17 The conception rates of bulls from which ejaculates were collected electrically were the same as when the ejaculates were collected in an artificial va- gina.527 Electroejaculation has become a useful adjunct to the artificial vagina in artificial insemination stations by al- lowing routine collections from crippled bulls without864 VETERINARY OBSTETRICS mounting. This is useful in utilizing injured bulls; and it can be used in cases of slow-breeding, impotent bulls. However, as pointed out previously impotency may be hereditary and perpetuating this condition may be det- rimental to the breed. This technique has proven of great value to veterinarians for obtaining semen from beef bulls, unaccustomed to handling and to the use of the artificial vagina, for evaluating semen of bulls before the breeding season when they go on range with cows.-17 It is doubt- ful if artificial insemination of cows with Brahman, Zebu or Santa Gertrudis semen would be possible without electroejaculation. The art of electroejaculating bulls can be mastered with practice. However certain bulls may not respond adequately and poor “semen” samples with oligospermia are obtained. In these bulls other collection techniques should be tried including the ring electrodes, the artificial vagina or massage of the internal genitalia. If an adequate sample cannot be obtained, the bull should not be classified as questionable or unsatisfactory.-4 Since semen could be collected by electroejaculation in nearly 100 percent of the attempts, this technique is superior to others for obtaining semen from untrained or intractable bulls refusing to ejaculate into an artificial vagina.15 The artificial vagina is the method generally pre- ferred and widely used for the collection of semen from dairy bulls and bulls in artificial insemination studs, and bulls on farms accustomed to being handled. Great care must be used in handling bulls as even fairly quiet ones can become dangerous in an instant. It is best to control them with two ropes, one fastened to a heavy nose ring, the other passing through the ring and tied around the horns. A metal bull staff is not safe for restraining a bull.19 By changing the mount, changing the environ- ment, allowing sexual rest, teasing or “stewing,” and other means, it will be found that there are relatively few bulls that cannot be kept in artificial service for many years. By the use of the artificial vagina a clean, com- plete ejaculate can usually be promptly obtained from properly trained bulls. The early models of the artificial vagina perfected by the Russians consisted of an artifi- cial vagina which fitted inside the vagina of a cow or a dummy. The present widely-used artificial vagina is modeled after the Cambridge type that was developed in England.-— The vagina consists of a heavy rubber cyl- inder about 7 cm. in diameter and 35.5 cm. long for young bulls, and 42 cm. long for older bulls; this is fitted with an inner rubber liner. The longer winter-type arti- ficial vagina is rather awkward and heavy and is seldom used except under farm conditions during the colder win- ter months.25b A rough-surfaced thick inner rubber liner apparently is preferred by bulls to a smooth, thin liner. The liner is longer than the heavy rubber cylinder and is turned back over the ends. There is usually a hole or valve in the heavy rubber cylinder for introducing and removing the hot water that is used to warm the vagina. The rubber liner is usually held in place by broad, flat, rubber bands. These should be tied to the vagina so that there is no danger of their slipping off and becoming fastened around the penis of the bull at the thrust of ejac- ulation and resulting in amputation of the penis if un- detected. A short rubber cone containing a glass or plas- tic collecting tube for semen is fastened to one end of the artificial vagina and is covered with a warmed in- sulating jacket. The proper pressure and warmth in the artificial va- gina is obtained by filling the water jacket, or the space between the inner liner and the heavy rubber cylinder, about one-half to two-thirds full of water depending on the size of the bull’s penis. The temperature of the water should be 125° to 180° F., 50 to 70° C. The colder the vagina and the outside temperature, the hotter should be the water that is added. At the time of collection the temperature inside the artificial vagina should be be- tween 105° to 125° F. or 40° to 52° C.20 Only a small amount of lubricant should be applied by means of a sterile glass rod to prevent an excess of lubricant mixing with semen. The lubricant can be a water-soluble lubri- cating jelly such as “K.Y.” jelly, which is readily ob- tained commercially. If the temperature of the artificial vagina is too low, the bull usually fails to thrust and ejaculate; if it is too hot, some spermatozoa may be killed, or it may cause the bull pain and he may develop a tem- porary fear of this method of collection. The glass tube on the rubber cone may be protected from breakage in the summer by having a piece of flannel or a paper hand towel fastened over it and in the winter a warm flannel of several thicknesses, an old coat-sleeve, or a special, quilted jacket with an impervious covering closed at one end can be slipped over that end of the vagina to keep the rubber cone and the collecting tube warm and protect the latter from accidentally breaking when the sample is collected. If collection is delayed during cold weather, this jacket and tube should be held under the arm or in the coat of the operator to keep the collecting tube warm. Either a cow, a bull or a steer that is trained and quiet may be used for a mount since metal or wooden dum- mies or phantoms even though they are heavily padded and covered by a hide, usually are not as satisfactory. If a bull is a slow-breeder, a cow in estrum is desirable, or a mount, either male or female, that is highly attrac- tive to bulls should be used. Bulls or steers are most desirable especially in an A.I. stud in order to prevent the possible spread of disease if the bull were to acci- dentally breed the cow used as a mount.INFERTILITY IN MALE ANIMALS 865 A few quiet and well-mannered beef and dairy bulls have even been trained to breed an artificial vagina with- out mounting or even having another animal close. The bull is brushed and stroked along the back and sides, and then along the abdomen, sheath, and testicles. When the penis is extended from the prepuce by this stroking, an artificial vagina is applied and ejaculation occurs. In artificial breeding studs all dairy bulls are teased before service to increase the total number of sperma- tozoa ejaculated. In slow breeding bulls this teasing prior to collection also makes mounting and ejaculation more prompt and rapid when the artificial vagina is heated and ready. The animal to be mounted is placed in a breeding rack or confined in a solid fence comer where the foot- ing should be good to prevent slipping. The mount an- imal if not in estms, should be restrained with a noselead to assist in its immobilization. The bull should be prop- erly restrained by ropes to his nose ring so when he dis- mounts he does not attack the collector.19 The underline and preputial hairs of the bull are brushed clean and if necessary washed and dried. Cleanliness and hygienic practices in the collection of semen from bulls is im- portant. The location for semen collection should be clean, dry, and free from dust, dirt, and mud. Douching the preputial cavity with a warm physiological saline solu- tion prior to service is of questionable value in reducing the bacteria present in the semen.8 If the semen collector is right-handed, it is easier for him to work on the right side of the bull. As the bull mounts, the prepuce enclosing the erect penis is drawn sidewise toward the collector by the cupped fingers of the left hand, thus deflecting the penis from the vulvar region or escutcheon of the mount animal. The sheath and penis should not be grasped tightly with the thumb and fingers. If the protruded penis is grasped, the bull usually retracts the penis and dismounts. The tip of the glans penis is introduced into the end of the artificial vagina that is held alongside the buttocks of the cow and tilted downward and backward so that the water collects in the lower or “caudal” end and provides the needed pressure and warmth to stimulate ejaculation on intro- mission. Swedish workers prefer to hold the vagina against the buttocks or ischial tuberosities of the cow, aiding the direction of the glans penis by the fingers on the prepuce but letting the bull seek, find and thrust into the artificial vagina.15 The bull should be allowed to thrust its penis into the vagina, since this thrust is necessary for ejacu- lation. If the operator prematurely pushes the vagina over the erect and extended penis, most bulls will not ejacu- late. After ejaculation the vagina should immediately be tipped in the opposite direction so that the semen will run into the collecting tube. If an excess of water has been used, it may be necessary to draw off a portion of that water before all the semen can drain from the arti- ficial vagina into the tube. A possible mishap from using an excess of water is to have the rubber liner burst or the rubber bands forced off at the time the penis is thrust into the vagina. If the latter happens, the rubber bands should be counted and penis should be examined. Some operators make a small nick or hole in the rubber col- lection cone to release air at the time of the thrust. For some bulls a heavy rubber band about 1-1/2 inches in diameter is placed around the liner, between it and the heavy rubber casing, at the open end of the vagina to provide more resistance to the entry of the penis and thus promote ejaculation. Since sperm cells are killed or injured by toxic sub- stances, it is necessary that all new rubber equipment which comes in contact with the semen be carefully cleaned and sterilized before using. New rubber equip- ment is often coated with a powder to prevent the rubber from sticking together. This powder or coating is often highly toxic to spermatozoa. After each collection the cone and rubber liner should be rinsed immediately in warm water. All glass, metal, and rubber equipment should be washed and brushed with a lukewarm solution of 0.2 to 0.3 percent sodium hexametaphosphate such as “Calgon,” or .3 to .5 percent tetrasodium pyrophos- phate, or a good glass cleaner and rinsed thoroughly with warm water. The synthetic organic detergents should not be used in washing and sterilizing artificial insemination equipment.10 If they are used, very careful rinsing is nec- essary. After draining, all parts of the equipment are then rinsed in 70 percent ethyl alcohol and permitted to dry in a dust-free, ventilated storage cabinet. Other types of alcohol such as methyl or denatured should not be used. Some workers use a final rinse of scalding distilled water, followed by a rinse in 70-percent ethyl alcohol. The drying may be aided by replacing the liners on the vagina but a better procedure is to distend the rubber liner with or- dinary clothes pins or a special metal rack. If equipment must be used before it has dried, the alcohol should be thoroughly washed away with physiological saline or a sterile citrate- or phosphate-buffer solution. The artificial vagina may be sterilized by boiling or by being placed in an autoclave but this hastens deterioration of the rub- ber parts. The artificial vagina method for the collection of bo- vine semen produces a clean concentrated semen sample with cheap, simple equipment and provides information on sex drive. It has the disadvantages of requiring a rel- atively trained cooperative bull and a suitable mount. The danger of injury of the operator is greater. While the electroejaculation method of collection gives good re-866 VETERINARY OBSTETRICS suits with few specialized facilities and even with un- trained bulls, it has the disadvantages of requiring more costly equipment, a greater chance of a contaminated sample with a low concentration of spermatozoa being collected, and no indication or determination of the sex drive, libido or ability to mount and ejaculate, or free- dom from lameness, of the bull is obtainable. The stallion may have his semen collected relatively easily by using a condom,9 or by the use of the artificial vagina.2'3'8'14 The former method is seldom used at pres- ent because of the excessive contamination of the ejacu- late by the penile skin. The collection of semen from the vagina or uterus of the mare after natural service is possible and has been described.4 However samples collected in this manner are not representative, are diluted and possibly contam- inated. This technique requires that the mare be healthy and free of any genital infection and not be in her foal heat. Strict hygienic and sanitary procedures should be followed in the collection of the semen by this method. After service by the stallion the hand encased in a sterile glove and sleeve is introduced into the vagina with a stiff rubber tube 3/16 inch in diameter and about 2 to 2-1/ 2 feet long. This tube is attached by a bent glass tube in a 2-holer rubber stopper to a 6-ounce sterile bottle and a 12- to 18-inch tube is similarly attached by a glass tube in the other hole of the stopper. By suction applied on the short tube with the mouth, semen is drawn into the bottle from the vagina and if necessary from the uterus. Another but less satisfactory method is to use a vaginal speculum and draw up the semen with a long nozzle at- tached to a syringe. These techniques are presently sel- dom used. Collection of the “dismount” or “tail-end” sample of stallion semen that drips from the glans and urethra after copulation can be easily accomplished by holding a warm enamel or plastic cup or large plastic funnel at- tached to a warmed tube or bottle under the vulva and glans penis as the stallion dismounts. This last portion of the ejaculate has a much lower concentration of sper- matozoa, has a different composition than the complete ejaculate, and is usually unsuited for predicting fertility and for inseminating purposes.9 The amount of semen collected in this manner is small, 10 to 30 ml., and it is commonly contaminated with smegma and dirt. Collec- tion and examination of this “tail-end” sample is usually performed to be certain that ejaculation occurred during intromission. Semen collected in this manner, is usually filtered through sterile gauze or a coarse-paper or milk filter into a vial before it is used for insemination or “impregnation” following a natural service. Massage of the ampullae and electroejaculation as described in bulls has been attempted in stallions without success by the author and others.5 With the horse com- pletely anesthetized electroejaculation is possible, as re- ported in swine, but it is not practical and urine often contaminated the sample.1 These above techniques, for obvious reasons, are not as satisfactory as collecting the entire ejaculate in an artificial vagina. The condom or breeder’s bag was used successfully on most Thoroughbred stallions.9* A mare in estrum, a mare that has been given 10 to 20 mg. of stilbestrol 24 to 48 hours previously to produce signs of estrus, or a very docile, trained older mare can be used with the usual restraints as a mount. A satisfactory condom for the stallion similar to that used by man was designed. Before use the breeder’s bag or condom should be thoroughly cleaned of all rubber preserving powder by thorough washing, rinsing with plain or distilled water and then rinsing with a physiological salt solution. If the condom is to be reused it should be sterilized after washing and rinsing by immersing in ethyl alcohol and dried. Before applying the condom the penis should be carefully washed and rinsed thoroughly sev- eral times with plain water and dried to remove dirt and smegma. The condom is fitted to the erect penis, but the left loose over the glans with the air squeezed out, just prior to service. It is held in place by rubber bands and removed immediately after service. If an excess of fluid collects in the condom before ejaculation empty it out. The ejaculate is poured into a sterile bottle or graduate warmed to about 100 to 102° F. Lubricating the outside of the breeder’s bag and vulva was not necessary if the stronger condoms were used. As previously indicated this technique is seldom employed at the present time be- cause nearly all stallions can be readily trained to ejacu- late into an artificial vagina. The artificial vagina has been widely used in En- gland, Russia, Japan, and the United States for the col- lection of semen from stallions. When this is performed regularly the stallion may be trained in its use. The artificial vagina is preferred to the condom because of more satisfactory results and less contaminated sam- ples.—'2’3'4’6'8’12 The equipment, however, is more ex- pensive. Some stallions that are collected regularly have been trained to mount dummies, manikins or phan- toms.710'" A mare in estrum or one in which estrum has been induced, is usually required. Strict hygienic pro- * Condoms for stallions may be purchased from the Pioneer Rubber Co., Willard, Ohio, Youngs Rubber Co., Trenton, N.J. and Dean Rubber Co., East Kansas City, Mo. (Texas Model.)INFERTILITY IN MALE ANIMALS 867 cedures should be followed, such as: bandaging the mare’s tail with a sterile bandage; careful and thorough wash- ing, disinfection and rinsing of her rear parts; and careful washing and rinsing of penis and sheath of the stallion. The usual precautions are taken to restrain the mare and to prevent injury to the stallion, the operator, or the mare.—6 The method of constructing the Missouri-USDA type of vagina has been described.*- The Mississippi model has been described by Berliner.3 Lighter more modem artificial vaginas for stallions are also available.** The diameter of the vagina is about 12.7 to 17.7 cm., 5 to 7 inches, and because of its increased size and weight a handle is provided. A dam is present at the closed end of the Nishikawa (Japanese)12 vagina that provides a place for contact for the glans penis. An equine artificial va- gina has been designed and used successfully for many years in Colorado.***— The outer casing is made from a nalgene pipette jar using rubber tubing similar to a bo- vine artificial vagina and the vagina is well-insulated. A built-in filter is provided that removes the gel from the ejaculate. A new vagina must be thoroughly washed, rinsed, disinfected with grain alcohol, and dried before it is first used, and following each use thereafter. The water-soluble lubricating jellies can be used sparingly to lubricate the opening of the vagina. The temperature of the vagina should be between 105 to 120° F. or 43 to 50° C. Temperature within a degree or two of 46° C. is desirable. This is provided by introducing hot water at 120° to 130° F. or 50 to 65° C., depending on the cli- matic conditions, between the jacket and the liner of the artificial vagina. Pressure in the artificial vagina simu- lating that of a mare’s vulva may be produced by a 2 inch wide rubber band, 3 inches in diameter, placed be- tween the jacket and the rubber liner near the open end of the vagina. Berliner advised manual pressure through the wall of the vagina. Some of the artificial vaginas such as the Japanese and Colorado types have rigid out- side walls. Air and water can be introduced into the ar- tificial vagina to produce adequate pressure on the penis. Although the operator may collect semen from either side of the stallion, most prefer the left or near side. The site * Haver-Lock hart Laboratories, P.O. Box 390, Shawnee, Mission, Kan., 66202. ** Artificial Vagina for obtaining stallion semen (Nishikawa Model) Fukihira Industry, Co. Ltd., 131 Morikawa-Cho, Bunkujoku, Tokyo, Japan, Goetze’s Artificial Vagina for Horses, H. Hauptner, Solingen, Germany. ***Colorado Equine Artificial Vagina, Lane Manuf., Co., 2057 S. Hudson St., Denver, Colo., 80222. for collection should be level and provide good footing. The artificial vagina should not be shoved over the stal- lion’s penis as he mounts but rather the stallion should be permitted with help to insert his penis into the vagina. On cold days the bottle receiving the semen should be warmed and protected. The vagina should be held firmly against the flank and buttock of the mare with the open end of the vagina held above the level of the plastic col- lecting bottle and pressure exerted against the penis equal to that exerted by the stallion. It usually requires about 20 to 30 seconds for ejaculation. The operator can place his fingers on the ventral surface of the caudal portion of the erect penis, to detect the pulsations of the urethra during ejaculation.—6 If the stallion or jack is not prop- erly trained or lacks desire, a quiet mare or jenny and quiet surroundings are necessary for collection with an artificial vagina. The author has successfully used a bo- vine artificial vagina for the collection of semen from small ponies. Stallions that require repeated intromis- sions before ejaculation or are slow to mount and cop- ulate at natural coitus act similarly when semen is col- lected by the artificial vagina. Patience and gentle training may be required, partic- ularly if a stallion is to be collected on a phantom.710 11 The use of a phantom eliminates most of the possibilities for injury to the mare, stallion and collector. Because of the lower height of the phantom and its immobility it is less stressful to the rear quarters of the stallion. The use of urine from an estrous mare on the phantom is of ques- tionable value as a sexual stimulant to the stallion.10 The ram and buck may have satisfactory semen sam- ples collected by removing the semen from the vagina of a ewe after coitus, by an artificial vagina or by elec- troejaculation. Rams may be mated to restrained diestrual ewes. The ewes’ vaginas are cleaned prior to use by repeatedly in- serting and withdrawing saline with a collecting pipette of glass or plastic 30 cm. long and 1.0 cm. in diameter attached to a syringe until no more mucus can be re- moved. If the ram refuses to breed a diestrual ewe, one in estrum may be used. After coitus semen is removed in a similar fashion. This is a simple method but the semen is usually contaminated. It is faster for collecting from shy, untrained rams than the artificial vagina method and it also detects rams that physically are unable to cop- ulate. Semen evaluation can be performed satisfactorily on such samples.4'11 The artificial vagina for rams and bucks is con- structed like the artificial vagina for bulls but it is smaller, about 20 cm. long and 5 cm. in diameter. The temper- ature of the vagina at the time of collection is critical for868 VETERINARY OBSTETRICS the ram and should be 41° to 44° C. or 106° to 112° F., with a pressure of 40 to 60 mm. of mercury.7,8'910 Rams and bucks may be readily trained in a suitable environ- ment, with a restrained ewe or doe preferably in estrum. Later any ewe or doe, an ovariectomized ewe or doe treated with estrogen, or even a dummy may be used as a mount. As the operator holds the vagina in his hand he should be crouched next to the rear parts of the ewe and doe and be alert as mounting and copulation is very rapid. False mounts without ejaculation are common. The penis should not be touched by the hand but the sheath may be grasped to direct the penis into the artificial va- gina. A refractory period of 20 to 30 minutes follows ejaculation in the ram and buck before he will mount again. A ram or buck may be collected 2 to 3 times a day for a number of days. Electroejaculation of rams was first described by Gunn in 1936.3 In recent years improved electroejaculators are available with bipolar rectal probes about 30 cm. long and 2 cm., in diameter.* (See footnote.) The ram re- sponds rapidly to electrical stimulation and often 3 to 5 stimulations of 3 to 5 seconds duration with 1 to 2 sec- onds rest, at 2, 5 and 8 volt peaks result in ejacula- tion.1'2,5,12 Thus fewer stimulations by the electroejaculator are needed in rams and bucks than in bulls. The insertion of the rectal probe to a depth of 15 cm. instead of 20 to 25 cm., improved the rapidity of response and produced a greater volume of semen. Rams and bucks may be elec- troejaculated in the standing position or restrained on their side with their legs extended. The latter position is more often recommended. The penis should be removed from the sheath and held with gauze so the urethral process is directed into the collection vial or tube to avoid ejacu- lation into the sheath. Often the penis will protrude from the sheath with electrical stimulation as in the bull. This method results in a great variation in semen volume and lower concentration than an ejaculate collected with the artificial vagina. Occasionally urine may contaminate the sample. If the first collection is unsatisfactory it is dif- ficult to get another satisfactory ejaculate until several hours have elapsed. Electroejaculation has the advan- tages that it may be used on untrained rams and bucks and is particularly valuable as a screening test of the se- men quality of large numbers of rams.z’5 Indiscriminate use of electroejaculation without re-examinations could *Nicholson Manufacturing Inc., Chicago, 111. Production Products, Inc., (Dzuik Model) 4607 Lyndale Ave. N., Minneapolis, Minn., Lane Manufacturing Co., Hudson St., Denver, Colo. Marden Electronics Co., Bryan, Texas. Standard Precision Electronics Co., Denver, Colo., (Battery operated). lead to the culling of many potential high fertility rams as occasional samples of semen obtained by electro- ejaculation from fertile rams and bucks were inferior in quality. The induction of erection and ejaculation in rams and bucks by the local massage of the sheath and penis has been described.6 The boar may have semen collected by a modified artificial vagina, the gloved-hand technique or by elec- troejaculation. Before collection by any of these proce- dures the contents of the preputial diverticulum should be expelled and the area of the preputial orifice should be cleansed and dried. The artificial vagina may be of various designs to pro- vide the necessary pressure to the spiraled glans penis so that it “locks” at complete erection as it does in the anterior vaginal and cervical folds of the sow. This may be accomplished most simply by a heavy rubber casing 4.5 cm. in diameter and about 12.5 cm. long with a rub- ber liner and small piece of sponge rubber between it and the casing where warm water at 45° to 50° C. or 113 to 122° F., is placed to heat the vagina. The sponge rub- ber causes increased pressure on the penis. A continu- ous, smooth, thin rubber liner or tubing 40 cm. long and 3 to 3.5 cm. in diameter with a small hole in the upper portion to allow air to escape is passed through the above vagina and fastened to the outer end of the vagina and lubricated. The other end is fastened to a plastic bottle or bag of 500 ml. capacity that is in a cup or thermos of warm water at 102° F. or 39° C. As the penis passes through the vagina pressure is applied to the glans by the hand of the operator through the thin rubber tub- ing.4,6,9,10 After several back and forth motions the penis “locks” in the fingers, continuous moderate pressure is applied, and ejaculation commences and continues for about 15 minutes with much of the sperm-rich fraction being emitted around the third or fourth minute. This is a somewhat similar procedure to the gloved-hand tech- nique but more cumbersome. Frequently there may be a series of sperm-rich fractions interspersed between pe- riods of thin sperm-poor fractions and gelatinous tap- ioca-like secretions. A slightly more complex model of artificial vagina the diameter of the artificial vagina for the bull, but only 18 cm. long designed to prevent con- tamination of semen with preputial secretions has been described.—'1 A very simple model consisting of only a 35 to 40 cm. rubber tubing as described above with a key ring for an orifice that is warmed before use has also been described.56 Other earlier types were similar to the artificial vagina for the bull but with attachments to it so air could be pulsated into the vagina.-11 Currently most workers collect semen from boars with only a gloved hand and a wide-mouthed thermos jugINFERTILITY IN MALE ANIMALS 869 containing warm water and lined with a plastic bag to prevent chilling of the semen. This technique is easy, inexpensive, and repeatable.7,8 After the boar mounts the estrous or restrained sow and protrudes the penis, the hand, encased in a surgical glove, is shaped like a cone to permit the entry of the glans penis and placed several inches cranial to the preputial orifice. After the penis enters the hand the fingers are gently closed locking the spiral penis in the hand. It is critical that the distal 2 to 3 centimeters of the penis be held quite firmly with the small, fourth, and third fingers with no pressure applied to the shaft of the penis. Full erection then occurs and ejaculation follows.8 The mouth of thermos jug may be covered with several layers of gauze or cheesecloth to separate the gel fractions from the rest of the semen. Usually ejaculation takes about 5 to 15 minutes and oc- casionally some boars will have a second ejaculatory cycle, shorter than the first, before dismounting. Boars are usually readily trained to mount a dummy composed of a metal or wooden frame covered with bur- lap or they may be allowed to mount a confined or re- strained sow or barrow. The former is preferable. The environment should be quiet and the footing non-slip- pery.7,10,6 Electroejaculation in boars has been described.3 5ab It is not as desirable as the gloved-hand or artificial va- gina for the collection of semen because mating behavior and ability to mate cannot be assessed and the procedure and equipment is costly and the ejaculate secured is not typical. The older Dzuik model or newer small bull or large ram probe is satisfactory if the rectum is evacuated of feces before the probe is inserted. Stimuli must be applied at gradually increasing voltage peaks in a rhythmical manner similar to the technique used in bulls to first induce erection and then by inserting the probe an additional 6 to 8 cm. into the rectum to produce ejac- ulation. The volume of semen obtained is low but the concentration is usually high because of a lack of ac- cessory gland secretions. Since boars must be forcibly restrained, the collection is a noisy drawn-out affair, often resulting in a heavily contaminated ejaculate. The elec- troejaculation of boars is not as satisfactory as in bulls and rams. For this reason the electroejaculator should be used on anesthetized boars. One to one and one-half grams of “Surital,” sodium thiamylal (Parke-Davis) given in- travenously in the ear vein through a 20 gauge needle produced good anesthesia for 15 to 30 minutes in 300 to 400 pound boars.3 5a The genital organs were easily and thoroughly cleansed and the penis was removed from the prepuce by the fingers or by gentle traction with forceps while the initial electroejaculating stimuli are applied re- sulting in erection. The penis was held by the hand and directed so the semen would flow into a warmed thermos jug lined with a plastic bag when ejaculation occurred. Under anesthesia the penis and testes are easily exam- ined. The above method was rapid and quiet and was preferred3 for the evaluation of the semen of boars to the use of the artificial vagina which required obtaining sows in estrum or training the boar to mount and use the ar- tificial vagina. Shy, slow, inexperienced, mean, lame or injured boars are difficult to train. Training procedures can't be standardized and are very time consuming. If a live mount is used there may be disease control problems to consider. In the dog semen may be obtained for examination or artificial insemination by digital manipulation of the penis or by an artificial vagina. A method of electroejac- ulation of the anesthetized dog modeled after the pro- cedure in rams has been described.1 This proved useful in a very few males that could not be collected by the former two methods. Most untrained dogs respond best to digital manipulation.-3'— 3 7 8 1 1 The collection area should be a small quiet room with minimal distractions. The dogs and teaser bitch should be handled quietly after they have become acquainted with the operators and the collection room. The footing should be nonslippery. The teaser bitch is usually fas- tened securely to a table leg or wall and held by an as- sistant with a hand under her chest and the other hand around her muzzle to prevent her from sitting down or possibly biting the male or the operator. Manipulation of the base of the penis is the sim- plest, cheapest, and commonest way to collect semen in the dog. A bitch, preferably in heat, should be presented to the male. When the dog shows sexual interest the pre- putial skin is pushed caudally, exposing one to two inches of the glans penis. The base of the penis behind the bul- bus glandis is grasped through the prepuce and moderate pressure is applied by the fingers. In an impotent male back and forth movement, masturbation, may aid in pro- ducing an erection. As erection occurs the prepuce is retracted behind the bulbus glandis and digital pressure is maintained caudal to the bulbus to simulate its en- gagement in the vulva. The dog during ejaculation will often step over the arm of the operator causing the penis to be extended caudally between the dog’s rear legs as he faces the opposite direction. Even though no teaser bitch is present some dogs can be trained to ejaculate by manipulation of the base of the penis until erection is induced, but sperm cell concentration is usually low. The semen is collected by means of a warm glass or plastic funnel into a 25 to 30 ml. warm tube or vial or the warmed barrel of a 20 to 50 ml. plastic or glass sy- ringe on which a rubber adapter has been placed and870 VETERINARY OBSTETRICS doubled over to prevent leakage of semen. Since glass collection equipment is difficult to handle with an active, thrusting dog and may break or traumatize the penis, a collection apparatus consisting of a rubber conical sheath, similar to the conical sheath used on a bovine artificial vagina but cut down or folded at the large end to reduce its size with a 15 ml. conical plastic centrifuge tube placed in the narrow end of the rubber sheath and warmed to 38 to 40° C. also prevents loss of semen during ejacu- lation.11 A very small amount of K.Y. jelly may be ap- plied to the inside of the rubber sheath. The first portion of the ejaculate may be lost due to a brief period of thrusting motions by the male. This is of little impor- tance, as few spermatozoa are present in this portion. When the ejaculation of sperm cells commences thrust- ing motions cease. The penis does not need to enter the tube or syringe barrel and in shy or impotent males the funnel, tube or syringe barrel should not be allowed to touch the penis. It is important to maintain constant pres- sure behind the bulbus glandis until sufficient semen has been collected.-’-,-,-,2,7,8,n The portion of the ejaculate containing the spermatozoa is a whitish-grey milky fluid. Ejaculatory action can be noted by feeling the pulsations of the urethra in the base of the penis. Ejaculation may last 5 to 15 minutes. An artificial vagina for the dog similar in size, 5 cm. in diameter and 19 cm. long, and similar in pattern to the artificial vagina for a ram has been described.4 5,6,9 A firm rubber diaphragm around the open end of the vagina to simulate a bitch’s vulva was recommended.4 The temperature of the vagina should be about 40° to 42° C. or 104° to 107° F., and no lubricant need be used. The penis is grasped behind the bulbus glandis as de- scribed above to produce erection before the vagina is applied. Semen motility may be adversely affected by this technique.2 Possibly this was due to the contact of the sperm cells with the heated walls of the artificial va- gina as this finding was not reported by others that used and preferred an artificial vagina for semen collection in the dog. In the tom cat semen collection has been described by the use of the artificial vagina12 or by electroejac- ulation under anesthesia.10 Male cats were selected for their calm temperament and for their strong libido. Teaser queens were either females in estrum or ovariec- tomized females given 12.5 mg diethylstilbestrol, Re- positol, every 10 days. It usually required about 2 weeks to train a tom cat for routine semen collection. The ar- tificial vagina was a 2 ml. rubber bulb from the end of a bulb pipette or “eye dropper” with the bulb end cut off and fitted over a 3 X 44 mm. test tube. This was placed in a 60 ml. plastic polyethylene bottle. The bottle was filled with water at 52° C so at the time of collection the temperature would be 44 to 46° C. The open end of the rubber bulb was rolled over the mouth of the bottle and smeared lightly with K.Y. jelly. The artificial va- gina was slipped over the penis of the tom as he mounted the teaser queen and developed an erection. The oper- ators other hand was used to steady the tom and teaser queen. Collection took from 1 to 4 minutes. Their study indicated that toms could be collected 3 times a week and daily use for a short period was possible without a great decline in semen quality. Daily collection did not affect the male cats’ libido. The electroejaculation pro- cedure required special equipment and rectal probe and after anesthesia was induced with Ketamine HCL the technique was similar to that used in the other domestic animals with a similar response.10 References Clinical Fertility Examinations and Semen Collection L Carroll, E. J., Ball, L. and Scott, J. A. (1963) Breeding Sound- ness in Bulls—A Summary of 10,490 Examinations, JAVMA, 142, 1105. 2. Elmore, R. G., Bierschwal, C. J., Martin, C. E. and Youngquist, R. S. (1975) A Summary of 1127 Breeding Soundness Exami- nations in Beef Bulls, Theriog. 3, 6, 209. 3. Foote, R. H. and Trimberger, G. W. (1968) Reproduction in Farm Animals, Edit, by Hafez, E. S. E., Lea and Febiger, Philadel- phia, Pa. 4. Frank, A. H. (1950) Artificial Insemination in Livestock Breed- ing. Circular 567 U.S. Dept, of Agric., Washington, D.C. 5. Gledhill, B. L. (1967) Swedish Methods for the Evaluation of Breeding Soundness in Bulls, (Mimeographed notes presented at the Amer. Vet. Soc. for the Study of Breeding Soundness, Univ. of Missouri). FAO/Swedish Intemat. Vet. Postgraduate Course on An. Reprod., Royal Vet. College, Stockholm, Sweden. 6a. Johnston, S. D., Larsen, R. E. and Olson, P. S. (1982) Canine Theriogenology, Soc. for Theriog. Jour. Vol. XI, 62-93 (Eval- uation of Fertility in the Dog). 6b. Larson, L. L., Bartlett, D. E. and Parker, W. G. (1972) Disease Incidence in Bulls, I. When Examined for Use in AI., Proc. 7th Intemat. Congr. on Animal Reprod. and Art. Insem., 1473. 7. Maule, J. P. (1962) The Semen of Animals and Artificial Insem- ination, Commonwealth Agric. Bureaux, Famham Royal, Bucks, England. 8. Nishikawa, Y. (1962) Fifty Years of Artificial Insemination of Farm Animals in Japan, Dept, of Animal Science, Kyoto Univ., Japan. 9. Ott, R. S. (1981) How to Examine Bulls for Breeding Soundness, Proc. Ann. Mtg. Soc. for Theriog., Spokane, Wash., 1. 10. Perry, E. J. (1960) The Artificial Insemination of Farm Animals, 3rd Ed., Rutgers Univ. Press, New Brunswick, N.Y. 11. Society for Theriogenology (1972) Compilation of Current In- formation on Breeding Soundness Evaluation Jour., Vol. XII 2nd Ed., Association Bldg. 9th and Minnesota, Hastings, Nebr., 68901.INFERTILITY IN MALE ANIMALS 871 The Bull 1. Aenhalt, E. and Dittmar, J. (1961) Arbeitsweise und Ergegnisse der Bullen-Prufstation Nordwestdeutschland, Proc. 4th Intern. Congr. on An. Reprod. The Hague, II. 2. Austin, J. W., Hupp, E. W. and Murphree, R. L. (1961) Com- parison of Quality of Bull Semen Collected in an Artificial Va- gina and by Electroejaculation, J. Dairy Sci., 44, 12, 2292. 3. Ball, L. (1980) Semen Collection by Electroejaculation and Massage of the Pelvic Organs, in Current Therapy Theriog., edit, by D. A. Morrow, W. B. Saunders Co., Philadelphia, 345. 4. Ball, L. and Furman, J. W. (1972) Electroejaculation of the Bull, Bov. Pract. 7, 46. 5. Ball, L., Nelson, L. D., Furman, J. W. and Seidel, G. E., Jr. (1974) Semen Collection and Evaluation of Bulls for Breeding Soundness, Proc. Ann. Mtg. Amer. Vet. Soc. for Study of Breeding Soundness, Columbia, Mo. 6. Bierschwal, C. J. (1976) Revised Breeding Soundness Exami- nation Procedures, Proc. Ann. Mtg. Soc. for Theriog., Lexing- ton, Ky., 128. 7. Case, C. H. (1925) Handling Cases of Sterility in Practice, Cor. Vet., 15, 1, 37. 8. Cembrowicz, H. J. and Osborne, A. D. (1961) Effect of Pre- putial Cavity Treatment on the Number and Types of Bacteria in Semen Samples and Sheath Washings, Proc. 4th Intemat. Congr. on An. Reprod. (The Hague) III, 468. 9. Chenoweth, P. J. (1978) New and Not-So-New Concepts in Bull Evaluation and Management, Proc. 11th Ann. Conv., AABP, Baltimore, Md. 104. 10. Chenoweth, P. J. and Ball, L. (1980) Breeding Soundness Eval- uation in Bulls, in Current Therapy in Theriog. edit, by D. A. Morrow, W. B. Saunders, Co., Philadelphia, 330. 11. Debruyn, R. (1961) The Collection of Semen in Bulls by Mas- sage of the Ampullae Through the Rectum, Proc. 4th Intemat. Congr. on An. Reprod., The Hague, II, 283. 12. Dzuik, P. J., Graham, E. F. and Petersen, W. E. (1954) The Technique of Electroejaculation and Its Use in Dairy Bulls, J. of Dairy Sci., 37, 9, 1035. 13. Easley, G. T. (1970) A Hand Electrode for the Electroejacu- lation of Bulls, Bov. Pract. 5, 12. 14. Furman, J. W., Ball, L. and Seidel, G. E., Jr. (1975) Electro- ejaculation of Bulls Using Pulse Waves of Variable Frequency and Length, J. An. Sci. 40, 4, 665. 15. Gledhill, B. L. (1967) Swedish Methods for Evaluation of Breeding Soundness in Bulls, Ann. Meeting Amer. Vet. Sco. for the Study of Breeding Soundness, Univ. of Missouri, Co- lumbia, Mo., Royal Vet. College, Stockholm, Sweden. 16. Gunn, R. M. C. (1936) Fertility in Sheep: Artificial Production of Seminal Ejaculation and the Characters of the Spermatozoa Contained Therein, Council of Sci. and Ind. Res. of Austral., Bull #94. 17a. Hill, H. J., Scott, F. S., Homan, N. and Gassner, F. X. (1956) Electroejaculation in the Bull, JAVMA, 128, 8, 375. 17b. Hahn, J., Foote, R. H. and Cranch, E. T. (1969) A Tonometer for Measuring Testicular Consistency of Bulls to Predict Semen Quality, J. An. Sci. 29, 3, 483. 18. Hahn, J., Foote, R. H. and Seidel, G. E., Jr. (1969) Testicular Growth and Related Sperm Output in Dairy Bulls, J. An. Sci. 29, 1, 41. 19. Larson, L. L. (1980) Physical Examination of the Reproductive System of the Bull, in Current Therapy in Theriog., edit, by D. A. Morrow, W. B. Saunders Co., Philadelphia, 307. 20. MacMillan, K. L., Hafs, H. D. and Desjardins, C. (1966) Some Semen Characteristics in Dairy Bulls Ejaculated with Artificial Vaginas at Varying Temperatures, J. of Dairy Sci. 49, 9, 1132. 21. Marden, W. G. R. (1954) New Advances in Electroejaculation of the Bull, J. of Dairy Sci. 37, 5, 556. 22. Megale, J. (1968) Induction of Erection and Ejaculation in the Bull by Local Massage, Cor. Vet. 58, 1, 88. 23. Miller, F. W. and Evans, E. I. (1934) Technique for Obtaining Spermatozoa for Physiological Dairy Studies and Artificial In- semination, Jour. Agric. Res. 48, 10, 941. 24. Murray, G. R. (1970) Personal Communication. 25a. Rowson, L. E. A. and Murdock, M. I. (1954) Electrical Ejacu- lation in the Bull, Vet. Rec. 66, 23, 326. 25b. Salisbury, G. W. and Willett, E. L. (1940) An Artificial Vagina for Controlled Temperature Studies of Bull Semen, Cor. Vet., 30, 1, 25. 26. Scott, J. A. (1966) The Electroejaculator: Its Use and Problem Bulls, Proc. 1st Tech. Conf. on Art. Insem. and Bovine Re- prod., NNAB. 27. Singleton, E. F. (1970) Field Collection and Preservation of Bo- vine Semen for Artificial Insemination, Austral. Vet. J. 46, 160. 28. Wells, M. E., Philpot, W. N., Musgrave, S. D., Jones, E. W. and Brock, W. E. (1966) Effect of Method of Semen Collection and Tranquilization on Semen Quality and Bull Behavior, J. Dairy Sci. 49, 5, 500. 29. Willett, E. L. and Ohms, J. I. (1957) Measurement of Testicular Size and Its Relation to Production of Spermatozoa by Bulls, J. Dairy Sci., 40, 12, 1559. 30. Williams, D. J. (1969) Electroejaculation in the Bull, Proc. of Conf. on Reproductive Problems in Animals, Univ. of Georgia, Nov., p. 38. The Stallion 1. Adams, W. M., Jr. (1968) Personal Communication. 2. Asbury, A. C. and Hughes, J. P. (1964) Use of the Artificial Vagina for Equine Semen Collection, JAVMA, 144, 8, 879. 3. Berliner, V. (1960) The Artificial Insemination of Farm Animals, 3rd Ed., Edit, by Perry, E. J., Rutgers Univ. Press, New Bruns- wick, N.Y. 4. Bielanski, W. (1963) Die Kuntsliche Besantung beim Pferd, from Die Kunstliche Besamung bie den Huastieren, Schaetz, F. Gustav Fischer Verlag, Jena, Germany. 5. Day, F. T. (1940) The Stallion and Fertility, Vet. Rec. 52, 34, 597. 6. Kenney, R. M. (1975) Clinical Fertility Evaluation of the Stal- lion, Proc. 21st Ann. Conv. AAEP, Boston, Mass. 7. Kenney, R. M. and Cooper, W. L. (1974) Therapeutic Use of a Phantom for Semen Collection from a Stallion, JAVMA, 165, 706. 8. Lambert, W. V. and McKenzie, F. F. (1940) Artificial Insemi- nation in Livestock Breeding, U.S. Dept. Agr. Cir. 567. 9. MacLeod, J. and McGee, W. R. (1950) The Semen of the Thor- oughbred, Cor. Vet. 40, 3, 233. 10. Pickett, B. W., Squires, E. L. and Voss, J. L. (1981) Normal and Abnormal Sexual Behavior of the Equine Male (Training to a Phantom) Animal Reprod. Lab., Colo. State Univ., Exper. Stat., General Series 1004, 25. 11. Richardson, G. F. and Wenkoff, M. S. (1976) Semen Collection from a Stallion Using a Dummy Mount, Canad. Vet. J. 17, 177.872 VETERINARY OBSTETRICS 12. Rossdale, P. D. and Ricketts, S. W. (1980) Equine Stud Farm Medicine, 2nd Ed., Lea and Febiger, Philadelphia, 140-142. The Ram and Buck 1. Barker, C. A. V. (1958) The Collection of Semen from Bulls, Rams and Bucks, Canad. J. of Comp. Med. 22, 1,3. 2. Dzuik, P. J., Graham, E. F., Donker, J. D., Marion, G. B. and Petersen, W. E. (1954) Some Observations on Collection of Se- men from Bulls, Goats, Boars and Rams by Electrical Stimula- tion, Vet. Med. 49, 11, 455. 3. Gunn, R. M. C. (1936) Fertility in Sheep, Council of Sci. and Ind. Res. of Australia, Bull #94. 4. Hulet, C. V. and Ercanbrack, S. K. (1962) A Fertility Index for Rams. J. An. Sci. 21, 489. 5. Hulet, C. V., Foote, W. C. and Blackwell, R. L. (1964) Effects of Natural and Electrical Ejaculation on Predicting Fertility in the Ram, J. An. Sci. 23, 2, 418. 6. Megale, F. (1968) Induction of Erection and Ejaculation in the Bull by Local Massage, Cor. Vet. 58, 1, 88. 7. Ott, R. S. and Memon, M. A. (1980) Breeding Soundness Ex- aminations of Rams and Bucks, A Review, Theriog., 13, 2, 155. 8. Ott, R. S. and Memon, M. A. (1980) Breeding Soundness Ex- aminations of Rams and Bucks, in Sheep and Goat Manual, Vol. X, Soc. for Theriog., Hastings, Nebr. 9. Rhodes, A. P. (1980) Semen Collection and Evaluation in Rams in Current Therapy in Theriogenology, Edit, by D. A. Morrow, W. B. Saunders Co., Philadelphia, 944. 10. Smith, M. C. (1980) Semen Collection in the Buck, in Current Therapy in Theriogenology, Edited, by D. A. Morrow, W. B. Saunders Co., Philadelphia, 922. The Boar 1. Aamdal, J. and Hogset, I. (1957) Artificial Insemination in Swine, JAVMA, 131, 1, 59. 2. Aamdel, J., Hogset, I., Sveberg, O. and Koppang, N. (1958) A New Type Artificial Vagina and a New Collection Technique for Boar Semen, JAMVA, 132, 3, 101. 3. Adams, W., Clark, T. L. and Evans, L. E. (1969) Electrojacu- lation of the Anesthetized Boar, An. Meeting, AVMA, Minne- apolis, mimeographed notes. 4. Bratton, R. (1967) Personal Communication, Cornell Univ. 5a. Clark, T. L. (1976) Electroejaculation of the Anesthetized Boar, Soc. for Theriog., Jour. Vol. VII, 2nd Ed., Hastings, Nebr. 5b. Dzuik, P. J., Graham, E. F., Donker, J. D., Marion, G. B. and Petersen, W. E. (1954) Some Observations in Collection of Se- men from Bulls, Goats, Boars, and Rams by Electrical Stimu- lation, Vet. Med. 49, 11, 455. 5c. Frank, A. H. (1950) Artificial Insemination in Livestock Breed- ing, USDA, Circular 567, Wash., D.C. 6. Hess, E. A., Ludwick, T. M. and Teague, H. S. (1960) Artificial Insemination in Swine, Ohio Agric. Expe. Stat., Res. Circ. #90, Wooster, Ohio. 7. Hughes, P. E. and Varley, M. A. (1980) Reproduction in the Pig, Butterworth and Co., London. 8a. Hurtgen, J., Crabo, B. and Leman, A. D. (1977) Fertility Ex- amination of Boars, Proc. Ann. Mtg. Soc. for Theriog., St. Paul, Minn. 11. 8b. Hurtgen, J. P. (1982) Reproductive Diseases (of the Boar), Vet. Clin, of N. Amer., Lg. An. Pract., 4, 2, 292-297. 9. Melrose, D. R. (1963) Artificial Insemination in the Pig, A Re- view of its Development, Brit. Vet. Jour. 119, 532 and World Review of Animal Production, 1966, II, 15. 10. Turkheimer, A. R., Young, D. C. and Foote, R. H. (1958) Tech- niques for Semen Collection; Semen Production in Young Boars, Cor. Vet. 48, 3, 291. 11. Rothe, K. (1963) Die Kunstliche Besamung beim Schwein, Ar- chiv. Fur. Exper. Veterinarmed. Bd. 16, 957. 12. Thompson, L. (1979) Check Boar Fertility, Swine Professional Topics, Univ. of Illinois, 4, 7. The Dog and Cat 1. Christensen, G. C. and Dougherty, R. W. (1955) A Simplified Apparatus for Obtaining Semen from Dogs by Electrical Stimu- lation, JAVMA, 127, 940, 50. 2. Boucher, J. H., Foote, R. H. and Kirk, R. W. (1958) The Eval- uation of Semen Quality in the Dog and the Effects of Frequency of Ejaculation Upon Semen Quality, Libido and Depletion of Sperm Reserves, Cor. Vet. 48, 1, 67. 3. Foote, R. H. (1965) Current Veterinary Therapy, 3rd Ed., R. W. Kirk, Editor W. B. Saunders Co., Philadelphia and London, p. 686. 4. Hancock, J. L. and Rowlands, I. W. (1949) The Physiology of Reproduction in the Dog, Vet. Rec. 61, 47, 71. 5. Harrop, A. E. (1954) A New Type Canine Artificial Vagina, Brit. Vet. Jour. 110, 194. 6. Harrop, A. E. (1954) Reproduction in the Dog, Williams and Wilkins Co., Baltimore, Md. 7. Kirk, R. W. (1959) Artificial Insemination in the Dog, Allied Vet., Mar-April. 8. Larsen, R. E. (1980) Infertility in the Male Dog, in Current Ther- apy in Theriogenology, edit, by D. A. Morrow, W. B. Saunders Co., Philadelphia. 9. Nooder, H. J. (1950 Enkele Mededelingen omtrent, de K. I. brij Teven en het Sperma van Reuen, Tijdschr. v. Diergeneesk, 75, 3, 81. 10. Platz, C. C., Jr. and Seager, W. J. (1978) Semen Collection by Electroejaculation in the Domestic Cat, JAVMA, 173, 1353. 11. Seager, S. W. J. and Platz, C. C. (1977) Collection and Eval- uation of Canine Semen, Veterinary Clinics of N. Amer., I, 4, 765, W. B. Saunders Co., Philadelphia. 12. Sojka, N. J., Jennings, L. L. and Hamner, C. E. (1970) Artificial Insemination in the Cat (Felis Catus L.) Lab An. Care, 20, 2, 598. SEMEN QUALITY EXAMINATION AND FERTILITY ASSESSMENT Examinations for semen quality can only be satisfac- torily performed on approximately normal ejaculates within a short period after collection. The ejaculates must be properly protected and handled until examined. Some factors to consider in the proper handling of semen are: (1) The artificial vagina or the container used for semen in electroejaculation should be clean and free from con-INFERTILITY IN MALE ANIMALS 873 taminants that might injure spermatozoa, such as: alco- hol, excessive petrolatum, powder present on new rub- ber liners, and antiseptics or chemicals of any kind; (2) at the time of collection excessive dirt or debris includ- ing preputial smegma and secretions should be kept out of the vagina; water and urine injure spermatozoa by cre- ating a different osmotic pressure; (3) excessive amounts of blood and serum may adversely affect spermatozoa; (4) overheating and too-rapid chilling injure spermato- zoa, (5) too much agitation and shaking of the semen damages spermatozoa; and (6) excessive exposure to sunlight should be avoided. It is important that the se- men sample be examined as soon as possible after col- lection.70 A good laboratory with the necessary very clean glass- ware and equipment and a well-trained technician, if it is within a few hours drive is the logical place to have the semen examination performed. However, all too often a semen sample is sent to a laboratory at some distance; and the motility and other qualities may be so affected during shipment that the value of such an examination is questionable or limited. In many of these instances only a morphological examination and density estima- tion of spermatozoa can be performed. Usually a warm “laboratory” at 60 to 80° F. can be set up in an auto- mobile with a good heater. Portable electric incubators that can be connected to a 110 volt circuit are now avail- able for the warming of equipment. For this reason the author firmly believes that by the use of a microscope most trained veterinarians can perform by means of a few simple laboratory procedures on the farm or ranch 3 or 4 semen tests on a male and more accurately de- termine his probable fertility than can a trained labora- tory technician receiving a single ejaculate by mail. The veterinarian also has access to the complete breeding his- tory, information on the male’s sexual desire and fre- quency of service, and other pertinent information, such as his performance during copulation, from a careful physical examination not known to a laboratory. In this testing procedure as in other laboratory techniques the results must be carefully evaluated on the basis of the information obtained and what is known concerning the case; too much reliance should not be placed on the re- sults of tests on a single ejaculate of semen. The best fertility evaluation test is the conception rate of the fe- males bred to the male. Semen examinations, if carefully done, may provide a ready and reasonably accurate mea- sure of whether the male is probably fertile or definitely infertile and be of value in determining the severity and the possible cause of infertility affecting a male. If spe- cial staining techniques, electron microscopy or other complicated procedures are necessary for morphological studies on certain semen samples these must be done in specialized laboratories under the supervision of skilled and knowledgeable technicians and scientists. Semen quality of the first ejaculate after a long period of sexual rest may have a lowered motility and an in- creased number of dead spermatozoa. Semen quality in many rams and a few bulls may be decreased during the hot summer months. Season of the year had a significant effect on semen quality in stallions with the best quality of semen produced late in the spring or early summer and the poorest quality semen in the winter months.94'95'96 Similar conditions prevail in the breeding and nonbreed- ing season of sheep and goats. The various common tests on semen are as follows: Volume—The usual volume of the ejaculate in the various domestic animals has been noted previously. Re- peated frequent ejaculations may temporarily lower the volume of the ejaculate. However, under the usual breeding conditions the amount of the ejaculate pro- duced remains fairly constant for each species of animal. (See Table 21.) Under conditions of artificial insemi- nation, teasing or “stewing” of bulls, dogs, boars and other species is often practiced to increase the numbers of spermatozoa and possibly the volume of the ejaculate. Restraining bulls for 2 to 5 minutes or more to induce sexual excitement before allowing ejaculation, was ac- companied by increases of about 40 percent in the num- ber of motile spermatozoa per ejaculate over unre- strained bulls.31 Small volumes of semen may be ejaculated in young males, in males used excessively, in incomplete ejaculation or failure of ejaculation, and in cases of bilateral seminal vesiculitis in bulls and stal- lions. An increase or decrease in volume of semen ejacu- lated is usually not correlated with fertility in a male un- less ejaculation fails to occur. Color—As described previously ram and bull semen is concentrated and the color is milky or creamy white and opaque. (See Tables 23 and 26.) It is normally like cream in consistency. In the stallion, boar, and dog the spermatozoa are much less concentrated and the color is pearly-white to grey and translucent. A creamy consis- tency of semen is present in bulls with spermatozoan concentrations of 1,000,000 to 1,200,000 per cmm. or higher; a thin milky consistency with spermatozoan con- centrations of 500,000 to 600,000 per cmm., and wa- tery, translucent or clear semen occurs with fewer than 300,000 spermatozoa per cmm.53 Brownish-colored se- men in bulls, probably due to blood pigment, may be observed in cases of orchitis.36 The light yellow color seen occasionally in the semen of some bulls at the time of collection is due to riboflavin secreted by the acces- sory glands and it has no significance.874 VETERINARY OBSTETRICS The presence of Ps. aeruginosa in bull semen may cause a change from a normal to a yellowish-green color when semen is left standing at room temperature.53 Clumps, clots or large flakes in semen are due to the presence of pus usually from the accessory glands or am- pullae. A dark red to pink color of the semen is due to the presence of varying amounts of blood from the gen- ital tract, urethra or penis. A light brown color may be due to the presence of feces in the semen. When the semen is not a normal color and consistency, further ex- amination should be made of the actual density or con- centration of the spermatozoa, since reduced fertility may accompany a reduced or low concentration of sperma- tozoa or severe contamination with substances or agents harmful to spermatozoa. Hydrogen ion concentration or pH value of the se- men of domestic animals has been reported previously. Measurements of the pH of semen at the time of collec- tion is of little practical value in the normal male for predicting fertility.-'114 In bulls, rams and dogs the pH of semen is neutral, about 6.7. A pH of 7.0 or higher in semen was observed in bulls used excessively, in in- complete ejaculates and in pathological or inflammatory conditions affecting the testes, epididymides, ampullae or vesicular glands.20 The semen of stallions, boars and cats is normally slightly alkaline in reaction, pH 7.4. First ejaculates from stallions had an average pH of 7.47 and second ejaculates collected soon after the first were more alkaline, pH from 7.5 to 8.0.94,95 The pH of semen may be measured with pH paper, with bromthymol blue or a pH meter. When an inflammatory condition affect- ing an accessory genital organ is suspected or present and characterized by an elevation of the pH of the ejacu- late, a catalase test is indicated. High catalase activity of semen, a reaction greater than 300 on the tube used for the test, is demonstrable in cases of acute seminal vesiculitis of bulls. Concentration or density of spermatozoa in semen has been cited previously for the various domestic ani- mals. (See Table 23.) The concentration of spermatozoa in ejaculates of fertile bulls varies from 300,000 to 2,000,000 per cmm. with an average of 800,000.74 Ejac- ulates collected with the electroejaculator frequently have a lower concentration and a greater volume than those collected with the artificial vagina due to an excess of accessory gland secretion. Spermatozoan density is within normal limits in many bulls with testicular degeneration and therefore other tests are usually necessary for an ac- curate evaluation of semen quality.53 It was indicated that concentrations of spermatozoa below 600,000 should be looked upon with suspicion. In 24 bulls with serious af- fections of the testes, 13 had oligospermia, fewer than 200.000 spermatozoa per cmm. and 7 of these had fewer than 10,000 spermatozoa per ml.16'20 Some watery translucent ejaculates in bulls were due to incomplete ejaculation.16,20,108 In humans low concen- trations usually were correlated with infertility but ex- ceptions were common.80 In fertile men with low sperm cell counts the motility and morphology of the sperma- tozoa were good. In general, however, there was a def- inite correlation between spermatozoan density, motil- ity, and morphology. In rams50 and boars58 testicular degeneration is characterized by a marked decrease in the spermatozoan concentration correlating with the se- verity of the degeneration. As reported previously, sper- matozoan concentration is usually very low, less than 75.000 per cmm., in testicular hypoplasia of bulls with complete or nearly complete sterility.53,74 Another char- acteristic of sperm cell concentration noted in many in- fertile or sterile bulls was the rapid decrease in sper- matozoan concentration between the first, second, and third successive ejaculates, indicating poor spermato- zoan reserves and reduced sperm cell production.53,99 Fertility declined in stallions when there were fewer than 2 billion spermatozoa in the ejaculate.35 The incidence of azoospermia or oligospermia in several thousand stal- lions examined was low, 0.04 to 0.14 percent.12'13 Fer- tility usually depends upon the total number of actively motile normal spermatozoa in the ejaculate. The techniques used for determining concentration of spermatozoa are as follows: 1. The color or macroscopic examination of semen in bulls and rams with concentrated semen is quite satis- factory for an approximation of the density of sperma- tozoa. (See Table 26.) In boars, stallions, and dogs gross examination of semen is not accurate even with the ge- Table 26. Sperm Cell Concentration and Semen Color in Bulls and Rams Bulls (per cmm) Rams (per cmm)* Color of Semen 2,500,000 Thick, creamy 2,000,000 2,000,000 Creamy 1,000,000 1,000,000 Light creamy 500,000 500,000 Milky 100,000 100,000 Cloudy, watery, translucent less than 50,000 less than 50,000 Almost clear, transparent, watery *Gunn and coworkers.50INFERTILITY IN MALE ANIMALS 875 latinous portion of the ejaculate of stallions and boars removed. Although as the examiner gains experience this method will give a fair indication of the spermatozoan concentrations in the more concentrated samples in bulls and rams; but in medium to lower ranges the visual es- timation of sperm cell concentration is subject to serious errors. 2. The enumeration of spermatozoa may be made with a hemocytometer in a manner similar to that used in making a red blood cell count.30 One procedure was to fill a red blood-cell pipette to the 0.5 mark with undiluted semen. A 3 percent chlor- azene solution was drawn up to the 1.01-mark in the pipette; this diluted the semen and killed the spermato- zoa. This mixture was shaken carefully but vigorously for 2 to 3 minutes. A few drops were released and the shaking was repeated. A few more drops were released and then a drop was placed under the cover slip in a Neubauer blood-cell counting chamber. Sperm cells in 5 large squares were counted in a diagonal direction and the total number of spermatozoa counted were multiplied by 10,000.105 This procedure rapidly gives an accurate indication of the sperm cell concentration per cmm if the mixing is thorough. 3. The concentration of spermatozoa may be obtained rapidly in a well-equipped laboratory by a photoelectric colorimeter that has previously been properly calibrated by known spermatozoan concentrations.121 After adding 1 part bovine semen to 40 parts of sodium citrate buffer, the diluted semen is placed in a special tube in the pho- telometer. By reading the dial on the photelometer and comparing this reading with a chart containing previous readings with known spermatozoan concentrations, the sperm cell concentration of the ejaculate in question can be determined very rapidly. This may be adapted to dogs or other species. In the dog a dilution rate of 1 to 4 to 1 to 16 was recommended.43 This technique is used in most bovine artificial breed- ing laboratories for determining the concentration of spermatozoa. This information is necessary for comput- ing the dilution or extension factor. 4. The comparing chamber described by B lorn16 may be used for a fairly accurate estimation of the concen- tration of spermatozoa by comparing the concentration of spermatozoa in a layer of semen 50 microns thick with pictures of known concentrations of 1, 0.5 and 0.2 million spermatozoa per cmm. 5. Other methods not so practical as the above for de- termining the concentration of spermatozoa include the measuring the packed cell volume, spermatocrit,41 and the use of the Coulter electronic counter.48 Motility of spermatozoa at the time of collection is commonly used and excellent measure of the fertilizing ability of spermatozoa. Care should be taken at the time of collection that the ejaculate is protected from “cold shock” or sudden reduction in temperature that has a marked depressing effect on motility. Excessive heat and chemicals or foreign agents, as well as urine or water, also affect sperm cells and reduce motility. The first ejaculate after a long period of sexual inactivity often has poor motility and increased numbers of dead sper- matozoa. For accurate results this test is best made with an elec- trically heated microscope stage at body temperature. Motility ratings can be made in the field by gently warm- ing the semen slide by placing it on a flat bottle con- taining warm water at body temperature. Cooling semen from body temperature down to refrigerator temperature causes a gradual loss of motility of spermatozoa until near immobility is reached. Therefore, semen should al- ways be examined at body temperature so that accurate and comparative readings can be made. It may be de- sirable to dilute the semen in warm Ringer’s saline or 2.9 percent sodium citrate solution to more easily ob- serve the individual spermatozoa so an estimate of the degree and percentage of motile spermatozoa can be made. A fast, accurate, photographic method of measuring the proportion of moving spermatozoa and their rate of pro- gression has been described.79 Motility of bovine sper- matozoa is more significant as a test for fertility after thawing following freezing. A motility rate less than 20 percent after thawing will contribute to a low non-return rate.77a A time-exposure photographic system with dark- field microscopy has proven a valuable procedure to de- termine spermatozoan motility and semen quality fol- lowing thawing of frozen bull semen.77b By this tech- nique the number of progressively motile cells, which varies widely between ejaculates and bulls, can be as- sessed with great accuracy. Motility is based on the estimated percentage of motile spermatozoa and their degree of motility. Most investi- gators described the various degrees of motility of sper- matozoa in undiluted semen as follows:53,55 0— spermatozoa are immotile 1— stationary bunting or weak rotary movements are exhibited by spermatozoa 2— oscillatory or rotary movements and fewer than 50 percent of the spermatozoa are in progressive mo- tion, with no waves or eddies 3— progressive rapid movement of spermatozoa, with slowly moving waves and eddies, usually 50 to 80 percent of the spermatozoa must be progressively motile to produce waves and eddies 4— vigorous, progressive movement with rapid and876 VETERINARY OBSTETRICS abruptly forming waves and eddies, indicating about 90 percent motile spermatozoa 5—very vigorous forward motion, extremely rapid waves and eddies, indicating about 100 percent ac- tively motile spermatozoa In the 350 micron thickness of undiluted semen in a comparing chamber at body temperature, 50 to 70 per- cent living spermatozoa produced rapid whirls and ed- dies and good to excellent motility; 30 to 50 percent pro- duced sluggish waves and fair motility; and 10 to 30 percent motile spermatozoa produced single propulsions with no waves or whirls and with poor motility.16 In nor- mal bovine semen initial motility of 40 to 45 percent or more was essential since lower rates of motility were associated with infertility. Most fertile bulls have 50 to 80 percent of their spermatozoa exhibiting active, pro- gressive motility.16,20 Good initial motility alone is not always an accurate indication of fertility in the bull.114 Examples of infertile bull semen with excellent initial spermatozoan motility that rapidly lost its motility when stored or highly motile spermatozoa that were infertile were cited. No difference was reported in conception rates of semen with 50 per- cent actively motile spermatozoa and higher percentages of motile sperm cells. Motility below 50 percent was often associated with lower conception rates or poor fer- tility. The motility of bovine spermatozoa in testicular hy- poplasia was much poorer than in testicular degenera- tion.53 Only 10 percent of the bulls with testicular de- generation showed motility above 70 percent and a rate or degree of motility of 3 or higher, which is the average requirement. The number of motile spermatozoa was less than 70 percent in 90 percent of the bulls with testicular degeneration but the degree of motility was below 3 in only 42 percent. Ninety-two percent of 100 normal fer- tile bulls had satisfactory motility whereas only 32 per- cent of the “problem” bulls had satisfactory motility.16,20 Congenitally sterile bulls with a very high percentage of abnormal sperm cells, especially those with defects of the midpiece and tail, had the lowest motility.53,99 It is generally assumed that the duration of motility of ab- normal spermatozoa is reduced. Normal stallion spermatozoa had a degree of motility of 3 to 4, and 48 to 75 percent of the spermatozoa in the semen were actively motile about 20 minutes after ejaculation.83 After the unextended semen had stood 8 hours at room temperature no reasonable degree of activity was observed.83 The percentage of motile spermatozoa in 54 fertile stallions ranged from 55 to 60 percent.12,13 In sev- eral thousand stallions examined low motility or as- thenospermia occurred in 0.8 to 3.4 percent and necros- permia occurred in 0.09 to 0.3 percent. Even with the minimum of handling, the motility of equine sperma- tozoa decreased rapidly in vitro.83 This is a possible re- flection of the inability of equine spermatozoa to survive in equine seminal plasma that has very low levels of re- ducible sugar for energy purposes in contrast to the rel- atively long viability of spermatozoa in seminal plasma of other animals. The addition of isotonic, 5 percent, glucose to equine semen with poor motility of the sper- matozoa, may result in marked improvement of the mo- tility.96 This is interesting, since in the genital tract of the mare equine spermatozoa survived 72 hours or more.35 (See equine reproductive physiology) In horses it is pos- sible that seminal plasma may have an adverse effect on spermatozoa while the environment of the mare’s genital tract is highly favorable for sperm cell survival. Thus some stallions with relatively poor motility in freshly ejaculated sperm may be quite fertile. Even so, in the stallion the spermatozoan motility and the quality of that motility are the most reliable estimates of fertility.118 In rams,50 boars58 and bulls a decreased motility of spermatozoa has been reported in experimentally-pro- duced testicular degeneration. Fertile boars have semen that usually contain 80 to 95 percent actively motile spermatozoa, while rams have about 60 to 70 percent motile cells. In man 50 to 60 percent active spermato- zoan motility was average and 75 percent was good.81,82 In men with less than 40 percent actively motile sper- matozoa the incidence of sterility rose sharply. Sperm cell defects involving the midpiece and tail are often characterized by poor motility. There is an intimate relationship between the epididymis and its secretions on sperm cell motility and tail defects as described under diseases of the epididymis. Pus and drops of vaseline in the semen reduced sper- matozoan motility.10,16,20 Care should be used in lubri- cating an artificial vagina not to apply an excess of lu- bricant that might melt and run into the semen-collecting tube or vial. The importance of the number of actively motile sperm cells in the ejaculate on the fertility of the male has been stressed in different species by many workers. This fact was well-illustrated by a valuable, 12-year-old Guernsey bull used in an artificial insemination stud that developed senile testicular degeneration associated with interstitial cell tumors. A progressive gradual decline occurred in motile spermatozoa in the ejaculate from 50 to 10 per- cent along with a gradual increase from 30 to 60 percent in the number of abnormal spermatozoa. Extending his semen on the basis of the numbers of actively motileINFERTILITY IN MALE ANIMALS 877 spermatozoa present in each ejaculate resulted in satis- factory conception rates even though the extension rates were as low as 1 to 10 in order to provide 6 to 10 million actively motile spermatozoa per ml. for each insemina- tion. Longevity, viability, or liveability of spermatozoa in semen or extended semen at refrigerator, room or in- cubator temperatures is another measure that can be used for testing or estimating the fertility of semen. A number of studies from 1940 to 1955 were summarized in the first edition of this text and others of work performed on this type of test for assessing semen quality and fertil- ity.-98 Since that time relatively few experimental stud- ies on these tests have been conducted because they are difficult to run as they extend over a period of hours or days, and thus are not adaptable to semen collected for artificial insemination purposes. Good quality equine se- men maintained reasonably good motility for up to 8 hours after collection at room temperature.85 Results and cor- relations with fertility of the male do not provide any greater predictive value than the current simpler tests of semen quality including concentration, motility, and morphology. Differential staining to determine live/dead sper- matozoa in an ejaculate was described using a vital stain such as eosin nigrosin stain.18,20,115 This stain, as the India ink, is a good background stain. To make the stain- ing solution, weigh out 3 gms. of sodium citrate dihy- drate and add to 100 ml. of sterile double distilled water. To this add 1 gm. eosin B and 5 gm. nigrosin and mix into solution. The eosin will stain the dead spermatozoa a pink or red color, live spermatozoa remain colorless, and nigrosin provides a blue-black background stain.18 This stain will remain stable for one year or more with- out refrigeration. Place a small drop of stain on a clean warm slide and add a small drop of semen to the stain and mix gently with a round glass rod or a platinum loop. After a few seconds to a minute or more smear out with the glass rod or another glass slide and dry rapidly near a flame. At least 100 to 200 cells, or preferably 500, should be counted by scanning the entire length of the semen smear. Morphologically abnormal cells may be counted at the same time. In a review on the assessment of semen quality, most workers found an average of about 20 percent dead cells in most normal bovine semen sam- ples and there was little correlation with fertility.- After a prolonged period of sexual rest the percentage of dead spermatozoa may be increased. The live/dead sperm cell count should be evaluated critically. Poor stain or stain- ing technique may greatly affect the findings. A high incidence of necrospermia is usually associated with poor motility and low fertility. However, poor motility may be associated with normal levels of live spermatozoa, which depending on the cause of the poor motility, may be characterized by either normal or low fertility. Pres- ently the live-dead spermatozoan ratio in ejaculates is seldom used to assess fertility. Examination of stained spermatozoa for morphol- ogy is of definite value in studying the severity of tes- ticular degeneration or testicular hypoplasia and the con- genital or hereditary defects of spermatozoa. Techniques for preparing and staining sperm cells for morphology examination—The importance of making smears, and fixing them by air-drying before the semen is cooled to prevent the development of secondary spermatozoan abnormalities has been emphasized.97 Storing semen a reasonable time had no effect on the primary spermatozoan abnormalities. Extended semen is not satisfactory for morphological examination because of the egg yolk or milk that is present. Semen samples could be diluted with a physiological saline solution to a concentration of about 200,000 per cmm. before a slide is prepared, so that the stained spermatozoa will not be too concentrated to permit observation of individual cells.18-20 All glass slides used in making semen smears should be thoroughly cleaned, soaked in alcohol, and dried. The plasma and gel fraction of semen may inter- fere or make difficult the staining of equine or porcine spermatozoa. The addition of one-half to one part of five percent of isotonic glucose solution to one part of horse semen was recommended.96 This mixture was centri- fuged at 1500 rpm in a clinical centrifuge for 5 minutes. After pouring off the plasma the sperm cells in the glu- cose solution are stained in the usual manner. India ink preparations, are probably the simplest and easiest for the veterinary practitioner to prepare.19,20 Five parts or drops of a high-grade India ink, such as Pelican Yellow Label, are gently mixed with 1 part or drop of semen. One should be careful not to contaminate the bot- tle of India ink with sperm cells or bacteria. A drop of this mixture is placed on the slide and spread by one of the following methods: blowing gently; drawing, not pushing, it out with a spreader as with a blood smear; or gently smearing it out with a 1/8 inch, rounded, glass rod. The smear is then air-dried or dried slowly over the warm air of a flame. The dried slide is examined under oil immersion or the high dry magnification. All abnor- malities of the spermatozoa and semen may be noted. Large round cells, if present, should be recognized as leukocytes or primordial germinal cells. Eosin-nigrosin stain is a widely-used simple and ef- fective vital stain.18,115 The technique for its use was de-878 VETERINARY OBSTETRICS scribed previously. It may be used for counting the num- bers of live/dead cells as well as the morphologically normal and abnormal cells. Wright’s stain, commonly used for staining blood smears, may also be used for semen examinations. This stain is not as satisfactory as Casarett’s stain because it tends to precipitate on the slide, producing artifacts, and it does not stain the spermatozoa as effectively. The semen should be smeared gently and thinly over a clean slide and fixed by air-drying. The slide should then be immersed in 0.5 or 1 percent chloramine T solution to remove the excess mucus, even though this procedure may cause some breakage of spermatozoa. After being immersed in this chlorine solution for 5 to 7 minutes, the film of semen on the slide is washed gently first with distilled water and then with 95 percent alcohol, and then dried. The semen film on the slide is covered with Wright’s stain for 60 seconds. Distilled water is then added until a metallic luster is produced. The stain is left on the slide for 2 to 5 minutes before being rinsed off with distilled water. After the stained slide is air-dried it can be examined under the oil immersion or the high dry power of the microscope. Hematoxylin and eosin and Giemsa’s stains are also satisfactory for the examination of semen smears for the presence of cells other than spermatozoa. Casarett’s stain is an excellent stain for semen slides.10 Thin films of fresh semen are fixed on glass slides by immersing them for 3 minutes in a mixture of equal parts of ethyl alcohol and ether; the slides are then air-dried. They are stained by immersion for 5 to 7 minutes in a dye solution heated to 40 to 60° C. The dye solution con- sists of 30 ml., or 2 volumes, of 5 percent watery eosin B. solution and 15 ml., or 1 volume, of 1 percent watery phenol solution. The stained smears are washed with dis- tilled water, air-dried, and mounted in balsam. The sper- matozoan structures are very clearly outlined. Other good staining techniques have been described including car- bolfuchsin and eosin stain and methylene blue.- For long term preservation of spermatozoa, especially for acrosomal examination, adding a few drops of semen to a small amount of buffered formo-saline made up and used as follows is recommended:47 51,52 Stock buffer soln* 100 ml. Stock NaCl soln.** 150 ml. Commercial formalin (37-40% 62.5 ml. formaldehyde) Aq. dist. ad. 500 ml. *Stock buffer soln. soln. A) Na2 HP04.2H2) 21.682 gm. Aq. dist. ad 500 ml. soln. B) KH2 P04 22.254 gm. Aq. dist. ad. 500 ml. Take 200 ml. of soln. A and mix with 80 ml. of soln. B. Then from the resultant 280 ml., take 100 ml. as stock buffer soln. ** Stock NaCl soln. NaCl 9.01 gm. Aq. dist. ad. 500 ml. Directions for use: Add 1 to 2 drops semen to about 5 to 10 ml. of buf- fered formo-saline, gently shake; add 1 to 2 drops of dihydrostreptomycin, incubate for 10 to 20 min. at 37° C and then refrigerate (about +4° C); this will preserve sperm cells for up to 18 months. Another method for fixing bull or boar spermatozoa for shipping or storing was to use glutaraldehyde in phosphate buffered saline with sodium cacodylate.65,68 Wet mounts for phase contrast microscopy are made in a suitably equipped laboratory from preserved sam- ples and are far superior to smeared and stained prepa- rations for estimating the percentage of spermatozoa with proximal protoplasmic droplets and acrosomal abnor- malities. A phase contrast effect can be partially achieved in a regular light microscope by reducing the amount of light permitted to come through the substage condenser. Following one or more of the several staining procedures 100 to 200 or more up to 500 to 1000 spermatozoa should be examined under oil immersion at 1,200 magnification and classified. An experienced technician could achieve as reliable results counting 100 cells as by counting 500 sperm cells.107 Spermatozoan abnormalities may be classified as head, body, and tail defects. These three anatomical groups of sperm cell abnormalities have been classified by Lagerlof and Blom19,20'47 in two further groups as pri- mary forms that occur due to disorders of the seminif- erous or germinal epithelium and as secondary forms that occur after they have left the germinal epithelium, dur- ing their passage through the mesonephric ducts, during ejaculation, or in manipulations of the ejaculate includ- ing excessive agitation, over-heating, too rapid cooling, due to the presence of water, urine or antiseptics in the semen, and etc. The primary anomalies occur during spermatogenesis either during spermatocytogenesis from spermatogonia to spermatids or during spermiogenesis from spermatids to spermatozoa. The author and others46,47 have serious reservations over using these latter two classifications of spermatozoan ab- normalities. If a sperm cell is defective and for that rea- son can’t fertilize an ovum it doesn’t matter whether it becomes defective in the seminiferous tubules or me- sonephric duct or at ejaculation. If sperm cell artifacts are due to accidents from improper handling of the ejac-INFERTILITY IN MALE ANIMALS 879 ulate or smearing or staining, a subsequent ejaculate, if handled properly, will usually lack such damaged cells. Furthermore, defects occurring in the germinal epithe- lium may not manifest themselves until later in the ma- turation of the cell such as separation of the head and neck described in Guernsey bulls5152 in which the sep- aration took place in the head of the epididymis at the time of the loosening of the cytoplasmic or protoplasmic droplet which up to this point had apparently prevented the separation. Chromosomal defects in apparently normal sperm cells have been discussed previously and are probably genetic in nature. (See prior discussion in this Chapter on ab- normal acrosomes, nuclear defects, intrachromosomal aberrations in spermatozoan development and hereditary or congenital sperm cell defects.) Spermatozoan head abnormalities include: (See Figures 198, 199, 200) Microcephalic heads Macrocephalic heads Double, or multiple heads Elongated or narrow heads Pyriform or pear-shaped heads with a narrow or ta- pering base Twisted, irregular-shaped heads and abortive forms Round short heads Abnormal acrosomes (Knobbed spermatozoa) “ruf- fled,” incomplete, flattened, or “bent-over” acro- somes Nuclear envelope invaginations “craters,” “pouches,” “erosions” (near equator) Detached or free heads (Guernseys and others) Detached galea capitis and acrosome The latter two are possible “secondary” abnormalities. Macrocephalic heads with a broader than normal base have been shown by various tests to probably be cells with a diploid chromosome content. These were found with an incidence of 0.104% in a group of inbred or closely line-bred Hereford bulls104 and as a rare occur- rence in six bulls with lowered fertility.46 Abnormal ac- rosomes and nuclear abnormalities may be difficult to observe or detect without phase contract microscopy, electron microscopy, or special staining procedures. A review has been compiled on recent studies on acroso- mal changes associated with aging of spermatozoa and in freeze-thawed spermatozoa as another indicator of sperm quality since penetration of the ovum depends on acrosomal enzymes.26'101 Detached or free heads may be due to excessive agitation of the semen sample or due to improper smearing of the spermatozoa on the slides. The detached galea capitis or head cap from dead sper- matozoa is seen mainly in India Ink preparations in the Figure 198. Normal Bovine Spermatozoa (Left) Normal Spermatozoa, (Center) Diagram of Dorsoventral Aspect, (Right) Diagram of Lateral Aspect.880 VETERINARY OBSTETRICS Normal Sperm Cells Microcephalic Sperm Cells Elongated Narrow Heads Pyriform or Pear- Shaped Heads Macrocephalic Sperm Cells Short Broad Heads Double Heads Double Middle Pieces and Tails Swelling of Middle Pieces Kinked and Coiled Middle Pieces and Tails Abaxial Attachments of Middle Pieces (may be normal in stallions and boars) Figure 199. “Primary” Spermatozoan Abnormalities.INFERTILITY IN MALE ANIMALS 881 Free Heads, Middle Pieces and Tails Proximal and Distal Protoplasmic Detached and Droplets and Bent Middle Pieces Loosened Galea Capitis (India Ink Stain) Figure 200. “Secondary” Spermatozoan Abnormalities. first ejaculate after a long period of sexual rest or in sper- matozoa after prolonged storage. They resemble a bath- ing cap in shape. Using a special stain, less than 5 per- cent of acrosomal abnormalities in sperm cells from bulls being collected regularly but an average of 21 percent abnormalities of the acrosome in the first ejaculates of 22 sexually-rested bulls was found.119 This may be an aging phenomena.101,106 An increased number of tailless heads occurred in the early stages of testicular degeneration in fertile bulls.19,20'53,99 Normal fertile bovine semen contained only 0.5 to 8.6 percent loose heads. The stallion and possibly the boar spermatozoan differs from other mammals by having an asymmetric head, an abaxial position of the tail and a small acrosome.14,15,646,65,66 Spermatozoan body or middle piece abnormalities include: (See Figures 199 and 200) Swollen neck Kinked neck with coiling of the middle piece and tail about head Stubby midpiece (“tail stump” defect) Naked or filiform neck Abaxial attachment of the neck and middle piece to the head, (normal in stallion and boar15,646) Swelling of the middle piece, either diffuse, localized, cranial or caudal Double middle piece Coiled middle piece Kinked middle piece with a tightly coiled tail “Corkscrew” middle piece Loose or free middle-pieces and tails; these may be weakly motile Kinked necks Middle pieces with proximal or distal protoplasmic or cytoplasmic droplets Bent middle pieces, with or without a protoplasmic droplet at the point of the greatest bending In counting abnormal sperm cells, loose or free middle pieces and tails should not be recorded if free heads are counted. The presence of a protoplasmic or cytoplasmic droplet on the middle piece has been described19,20,74,97 and is considered to be normally present on spermatozoa from the head of the epididymis. As the spermatozoa mature in their passage through the epididymis this pro- toplasmic drop recedes from the neck down the middle piece and is usually lost before the spermatozoa are ejac- ulated. The migration of the propoplasmic droplet from the proximal to the distal portion of the middle piece occurred in the head of the epididymis. These were con- sidered to be immature sperm cells when seen in ejacu- lated semen.74 No more than 2 to 3 percent of normal spermatozoa should have this protoplasmic drop on the proximal part of the middle piece.16,20,74 Other authors indicated that the presence of a high percentage of mid- dle pieces with protoplasmic droplets may possibly be due to overuse of the male and to too rapid passage of spermatozoa through the epididymis. In boars this con- dition was associated with testicular degeneration and882 VETERINARY OBSTETRICS hypoplasia.58 A localized swelling of the middle piece should be differentiated from an attached protoplasmic or cytoplasmic droplet. The true developmental abnor- mality of a swelling of the middle piece is an irregular enlargement which stains darkly, in which no differen- tiation can be seen between the swelling and the central fibril; and the ends of the swelling are tapered." The protoplasmic droplet, by contrast, stains less intensely and is quite spherical. The corkscrew and “stubby” mid- dle piece are unusual abnormalities.2l,22b,32b Abnormali- ties of the middle piece and tail interfere with fertility by reducing motility; the swollen and thickened types of midpiece abnormalities were most serious.53'" A con- stant content of 30 to 50 percent of bent middle pieces was usually associated with impaired fertility.- An ab- normal environment in the epididymis may result in mid- piece or tail defects. An abaxial location of the midpiece on the head of the spermatozoa is common in stallions and possibly boars and is not associated with infertility in those species.14’15'65,66 An incidence of 35 to 47 per- cent abaxial midpieces in stallions was reported.13 Spermatozoan tail abnormalities include: (See Fig- ures 199 and 200) Tightly coiled tails (Dag defect) Double tails Distal cytoplasmic or protoplasmic droplets (common in boar semen) Absent or shortened tails, seen most often in stallions Coiled tails Bent, “hairpin” tails, with or without a protoplasmic drop at the bend Broken tails The latter two conditions66 72 are possible “secondary” abnormalities in boars associated with infrequent use rather than overuse. Proximal protoplasmic or cytoplasmic droplets on the body or midpiece if present on a high percentage of cells is usually associated with infertility, especially in boars. Distal protoplasmic droplets are common, about 10 to 12 percent, in boar semen and are not associated with infertility.646 In general abnormalities of the tail are infrequent and of little importance. Tails bent at the junction of the tail and middlepiece; either with or without a protoplasmic droplet, are fairly com- mon. They are usually caused by cold shock or osmotic shock due to the presence of water or urine in the eja- culate. The presence of 10 percent or more of any single type of the above head, body or tail abnormalities, normally absent from semen of males, is often associated with re- duced fertility.52 Cells other than spermatozoa in semen smears in- clude: Leucocytes are found in cases of inflammation or in- fection of the reproductive tract; there are very few in normal semen Erythrocytes Squamous epithelial cells—both nucleated and non- nucleated. These usually come from the epithelium of the prepuce or the urogenital ducts. Boat-shaped spermatogenic cells—These are more common in abnormal than in normal semen and are more likely to be associated with deformed heads than with deformed middle pieces.53’99 Spermatids—nucleated, non-nucleated, and multi-nu- cleated. Spermatocytes—primary and secondary, often called Figure 201. Miscellaneous Cells Found in Semen 1. Leukocytes 2. Erythrocytes 3. Medusa Formations 4. Protoplasmic Droplets 5. De- generating Sperm Cell Cluster 6. Primordial Spermiogenic Cells 7. Giant or Multinucleated Cells 8. Squamous Epithelial Cells.INFERTILITY IN MALE ANIMALS 883 Figure 202. Normal Bovine Spermatozoa Figure 203. Normal Canine Spermatozoa (India Ink Stain) (Cour- tesy K. McEntee). Figure 204. Proximal Protoplasmic Droplets on Bull Spermatozoa (India Ink Stain) (Courtesy K. McEntee). Figure 205. Coiled Tails and Middle Pieces in an Infertile 11-year- old Bull. (The motility rate was between 5 and 10 percent, yet the conception rate was 50 percent with liquid semen extended 1:10 to 20.)884 VETERINARY OBSTETRICS “spheroids” or primordial spermatogenic cells. Medusa cells or bodies—Medusa formations are por- tions of ciliated epithelial cells from the efferent ducts of the testis.17 They are deeply-staining cells about the size of the head of the spermatozoa, with 10 to 30 fili- form, or long brush-like, projections or cilia. These cells are seen only in rare instances in the usual sperm cell preparations but may be seen in much greater number in semen preparations from males with severe testicular hy- poplasia when the semen is centrifuged and the sediment is placed on a slide and stained. This finding may aid in differentiating between an incomplete ejaculation of a normal bull and a complete ejaculation of a bull with nearly completely suppressed spermatogenesis. These medusa formations are seen at a rate of about 1 to 10,000 spermatozoa in normal bulls. In stallions the incidence is higher. Protoplasmic or cytoplasmic droplets; floating free in semen, are often observed in fertile semen and are of no significance. Bacteria, molds, and protozoa are usually contami- nants from the prepuce. Degenerating spermatozoan clusters—were observed in 19 percent of fertile bulls and 79 percent of bulls with testicular degeneration.53 Occasionally they were seen in bulls with testicular hypoplasia. These clusters of sper- matozoa are apparently produced by a disturbance in spermatogenesis. Multinucleated giant cells with 6 to 8 nuclei are seen occasionally in males with testicular hypoplasia or de- generation and are due to abnormalities in the divisional mechanism of the primary spermatocytes.33 The cause of these latter two conditions might be similar. The determination of the number and type of abnormal sperm cells in an ejaculate should be used along with other examinations conducted immediately after collec- tion such as those for motility and concentration. There is a divergence in opinion as to the importance of the presence of varying numbers of abnormal spermatozoa seen on stained semen preparations. If the percentage of abnormal spermatozoa is not above 30 to 35 percent it is not correlated with fertility in the relatively fertile bulls.25114 An average of 31.4 percent abnormal sper- matozoa was reported with a range of 15 to 48 percent in 19 bulls with testicular degeneration53 and an average of 39.1 percent abnormal spermatozoa with a range of 22 to 58 percent in 4 bulls with testicular hypoplasia. Normal fertile bulls had an average of 15.1 percent ab- normal spermatozoa with a range of 6 to 26 percent. The semen of normal fertile bulls should not have more than 3 to 4 percent abnormal heads, 4 to 10 percent abnormal middle pieces, 0.5 to 2 percent abnormal tails, and 0.5 to 6 percent, tailless heads.53,99 Similar values of 1.2 to 10.4 percent, with an average of 4.6 percent, primary spermatozoan abnormalities and an average of 2.1 per- cent, with a maximum of 8.6 percent, loose heads and other secondary abnormalities were reported in normal fertile bulls.19,20 Rams and bucks have very similar semen character- istics including, volume, concentration and motility pa- rameters.87,91 Rams having more than 14 percent abnor- mal spermatozoa in their semen are probably of reduced fertility providing the ejaculate was not taken after a long period of sexual rest.87 Normal fertile ram semen should not contain more than 5 to 15 percent abnormal sper- matozoa.117 Rams having 0.1 percent abnormal sper- matozoa in their semen had an approximate fertility of 80 to 100 percent; those with 1 percent abnormal sper- matozoa had fertility rates of 60 percent; rams with 10 percent abnormal spermatozoa had fertility rates of 45 percent; those with 30 percent abnormal spermatozoa had a fertility rate of 20 percent; and rams with more than 50 percent abnormal spermatozoa were sterile.50 Less than 14 to 17 percent with a range of 6 to 10 percent abnormal spermatozoa was observed in the se- men of fertile boars.58,92 In 13 boars with testicular de- generation the abnormal spermatozoa varied from 3 to 36 percent and immature spermatozoa with proximal protoplasmic droplets from 1 to 95 percent. The number of abnormal sperm cell heads was over 20 percent in 5 of the 13 boars and in 5 others the percentage varied from 3 to 8. The numbers of immature spermatozoa with proximal droplets were high in most cases of porcine testicular degeneration.53 Conception rates were 67.7 percent, 57.3 percent and 45.5 percent with boars with 80 to 100 percent, 60 to 79 percent and 40 to 59 percent normal spermatozoa, respectively, including sperm cells with distal protoplasmic droplets.14 The number of cells with distal and even proximal protoplasmic droplets were extremely variable between boars and between ejacu- lates. Tightly coiled tails appeared to be a defect in sper- matogenesis and doubling of a portion of the cells oc- curred at a level of 0.3 percent. A majority of midpiece attachments were slightly abaxial in the boar and this defect should not be considered as a primary sperm cell defect in the boar as it is in the bull.14 Many workers have reported that it was more difficult to evaluate the spermatozoa of stallions than of bulls, rams, boars and dogs.12-14,71 74,83,100 In the Thoroughbred stallion infertility can exist in the presence of appar- ently normal semen quality and it was concluded that the actual fertility of a stallion cannot always be pre- dicted on the basis of a semen examination.83,100 Other authors35,12-14 reported on sterile stallions with semenINFERTILITY IN MALE ANIMALS 885 containing only dead spermatozoa (necrospermia) at the time of ejaculation. In stallions of low fertility the con- centrations of spermatozoa and the volume of semen were low, 10,000 to 15,000 per cmm. and about 10 to 25 ml., respectively. A fertile stallion was described with good sperm motility but with 35 to 45 percent of the sper- matozoa having a proximal protoplasmic droplet and 4 to 6 percent having double heads.35 Bielanski12,13 re- ported on 54 stallions with conception rates from less than 25 percent to nearly 100 percent and the primary spermatozoan abnormalities varied from 2.5 to 10 per- cent and the secondary abnormalities from 22 to 39 per- cent. The most fertile stallions had less than 3 percent primary abnormalities. The author observed a young Standardbred stallion with 60 to 70 percent grossly ab- normal middle pieces and associated poor motility. Un- der regular handling infertility was evident but by good management, controlled breeding and breeding at the proper time of estrum he achieved a 70 percent concep- tion rate the next four years. In general the presence of more than 20 percent abnormal spermatozoa in equine semen may be interpreted as indicating low fertility but there were many exceptions.37 Some stallions may have apparently normal spermatozoa and low fertility; others are highly fertile even though a rather high percentage of spermatozoa are abnormal. Five to 13 percent abnor- mal spermatozoa in semen of fertile stallions was re- ported.86 Up to 30 percent abnormal spermatozoa may be present in fertile equine semen.11 Less than 20 percent abnormal spermatozoa were pres- ent in dogs producing good quality, fertile sperm.543,69 903 Only 0 to 10 percent abnormal spermatozoa with an av- erage of 4.8 percent in fertile canine semen was reported in another study.526 Ten to 15 percent abnormal sperm cells were reported by other authors in 11 normal dogs.5,24 Four to 10 percent abnormal spermatozoa were reported in ejaculates of 6 fertile male cats.111,3,6 The most com- mon abnormalities were cytoplasmic droplets, double, bent, dubbed or shortened tails and enlarged middle pieces. It is obvious from the above discussion that great care must be used in the interpretation of the morphology of spermatozoa in semen samples. Technicians differ in their classification of sperm cells, some classifying certain cells as abnormal that others would classify as normal. Dif- ferences arise due to variations in the technique of han- dling and preparing slides. There is probably no distinct line of demarcation between animals of good and poor fertility. The morphological examination of semen as an aid in evaluating fertility is apparently of greatest value in the detection of males whose fertility is unsatisfactory in natural matings. It is of limited or questionable value in determining fertility in individual ejaculates from males of fair to good fertility used in artificial insemination. The revised criteria (1976) of the American Society of Theriogenology110 for the evaluation of the breeding soundness (BSE) in bulls is scored or based on three re- liable characteristics that have been correlated to fertil- ity. These are: 1. scrotal circumference (based on 10 to 40 the age of the bull) 2. percent abnormal spermatozoa 3 to 40 (primary and total) 3. motility (gross and individual) 3 to 20 Total score 16 to 100 Bulls receiving scores from 60 to 100 are graded as satisfactory, 30 to 60 as questionable and below 30 as poor potential breeders. This presumes that the bull is normal physically, has satisfactory libido and is man- aged properly. In a Nebraska breeding trial with 57 sat- isfactory bulls, 22 questionable and 22 poor potential breeders, the conception rates were 60, 48 and 30 per- cent, respectively.110 The current, revised (1976) values for these three cri- teria are as follows: Scrotal circumference (given previously in this Chap- ter, page 860) Percent Abnormal Spermatozoa Classification Primary (%) Total (%) Score Very good 10 25 40 Good 10-19 26-39 25 Fair 20-29 40-59 10 Poor 29 59 3 Motility (Vigor of Movement) of Spermatozoa Classification Gross Individual* Score Very good rapid swirls rapid, linear 20 Good slower swirls moderately fast, linear 12 Fair shaky slow, linear 10 Poor flickers very slow, erratic 3 *Must evaluate in a compatible diluent Although these current criteria and tests used for the evaluation of the breeding soundness of bulls have been simplified and made more repeatable, it is probably ad- visable to continue the “battery” of semen tests, partic- ularly on certain bulls to identify those with unusual se- men characteristics. Bacteriological or virological examination of semen886 VETERINARY OBSTETRICS may be indicated under certain circumstances, especially when evidence of genital inflammation or infection is present in females following breeding to a male, a rapid decline in motility of the spermatozoa occurs on storage, or an increase in pH or the presence of leukocytes or frank pus are present in the ejaculate or in the semen smear. Organisms or viral agents in the semen may come from the testes or epididymides, the accessory glands, the vas deferens, the urethra, or the prepuce or penis. Semen examination of bulls by cultural methods or by the injection of semen into test animals may reveal in- fection with brucellosis, trichomoniasis, vibriosis, my- coplasmosis and others. In cattle the fluorescent anti- body test has proven useful in the examination of preputial smegma samples for vibriosis. In brucellosis, semen plasma agglutination tests may be indicated if the blood test reveals a positive or suspicious titer. Besides the possible danger to the female by introducing infection at the time of coitus, bacteria and their products may injure the spermatozoa and result in a rapid decline in the mo- tility of stored sperm cells, especially in liquid or frozen extended semen. (See prior discussion in this Chapter on genital infections of the male.) A brief summarization of the infectious organisms, either venereal, systemic, or “opportunistic” found in the semen of bulls include: diptheroids, C. renale, strep- tococci, B. pyocyaneus, Leptospira spp., staphylococci, E. coli, C. pyogenes, Br. abortus, Mycobacterium tu- berculosis (bovine and avian types) Mycobacterium paratuberculosis,75 Ps. aeruginosa, actinomycetes, Proteus, micrococci, yeasts, bacilli and molds. Myco- plasma were found in 94 percent of the semen samples from bulls.2 This organism was a saprophyte in the pre- puce of nearly all bulls. Mycoplasma were readily re- covered from the sheaths of 80 percent of 160 bulls, and less commonly from the semen.la 67a 90b Which of these mycoplasma are pathogenic remains to be determined. The pathogenic Mycoplasma bovigenitalium has been reported from semen from bulls with seminovesiculi- tis.Ib'23'57 Viruses including enteroviruses, genital fibro- papilloma virus, foot and mouth disease virus,323'45 Chla- mydia, epivag, parainfluenza III virus, and IBR-IPV virus have been recovered from the semen or testes of bulls. Freezing semen for the preservation of sperm cells will also preserve most infectious agents including viruses.6a'b 47'84'112 Liquid nitrogen used for the storage of frozen semen may also become contaminated with a va- riety of organisms and viruses and thus be a source of infection for the cow. Bulls clinically infected with Johnes’ disease usually have the organism in the semen.75 Similar types of organisms as well as those respon- sible for venereal diseases in each species may also be found in other male animals, for example Br. suis in swine, Br. canis in dogs, Br. ovis in sheep, Trypa- nosoma equiperdum (dourine) and possibly influenza and infectious equine anemia viruses and the herpesvirus of coital exanthema in horses. A vaginitis and vulvitis are commonly observed in heifers or cows after natural service, especially to older bulls caused by ureaplasma and possibly H. somnus. Mares may become infected with streptococci, Klebsiella and Pseudomonas organ- isms by being bred to stallions that have large numbers of these organisms in the sheath or semen. Except for vibriosis, brucellosis, IBR-IPV and tricho- moniasis, infections in most cows transmitted to them by natural breeding are not serious and seldom prevent conception or cause subsequent abortion. Many bulls with a seminovesiculitis may have nearly normal conception rates. However, in artificial insemination the author and others have observed several bulls with Ps. aeruginosa, C. pyogenes or M. bovigenitalium infection of the ve- sicular glands that caused a rapid loss of motility of the spermatozoa probably due to the inflammatory products in the ejaculate. The presence of pus in stallion semen caused a much more rapid decline in motility of the sper- matozoa than occurred in normal semen.37 Pseudomonas was recovered from semen of 25 of 70 stallions.59 No lesions were observed in the stallions, no leukocytes were present in the semen and conception rates were com- parable to stallions not harboring the organism. However infected stallions could produce genital disease in mares having a lowered resistance to infection. In the collection of semen samples for bacteriological or viral studies it is essential that strict sanitary and hy- gienic practices be observed. Even if the semen is col- lected in a sterile vagina, contamination usually occurs. Taking a bacteriologically sterile semen sample in the artificial vagina or by electroejaculation is impossible because of contamination from the urethra, prepuce, penis and air. The method of taking a satisfactory sample of secretion from the accessory glands for culture as de- scribed in the discussion on seminal vesiculitis is most satisfactory. Briefly this consists of exteriorizing the penis and after careful washing and disinfection of the exposed penis, sheath and lower portion of the urethra, a sterile cannula is passed up the urethra and a sample is col- lected in a sterile vial by massage of the accessory glands. At present this test is seldom used except to determine the causative agent of inflammatory processes of the up- per reproductive tract or accessory glands. Disease Control in Bulls and Semen—Many studies over the past 40 years on micro-organisms that may con- taminate semen and, like spermatozoa, survive process- ing, freezing and storage and result in transmission of disease have been reported in this and prior Chapters on infertility in female animals and have been recently re-INFERTILITY IN MALE ANIMALS 887 viewed in respect to cattle.6bc,108b c The world wide use of bovine artificial insemination requires herd owners, veterinarians and regulatory officials be cognizant of the current status of these infectious organisms for cattle. The semen-borne pathogens may be classified into four control-related categories of: 1. Specific pathogen-free category requiring the elimination of these organisms from the AI stud fol- lowed by routine testing: viruses of foot and mouth disease and rinderpest and Mycoplasma mycoides (contagious pleuropneumonia), Mycobacterium bovis, Mycobacterium paratuberculosis, Brucella abor- tus, Leptospira spp., Campylobacter fetus vene- realis and Trichomonas fetus (The last three organ- isms are treatable. Further studies on improved diag- nostic tests for M. paratuberculosis are indicated.) 2. Control by surveillance category requiring fre- quent serologic tests of bulls, cultures of semen and close clinical observation to recognize these organ- isms in a bull or stud: viruses of BVD-MD, IBR/IPV/ IPB (infectious bovine rhinotracheitis, infectious pus- tular vulvovaginitis, infectious pustular balanoposthi- tis), parainfluenza, fibropapillomatosis, blue tongue, bovine leukemia, Chlamydia, Bedsonia, and Coxiella burnetii. [Although as stated previously in this Chap- ter and in a recent review,"7b there is no evidence that the bovine leukemia virus (BLV) present in lympho- cytes of serologic-positive, infected animals can be transmitted venereally by natural or artificial service or embryo transfer. Because of the potential for such transmittal many countries importing semen or cattle from the United States require that such donor animals and imported cattle be free of the infection based on the agar-gel immunodiffusion test.] 3. Control by Sanitation/hygiene of ubiquitous, op- portunistic pathogenic or nonpathogenic organisms in- cluding: Pseudomonas aeruginosa, Corynebacte- rium pyogenes, Staphylococcus spp., Streptococcus spp., Escherichia coli, Proteus, Mycoplasma bovi- genitalium and bovis, ureaplasma, molds, yeasts and others. 4. Further control of organisms in the above 3 cate- gories may be enhanced or made more certain by the addition of antibiotics to semen for the following or- ganisms: Leptospira, Campylobacter, M. bovigeni- talium and bovis and other susceptible organisms in category 3. (This is accomplished by adding penicil- lin, dehydrostreptomycin, polymyxin B, sulphate and possibly lincomycin, spectinomycin and minomycin in various combinations and concentrations to the ex- tended semen.) To realize the strict control or elimination of these in- fectious organisms from bovine semen a number of rig- idly enforced procedures of quarantine, isolation, routine serologic testing of bulls and culturing of semen and even certain vaccination practices may be required.6b c'108b'c If artificial insemination becomes wide spread in other spe- cies as it has in cattle, similar in depth studies of the infectious organisms and diseases transmitted in semen would be necessary. Total solids in the bull semen may be rapidly deter- mined and those samples with less than 4 to 5 percent solids, often indicative of incomplete ejaculation or sem- inal vesiculitis, should be closely examined.2042 Normal ejaculates from fertile dairy bulls averaged 8.8 to 10.0 g. of solids per 100 g. of plasma. Semen obtained by electroejaculation averaged 2.0 to 6.7 percent solids and semen in older bulls averaged 8.9 percent solids com- pared to 10.2 percent solids in young bulls. Enzyme determination of semen plasma has proven of limited value in measuring degrees of damage to sperm cells before ejaculation and during the freezing process. Enzymes such as GOT, LDH, chlolinesterase and al- kaline or acid phosphatase and others are intimately re- lated to the sperm cell. When the sperm cell dies these enzymes pass into the plasma. The levels of enzymes are highest in the bull, intermediate in the stallion and lowest in the boar.49 Other tests for semen quality and fertility—in par- ticular rapid tests that would be of value in determining the fertility of semen used in artificial insemination— have been developed and tried. These laboratory tests include those that measure the resistance of spermatozoa to temperature shock, hypertonic salt solutions, or to other inimical influences, and tests for measuring the fructo- lysis or oxidation rate of semen. The methylene-blue re- duction test based on the dehydrogenase activity of se- men was found to be closely correlated with motility and concentration.9 Other biochemical tests for semen qual- ity were developed and reported by many workers and reviewed.- But as stated by Mann, “On the whole, the metabolic processes in semen are more often related to sperm density and motility than they are to the fertilizing power of spermatozoa.” Semen evaluation is indicative for, but not a test of, fertility in a male animal. Conclusions on the Assessment of Semen Quality as it is Related to Fertility. Excellent reviews and sum- maries of much published data have been presented-15’25,27 on the relationship of semen quality to fertility in the relatively fertile males present in artificial insemination bull studs. Many semen quality tests and evaluations have been reported by many workers on known sterile or in- fertile males from which certain general conclusions can be drawn. Extensive surveys of semen quality in popu- lations of males of known and unknown fertility have been performed in bulls,2974 in stallions, 12“14’35,83 in888 VETERINARY OBSTETRICS rams,39,50'60,61 and in men.44,80-82 But fewer controlled studies have been conducted such as those in rams where semen examinations of males were followed by fertility trials in an evaluation of the factors of semen quality that were related to fertility or infertility in males.61'109 Differences have long been observed between males in their apparent fertility. Bovine and porcine artificial insemination of numerous females have emphasized these differences. In a recent report 18 bulls from 7 AI or- ganizations were used artificially in a 2500 cow dairy. Five low-fertility bulls, 7 medium-fertility bulls and 6 high-fertility bulls had conception rates of 38, 56 and 66 percent, respectively. The minimum number of 36 ser- vices was needed to determine correctly the level of a bull’s fertility.34 Another method for assessing the fertility of male an- imals, that has been shown not to be highly correlated to various semen examinations but is more accurate, is the competitive matings between two males in which equal numbers of spermatozoa from each male are mixed and inseminated into the same females (heterospermic matings). Thus differences in fertility of males can be determined using fewer females.8,38102 This method is particularly useful in boars because the large number of offspring requires fewer females in the trial.85 The non-return rate of bulls used in AI studs is a valid method for assessing fertility between the bulls and a basis for eliminating the bulls with low fertility. How- ever a more rapid and reliable method of fertility pre- diction is desirable. In one report28 160 beef heifers were synchronized and superovulated and bred artificially to 8 sires, 5 of which were consistently above and 3 con- sistently below the average 68 percent nonreturn rates. The heifers were slaughtered 3 to 4 days after insemi- nation and the ova were recovered and examined. The fertilization rates of the ova from the heifers bred to the above and below average fertile bulls was 89 (355 ova) and 70 percent, (155 ova), respectively. In another similar study89 with superovulated heifers bred to 7 bulls with specific morphological sperm cell defects compared to heifers bred to 4 normal bulls the percent of fertilized ova were 33 vs. 72, respectively. From the above references several generalizations can be made concerning the relationship of semen quality tests and fertility in relatively fertile males used in bo- vine artificial insemination. The physical activity of se- men was more closely related to fertility than was met- abolic activity but both were closely related to each other. Presently it is doubtful if more than 20 percent of the differences in fertility can be accounted for by these se- men quality tests especially in artificial insemination bulls where the fertility of bulls usually is in a narrow range of 15 percent difference in conception rates from the most fertile to the least fertile bull. In most cases very poor quality semen resulting in a nonreturn rate of less than 45 percent would be evident and be discarded by the laboratory tests routinely used for semen evaluation.77 For this reason in artificial insemination centers good fertility results are based on providing each cow a certain number, about 6 to 10 million, of actively motile sper- matozoa. Dead, or immotile spermatozoa have no effect on the normal viable spermatozoa. For an ejaculate to be satisfactory for use in bovine artificial insemination it must have a volume of at least 2 ml. and be of normal consistency and color, a sperm cell concentration of over 500 million per ml., motility of at least 40 percent with distinct progressive movement of cells, less than 15 per- cent primary abnormalities and a pH of 7.0 or below. The close correlation in swine between conception rate and litter size is well documented116 and further confirms observations made with uniparous species that there is a wide and definite range in fertility between males. Young, 8 to 12 month old boars should produce 80 to 150 ml. of gel-free semen, opalescent to milky in color, 60 per- cent motility, less than 10 percent primary defective sperm cells, less than 10% secondary sperm abnormalities and more than 10 x 109 (10 billion) spermatozoa per ejac- ulate. Older boars will produce to to 400 ml. of semen and have about 10 percent more abnormal sperm cells.66 Breeding on 2 consecutive days of estrus will increase conception rates 10 to 25 percent and an additional 4 to 8 percent if different boars are used.64 Only a certain minimum quality for each semen trait is needed for maximum fertility. Once this threshold has been reached the association between fertility and semen quality is nearly random, but below this threshold the correlation between fertility and semen quality is im- portant. The semen quality tests most correlated with fertility in males are the concentration or numbers of spermatozoa, the percent of motile spermatozoa and par- ticularly the rate, degree or vigor of motility. In rams the combined physical examination including the palpation and serologic test for epididymitis due to Br. ovis, the assessment of libido and semen evaluation has been closely correlated to the fertility of the ram. When the fertility of rams was categorized on the basis of semen scores as very good, good, satisfactory, poor and very poor and rams in each category were bred to adequate numbers of fertile ewes, the percentage of rams in each category achieving an 80 to 100 percent con- ception rate was 94, 97, 97, 35 and 25, respec- tively.60,61,88 In 31 rams the scrotal circumference, which ranged from 31 to 42 cm., and semen tests were not related to fertility. However the rams with the highestINFERTILITY IN MALE ANIMALS 889 conception rate on first service sired significantly more lambs 1.04 vs. 0.89.88 Thus, as in swine, the higher the fertility of the male the larger the “litter” size. Rams with satisfactory to very good fertility had 60 to 90 per- cent motile sperm cells with a moderate to high degree of vigor and progressive movement, 70 to 90 percent live normal spermatozoa and sperm cell concentrations of 1.0 to 1.8 billion/ml.60-62 Rams with poor fertility on the basis of actual fertility trials had 15 percent or less motility with no progressive movement and little or no activity of the spermatozoa, 40 percent or less normal live spermatozoa with sperm cell concentrations of 0.1 billion per ml. or less. No male should be permitted to score higher than his poorest semen character. About 6 percent of range bulls had poor fertility and 7 percent had questionable fertility based on essentially the same above BSE criteria for semen quality but also including a careful physical examination.29 One report on 29 bulls with normal or satisfactory semen averaged 60 percent conception, range 14 to 100 percent, to the first service, bulls with questionable semen quality had a 48 percent conception rate, range 31 to 57 percent, on first service; and 11 bulls with poor or unsatisfactory se- men had a 30 percent conception rate, range 0 to 69 percent, on first service.40 In another report, forty 2-year-old Santa Gertrudis bulls were evaluated for breeding soundness. Each of the bulls was exposed to 100 cyclic Santa Gertrudis heifers for a 4 day breeding period with about 12 to 27 estrous fe- males available to each bull. The percent of pregnant estrous females and percent of mated females was re- corded. Libido was positively correlated with the per- centage of pregnant females in estrus but the scrotal cir- cumference, the spermatozoan abnormalities or motility was not significantly correlated with the conception rates of estrous or mated heifers.109 In a third report beef heif- ers bred to 12 Angus bulls with apparently similar semen quality by single or multiple services each estrous period had a conception rate of 62.1 and 62.9 percent, respec- tively with a range of 0 to 95 percent in single sire mat- ings.78 In multiple (3) sire matings the conception rate in the heifers was 74 percent, with a range of 68 to 84 percent, or significantly higher than single sire matings. Except for the one bull, the breeding soundness evalu- ation tests had low correlations with the conception rates and fertility in the other 11 bulls which ranged from 12 to 95 percent. If the least fertile bull and most fertile bull were removed, the remaining 9 bulls had conception rates ranging from 61 to 80 percent.78 If the first semen test reveals poor semen quality, sub- sequent tests seldom show any improvement except pos- sibly in very young immature males or males recently affected with a severe stress or disease. However in val- uable males with poor quality semen a number of tests including breeding trials over a period of 6 months to one year may be indicated before the male is pronounced infertile or sterile. If semen collected by means of elec- troejaculation is of poor quality at least 3 more samples at weekly or greater intervals should be collected and evaluated especially if no physical defect is detected. Even then the ejaculator and the collection technique should be checked carefully. Evaluation of semen of range bulls, rams and possibly range stallions, is desirable before the breeding season because these males may collect and guard a “harem” of females and if they are sterile or infertile the pregnancy rate is greatly reduced even if an adequate ratio of males to females is present. Several recent reviews on the fertility evaluation of stallions recognized that no single test is adequate, that infertility can occur in the presence of normal numbers, motility and morphology of spermatozoa in the ejaculate and that conversely stallions having poor semen quality are able to produce satisfactory conception rates if prop- erly managed.71 100 122 As a practical guide to what would constitute a normal fertile stallion it was concluded that the stallion would have to demonstrate normal libido, mating behavior and ejaculation. His reproductive or- gans should be visibly and palpably normal and free of inflammation or signs of infection or disease. He should be able to ejaculate 400 X 106 (4 x 109) sperm cells in a first ejaculate during the breeding season with 50 per- cent motility and 60 percent normal morphology.14 The motility should not drop below 10 percent in fresh semen after 6 hours at 22° C. If a stallion meets these criteria he may be considered a satisfactory potential breeder. If he is borderline in 2 or more criteria or definitely un- satisfactory in 2 or more criteria or has serious perma- nent disabilities or imperfections he should be consid- ered either a questionable or unsatisfactory potential breeder.71100 However in a stallion the ultimate defini- tion and prediction of fertility, as in other males, is the conception rate after breeding to normal healthy mares in a properly managed breeding program. Sterility or complete failure to settle any of a number of fertile mares is rare in stallions, probably about 3 to 5 in over 5000 Thoroughbred stallions.103 Probably very few stallions physically acceptable as breeders would have a failure of libido or complete sterility due to chromosomal ab- normalities. Only males with azoospermia or necrospermia should be pronounced sterile. Even if the semen quality is poor, if normal motile spermatozoa are present in sufficient numbers conception can occur. This is especially true in boars, stallions and dogs where the ejaculate is delivered890 VETERINARY OBSTETRICS into the uterus at coitus and the few motile cells more readily gain access to the uterine tubes. In the other spe- cies, cattle, sheep, and humans, larger numbers of mo- tile spermatozoa appear to be required as many are lost in the vagina and never traverse the cervix to the uterine cavity. There is probably no single criterion aside from actual breeding tests that can be used as an accurate overall measure of sperm quality. All facets of the examination of a male should be considered in the evaluation of his fertility including the physical examination, his sex drive and ability to mount and copulate readily, and the ex- amination of his semen. Other considerations might well include the male’s genetic merit and his freedom from disease. As a result of the widespread use and benefits of ar- tificial insemination in the diary and beef and swine in- dustries, progeny testing of young males is providing needed genetic information to guide farmers and veter- inarians in their selection of sires. The “genetic profile” of bulls maintained by progressive AI organizations in- cludes information on production of milk or meat, type and conformation, especially of the feet, legs and udder, disposition, ease of calving and anomalies or defects of their offspring. Additional information is available on the fertility (conception or nonreturn rate) of the males. The above “genetic profile” could be significantly im- proved by the addition of several other items, with a ge- netic component, namely: liveability of a male’s off- spring including stillbirths and postnatal deaths (within one month) and the incidence of twinning and cystic ovaries in a bull’s daughters which are of the causes of concern in certain dairy herds. Such above significant genetic information obtained by extensive progeny testing, which is necessary for the improvement of a breed or species, is regretably not gen- erally available for the selection of sires in the other spe- cies of domestic animals. References Semen Quality Examination and Fertility Assessment la. Afzelius, B. A. (1979) The Immotile-Cilia Syndrome and Other Ciliary Diseases, Intemat. Rev. of Exp. Path., 19, 1-43. (Kar- tagener’s Syndrome) lb. Al-Aubaidi, J. M. and Fabricant, J. (1968) Techniques for the Isolation of Mycoplasma from Cattle, Cor. Vet., 58, 4, 555. 2. Albertsen, B. E. (1955) Pleuropneumonia-like Organisms in the Semen of Danish Artificial Insemination Bulls, Nord. Vet. Med., 7, 3, 169. 3. Ball, L. (1969) Symposium on Management of Beef Cattle for Reproductive Efficiency, Ft. Collins, Colo., mimeographed notes. 4. Ball, L., Nelson, L. D., Furman, J. W. and Seidel, E., Jr. (1974) Semen Collection and Evaluation of Bulls for Breeding Soundness, Proc. Ann. Mtg. Amer. Vet. Soc. for the Study of Breeding Soundness, Columbia, Mo. 5. Bartlett, D. (1962) Studies on Dog Semen, I Morphological Characteristics J. Reprod. and Fertil., 3, 173. 6a. Bartlett, D. E. (1968) The AVMA/NAAB Code and the U.S.L.S.A. Recommended Regulations, Proc. 2nd Tech. Con- fer. on Art. Insem. and Reprod., Chicago, 37. 6b. Bartlett, D. E. (1980) Health Management of Bulls Used in AI, in Current Therapy in Theriogenology, edit, by D. A. Morrow, W. B. Saunders Co., Philadelphia, 405-410. 6c. Bartlett, D. E., Larson, L. L., Parker, W. G. and Howard, T. H. (1976) Specific Pathogen Free (SPF) Frozen Bovine Se- men: A Goal? Proc. 6th Techn. Conf. on AI and Reprod., Nat. Assoc, of Animal Breeders, Milwaukee, Wise. 7. Bartlett, D. E. and Elliott, F. I. (1960) The Constancy of Fer- tility in “Normal” Bulls as Expressed in Artificial Insemina- tion, Intemat. Jour, of Fert., 5, 3, 307. 8. Beatty, R. A., Bennett, G. H., Hall, J. G., Hancock, J. L. and Stewart, D. L. (1969) An Experiment with Heterospermic Insemination in Cattle, J. Reprod. Fert., 19, 491. 9. Beck, G. H. and Salisbury, G. W. (1943) Rapid Methods for Estimating the Quality of Bull Semen, J. of Dairy Sci., 26, 6, 483. 10. Bentinck-Smith, J. (1955) Personal Communication. 11. Berliner, V. R. (1946) The Biology of Equine Spermatozoa, in the Problem of Fertility, Princeton Univ. Press, Princeton, N.J. 12. Bielanski, W. (1960) Reproduction in Horses I. Stallions, Pub- lic. #116, Institute of Zootechnics at the Agric. College in Krakow, Poland. 13. Bielanski, W., Wierzbowski, S. and Zakrewska, I. G. (1957) The Results of Mass-Wise Evaluations of the Semen and Sex- ual Reflexes of Stallions, Dept, of Animal Hygiene and Zoo- technical Institute. Lab. of An. Reproduction, Krakow, Po- land, Zootechnica Z. 1, 3, 97. 14. Bierschwal, C. J. and Hendrikse, J. (1969) Preliminary Report of Variations in Morphology of Boar Sperm and its Importance in Evaluation of Fertility of Yorkshire Boars Used in Artificial Insemination, Proc. of Conference on Reproductive Problems in Animals, Univ. of Georgia, Nov., 21. 15. Bishop, M. W. H. and Hancock, J. L. (1955) The Evaluation of Bull Semen, Vet. Rec., 67, 363. 16. Blom, E. (1946) Kompartionskammeret, et Hjaelpe Middel tel Forbedret Microscopisk Undersolgelse of Ufortyndel Tyre- sperma, Skand. Vet. Tidskr., 36, 613. 17. Blom, E. (1947) On Medusa Formations (Detached Ciliated Borders) in Bull and Stallion Semen and Their Diagnostic Sig- nificance, Skand. Vet. Tidskr., 37, 257. 18. Blom, E. (1950) A Simple Rapid Staining Method for the Dif- ferentiation Between Live and Dead Sperm Cells by Means of Eosin and Nigrosin, Nord. Vet. Med., 2, 58. 19. Blom, E. (1950) Interpretation of Spermatic Cytology in Bulls, Fert. and Steril., 1, 3, 233. 20. Blom, E. (1950) On the Evaluation of Bull Semen, Thesis, C. Mortenseri, Copenhagen, Denmark. 21. Blom, E. (1959) A Rare Sperm Abnormality “Corkscrew- Sperms” Associated with Sterility in Bulls, Nature, 183, 1280. 22a. Blom, E. (1968) Rapid Refractometric Determination of TotalINFERTILITY IN MALE ANIMALS 891 Solids in Bull Seminal Plasma and its Possible Diagnostic Value, Nord. Vet. Med., 20, 361. 22b. Blom, E. and Birch-Andersen, A. (1978) Ultrastructure of the “Tail Stump” Sperm Defect in the Bull, Proc. 13th Nord. Vet. Congr., Finland, 305. 23. Blom, E. and Erno, H. (1967) Mycoplasmosis Infections of the Genital Organs of Bulls, Acta Vet. Scand., 8, 186. 24. Boucher, J. H., Foote, R. H. and Kirk, R. W. (1958) The Evaluation of Semen Quality in the Dog and the Effects of Frequency of Ejaculation upon Semen Quality, Libido and De- pletion of Sperm Reserves, Cor. Vet., 48, 1, 67. 25. Bratton, R. W., Foote, R. H., Henderson, C. R., Musgrave, S. G., Dunbar, R. S., Jr., Dunn, H. O. and Beardsley, J. P. (1956) The Relative Usefulness of Combinations of Laboratory Tests for Predicting the Fertility of Bovine Semen, J. Dairy Sci., 39, 11, 15, 42. 26. Britt, J. H., Cox, N. M. and Stevenson, J. S. (1981) Advances in Reproduction in Dairy Cattle, J. Dairy Sci., 64, 1378. 27. Buckner, P. J., Willett, E. L. and Bayley, N. (1954) Labo- ratory Tests, Singly and in Combination for Evaluating Fertil- ity of Semen and of Bulls, J. Dairy Sci., 37, 9, 1050. 28. Callaghan, B. D. and King, G. J. (1980) Determination of the Fertilization Rate of AI Sires, Theriog., 14, 6, 403. 29. Carroll, E. J., Ball, L. and Scott, J. (1963) Breeding Sound- ness in Bulls: A Summary of 10,940 Examinations, JAVMA, 142, 10, 1105. 30. Coffin, D. L. (1953) Manual of Veterinary Clinical Pathology, 3rd Ed. Comstock Publ. Co., Ithaca, N.Y. 31. Collins, W. J., Bratton, R. W. and Henderson, C. R. (1951) The Relationship of Semen Production to Sexual Excitement of Dairy Bulls, J. Dairy Sci., 34, 3, 224. 32a. Cottral, G. D., Gailiunis, P, and Cox, B. (1963) Foot and Mouth Disease Transmitted in Bull Semen, JAVMA, 143, 784. 32b. Coubrough, R. I. and Barker, C. A. V. (1964) Spermatozoa: An Unusual Midpiece Abnormality Associated with Sterility in Bulls, Proc. 5th Intemat. Congr. on An. Reprod., Trento, Vol. 5, 219. 33. Cupps, P. T. and Laben, R. C. (1960) Spermatogenesis in Bulls in Relation to Semen Production, J. Dairy Sci., 43, 6, 782. 34. Davidson, J. N. and Farver, T. B. 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Sci., 39, 2, 561. 43. Foote, R. H. and Boucher, J. H. (1964) A Comparison of Sev- eral Photoelectric Procedures for Estimating Sperm Concen- tration in Dog Semen, Am. J. Vet. Res., 25, 105, 558. 44. Freund, M. (1966) Standards for the Rating of Human Sperm Morphology, A Cooperative Study, Intemat. J. of Fertil., 11, 1 (Part 2) 97. 45. Gierloff, B., Chr. H. and Jakobsen, K. F. (1961) On the Sur- vival of Foot and Mouth Disease Virus in Frozen Semen, Acta. Vet. Scand., 2, 210. 46. Gledhill, B. L. (1965) Cytophotometry of Presumed Diploid Bull Spermatozoa, Nord. Vet. Med., 17, 328. 47. Gledhill, B. L. (1967) Swedish Methods for the Evaluation of Breeding Soundness in Bulls, An. Meeting Amer. Vet. Soc. for Study of Breeding Soundness, Univ. of Missouri, Colum- bia, Mo. FAO-Swedish Intemat. Post-Graduate Course on An- imal Reproduction, N. Lagerlof. Mimeographed Notes. 48. Glover, F. A. and Phipps, L. W. (1962) Preliminary Study of an Electronic Method of Counting and Sizing Bull Spermato- zoa, J. Reprod. and Fertil., 4, 2, 189. 49. Graham, E., Pace, M. M. and Gibson, C. D. (1969) Some Different Methods for Measurement of Bovine Semen Quality, Proc. Ann. Meeting AVMA, Minneapolis, Lecture Notes. 50. Gunn, R. M. C., Sanders, R. N. and Granger, W. (1942) Studies in Fertility in Sheep, Commonwealth of Austral. Council for Scient. and Indust. Res. Bull., 148. 51. Hancock, J. L. (1955) The Disintegration of Bull Spermato- zoa, Vet. Rec., 67, 44, 825. 52a. Hancock, J. L. (1955) The Morphologic Characteristics of Spermatozoa and Fertility, Intemat. J. of Fertil., 4, 4, 347. 52b. Hancock, J. L. and Rowlands, I. W. (1949) The Physiology of Reproduction in the Dog, Vet. Rec., 61, 47, 771. 53. Haq, I. (1949) Causes of Sterility in Bulls in Southern En- gland, Brit. Vet. Jour., 105, (3, 4, 5, 6), 71, 114, 143, 200. 54a. Harrop, A. E. (1955) Some Observations on Canine Semen, Vet. Rec., 67, 26, 494. 54b. Hartman, C. G. (1965) Correlations Among Criteria of Semen Quality, Fert. and Steril., 16, 5, 632. 55. Herman, H. A. and Swanson, E. W. (1941) Variations in Dairy Bull Semen with Respect to its Use in Artificial Insemination, Mo. Agr. Expt. Stat. Res. Bull., 326. 56. Herrick, J. B. and Self, H. L. (1962) Evaluation of Fertility in the Bull and Boar, Iowa State Univ. Press., Ames, Iowa. 57. Hirt, R. S., Plastridge, W. N. and Tourtellette, M. C. (1967) Survival of Mycoplasma in Frozen Bovine Semen, Amer. J. Vet. Res., 28, 97. 58. Holst, S. J. (1949) The Semen of Sterile Boars, Proc. 14th Intemat. Vet. Congr. Ill Sect. 4 (C), 118. 59. Hughes, J. P., Asbury, A. C., Loy, R. G. and Burd, H. E. (1967) The Occurrence of Pseudomonas in the Genital Tract of Stallions and its Effect on Fertility, Cor. Vet., 57, 1, 53. 60. Hulet, C. V. (1977) Prediction of Fertility in Rams, Vet. Med./ Sm. An. Clin., 72, 8, 1363. 61. Hulet, C. V. and Ercanbrack, S. K. (1962) A Fertility Index for Rams, J. An. Sci., 21, 3, 418. 62. Hulet, C. V., Foote, W. C. and Blackwell, R. L. (1964) Ef- fects of Natural and Electrical Ejaculation on Predicting Fer- tility in the Ram, J. An. Sci., 23, 2, 418. 63. Hulet, C. V., Foote, W. C. and Blackwell, R. L. (1965) Re- lationship of Semen Quality and Fertility in the Ram to Fe- cundity in the Ewe, J. Reprod. and Fertil., 9, 311. 64a. Hurtgen, J. P. (1981) Influence of Housing and Management Factors on Reproductive Efficiency of Swine, JAVMA, 179, 1, 74. 64b. Hurtgen, J. P. (1982) Reproductive Diseases (of Boars) Vet. Clin, of N. Amer., Lg. An. Pract., 4, 2, 292-299.892 VETERINARY OBSTETRICS 65. Hurtgen, J., Crabo, B. and Leman, A. D. (1977) Fertility Ex- amination of Boars, Proc. Ann. Mtg., Soc. for Theriog., St. Paul, Minn., 11. 66. Hurtgen, J. P. and Leman, A. D. (1976) Management of Boar Fertility and Boar Evaluation, the Soc. for Theriog. Jour. Vol. VII, 2nd Ed. 67. Jasper, D. (1969) Personal Communication. 68. Johnson, L., Bemdtson, W. E. and Pickett, B. W. (1975) An Improved Method for Evaluating Acrosomes of Bovine Sper- matozoa, J. An. Sci., 42, 4, 951. 69. Johnston, S. D., Larsen, R. E. and Olson, P. S. (1982) Canine Theriogenology Soc. for Theriog. Jour. Vol. XI, 62-93, (Evaluation of Fertility in the Dog). 70. Kendrick, J. W. (1979) Semen Handling and Evaluation, Classroom Notes. 71. Kenney, R. M. (1975) Clinical Fertility Evaluation of the Stal- lion, Proc. 21st Ann. Conv. AAEP, Boston, Mass., 336. 72. Kojima, Y. (1977) Light and Electron Microscopic Studies of “Hairpin Curved Deformity” on Boar Spermatozoa, Jap. J. Vet. Sci., 39, 3, 265. 73. Kojima, Y. and Konoshita, Y. (1975) Fine Structure of Mul- tiple Sperm Syncytium in the Boar Testes, Jap. J. Vet. Sci., 37, 555. 74. Lagerlof, N. (1934) Morphologische Untersuchungen uber Veranderungen im Spermabild und in den Hoden bie Bullen mit vesminderter Oder Aufgehabener Fertilitat, Acta Pathol, et Microbiol. Scand. Suppl. XIX. 75. Larsen, A. B. and Kopecky, K. E. (1970) Mycobacterium paratuberculosis in Reproductive Organs and Semen of Bulls, Amer. J. Vet. Res., 31, 2, 255. 76. Larsen, L. L. (1960) Semen Collection and Its Evaluation in the Bull, Southwest Vet. Spring, 187. 77a. Linford, E., Glover, F. A., Bishop, C. and Stewart, D. L. (1976) The Relationship Between Semen Evaluation Methods and Fertility in the Bull, J. Reprod. Fert., 47, 283. 77b. Lorton, S. P. (1982) Sperm Motility, A.B.S. Breeder Jour., Winter, 7. 78. Lunstra, D. D. and Laster, D. B. (1982) Influence of Single Sire and Multiple Natural Mating on Pregnancy Rate in Beef Heifers, Theriog., 18, 4, 373. 79. Lustig, G. and Lindahl, P. E. (1970) Activation of Motility in Bull and Rabbit Spermatozoa by Ultrasonic Treatment Re- corded by a Photographic Method, Intemat. J. of Fert., 15, 3, 135. 80. MacLeod, J. (1950) Semen Quality in One Thousand Men of Known Fertility and in Eight Hundred Cases of Infertile Mar- riage, Fert. & Steril., 2, 115. 81. MacLeod, J. and Gold, R. Z. (1956) The Male Factor in Fer- tility and Infertility VIII, A Study of Variation in Semen Qual- ity, Fert. and Steril., 7, 5, 387. 82. MacLeod, J. and Gold, R. Z. (1958) An Analysis of Human Male Fertility, Intemat. J. of Fertil., 3, 382. 83. MacLeod, J. and McGee, W. R. (1950) The Semen of the Thoroughbred, Cor. Vet., 40, 3, 233. 84. MacPherson, J. W. and Fish, N. A. (1954) The Survival of Pathogenic Bacteria in Bovine Semen Preserved by Freezing, Amer. J. Vet. Res., 15, 548. 85. Martin, P. A. and Dzuik, P. J. (1977) Assessment of Relative Fertility of Males by Competitive Mating, J. Reprod. Fert., 39, 251. 86. McKenzie, F. F. (1940) Recent Reproduction Studies on Equines Proc. Amer. Soc. of An. Prod., 98. 87. McKenzie, F. F. and Phillips, R. W. (1934) Measuring Fer- tility in the Ram, JAVMA, 84, 189. 88. Mickelsen, W. D., Paisley, L. G. and Dahmen, J. J. (1981) The Effect of Scrotal Circumference, Sperm Motility and Sperm Morphology in the Ram on Conception Rates and Lambing Percentage in the Ewe, Theriog., 16, 53. 89. Miller, D. M., Johnson, W. H., Cates, W. F. and Mapletoft, R. J. (1981) Superovulation Studies in Heifers to Determine Fertilization Rates of Bulls with High Levels of Certain Sperm Defects, Theriog., 15, 1, 122. (Abstr.) 90a. Nooder, H. J. (1950) Enkele Mededelingen Omtrent De KI by Teven En Het Sperma Van Reuen, Tijdschr. v. Diergeneesk., 75, 3, 81. 90b. O’Berry, P. A. (1967) Isolation of Mycoplasma spp. from Bull Semen and Its Role in Infertility, JAVMA, 150, 11, 1314. 91. Ott, R. S. and Memon, M. A. (1980) Sheep and Goat Manual, Soc. for Theriog. Jour. Vol. X., Assoc. Bldg., Hastings, Nebr. 68001. 92. Phillips, R. W. (1935) The Physiology of Spermatozoa, Proc. Amer. Soc. of An. Prod., 222. 93. Pickett, B. W. (1969) Personal Communication. 94. Pickett, B. W., Faulkner, L. C. and Sutherland, T. M. (1969) The Effect of Season on Equine Semen Characteristics, J. An. Sci., 29, 1, 196. 95. Pickett, B. W., Faulkner, L. C. and Sutherland, T. M. (1970) Effect of Month and Stallion on Seminal Characteristics and Sexual Behavior, J. An. Sci., 31, 4, 713. 96. Rajamannan, A. (1969) Personal Communication. 97. Rao, C. K. and Hart, G. H. (1948) The Morphology of Bovine Spermatozoa, Amer. J. Vet. Res., 9, 117. 98. Roberts, S. J. (1956, 1971) Veterinary Obstetrics and Genital Diseases, 1st and 2nd Ed., Woodstock, Vt. 05091. 99. Rollinson, D. H. L. (1951) Studies on Abnormal Spermatozoa of Bull Semen, Brit. Vet. Jour., 107, (5, 6, 11); 203, 251, 258. 100. Rossdale, P. D. and Ricketts, S. W. (1980) Equine Stud Farm Medicine, 2nd Ed., Lea and Febiger, Philadelphia. 101. Saacke, R. G., Amann, R. P. and Marshall, C. E. (1968) Ac- rosomal Cap Abnormalities of Sperm from Subfertile Bulls, Jan. Sci., 27, 5, 1391. 102. Saacke, R. G., Marshall, C. E., Venson, W. E., O’Connor, M. L., Chandler, J. E., Mullins, J., Amann, R. P., Wallace, R. A., Vincel, W. N. and Kallgren, H. C. (1980) The Rela- tionship of Semen Quality and Fertility: a Heterospermic Study, Proc. 8th NAAB Tech. Conf. Art. Insem. and Reprd. 103. Sager, F. (1969) Personal Communications. 104. Salisbury, G. W. and Baker, F. N. (1966) Nuclear Morphol- ogy of Spermatozoa from Inbred and Line Cross Hereford Bulls, J. An. Sci., 25, 2, 476. 105. Salisbury, G. W., Beck, G. H., Elliot, J. and Willett, E. L. (1943) Rapid Methods of Estimating the Number of Sperma- tozoa in Bull Semen, J. Dairy Sci., 26, 1, 69. 106. Salisbury, G. W. and Flerchinger, F. H. (1967) Aging Phe- nomena in Spermatozoa I, II, III, J. Dairy Sci., 50, 10, 1675, 1679, 1683. 107. Salisbury, G. W. and Mercier, E. (1945) The Reliability of Estimates of the Proportion of Morphologically Abnormal Sperm in Bull Semen, J. An. Sci., 4, 2, 174. 108a. Seidel, G. E., Jr. and Foote, R. H. (1969) Motion Picture Analysis of Ejaculation in the Bull, J. Reprod. and Fert., 20, 313. 108b. Schultz, R. D. (1977) When Can We Achieve Our Goal ofINFERTILITY IN MALE ANIMALS 893 Providing Specific Pathogen-Free Bovine Semen, Proc. 81st Ann. Mtg., USAHA, Minn., Minnesota. 108c. Sire Health and Management Committee, Nat. Assoc, of An- imal Breeders. (1976) Code of Minimum Standards for Health of Bulls and Hygiene of Bull Studs Producing Semen for Ar- tificial Insemination, NAAB, P. Conv., Seattle, Wash. 109. Smith, M. F., Morris, D. L., Amoss, M. S., Parish, N. R., Williams, J. D. and Wiltbank, N. N. (1981) Relationships Among Fertility, Scrotal Circumference, Seminal Quality and Libido in Santa Gertrudis Bulls, Theriog., 16, 4, 379. 110. Society for Theriogenology (1976) Breeding Soundness Eval- uation in Bulls, Jour. Vol. VII, 2nd Edit., Assoc. Bldg., Has- tings, Nebr. 68901. 111b. Sojka, N. J., Jennings, L. L. and Hamner, C. E. (1970) Ar- tificial Insemination in the Cat (Felis Catus L.), Lab. An. Care, 20, 2, 198. 111a. Sojka, N. (1980) Feline Semen Collection, Evaluation and Ar- tificial Insemination, in Current Therapy in Theriogenology, edit, by D. A. Morrow, W. B. Saunders Co., Philadelphia, 848. 112. Spradbrow, P. B. (1968) The Isolation of IBR Virus from Bo- vine Semen, Austral. Vet. J., 44, 9, 410. 113. Squires, E. L., Amann, R. P., Pickett, B. W., Bemdtson, W. E., Shideler, R. K. and Voss, J. L. (1978) Effect of Fenben- dazole on Reproductive Function in Stallions, Theriog., 9, 5, 447. 114. Swanson, E. W. and Herman, H. A. (1944) The Correlation Between Some Characteristics of Dairy Bull Semen and Con- ception Rate, J. Dairy Sci., 27, 4, 297. 115. Swanson, E. W. and Bearden, H. J. (1951) An Eosin-Nigrosin Stain for Differentiating Live-Dead Bovine Spermatozoa, J. An. Sci., 10, 4, 981. 116. Swierstra, E. E. and Dyck, G. W. (1976) Influence of the Boar and Ejaculation Frequency on Pregnancy Rate and Embryonic Survival in Swine, J. An. Sci., 42, 2, 455. 117a. Terrill, C. E. (1960) Artificial Insemination of Farm Animals, Edit, by Perry, E. J., Rutgers Univ. Press, New Brunswick, N.J. 117b. Thurmond, M. C. and Burridge, M. J. (1982) Application of Research to Control of Bovine Leukemia Virus Infection and to Exportation of Bovine Leukemia Virus-free Cattle and Se- men, JAVMA, 181, 12, 1531. 118. Voss, J. L., Pickett, B. W. and Squires, E. L. (1981) Stallion Spermatozoal Morphology and Motility and Their Relation to Fertility, JAVMA, 178, 3, 287. 119. Wells, M. E., Awa, O. A. and Wondafrash, J. (1969) Eval- uation of Acrosomal Morphology with the Wells-Awa Stain, J. Dairy Sci., 52, 4, 563. 120. Wenkoff, M. S. (1976) Bovine Sperm Cell Morphology, with Special Emphasis on Mid-piece Defects, Ann. Mtg. Soc. for Theriog., Lexington, Ky., 123. 121. Willett, E. L. and Buckner, P. J. (1951) The Determination of Numbers of Spermatozoa in Bull Semen by Measurement of Light Transmission, J. An. Sci., 10, 1, 219. 122. Worthington, W. E. (1968) Evaluation of Stallion Fertility, 14th Ann. Conf. AAEP, Philadelphia, 133. 123. Williams, W. W. (1961) The Enigma of Male Infertility, In- ternal. J. of Fertil., 6, 3, 311.Chapter XIX ARTIFICIAL INSEMINATION By Robert H. Foote, B.S., Ph.D.* Artificial insemination, using the semen of highly se- lected males, has been the most powerful tool for live- stock improvement ever available to the breeder. In the early days of development many books were written on the subject. However, other than in dairy cattle,13 there have been no recent treatises on the subject. Conse- quently, some historical perspective will be included here. Added information can be found in older texts and sev- eral recent reviews.--— History Isolated cases of artificial insemination of domestic animals have been reported for centuries. In the four- teenth century an Arab was alleged to have taken semen by means of a pledget of cotton from the vagina of a mare recently bred to a famous stallion; then by inserting this cotton into the vagina of his own mare conception was produced. Leeuwenhoek and Hamm observed sper- matozoa as early as 1677.12 The first scientific research in artificial insemination of animals was performed on dogs in 1780 by the Italian scientist, Spallanzani. This was confirmed in 1782 by Rossi. Although Spallanzani demonstrated that the fertilizing power of semen resided in the spermatozoa, few further studies or attempts at artificial insemination were conducted until the latter part of the nineteenth century. Heape reported that a dog breeder, Millais, between 1884 and 1896, artificially in- seminated 19 bitches, of which 15 produced young. Iso- lated cases of artificial insemination in the horse about this time also were reported. In the early 1900’s workers were beginning to realize the possible value of artificial insemination. In 1907 Ivanov reported the successful re- sults of a series of artificial inseminations in mares, cows, and ewes as a means for the widespread improvement ♦Jacob Gould Schurman Professor of Animal Physiology, Dept, of Animal Sciences, N.Y.S. College of Agriculture and Life Sciences, Cornell University, Ithaca, N.Y. of farm animals. As a result a laboratory was established in Russia and several hundred men were trained in the techniques of artificial insemination prior to 1914. Jap- anese researchers also were particularly active during this period. After the first World War, activities in this field in Russia increased greatly and by 1938 the number of animals inseminated in that country was reported as 120,000 mares, 1,200,000 cattle, and 15 million sheep. In 1936 Sorenson and Gylling-Holm organized the first cooperative artificial breeding association in Denmark and by 1958 nearly 100 percent of the cows in Denmark were bred artificially. Artificial insemination was first performed on cattle in the United States in 1937 and 1938 at the Agricultural Experiment Station in Minnesota. The first cooperative cattle artificial breeding association was organized by E. J. Perry in New Jersey in 1938, with Dr. J. A. Hen- derson as the first veterinary technician. Artificial insemination in dairy cattle grew rapidly. In 1956, 21 percent of the dairy cows in the U.S. were bred artificially; in 1969 about 52 percent or 8,000,000 cattle, including 750,000 beef cattle, were bred artificially. Most smaller AI organizations in the U.S. merged into a few large ones. By 1982 artificial insemination had plateaued for several years at about two-thirds of the nearly 11,000,000 dairy cows. Only about 4% of the beef cows are inseminated artificially. Several countries, including Denmark, Japan and Israel breed nearly 100 percent of their dairy cattle artificially. In species such as cattle, where frozen semen is readily available, semen is cur- rently being shipped by air throughout the world. Artificial insemination in swine has been developed and used extensively in Europe, the middle east and Asia.7 Only about 20,000 sows are inseminated in the U.S. Ar- tificial insemination in horses has received widespread attention, but has limited commercial use. The devel- opment of frozen semen in horses and the newer ther- apeutic methods for the control of estrus and ovulation could increase the use of artificial insemination in the future. 894ARTIFICIAL INSEMINATION 895 Advantages and Disadvantages The advantages of artificial insemination are well known, and greatly outweigh the disadvantages; if this were not so, the rapid growth of the artificial insemi- nation would not have continued. 1. Artificial insemination greatly increases the utili- zation of proven sires. The services of outstanding, su- perior sires are made available to many more owners. Milk production has doubled since artificial insemination was introduced through better genetics, feeding and management.315 This has been of economic benefit to the owner and the country. Many proven bulls have ar- tificially sired between 100,000 and 200,000 calves in their lifetime. This use of outstanding sires is further in- creased by the ability to ship frozen semen of some spe- cies worldwide. Stallions potentially may sire over 100 foals in a short breeding season. Boars may sire over 1,000 litters of pigs per year. 2. Bulls used in artificial insemination are more care- fully and scientifically selected from outstanding cows and proven sires than is possible in individual dairy herds. Computers scan the records of all the top tested cows and matings are made with the best sires available. About 90 percent of the possible genetic improvement in a commercial herd depends on the genetic improvement through artificial insemination. Artificial insemination permits earlier and more rapid proving of young bulls on a greater number of cows under varied conditions. This gives a more accurate proof of a male’s transmitting ability than can the testing of a bull on only one small group of females in a herd under similar conditions of management and feeding. This mode of testing also dis- tributes the risk so that inferior bulls cause little loss to individual owners. In bull studs it costs about $10,000 to prove the genetic worth of a young bull even when his initial purchase price may be small. Because only about one out of seven to ten bulls tested is usually kept as a proven sire, each of these represents an average in- vestment of about $75,000. 3. The danger, work, and expense of keeping and handling, what in many cases proved to be, an inferior male is eliminated for the average dairyman. This added saving by the use of artificial insemination can be spent on maintaining an additional cow, which, may defray part or all of the yearly cost of breeding a herd artifi- cially. 4. If the males are handled carefully, examined closely from a health standpoint to make certain that they are free from disease, if regular semen examinations are made and accurate breeding records maintained, artificial in- semination lessens or eliminates the occurrence of ve- nereal diseases such as vibriosis, trichomoniasis, and brucellosis. Large AT. organizations are members of the National Association of Animal Breeders and they rou- tinely test their bulls for a battery of diseases (see Chap- ter XVIII). When semen is obtained from a member of the National Association of Animal Breeders, one can be assured that bulls have been carefully screened for disease. Because only high quality semen is shipped to breeders, conception rates can be improved if the semen is handled properly and the cows are bred at the proper time. Artificial insemination frequently results in im- proved record keeping, and in heightened interest on the part of the farmer in having cows conceive promptly. This has been helpful in the early diagnosis and treat- ment of genital abnormalities and has often resulted in an improved breeding efficiency in the herd. In herds affected with vibriosis and trichomoniasis, artificial in- semination, may be a valuable means or aid in overcom- ing the disease. In fact, in herds using artificial insem- ination for many years, vibriosis and trichomoniasis are not found. In an emergency, such as an outbreak of foot and mouth disease, previously stored frozen semen can be used safely by an A.I. Stud. 5. With the advent of the widespread use of frozen semen and the classification of the physical character- istics of a proven sire’s daughters, careful selection of bulls for type and line breeding is possible for the breeder who so desires. 6. The intensive selection and record keeping has re- duced the incidence of lethals and other genetic defects. 7. Miscellaneous advantages of artificial insemination include the following: a) It makes possible the mating of animals with a great difference in size without injury to either animal. b) It may extend the usefulness of sires which for some physical reason are unable to copulate normally. c) It may be used to increase the usefulness of males of monogamous species such as the fox. It is of value in experiments on hybridization where natural mating cannot take place. d) Artificial insemination usually stimulates greater interest in livestock breeding and in better management practices. e) Artificial insemination has proved to be of value for male dogs that are timid or have premature erection, as complete erection of the canine penis does not ordi- narily occur until after entry into the female’s vagina. In toy breeds of dogs it may be used to prevent exhaustion due to repeated attempts to copulate during hot weather. It may also be of value in relatively impotent male dogs. f) It may be helpful when used in females which are in true estrum and ovulate but refuse to stand or ac-896 VETERINARY OBSTETRICS cept the male. An example of this is in zoo animals where pairs refuse to mate. Semen can be collected by elec- troejaculation, frozen and used when the female is in estrus. The disadvantages of artificial insemination should be recognized and carefully considered. 1. Well-trained operators are required to supervise the collection, examination, extension, freezing, shipping, and the insemination of the females in order to ensure that infectious diseases such as brucellosis, vibriosis, tri- chomoniasis and others are not spread. All major A.I. organizations in the U.S. maintain studs free of these diseases. If semen is not collected, extended and handled properly, poor breeding efficiency results. Careful ob- servations for estrum and insemination at the proper time is important. Careful, complete records must be kept. Inseminators, if they are not careful, could be a means of spreading infectious diseases from one farm to an- other. 2. There is a possibility of spreading genetic abnor- malities in cattle, such as: cystic ovaries, spastic syn- drome, poor conformation, especially of feet and limbs, and lack of libido. However, large artificial insemination organizations have systems for routinely evaluating udder, legs, feet and other type traits. Only those sires passing this evaluation are used to produce sons for further test- ing. The increase in cystic ovaries in dairy cattle may be due partly to the wide use of certain bulls by means of artificial insemination. Improved feeding practices and successful treatment of cows with cystic ovaries also may have increased the incidence of cystic ovaries. 3. Miscellaneous disadvantages: a) Intrauterine insemination of a pregnant female may result in abortion. b) Uncontrolled or unscrupulous operators or own- ers could substitute sperm of less valuable animals un- less blood typing is routinely employed. However, few errors have been found, so this seems to be a minor problem. c) Service is not always available. Many dairymen take training to do their own insemination. d) Artificial insemination cannot be used conve- niently on all species or breeds of animals. In some spe- cies much more work must be done before artificial in- semination becomes practical. References General Background and History of Artificial Insemination L Cole, H. H. and Cupps, P. T. (1959) (1969) Reproduction in Domestic Animals, 2nd and 3rd Edit., Academic Press, N.Y.C. 2. Foote, R. H. (1969) Physiological Aspects of Artificial Insemi- nation, in Reproduction in Domestic Animals, Edit, by H. H. Cole and P. T. Cupps, Academic Press, N.Y.C., 2nd Edit. 3. Foote, R. H. (1981) The Artificial Insemination Industry in New Technology in Animal Breeding, Edit, by B. G. Brackett, G. E. Seidel, Jr. and S. M. Seidel. Academic Press, N.Y.C. 4. Gomes, W. R. (1971) Artificial Insemination, in Reproduction in Domestic Animals, Edit, by H. H. Cole and P. T. Cupps. Academic Press, N.Y.C., 3rd Edit. 5. Hafez, E. S. E. (1980) Reproduction in Farm Animals, 4th Ed., Lea and Febiger, Philadelphia. 6. Herman, H. A. (1981) Improving Cattle by the Millions. Univ. of Missouri Press, Columbia, Mo. 7. Iritani, A. (1980) Problems in Freezing Spermatozoa of Different Species. 9th Intern. Congr. Anim. Reprod. & A.I., Madrid. I, 115. 8. Maule, J. P. (1962) The Semen of Animals and Artificial Insem- ination, Tech. Communic. No. 15, Commonwealth Agricultural Bureau, Famham Royal, Bucks, England. 9. Morrow, D. A., edit. (1980) Current Therapy in Theriogenology. W. B. Saunders Co., Philadelphia. 10. NAAB (1982) Proc. 9th Tech. Conf. on A.I. and Reprod. 1- 118. National Assoc. Animal Breeders, Columbia, Mo. 1L Nishikawa, Y. (1962) Fifty Years of Artificial Insemination of Farm Animals in Japan. English Bui. 2, Dept, of An. Sci., Fac- ulty of Agric., Kyoto Univ., Japan. ]2. Perry, E. J. (1968) The Artificial Insemination of Farm Animals, 4th Edit., Rutgers Univ. Press, New Brunswick, N.J. J3. Salisbury, G. W., VanDemark, N. L. and Lodge, J. R. (1978) Physiology of Reproduction and Artificial Insemination of Cattle. 2nd Edit., W. H. Freeman & Co., San Francisco. 14. U.S. Dept, of Agr. Reports. (1967) Artificial Insemination Rises, An. Health News 1, 2, 22. 15. Van Vleck, L. D. (1981) Potential Genetic Impact of Artificial Insemination, Sex Selection, Embryo Transfer, Cloning and Self- ing in Dairy Cattle. In: New Technologies in Animal Breeding. Edit, by B. G. Brackett, G. E. Seidel, Jr. and S. M. Seidel. Academic Press, N.Y.C. AI in Cattle: General and Liquid Semen Few advances in livestock production have been so rapidly accepted and have had such a profound influence on dairy cattle improvement as has the use of artificial insemination. The ability of bull semen to be stored for long periods and the confined management conditions under which dairy cattle are kept, have made artificial insemination very adaptable to this segment of the live- stock industry in the United States and other countries. Artificial insemination has been commonly used on val- uable purebred beef cattle, especially on small farms or in foundation herds. It provides a convenient means of crossbreeding. Because of the large number of beef cat- tle scattered over a large area when on range, the prin- cipal problem and cost is that of finding cows during estrum and driving them to a central point for insemi- nation. Most ranchers prefer to let the bull manage re-ARTIFICIAL INSEMINATION 897 production, despite its many disadvantages. Methods of synchronization of estrus may increase numbers of beef cattle inseminated. At present many owners of larger farms are breeding artificially to their own bulls using frozen semen or they are purchasing semen from other sources. The collection of semen from the bull for use in ar- tificial insemination is usually accomplished with the ar- tificial vagina and occasionally where necessary with electroejaculation as described in Chapter XVIII. Semen collected by personnel experienced with electroejacula- tion equipment is comparable in quality to that collected by the artificial vagina. The concentration of sperma- tozoa per ml by electroejaculation often is about one-half that of semen collected by the artificial vagina, but the volume of semen is twice as large. The pH usually is higher. Thus, the motility of the spermatozoa and the total numbers of sperm cells per ejaculate were the same for the two methods of collection, and this is most im- portant. Semen collection from Brahman and Santa Gra- trudis is difficult as they are shy. With proper manage- ment most mature bulls in artificial insemination studs may be collected up to four times weekly over an ex- tended period of time. It is important to have a properly designed place for semen collection, providing safety for the handlers as well as for the bull. Good footing is important. Proper restraint of teasers and a place to sexually prepare a bull with more than one teaser can facilitate obtaining the best semen possible. Only bulls, steers or dummies should be used for mounts and these should be cleaned or cov- ered between each semen collection to prevent any pos- sible transmission of disease amoung bulls. All collec- tion equipment should be sterilized and aseptic techniques of semen collection used. Obviously, only bulls with ex- cellent reproductive characteristics producing high qual- ity semen should be selected for A.I.10and-~-. Semen Evaluation This is covered in Chapter XVIII. However, it should be mentioned here that all major suppliers of semen col- lect and examine semen carefully.19 Each ejaculate must pass a test for semen volume, sperm motility, sperm concentration and general appearance. Frozen semen must meet rigid motility standards after freezing and thawing. Various more detailed tests are included with problem bulls. Semen that is contaminated should be discarded. Most semen collected from mature bulls trained to serve the artificial vagina should have at least 50% of the sper- matozoa motile and a concentration that usually exceeds 500 million/ml. Liquid Semen Handling the semen after collection is very impor- tant. It should not be allowed to cool below 20° C with- out adding medium such as buffered egg yolk or heated milk to avoid coldshock.111315 The dilution of semen with proper extenders protects against coldshock and prolongs the viability and fertility of the spermatozoa. Cooling the semen from body temperature of about 38° C to 5° C over a period of two hours should be done in protected containers placed in a coldroom at about 5° C.— The ex- tender should include penicillin, streptomycin and po- lymyxin B.2A7’lla'20 Extenders for Liquid Semen. Most bull semen for commercial use is frozen. However the extenders used for frozen semen were modified from liquid semen ex- tenders, primarily by adding the cryoprotectant, glyc- erol. Consequently, brief coverage of these extenders will provide a background for the discussion of frozen se- men 1-3’5'9’14>15’18’21’25'26 A semen extender should have the following charac- teristics: 1. Provide nutrients. 2. Protect against the harmful effects of cooling (coldshock). 3. Be buffered at the proper pH for bull semen of about 6.7-7.0. 4. Have the proper osmotic pressure and balance of ingredients. 5. Inhibit bacterial growth. 6. Increase the volume (dilute the sperm cells) with- out reducing sperm cell viability. 7. Protect sperm cells during freezing. A common cryoprotectant is glycerol. The most common extenders contain either egg yolk or milk. Buffered egg yolk extender was first described by Phillips and Lardy in 1940 who used a phosphate buf- fer with egg yolk. In 1941 Salisbury et al. described the egg yolk citrate buffer extender which presently is wide- ly used with glycerol as an extender for frozen semen. This extender made possible the rapid advance of arti- ficial insemination. The egg yolk citrate diluter is pre- pared by adding 2.9 gms of sodium citrate dihydrate (Na3C6H50 • 2H20) to 100 ml of double distilled water and mixing it at a rate of one part egg yolk to one to five parts of buffer solution. To prepare the egg yolk for the buffered egg yolk extender, fresh eggs should be washed in water and wiped with 70 percent grain alco- hol. After allowing the egg to dry, the shell is broken with a sterile knife in a dustfree room. Egg yolks are separated from the egg white aseptically. The protective value of the egg yolk is largely due to the lecithin and898 VETERINARY OBSTETRICS lipoproteins.-— Most extenders are prepared fresh each day in artificial insemination centers. Egg yolk-tris also has been used widely for liquid and frozen semen.Uc The buffer is made with 24.2 grams of Tris, 15 grams of citric acid monohydrate and 12.5 grams of glucose per liter of double distilled water. To this 20% egg yolk (1 part egg yolk:4 parts of Tris buffer) is added, along with penicillin, streptomycin and polymyxin B. This extender has been used for frozen semen by adding about 7% glycerol by volume. With this extender, semen extension and filling of straws can be done at room tem- perature before cooling, thus being more comfortable for the laboratory personnel. Boiled, pasteurized, homogenized milk, and boiled, pasteurized skim milk1'318 have been reported to be as satisfactory as the buffered egg yolk extenders as an ex- tender for bull semen. These extenders are prepared by placing fresh homogenized or skim milk in the top por- tion of a covered Pyrex glass double boiler and heating it to 95° C or 203° F. The thermometer is removed, the lid replaced to avoid water loss and gentle boiling is continued for ten minutes. The boiling period should not be excessively prolonged. The boiled milk is cooled to the same temperature as the semen to be diluted. The milk can be filtered or poured slowly from the boiler leaving the surface scum of albumin on the sides of the boiler. No unboiled or improperly heated milk should be added to the boiled milk, as relatively small amounts of unboiled milk exert a harmful effect on spermatozoa. Copper-lined utensils should not be used. Ordinary fresh pasteurized milk or fortified skim milk has not proven as satisfactory as pasteurized homogenized or skim milk as a semen extender and their use is not recommended. The milk can be boiled the day before use and stored in a refrigerator. The satisfactory use of 9 percent homog- enized sterilized cream was reported.1 Skim milk pow- der, if of a good grade, may be used in preparing a sat- isfactory extender.18 The toxic fraction in milk is ap- parently the lactenin that is destroyed by heating.1 The protective fraction is composed of the phospholipids. It is easier to view sperm in skim milk but whole homog- enized milk often is used. Controlled fertility trials reported by various workers using egg yolk buffer and milk extenders have been sum- marized.-— The results with both extenders on the same ejaculates of semen were similar. Antibiotics added to semen extenders have been shown to increase the viability of spermatozoa and to eliminate V. fetus organisms in the extended semen.17 It was found that 1,000 units of penicillin and 1,000 mi- crograms of streptomycin per ml of extender had no ad- verse effect on the spermatozoa and effectively con- trolled bacterial growth in the diluted semen.2 The addition of antibiotics to semen of low-fertile bulls improved their conception rates 10 to 15 percent.113 Foote et al.lla com- pared the combination of penicillin, streptomycin and polymyxin with individual antibiotics and obtained the best results with the combination. This is still the pres- ently recommended combination of the National Asso- ciation of Animal Breeders. This definite improvement in conception rates was possibly due to better control of vibriosis found to be present in the semen in many older bulls17 20 (see Chapter XIV). Five hundred units of pen- icillin and 500 micrograms of streptomycin per ml were found to be as satisfactory as the higher concentrations if semen was extended at least 1:25 times and held for 6 hours before use.17 Non-contaminated buffer solutions containing antibiotics for the egg yolk extender may be stored for one week at 5° C. For liquid semen extenders sulfanilamide may be added at a concentration of 0.03 gms per ml. Sulfanilamide should not be used for ex- tenders for frozen semen. Excessive levels of antibiotics in semen may be toxic to spermatozoa and amounts above those recommended have no additional beneficial effect. It should be noted and emphasized that although an- tibiotics will eliminate some bacteria in semen such as V. fetus17 and reduce the numbers of certain susceptible bacteria such as streptococci and staphylococci it will not eliminate such organisms as C. pyogenes, Brucella spp., Trichomonas fetus, Leptospira spp., myco- plasma, Mycobacterium tuberculosis, Pseudomonas, Listeria, and viruses such as IBR-IPV, Chlamydia, epivag, and others. Freezing of semen to which anti- biotics have been added will further preserve nearly all of the above organisms for long periods of time. Other antibiotics have been tried in semen extend- ers,-—’6,7’27 and some are definitely harmful while others were no better than the penicillin and streptomycin com- bination. Currently many others are under test, partic- ularly those which may control mycoplasma.24 The ad- dition of antibiotics to semen cannot be a substitute for the careful, sanitary collection of semen with a low bac- terial content from healthy disease-free males. Modifications of the above egg yolk buffer and milk extenders that have shown possible advantages include the addition of: Catalase, at a level of 20 to 100 mg per ml,14 affords protection to extended semen, especially in yolk citrate buffers. Catalase prevents the formation of hydrogen peroxide due to the effect of light9 and agitation on se- men, but its effect on fertility was not significant.15 Enzymes (with the possible exception of amylase), hormones, tranquilizers, vitamins, glucose, fructose, and other substances have been added to extenders withoutARTIFICIAL INSEMINATION 899 noticeable success in improving the fertility rate. Am- ylase added to semen has been reported to increase con- ception rate, but its possible beneficial effects were not repeatable in other trials.llb VanDemark and co-workers25'26 described a modified egg yolk buffer semen extender in which carbon dioxide was bubbled through the buffer solution until the pH reached 6.3. The diluted semen was sealed in ampules and stored in the dark at room temperature. Although the results were inconsistent, some workers reported good conception rates for up to 7 days. Foote et al.15 described an improved semen extender called C.U.E. (Cornell University Extender) that con- tained one part egg yolk to four parts of a special buffer containing sodium bicarbonate, potassium chloride, glu- cose, glycine, sodium citrate and antibiotics. This gave 66% pregnancy rates. However this extender is not good for freezing semen. Extending Semen The extension rate of semen is designed to give the optimal sperm per insemination dose. In practice this usually is the minimum number consistent with main- taining maximum fertility. By determining the volume of an ejaculate of semen and sperm cell concentration per ml., one can calculate the number of ampules or straws that can be filled with a standard number of sperm cells per breeding unit. The percentage of motile spermatozoa also is considered. Good quality bull semen, as ejacu- lated, should have at least 50% motile sperm and a con- centration of 500 million sperm per ml. Work by Foote and others111314 indicated that 5 mil- lion motile sperm per ml. was about the minimum in- semination dose when one ml was used for insemination. The 60 to 90 day nonreturn rate was 75 percent, with a pregnancy rate about 10 percent lower. If a sample of semen was 7.0 ml, had 60% motile sperm and a sperm concentration of 1,500 million sperm per ml., this would be enough to inseminate 630 cows with 10 million sperm per cow. With 5 million sperm per cow the total possible number would be 1260. Extension rates with liquid se- men as high as 1 part of semen to 200 parts of extender were common. In New Zealand the cows are insemi- nated with about 2.5 million freshly collected sperm in the short breeding season. Excessive light should be avoided during semen pro- cessing. This can cause photoxidation which is harmful to the sperm cells whether they are to be used with or without freezing.9 When numbers of spermatozoa per insemination de- creased from 10 to 6 million there was a 0.5 percent drop in conception rate per each million decrease.28 When one breeding unit (one ml) of extended semen contained fewer than 6 million spermatozoa there was a decrease of about 2.6 percent for each million decrease in spermatozoa. When not all of the semen is needed for use, the dilution rate to control vibriosis should be at least 1:25 and the semen should be in contact with the antibiotics for at least 6 hours.17 After the gradual cooling period, the semen is ex- tended by adding a calculated amount of extender, also at refrigerator temperature, 35 to 45° F or 3 to 8° C, to bring the amount of previously slightly diluted semen to the final volume needed. The semen and extender are gently mixed by tilting the container back and forth. Nearly all bull semen today is processed for freezing. However, when liquid semen was used the extended se- men often had colored coal-tar dyes added to aid in iden- tification of breeds.4 Each bull was carefully identified on labeled tubes and the semen was packaged and kept at 3 to 8° C until used or discarded. Best fertility was obtained within 48 hours of collection. A veterinarian could prepare his own egg yolk-citrate, egg yolk-tris or more conveniently boiled milk. This can be frozen in aliquots and stored.16 Selected references to the earlier literature on liquid semen are included to in- dicate the variety of combinations of balanced ingredi- ents that were used successfully.- —- Thus, on an average farm, a semen sample would be collected, 1 ml of semen would be added to 25 ml of diluter, or 1/2 ml semen to 12 1/2 to 15 ml of diluter. Even if the sperm cell concentration were only 500,000 per ml, this would still provide over 10 million sper- matozoa per ml if only 60 percent were actively motile. Proper antibiotic concentrations may be added to this small amount of prepared extender by making a stock solution of 100,000 units of crystalline penicillin and 100,000 micrograms (100 mg) of dihydrostreptomycin in 10 ml of a citrate buffer solution. To obtain a final concentra- tion of 500 units or micrograms of each antibiotic per ml of egg yolk buffer or milk extender, 0.5, 1.25 or 2.5 ml of the antibiotic stock solution should be added to 10, 25, or 50 ml of extender, respectively. To obtain a final concentration of 1,000 units of each antibiotic in the extender the amounts of the added stock solution should be doubled. Although it is possible for a dairy- man to manage his or her own A.I. program, they must be very skillful in estrus detection and all aspects of re- productive management.8 References Artificial Insemination in Cattle; General and Liquid Semen 1. Adler, H. C. and Rasbech, N. O. (1956) Skim Milk and Cream as Semen Diluents, Nord. Vet. Med. 8, 497.900 VETERINARY OBSTETRICS 2. Almquist, J. O. (1951) A Comparison of Penicillin, Strepto- mycin and Sulphanilamide for Improving the Fertility of Semen from Bulls of Low Fertility. J. Dairy Sci. 34, 819. 3. Almquist, J. O. (1954) Diluters for Bovine Semen V, A Com- parison of Heated Milk and Egg Yolk-Citrate as Diluters for Semen from Bulls of High and Low Fertility. J. Dairy Sci 37, 1308. 4. Almquist, J. O. (1964) The Effect of Certain Coal-Tar Dyes Used for Semen Identification on the Livability and Fertility of Bull Spermatozoa, J. Dairy Sci. 29, 554. 5. Almquist, J. O. and Wickersham, E. W. (1962) Diluents for Bovine Semen XII, Fertility and Motility of Spermatozoa in Skim Milk with Various Levels of Glycerol and Methods of Glycer- olization, J. Dairy Sci. 45, 6, 782. 6. Almquist, J. O. and Zaugg, N. L. (1974) Fertility of Bovine Semen in Milk Diluent Containing Combinations of Penicillin- Neomycin and Lincomycin-Spectinomycin. J. Dairy Sci. 57, 1211. 7. Bemdtson, W. S. and Foote, R. H. (1976) Survival and Fer- tility of Antibiotic-Treated Bovine Spermatozoa. J. Dairy Sci. 59, 2130. 8. Britt, J. H. (1981) Six Steps to Successful A.I. in Herds. Hoard’s Dairyman June 10, 852. 9. Coulter, G. H. and Foote, R. H. (1977) Effects of Package, Extender and Light on Stored Frozen Bull Spermatozoa. J. Dairy Sci. 60, 1428. 10. Coulter, G. H. and Foote, R. H. (1979) Bovine Testicular Mea- surements as Indicators of Reproductive Performance and Their Relationship to Productive Traits in Cattle. A Review. Theri- ogenology 11, 297. 1 la. Foote, R. H. and Bratton, R. W. (1950) The Fertility of Bovine Semen in Extenders Containing Sulfanilamide, Penicillin, Strep- tomycin and Polymyxin. J. Dairy Sci. 33, 544. 1 lb. Foote, R. H. (1967) Influence of Light and Agitation on Bovine Spermatozoa Stored with Protective Agents. J. Dairy Sci. 50, 1468. 1 lc. Foote, R. H. (1970) Fertility of Bull Semen at High Extension Rates in Tris-buffered extenders. J. Dairy Sci. 53, 1475. 12. Foote, R. H. (1975) Estrus Detection and Estrus Detection Aids, J. Dairy Sci. 58, 248. 13. Foote, R. H. (1981) The Artificial Insemination Industry. In: New Insemination Industry. In: New Technologies in Animal Breeding. Edit., Brackett, B. G., Seidel, G. E., Jr. and Seidel, S. M. Academic Press, Inc., N.Y. 14. Foote, R. H. and Dunn, H. O. (1962) Motility and Fertility of Bull Semen Extended at High Rates in Yolk Extender Contain- ing Catalase, J. Dairy Sci. 45, 10, 1237. 15. Foote, R. H., Young, D. C. and Dunn, H. O. (1958) Fertility of Bull Semen Stored One and Two Days at 5°C in 20 Percent Yolk Citrate-Glycine-Glucose Extenders, J. Dairy Sci. 41, 732. 16. Hurst, V. (1953) Dilution of Bull Semen with Frozen Egg Yolk- Sodium Citrate, J. Dairy Sci. 36, 2, 181. 17. McEntee, K., Hughes, D. E. and Gilman, H. L. (1954) Pre- vention of Vibriosis in Inseminated Heifers by Treating the Se- men from Vibrio-infected Bulls with Penicillin, Streptomycin and Sulphanilimide, Cornell Vet. 44, 3, 395. 18. Melrose, D. R. (1956) Skim Milk Powder as a Semen Diluent, Proc. 3rd Intemat. Congr. on Reprod., Cambridge, Sect. 3, 68. 19. Miller, P. D. (1981) Artificial Insemination Organizations, J. Dairy Sci. 64, 1283. 20. Orthey, A. E. and Gilman, H. L. (1954) The Antibacterial Ac- tion of Penicillin and Streptomycin Against Vibrio fetus In- cluding Concentrations Found in Naturally Infected Semen, J. Dairy Sci. 37, 4, 416. 21. Phillips, P. H. and Lardy, H. O. (1940) A Yolk-Buffer Pabu- lum for the Preservation of Bull Semen. J. Dairy Sci. 23, 399. 22. Rasbech, N. O. (1953) Influence of Antibiotics on Fructolysis in Varied Dilutions of Semen, Nord. Vet. Med. 5, 193. 23. Salisbury, G. W., Fuller, H. K. and Willett, E. L. (1941) Pres- ervation of Bovine Spermatozoa in Yolk Citrate Diluent and Field Results from its Use, J. Dairy Sci. 24, 905. 24. Truscott, R. B. and Abreo, C. (1977) Antibiotics for Elimina- tion of Mycoplasma and Ureaplasma from Bovine Semen. J. Dairy Sci. 60, 954. 25. VanDemark, N. L. and Bartlett, F. D., Jr. (1958) Prolonged Survival of Bull Sperm in the Mini Variable Temperature Dilu- ent. J. Dairy Sci. 41, 732. 26. VanDemark, N. L. and Sharma, U. O. (1957) Preliminary Fer- tility Results from the Preservation of Bovine Semen at Room Temperatures, J. Dairy Sci. 40, 438. 27. VanVleck, L. D. (1981) Potential Genetic Impact of Artificial Insemination, Sex Selection, Embryo Transfer, Cloning, and Selfing in Dairy Cattle. In: New Technologies in Animal Breeding. Edit., Brackett, B. G., Seidel, G. E., Jr. and Seidel, S. M. Academic Press, Inc., N.Y. 28. Willett, E. L. (1950) Fertility and Livability of Bull Semen Di- luted at Various Levels to 1:300. J. Dairy Sci. 33, 43. Frozen Semen For many years frozen semen has largely supplanted liquid semen for artificial insemination of cattle in the U.S. and around the world.1 The chief advantages of frozen semen are: 1. More efficient year round use can be made of se- men from proven or injured sires. 2. Selected matings can be made at any place at any time to a large number of available proven sires. Custom freezing of semen makes frozen semen available from farmer-owned bulls. The latter also can be a disadvan- tage when bulls are not carefully screened genetically or for disease.4’5,6'65 3. Semen can be stored for months to many years at -320° F (-196° C) in liquid nitrogen as a refrigerant. Frozen semen has been reported to have a slight decline in fertility38,70 after long-time storage. This was probably due to problems of handling in the field, as semen kept continuously at —196° C does not decrease in fertility for years.18,25 4. Shipping costs are reduced from the bull stud to the technician in the field because semen supplies and liquid nitrogen supplies only need replenishment about once a month. Semen may readily be shipped anywhere in the world.23 5. Great care is taken by major suppliers of frozen semen to insure that each package of frozen semen is carefully labeled and controlled.20ARTIFICIAL INSEMINATION 901 6. Sperm cell output, percentage of morphologically normal spermatozoa and percentage of motile sperm after freezing was lower in bulls 6 to 12 years of age than in bulls 3 to 6 years of age.30 Thus semen quality was high- est in bulls not yet old enough to complete the progeny test. It might be desirable in certain young bulls with lower quality semen to freeze a supply before it reached an older age and the semen becomes relatively infertile. Banking of semen18 is followed on some bulls, partic- ularly those breeds with few cow numbers. The major disadvantages of frozen semen are: 1. Semen from about 10 to 20 percent of the bulls does not freeze well. These are often bulls with poor semen quality and low fertility even if semen was used in liquid form. 2. In the freezing process about 40 to 50 percent of the spermatozoa are killed so increased numbers of sper- matozoa per insemination are required.23,28,64 When a proven sire is in great demand fewer cows can be bred compared to extended liquid semen. However, 6 to 8 million motile sperm after freezing are sufficient per in- semination.16,17,54,55 3. If proper bull health is not maintained, frozen se- men has great potential for the spread of viral and bac- terial diseases. Major bull studs are under continuous health tests.33 4. Heavy use of frozen semen could limit the number of sires used, and possibly result in narrowing the ge- netic base of a breed. However, the actual increase in exchange of semen possible with frozen semen also has increased the number of sires used to produce sons, so this has not happened generally. History In 1949 Polge et al.62 reported that spermatozoa of several species, including cattle, could be treated with glycerol and survive at a temperature of -19° C. They showed that the protective action of glycerol, by modi- fying the type of crystal formed during freezing, resulted in less harm or injury to the cells and thus survival of spermatozoa could be greatly improved by the slow cooling and freezing process which they perfected. In 1951 the first calf was reported bom from insemination with frozen semen. Thereafter interest in the application of frozen semen spread rapidly. Additional calves were bom in England the following year. The first calf in the United States resulting from the use of frozen semen was bom in May, 1953. The early work with frozen semen used solid carbon dioxide (“dry ice”) as a refrigerant at -19° C. Extensive studies by American Breeders Ser- vice resulted in the development of liquid nitrogen stor- age units which were very efficient and prolonged the storage life of spermatozoa.61 Details of the development of frozen semen and other associated historical events have been published.34 Today it is clear that genetic ma- terial may be preserved in the form of properly frozen sperm cells for a lifetime, probably for centuries and perhaps for milleniums. Extenders for Freezing Bull Semen Bull semen for freezing is usually processed in an egg yolk-citrate, or an egg yolk-tris or milk extend- er 8,19,23,28,73 m|]k can either be skim milk or ho- mogenized whole milk. These extenders are prepared the same way initially as for liquid semen (see previous sec- tion). However, before freezing glycerol is added in var- ious ways (described later) so that this cryoprotectant is present during freezing. Also, in a few countries where semen is processed in pellets, a sugar solution (lactose or raffinose) is combined with 20% egg yolk by volume plus 4 to 5% glycerol for freezing semen.49,50 Extending and Cooling Semen When semen is collected it is about 38 to 40° C in the collection tube. It is protected against the cold and usu- ally brought into the semen processing laboratory at about 37 to 38° C. The semen is placed in a water bath at 35 to 37° C. Raw semen has antibiotics added in concen- trated form at this point to provide maximum effect against microorganisms which may be present. The recom- mended concentrations of antibiotic are added in a vol- ume of .02 ml to each ml of raw semen—so as to give 1,000 IU of penicillin, 1,000 ug of streptomycin and 500 ug of polymyxin B per ml. Then the raw semen is mixed about 1 part of semen with 3 to 4 parts of any of the extenders listed previ- ously. Whatever extender an A.I. organization has had most experience with they should continue to use under normal circumstances. However, one study indicates that much less than 20 percent egg yolk may be necessary.73 It is important that the semen and extender be the same temperature when they are combined. The two parts should be mixed thoroughly by gentle swirling or in- version of closed tubes. This mixture often is referred to as the Pre-X (pre-extended semen). It is placed in a water jacket at the same temperature to protect against rapid cooling. The unit is placed in the coldroom at about 5° C where cooling takes place over a period of about 2 hours. After this time it is brought to one-half of the final vol- ume with the same extender as used previously, ex- cepting the antibiotics sometimes are reduced to about 500 units of penicillin, 500 ug of polymyxin B and 500902 VETERINARY OBSTETRICS ug of streptomycin per ml. Up to this point no glycerol normally has been included, except in extenders con- taining tris buffer. One-half the final volume without glycerol provides an opportunity to add glycerol slowly using a similar ex- tender containing double the final concentration of glyc- erol by adding a volume equal to the first half. The ac- tual volume of extender required depends upon the number of sperm cells available in the collection. This collection may represent more than one ejaculate from a bull. For example, two ejaculates collected the same morning may be combined after cooling and processed as one collec- tion. Supposing there are 10 billion motile cells in the col- lection from a particular bull and it is estimated that 50% of these cells will survive freezing and thawing. Thus, we would expect this collection to have 5 billion motile sperm after freezing. If the goal was to have 10 million motile sperm cells per breeding unit (straw, ampule or pellet) this would make potentially 500 breeding units. Of course, a small percentage is lost in processing, so the actual number of breeding units would be slightly less. Assume that semen is being processed for the 0.5 ml straw. This is very common in the U.S.A., although there also are straws holding about 0.25 and 0.3 ml of se- men.354857 When packaging in 0.5 ml straws the 500 straws represent 250 ml of extended semen. So the first half of the extended semen without glycerol would be 125 ml. Then 125 ml of extender, usually containing about 14% glycerol by volume, would be added drop- wise or stepwise over a period of about 30 minutes. Another way of calculating the straws that could be filled with 0.5 ml and the volume of extender required would be as follows: Supposing the 10 billion motile cells, to start with, was made up of two ejaculates combined as one collection totaling 10 ml. This collection had 70% motile sperm with a sperm concentration of 1.428 billion cells per ml. This would be 1.000 billion motile sperm per ml. If freezing will kill 50%, there will be 500 mil- lion motile cells after freezing. Each straw with 0.5 ml has 10 million motile sperm per straw packaged at a con- centration of 20 million motile sperm per ml. The arith- metic is quite simple, as 500 million divided by 20 mil- lion is a 25-fold dilution. Then 10 ml of semen diluted 25 x gives 250 ml, one-half of which is without glycerol and the final one-half added with glycerol. The actual number of sperm per ml varies with or- ganizations and demands for semen from particular bulls. Usually it is desireable to extend semen at a rate to give 6 to 12 million motile sperm per breeding unit.16’23'54'55-60 High extension rates also reduce numbers of contami- nating microorganisms, reducing the chances for infec- tion. Equilibration time is the period needed before freezing for the sperm cells to become adjusted to the extender so that upon freezing excessive loss of sperm cells does not occur. This time varies greatly between species. It is not necessary that bovine sperm cells equilibrate with or be in the presence of the glycerol for a period of time before freezing. Recent experiments, including fertility trials have indicated that the semen should be in the ex- tender with or without the glycerol for about 4 hours at refrigerator temperature. Because of the adverse effects of glycerol on antibiotics, equilibrating for at least 4 hours in glycerol-free extender is desirable.10 The second half of the egg yolk extender should contain about 14 percent glycerol by volume, making a final dilution rate of 7 percent. If sterilized milk is used as the extender the sec- ond half of the extender should contain 14 to 20 percent glycerol so the final concentration will be 7 to 10 per- cent. Glycerol should be added gently by dripping or in small increments, usually in the cold room. The diluted semen is then placed in 1 ml amounts of glass ampules or more commonly in 0.5 ml straws that are sealed after being filled. Freezing should be accomplished within 4 to 20 hours of collection of the semen. A recent study10 reported on bull spermatozoa from 10 bulls exposed at 5° C to extenders containing glycerol for 6 hours, 30 minutes and 10 seconds before freezing. The latter very short equilibration time resulted in a highly significant improvement in sperm motility following freezing and thawing. More study is obviously indicated especially since the Milk Marketing Board in England reported that 6 highly fertile bulls whose semen following freezing had poor conception rates could be improved by a shorter equilibration time. Freezing Semen Freezing rates vary depending upon the kind of ex- tender used. The principle is to freeze as rapidly as pos- sible to avoid the osmotic shock of water freezing out (thereby increasing the salt concentration), but not so fast as to cause marked thermal shock with intracellular ice formation.28 64 Freezing is usually done in liquid nitrogen freezers. The temperature is lowered from +5° C to about -100° C in 8 to 10 minutes by controlling the flow of nitrogen vapor over the straws or ampules. Ampules freeze a little more slowly than do straws. Anytime after the semen reaches -100° C it can be placed directly into the liquid nitrogen for storage at —196° C. This storage temperature was preferable to dry ice at -19° C61 so liquid nitrogen is used almost universally.ARTIFICIAL INSEMINATION 903 Semen can be stored for years at -196° C.25 Normally there is no point in storing semen longer than necessary to use it for insemination. An exception is to preserve certain banks of germ plasm. However, frozen embryos may be used for this purpose. It is very important to keep frozen semen immersed in liquid nitrogen. This way there is no chance that se- men will be warmed at all during storage. This aspect, along with thawing will be discussed further, under ship- ping and handling. Ampules and Straws The first sealed packages for freezing semen were am- pules which held 1.0 ml of extended semen. These have been largely replaced with straws holding from 0.25 to 0.5 ml. The advantage of the straw over the ampule is that the sperm cells can be frozen more uniformly, and less storage space is required. In fact storage is greatly increased with the .25 ml straw. A typical field unit which would hold 1,512 1 ml ampules will hold up to 3,000 0.5 ml straws. Also, fewer sperm are left in the straw than in the ampule upon insemination. All major suppliers of semen ran quality control checks on semen after freezing. If it has been stored for a long time they check it again for the percentage of progres- sively motile cells. Normally semen must have 25% or more progressively motile sperm cells to be shippable. Some sperm cells are killed in freezing and the general viability of sperm when incubated after freezing is not as good as before freezing. Nevertheless the conception rates with frozen semen are only slightly below those achieved previously with liquid semen. A 60 to 90 day nonreturn rate of 74.5 percent was reported17 with con- trol liquid semen. Frozen semen stored 1 day and 103 days at -79° C resulted in nonreturn rates of 72.7 and 71.0 percent, respectively. Semen frozen, thawed and subsequently shipped for use 24 to 60 hours later aver- aged only 51.7 percent nonreturns. Most bull studs today are averaging just a little under 70 percent 60- to 90-day nonreturn rates with sperm frozen in straws and stored continuously in liquid nitrogen at 196° C. A comparison of ampules and straws with about 8 million motile sperm per insemination dose showed the nonreturn rates for straws was slightly higher than for ampules, but the dif- ference was not significant.54 A review of the fertility of semen packaged in straws and ampules57 slightly favored the straw. Freezing in Pellets The extender for the pellets is composed of lactose, 11 percent, or raffinose, 18.5 percent in distilled water and 20 percent egg yolk, 4 to 5 percent glycerol, and antibiotics.49'50About 3 parts of warm extender are added to semen at 35° C and cooled to 5° C in about 1.5 hours. Three or four hours are provided for equilibration. About 0.1 to 0.2 ml of the extended semen containing 12 to 30 million spermatozoa is put directly in depressions made in a block of dry ice for 5 minutes to freeze. Then the pellets are transferred to storage tubes and put directly into liquid nitrogen. The pellet usually is thawed just before use in 1 ml of 3.2 percent sterile sodium citrate solution at 35° C. Then it is handled for insemination as liquid semen. The advantages of such techniques are: the obvious savings in cost of storage and sometimes better survival of sperm from bulls whose semen freezes poorly oth- erwise. At present these methods lack automation and are slightly cumbersome. Sanitation is questionable and contamination in the liquid nitrogen is theoretically pos- sible with pellets of semen. Identification methods for the semen are not as good as with ampules and straws. However, techniques have been developed for freezing the code number of the bull printed on thin paper as a part of the pellet. Antibiotics added to semen to be used in the liquid or frozen form has limited value against most pathogenic organisms often present in the semen. As mentioned pre- viously, penicillin at levels of 500 to 1,000 units and streptomycin at levels of 500 to 1,000 micrograms per ml. of liquid semen extended 1:25 or more times and stored for 6 hours before use controlled V. fetus present in the sheath and semen of bulls. Semen from infected bulls when treated with penicillin and streptomycin, ex- tended, frozen in the usual manner and stored for one week before use was unable to produce infection in sus- ceptible cows.39,44 Later it was shown the addition of polymyxin B sulfate (see previous section on use with liquid semen) at a level of 500 units per ml of extended semen along with 50 units of penicillin and 2,000 mi- crograms of streptomycin controlled V. fetus in the se- men.21 The extended semen was incubated at 37° C for 30 minutes before cooling and freezing. The protozoan, Trichomonas fetus can remain viable and infective es- pecially in liquid extended semen, but also in frozen se- men containing antibiotics. The chances of survival of the organism are markedly reduced in semen containing glycerol and experiencing a long equilibration period be- fore freezing. Br. abortus, Listeria monocytogenes, C. pyogenes, L. pomona and other such organisms are not affected by the antibiotics at levels that can be used in either liquid or frozen semen.40,42,47 Of course the viral agents of disease that may be in semen such as IBR-IPV and others are not affected by antibiotics added to the semen. Therefore, it is imperative that bull studs main-904 VETERINARY OBSTETRICS tain bulls free of brucellosis, tuberculosis, trichomon- iasis, leptospirosis, vibriosis (campylobacteriosis), and virus diseases. All major artificial insemination organi- zations carry out extensive disease control programs. New antibiotic combinations2 are being tested to assist in con- trolling the presence of possible organisms such as my- coplasma.77 For the individual owner of purebred bulls, used both naturally and artificially, and employing cus- tom-freezing and for persons using such semen, the problems of disease control are complex. They are dif- ficult to overcome even with highly competent veteri- nary and laboratory service. Freeze-drying of bovine spermatozoa, as is em- ployed extensively for the storage of bacteria at room temperature has been attempted by a number of workers but without reproducible success.46 Shipping and Handling Semen This discussion is limited to frozen semen as so little semen is shipped in any other form. The only exception is the use of highly extended liquid semen during the short breeding season in New Zealand. Also, if a spec- imen is obtained for diagnostic purposes it could be ex- tended, cooled to 5° C, packed with a bottle of ice at 3 to 5° C and brought to a Diagnostic Laboratory. Frozen semen can be transported by car, truck, bus, railroad or airplane. Most A.I. organizations have trucks carrying frozen semen and liquid nitrogen. They resupply dis- tributor or inseminator tanks, or on-the-farm units about every 4 weeks. Some of the newly engineered tanks will hold liquid nitrogen for several months, depending upon the model and conditions of use. Semen handling in the field is very important.12,58,69 The tank should always contain several inches of liquid nitrogen. Preferably it should be filled whenever the ni- trogen tank is half empty. The semen should be orga- nized with a well arranged inventory.71 This avoids hav- ing to pull canes of semen out far enough to check the bull number and possibly damage the semen. Never pull a canister or cane of semen above the edge of the liq- uid nitrogen tank to remove a breeding unit of semen. Never take more than 15 seconds to remove the unit wanted. If possible, keep the goblets containing straws filled with liquid nitrogen so that they will be surrounded by the nitrogen even in the neck of the tank. Always return the canister back to the lower level position in the tank as soon as possible. Never thaw out more ampules or straws than will be used within 15 minutes of thaw- ing. Most problems with poor semen quality result from improper field handling of semen. Large A.I. organi- zations have extensive quality control procedures and a reputation they protect by insuring that all semen leaving their premises is of high quality. Thawing of semen for insemination is very impor- tant.58,68,69 The optimal rate depends upon the kind of extender used for freezing. One should follow the rec- ommendations of the semen supplier in thawing the se- men. Some who use milk extender recommend a pocket thaw. Thawing time is the time required to thaw frozen semen in a water bath at about 30° C. Most organiza- tions recommend a thaw bath of 35 to 40° C. Automatic thawing devices that plug into cigarette lighters in cars have been developed. Straws will thaw in less than one minute. Ampules take several minutes to thaw. Once the semen is thawed it should not be loaded into a very cold gun in a cold bam. The inseminating gun can be warmed slightly with the hand under cold con- ditions before covering with a sterile sheath. Then in- semination should proceed promptly. This avoids any possible freezing of the semen after thawing which would be damaging to the sperm cells. A slight amount of cool- ing does not seem to be detrimental. Nevertheless it is always good practice to avoid warming, cooling and re- warming frozen-thawed semen. If there is any doubt about how well the semen has been stored, it should be checked microscopically for the proportion of motile sperm cells. If fertility is poor this check is most important. Some semen from individual bulls may have passed through the storage tanks of sev- eral distributors. It is especially important to check the quality of this semen, particularly if it has been pur- chased at a premium price. In countries or areas where liquid nitrogen is avail- able, several manufacturers1 provide excellent insulated tanks at a cost of $300 to $700 which hold up to several thousand breeding units. Smaller tanks are used for ship- ping frozen semen. Old tanks require refilling with liq- uid nitrogen every 4 weeks, depending on their size and frequency of use, and some newly designed tanks may be safe for 4 months between refills. Thus, semen may be shipped long distances by air or other means of trans- portation over a period of several days. Semen is a living biological product and could carry such diseases as foot and mouth disease and other cattle diseases.3'6,40,42,65 Health regulations have been estab- lished in certain states and in most countries regarding the importation of semen.3,4,33 For those desiring to im- port or export semen, information and permission should 1. Cryogenic Engineering Co., 4595 Bannock St., Denver, CO 80216; Linde Co., Div of Union Carbide Co., 270 Park Ave., N.Y.C. 10017; Minnesota Valley Engineering, Inc., New Prague, MI 56071.ARTIFICIAL INSEMINATION 905 be requested from either the Animal Inspection and Quarantine Division, Agricultural Research Service, U.S. Department of Agriculture, Washington 25, D.C. or from the Federal or State Veterinarian located in each state. Each semen shipment must be accompanied by the proper official health charts to comply with the regulations of the country of its destination. Semen shipped intrastate usually has no restrictions placed on it unless the herd is under quarantine for an infectious disease. Successful insemination of the cow depends upon (1) the quality of the semen used, (2) proper storage and handling of the semen, (3) a cow being reproductively healthy and in estrus and (4) use of proper insemination procedures.27 Following is a discussion of the latter two points, as the first two were discussed previously. The optimal time to inseminate a cow is from the middle to the end of estrum.76 This is about 6 to 24 hours before ovulation, as discussed in Chapter XIV. With good detection of estrus near optimal conception rates were found by Foote26 following the so-called A.M.-P.M. rule. Cows first seen in estrum in the morning were best in- seminated the afternoon of the same day. Cows first seen in estrum in the evening should be inseminated the next morning. Conception rates were lower when cows first seen in estrus in the evening were not inseminated until the next afternoon or cows first seen in estrus in the morning were not inseminated until the next morning. In another study29 cows were inseminated when first seen in heat versus a delay of 12 hours when the next heat check was made. This did not result in a statistically sig- nificant difference in conception rate. However, the pregnancy rate at the early insemination was 48 percent versus 53 percent for the insemination 12 hours later. Cows still in estrum 12 hours after insemination had a 57 percent conception rate as compared to 48 percent for those not in estrum 12 hours later. Pregnancy rates for heifers and cows in first, second, third or fourth and more lactations were 59, 51, 49, 48 and 38 percent, respec- tively. Ambient temperatures below 10° C or above 23° C at the time of insemination were associated with a de- cline in pregnancy rates. As sperm live in the cows re- productive system for 30 hours-- there does not seem to be a specific optimum time to inseminate. Also, in practice the exact time of onset of heat usually is not known. Nevertheless, with frozen sperm which do not survive as long in a test tube after freezing and thawing, it is thought that a slightly late insemination may have better chances of initiating pregnancy than an earlier one. Semen placement also affected fertility.41,78 There is no doubt but what the whole aspect of cow management at insemination is important. Increased pregnancy rate occurred in beef cattle by applying cli- toral massage immediately after insemination.63 This has been confirmed with other studies in beef cattle. The technique did not affect fertility in dairy cows.43 Many diarymen inseminate their own cows. If profes- sional insemination service is not available this may be desirable. The dairymen feels that the insemination can be better timed.79 However, it is then important for the owner to perform large numbers of inseminations and keep in practice, because many studies reveal that this is essential for best semen placement. Also, it is impor- tant that the semen inventory and liquid nitrogen level in the semen tank be carefully maintained.71,72 Under these circumstances the tradeoffs of convenience or inconven- ience of doing one’s own inseminations and conception rates that may be achieved probably balance out. But if herd fertility is low and a person on the farm is doing the inseminations, one of the possible problems is in- semination techniques or improper storage of semen. This is much less likely to be the case with a professional full- time inseminator, especially if good results are being achieved in surrounding herds serviced by the same per- son. Regardless of who does the insemination, the proce- dure is very important. One should be well-organized and have all equipment ready when thawing the semen. Thaw the semen according to the directions of the sup- plier. This usually will be at a temperature around 35° C. Then proceed carefully. NAAB has a checklist for new inseminators. A comfortable clean place to restrain the animal for insemination also is important. An atmosphere of calm- ness is important. Sanitation also is important.37 By car- rying out hygienic procedures the inseminator protects the semen, the cow and himself or herself. One should not allow any contaminating materials to come in contact with the inseminating gun. The cow should be ap- proached gently. At the present time nearly all cows are being insem- inated by the operator inserting one hand and arm en- cased in a rubber or plastic glove and sleeve into the rectum and grasping the cervix. Excess fecal material is paddled out. The vulva and vulvar lips are carefully wiped or, if necessary, washed and then wiped dry with cotton or a paper towel, precautions being taken to make certain that no feces are wiped between the vulvar lips. An in- seminating pipette, such as the Cassou gun for straws, is inserted through the vulva dorsally and forward through the vagina and into the external os of the cervix. If folds of the vaginal wall interfere, the cervix is pulled or pushed forward to straighten the lumen of the vagina. If the ex- ternal os is hard to locate, the cervix may be held by the fingers and the thumb placed over the external os; the906 VETERINARY OBSTETRICS pipette is manipulated to touch the thumb and then into the cervix. By a combination of gently inserting the pi- pette and working the cervix over the pipette, it is usu- ally readily passed one-half to two-thirds of the distance through the cervix, or into the uterine body on first ser- vices. The semen should be deposited slowly over a pe- riod of about 5 seconds. The body of the uterus is very short, so the objective is to deposit the semen on first service just through the cervix. There has been general acceptance of the placement of the forefinger over the cranial end of the cervix on first service. As soon as the tip of the inseminating gun touches the finger, stop. Most technicians tend to insem- inate too deeply. A variety of studies with dye placement and x-rays have been carried out. In one study only 42 percent of the inseminations were in the anterior cervix or body of the uterus, 42 percent were in the right horn and 4.4, 7, and 3 percent were in the left horn, posterior cervix and anterior vagina, respectively.573 Although there was no significant difference in the conception rates between the cervical or uterine body de- position of semen, semen deposition should be in the cervix when cows appear to be in diestrus, pregnant, or the cervix is otherwise difficult to pass. Intrauterine in- semination could result in endometritis and a shortened cycle (Chapter XIV). If insemination occurred during the luteal phase of the cycle it could cause pyometra. Fur- thermore if non-motile organisms such as Br. abortus are placed in the cervix they do not readily become es- tablished in the uterus.42 The endometrium of the uterus may be injured by the pipette causing an abscess of the uterine wall. The intrauterine deposition of semen could result in abortion in pregnant cows.66,74,75 As many as 10 percent of pregnant cows, especially the first three months of pregnancy, show estrus.74 Lastly, intracervical de- position of semen is more easily and quickly accom- plished than is intrauterine deposition. If semen is deposited into the uterus on first service it should be placed in the body or in both horns, or the ovaries should be examined to detect the location of the mature follicle and semen placed in the corresponding horn. This latter procedure requires great care not to rup- ture the follicle manually as this is usually followed by a failure to conceive. Most inseminators require about 2 to 3 months to become adept at inseminating cows. Each person should inseminate at least 500 cows to achieve high competence under different conditions. There is a significant difference between technicians and their in- semination results. Conception rates may vary from 15 to 20 percent between technicians depending on their at- titudes, methods of handling the cow, timeliness of in- semination, care of handling semen, their techniques of insemination and the method of record keeping.58 Traumatization of the cervix is unnecessary and dan- gerous. If the pipette will not pass readily into the cervix due to its small size in virgin heifers or due to pathologic lesions or defects, the operator should make certain that the animal is in estrum, and, especially if it is a heifer, the semen should be deposited as far into the cervix as the tube can be gently or readily passed. In such in- stances it is probably desirable to use larger amounts of semen as some may be lost into the vagina. Using a pi- pette of smaller diameter might be helpful. The straw inseminating gun is smaller in diameter than the older plastic rods. Complete obstruction of the cervix or uter- ine horn is characterized by mucometra. It has been re- ported that penetration of the cervix with a pipette was not possible in 1.1 percent of 11,112 cows and 11.7 per- cent of 1,711 heifers, but conception on A.I. service oc- curred in 36.5 percent and 54 percent of these animals, respectively.52 For good conception rates in herds bred artificially close cooperation and consultation is necessary between a competent veterinarian, a good herdsman, owner or manager, and the A.I. technician. If the herdsman, owner and A.I. technician are the same person then one has fewer people observing the animal. The herd should be placed on a routine reproductive examination program accompanied by good records that are reviewed period- ically. Regular prebreeding or postpartum examinations of cows, pregnancy examinations, twice daily careful heat checks and records, prompt treatment of reproductive abnormalities of the estrous cycle and genital tract, and insemination of cows at the proper time of estrum with highly fertile semen are all important parts of a complete reproductive health program. With increasing herd size this becomes even more important. A good manager will find that no other program will pay greater dividends. Measurement of the success of the insemination, such as regular pregnancy diagnoses, are important for the dairyman, inseminator and veterinarian in herd health and A.I. programs. It is also important for the semen sup- plier to be able to evaluate fertility of bulls and compare A.I. technicians they employ. Pregnancy results (pal- pation per rectum) are usually not available for this pur- pose. A nonreturn rate has been developed in A.I. to provide a regular basis for evaluating the reproductive efficiency of bulls and technicians.7 This nonreturn rate measures the proportion of cows inseminated which have not been resubmitted (returned) for another insemination within a certain time. For cows inseminated in a partic- ular month, the nonreturn rate after two to three months (two months from the end of a particular month and three months from the beginning) is known as a 60- to 90-dayARTIFICIAL INSEMINATION 907 nonreturn rate. A faster cutoff in time at 30- to 60-days after insemination or with a fixed cutoff interval can be programmed easily with the high speed computers used today. Typical 60-90 day nonreturn rates with liquid se- men for first services were in the low 70’s and with fro- zen semen ran just below 70.- Second service cows have about the same nonreturn rate and pregnancy rate as first service cows, but conception rates decline with succes- sive services in repeat breeders. There has been some concern that repeat inseminations with a foreign protein, such as egg yolk could cause immune reactions and in- fertility. However, studies55 indicate that this is not a problem. The submission of breeding records to an A.I. orga- nization is essential for calculating nonreturn rates and this can provide relatively accurate information.53 Nonreturn rates are higher than true pregnancy rates re- sulting from a particular insemination.7,45,53 This is be- cause some cows are sold that are not pregnant, cows are rebred to a bull or some other source of semen is used. Because more and more semen is sold directly to herds and distributors, where there is no feedback, the fertility of semen used and general success rate achieved by an organization in the field is less well established. A.I. organizations do a rigorous quality control on se- men, and this becomes more important as less reporting of fertility occurs. A.I. organizations that continue to employ their own full time inseminators have an advan- tage in this regard. They can maintain accurate records to compare bulls and inseminators. Special fertility testing may also be done. Various ex- perimental procedures are being researched to evaluate the fertility of bulls in highly efficient designs requiring fewer cows. One of the techniques is to use competitive fertilization.51 In this test semen from 2 to 3 sires is mixed and the proportion of progeny from each sire is deter- mined later. Either color markings or blood type must be used to identify which sire produced the sperm that resulted in the calf. These types of tests require special followup and are not used with registered cattle. Some in vitro tests, using zona-free hamster eggs, to estimate the fertilizing ability of bull sperm or sperm from other valuable males of domesticated species are promising. Artificial insemination in range beef cattle, if it is to be successful, requires excellent management and fol- lowing practices to which many ranchers are unaccus- tomed. The principles are the same as for dairy cattle. Cattle in the herd are usually bred artificially with frozen semen for a period of 24 days, slightly longer than one normal estrous cycle, or preferably 45 days, two estrous cycles, with semen from a proven beef bull. The tech- nician must be experienced. The cows or heifers to be bred must be placed in a fairly level lush pasture con- fined area, free of bushes and trees and gullys so cows is estrus can be easily observed. Cows must be well fed during the last part of the previous pregnancy as well as after calving. Heifers nursing calves may require added grain or forage so that estrus will occur regularly. At least 3 pens large enough to hold 5 percent of the herd in each pen should be built near the water supply or where cattle are accustomed to feed. Connected to these pens should be a chute to hold 6 to 8 cows with a step-in gate to allow the technician access to the cows. Well-trained and experienced ranch hands who will handle cattle qui- etly should examine the herd carefully early in the morn- ing when the cows first move about and again in the late afternoon or early evening. Otherwise many heats will be missed. One rider can usually observe about 200 cows in a good pasture arrangement. During the middle of the day beef cows are usually rather inactive. Beef cows in estrus are much more quiet than dairy cows and ranch hands should observe that cows in heat tend to group together, may be nervous and walk around, tails may be slightly elevated, and mucus may be present at the vulva which may be edematous. They tend to stand behind other cows. Mounting in beef cows is much less frequent than in dairy cattle so it is harder to note cows standing to be ridden. Often the periods of estrus in the southern states and in Brahman or Zebu cattle are shorter than the estrous periods in the English beef breeds in the more northern states. Cows in estrum should be hazed slowly into the corral and holding pens for breeding. Cows must be identified and records maintained of the dates of service and the bull used. Long hard hours plus care- ful attention to details are highly important to good con- ception rates in beef cattle.13,14 The use of “teaser” or vasectomized bulls has not gen- erally been very satisfactory although some ranchers have reported succsss with them. The presence of a bull can increase sexual activity among cows and increase heat detection.9 Some use young 3- to 5-month-old beef bull calves; others use vasectomized bulls; while others use bulls with the penis truncated or deviated by various pro- cedures which prevents copulation but does not interfere with libido. Also, a “Pen-O-Bloc,” device has been used by some with variable results for detecting estrum. This device in the sheath (which is designed to block protru- sion of the penis) is later removed to use the bull as a “cleanup” bull. These bulls are most effective if not al- lowed to run continually with the herd, but are turned out in the morning or evening whenever heat checking is done. Some ranchers use commercial “heat detector” patches (“Kamar”) that may be glued to the sacrum. If the cow is mounted by another cow a dye is released908 VETERINARY OBSTETRICS that can be easily observed. With such detectors on the rump of a cow it is desireable to run heat checking bulls or testostrone-treated steers with the cows continuously to detect cows in estrum at times cows are not observed directly. After two inseminations about 80 to 85 percent of the cows should be pregnant and one “clean up” bull for every 100 head should be turned in to breed the re- maining unbred cows. Estrous cycle regulation, with the objective of in- ducing animals to ovulate at a preset time has been in- vestigated extensively.24,31,32 Many products have been approved for use in recent years. These include the nat- ural prostaglandin F2a (Lutalyse, The Upjohn Company) and analogs of prostaglandin such as “Estrumate.” Var- ious progestational agents are available. These include a silastic coil impregnated with natural progesterone (pro- gesterone releasing intravaginal device, PRID), and a synthetic progestogen, “Norgestomet,” which is com- bined with estradiol valerate in a commercially available product called “Synchro-mate B” (Ceva Labs.). There are many other combinations which have been tested.24,31 These hormonal treatments are not cures for infertility. However, the progestational agents tend to increase the proportion of suckled beef cows which will be induced to ovulate in the normal postpartum breeding period of about 50 to 100 days. Removing the calf from the mother for 48 hours has been studied extensively by Wiltbank,80 and this increases the synchrony and number of cows that can be impregnated in a short period of time. It is very important that animals be well-fed and managed for synchronization to be effective. Recommendations of the manufacturer of each product must be followed care- fully. When this is done recent studies indicate that con- ception rates can be as high as breeding cows and heifers at naturally occurring heats. This is in contrast to the first 20 years of work with estrous cycle regulation, when conception rates in treated groups of animals often were 10 to 20% below controls. As a consequence of current technology it is possible to group beef cattle into a tight- er calving pattern and use semen from genetically su- perior sires by careful application of drugs to synchro- nize ovulation. These same techniques work especially well with dairy heifers. Artificial insemination organizations. The large number of 100 or so small A.I. organizations in the U.S. which developed as A.I. first grew in the 1940’s and 1950’s have decreased due to many mergers.34 Most of the semen today (outside of custom freezing) in the U.S. and Canada is supplied by about 10 large organizations. The proportion of registered cattle resulting from A.I. has increased over the years so that this technology pre- dominates in producing dairy cattle that are registered. The A.I. organizations and various colleges have inten- sive training programs to train full-time inseminators as well as herdsman’s schools to train farm personnel to inseminate cows. The latter have been increasing, so a substantial part of the semen produced by these few large A.I. organizations is sold for direct service. In the high concentration areas of dairy cattle of the northeastern, midwestem and western parts of the U.S. there are still many full-time inseminators. The development and cur- rent status of organizations affiliated with the National Association of Animal Breeders (NAAB) has been de- scribed recently.34 A full-time inseminator may inseminate between 2,500 and 4,500 cows per year, depending upon the density of the cow population in the area and the inseminator’s rep- utation as a top performer. Charges for insemination ser- vice vary from about $8 to $10 per cow, and a second or third service may be free. However, the semen must always be purchased. This cost usually ranges from about $5 to $30. Semen from a few bulls highly sought be- cause of pedigree and type, as well as production may be priced considerably higher. At large bull studs complete uniform and regular health tests and procedures are carried out under the supervi- sion of a competent veterinarian. The National Associ- ation of Artificial Breeders in the U.S. has adopted a Health Code of Minimum Standards33 (obtainable from NAAB), that requires bulls to be negative to the follow- ing tests: tuberculosis, once or twice annually; brucel- losis, blood tests and semen plasma tests twice annually; trichomoniasis, twice annually; and leptospirosis, twice annually. All bulls should be tested before coming from the farm to the stud; and should be placed in isolation for 4 to 8 weeks on arrival and retested. Many bulls are purchased as calves. If the bull is of breeding age six negative sheath tests for trichomoniasis are requested. For vibriosis control all studs must add the proper amounts of penicillin, dihydrostreptomycin and polymyxin B to the extended semen. Vibriosis should be eliminated from the stud since practical methods have been devised.39 All A.I. studs in the U.S., Canada and several European countries are free of vibriosis (Campylobacteriosis). If a bull develops a blood titer for leptospirosis he should be isolated for 4 months and treated with parenteral dihy- drostreptomycin and his blood titer should be stabilized before his semen is used. Many other diseases, partic- ularly viruses are of considerable concern (See Chapter XVIII) to A.I. studs, regulatory officials, cattle farmers, and veterinarians. Many purebred breeders use artificial insemination within the herd to control genital disease and to be able to offer for sale semen from valuable sires. Often this is coupled with embryo transfer to produceARTIFICIAL INSEMINATION 909 sons for sale and daughters for herd replacements or sale. There is an increasing demand for veterinarians to pro- vide or advise on this type of service. Further health requirements include general recom- mendations as to sanitation, investigation into the dis- ease problems of herds of origin of newly purchased males, and elimination of bulls found to harbor genetic recessive defects. As newer knowledge concerning older diseases becomes available and new disease entities that might be spread by semen are reported, steps must be taken by the bull studs to incorporate and use this in- formation to further protect the health of their valuable bulls and the herds of patrons using their semen. This is under continuous investigation. Monoclonal antibodies against viral diseases currently are being studied. In the U.S., custom freezing and uncontrolled sale of semen from bulls in private small herds provides a potential for wide-spread dissemination of infectious diseases. Such bulls are seldom subject to the rigid, continuing health standards enforced in most of the large A.I. studs. With the growth of the large A.I. organizations and their major investments in genetic testing and disease control programs, the small bull rings have largely dis- appeared. The large organizations have highly trained personnel, well-equipped laboratories and careful quality control procedures. Thus, these are sources of semen which represent known quality. Another valuable service of the large central breeding units is the detailed record- ing of the fertility rates of bulls, and the collecting of data on the proof of production and the type transmitted by the bulls, so that intelligent selection of known proven sires can be made. In the large organization this makes possible the development of proven bulls and rapid im- provement of the genetic makeup of cows sired by them, providing that participating members recognize the need and value of this service and cooperate with it. For fur- ther information on artificial breeding organizations the reader is referred to several of the general references listed earlier. Blood typing of all bulls used artificially is required by the purebred beef and dairy cattle associations. There are about 70 known antigens in bovine blood of which about 50 are used routinely for blood typing. The com- binations of blood antigens possible are so great that no two animals are similar unless they are identical twins. In questionable parentage cases the cow’s and her calf’s blood are typed. Then by a check of the blood types of the two bulls in question, one of the bulls can usually be excluded. Based on parentage tests 20 percent of cows bred artificially to two different bulls within an eleven day period conceived on the first service, while only 1 percent of cows bred to two different bulls at an 18 to 24 day interval conceived to the first service.66 This study suggested that parentage tests are indicated when cows are bred to different bulls on consecutive heat periods, when the intervals between service dates are less than 16 days or when the gestation length from the last ser- vice for normal sized calves is shortened 8 to 10 days or more. Blood typing assures the accuracy of pedigrees and the maintenance of the purity of purebreds and has been an important factor in the growth and confidence in artificial insemination of cattle. References Frozen Semen Processing and Insemination in Cattle 1. Adler, H. C. and Lindegaarde, L. E. (1965) Bovine Genital Vibriosis, Eradication from Danish A.I. Centers, Nord. Vet. Med. 17, 237. 2. Arriola, J. and Foote, R. H. (1982) Effects of Amikacin Sulfate on the Motility of Stallion and Bull Spermatozoa at Different Temperatures and Intervals of Storage, J. Anim. Sci. 54, 1105. 3. Bartlett, D. (1968) The A.V.M.A./N.A.A.B. Code and the U.S.L.S.A. Recommended Regulations, Proc. 2nd Tech. Conf. on Art. Insem. and Reproduct., Chicago, 37. 4. Bartlett, D. (1980) Facts of Veterinary Science as They Relate to Contemporary Regulations for Importation of Bovine Semen and to International Standards for Semen Exchange, 9th Intern. Congr. Anim. Reprod. and A.I., Madrid II, 271. 5. Bartlett, D. and Larsen, L. L. (1960) Veterinary Problems in Artificial Insemination, JAVMA 137, 8, 453. 6. Bartlett, D. and Larson, L. L. (1968) Disease and Artificial Insemination, in The Artificial Insemination of Farm Ani- mals, ed. by E. J. Perry, 4th Ed., Rutgers Univ. Press, New Brunswick, New Jersey. 7. Barrett, G. R., Casida, L. E. and Lloyd, C. A. (1948) Mea- suring Breeding Efficiency by Pregnancy Examinations and by Non-returns, J. Dairy Sci. 31, 682. 8. Bean, B. H., Pickett, R. W. and Martig, R. C. (1962) Some Factors Affecting the Motility and pH of Frozen Bovine Semen, J. Dairy Sci. 45, 15, 78. 9. Belling, T. H., Jr. (1961) Preparation of a “Teaser” Bull for Use in a Beef Cattle Artificial Insemination Program, JAVMA 138, 12, 670. 10. Bemdtson, W. E. and Foote, R. H. (1969) The Survival of Fro- zen Bovine Spermatozoa Following Minimum Exposure to Glycerol, Cryobiology 5, 6, 398. 11. Bemdtson, W. E., Olar, T. T. and Pickett, B. W. (1981) Cor- relation Between Post-thaw Motility and Acrosomal Integrity of Bovine Sperm, J. Dairy Sci. 64, 346. 12. Bemdtson, W. E. and Pickett, B. W. (1978) Techniques for the Cryopreservation and Field Handling of Bovine Spermatozoa, in: The Integrity of Frozen Spermatozoa, Washington, D. C., Conf. Natl. Acad. Sci., 53. 13. Bemdtson, W. E. and Pickett, B. W. (1980) Factors Affecting Fertility in an Artificial Insemination Program for Beef Cattle: Part 1. In: Bovine Practice, March-April. 14. Bemdtson, W. E. and Pickett, B. W. (1980) Factors Affecting Fertility in an Artificial Insemination Program for Beef Cattle:910 VETERINARY OBSTETRICS Part 2. In: Bovine Practice, May-June. 15. Bemdtson, W. E., Pickett, B. W. and Rugg, C. D. (1976) Pro- cedures for Field Handling of Bovine Semen in Plastic Straws. Proc. VI. Tech. Conf. A.I. & Reprod. 16. Boyd, L. J. and Hafs, H. D. (1970) Fertility of Frozen Semen Containing 12, 24 or 35 Million Sperm Extended to 0.5 or 0.9 ml Volume in Yolk Citrate, J. Dairy Sci. 53, 5, 660. 17. Bratton, R. W., Foote, R. H. and Cruthers, J. C. (1955) Pre- liminary Fertility Results with Frozen Bovine Spermatozoa. J. Dairy Sci. 38, 1, 40. 18. Coulter, G. H. and Foote, R. H. (1974) The Economics of Se- lected Systems by Banking Semen vs. Maintaining Bulls. Proc. Vth Tech. Conf. Anim. Reprod. & A.I., NAAB, 67. 19. Crowe-Swords, P. (1979) Bovine Semen Collection and Pro- cessing Techniques. Edit, by Taylor, J. Alberta, Canada. 20. Doak, G. and Poage, P. (1978) CSS Assures High Standards for Semen Identification. Sept. 10, 1978, 1036. 21. Elliott, F. I., Murphy, D. M., Bartlett, D. E. and Kubista, R. A. (1961) The use of Polymyxin B. Sulfate with Dihydrostrep- tomycin and Penicillin for the Control of Vibrio fetus in a Fro- zen Semen Process, Proc. 4th Intemat. Congr. on An. Reprod., the Hague. 22. Everett, R. W. (1975) Income Over Investment in Semen. J. Dairy Sci. 58, 1717. 23. Foote, R. H. (1975) Semen Quality from the Bull to the Freezer: An Assessment. Theriogenology 3, 219. 24. Foote, R. H. (1978) General Principles and Basic Techniques Involved in Synchronization of Estrus in Cattle. Proc. 7th Tech. Conf. on A.I. and Reprod., 74. 25. Foote, R. H. (1978) Maintenance of Fertility of Spermatozoa at -196°C. In: The Integrity of Frozen Spermatozoa, Rinfret, A. P. and Petricciani, J. C., edit., Nat’l Acad. Sci. 144. 26. Foote, R. H. (1979) Time of Artificial Insemination and Fer- tility in Dairy Cattle, J. Dairy Sci. 62, 355. 27. Foote, R. H. (1980) Artificial Insemination, in Reproduction in Farm Animals, edit, by Hafez, E. S. E., 4th Ed., Lea & Febiger, N.Y. 28. Graham, E. F. (1978) Fundamentals of the Preservation of Sper- matozoa, in: The Integrity of Frozen Spermatozoa, Rinfret, A. P. and Petricciani, J. C., edit., Nat’l. Acad. Sci., Washing- ton, D.C., 4, 44. 29. Gwazdawskas, F. C., Lineweaver, J. A. and Vinson, W. E. (1981) Rates of Conception by Artificial Insemination of Dairy Cattle. J. Dairy Sci. 64, 358. 30. Hahn, J., Foote, R. H. and Seidel, G. E., Jr. (1969) Quality and Freezability of Semen from Growing or Aged Dairy Bulls, J. Dairy Sci. 52, 11, 1843. 31. Hansel, W. and Beal, W. E. (1979) Ovulation Control in Cattle, in: Beltsville Symposia in Agricultural Research. 3. Animal Reproduction, H. W. Hawk, edit., Allenheld Osmum & Co., Montclair, N.J. 91. 32. Hansel, W. and Convey, E. M. (1983) Physiology of the Es- trous Cycle, J. Anim. Sci. 57, 404. 33. Health code of Minimum Standards for Bulls Producing Semen for Artificial Insemination (1962) A.I. Digest Dec., 17. 34. Herman, H. A. (1981) Improving Cattle by the Millions. Univ. of Missouri Press, Columbia, Mo. 35. L’Aigle Artificial Insemination Center (1969), Straw Method of Freezing, L’Aigle France. 36. Larson, G. L. and Bayley, N. D. (1955) The Fertility of In- seminations Made in Cows Showing Postestrous Hemorrhage, J. Dairy Sci. 38, 549. 37. Larson, L. L. (1981) Practice Careful Hygiene While Insemi- nating, Holstein World, Feb. 25, 1981, 45. 38. Lee, A. J., Salisbury, G. W., Boyd, L. J. and Ingalls, W. (1977) In Vitro Aging of Frozen Bull Semen, J. Dairy Sci. 60, 89. 39. Lein, D., Erickson, I., Winter, A. J. and McEntee, K. (1968) Diagnosis, Treatment and Control of Vibriosis in An Artificial Insemination Center, JAVMA 153, 12, 1574. 40. MacPherson, J. W. and Fish, N. A. (1954) The Survival of Pathogenic Bacteria in Bovine Semen Preserved by Freezing, Am. J. Vet. Res. 15, 548. 41. MacPherson, J. W. (1968) Semen Placement Effects on Fertility in Bovines, J. Dairy Sci. 51, 5, 807. 42. Manthei, C. A., DeTray, D. E. and Goode, E. R. (1950) Bru- cella Infection in Bulls and the Spread of Brucellosis in Cattle by Artificial Insemination I Intrauterine Injection, JAVMA 117, 106. 43. McDonnell, W. E., Edgerton, L. A., Olds, D. and Harned, F. D. (1977) Clitoral Stimulation and Non-Return Rate in the Bo- vine. J. Dairy Sci. Abstr. No. 46. 44. McEntee, K., Gilman, H. L., Hughes, D. E., Wagner, W. C. and Dunn, H. O. (1959) Insemination of Heifers with Penicillin and Dihydrostreptomycin-Treated Frozen Semen from Vibrio Fetus Carrier Bulls, Cornell Vet. 49, 1, 175. 45. McSparrin, B. H. and Patrick, T. E. (1967) Relationships Among 60 to 90 Day Non-returns, Diagnosed Pregnancies and Actual Calvings of Cows Bred Artificially, J. Dairy Sci. 50, 4, 612. 46. Meryman, H. T. and Kafig, E. (1963) Freeze-Drying of Sper- matozoa, J. Reprod. and Fertil. 5, 87. 47. Morrow, D. A. (1970) Bovine Diseases and the A.I. Industry, Proc. 3rd Tech. Conf. on Artif. Insem. and Reprod., N.A.A.B., February, Columbia, Mo., 79. 48. Mortimer, R. G., Bemdtson, W. E., Pickett, B. W. and Ball, L. (1976) Fertility of Frozen Bovine Spermatozoa Packaged in Continental Straws or Ampules. J. Dairy Sci. 59, 1595. 49. Nagase, H. and Niwa, T. (1964) Deep Freezing Bull Semen in Concentrated Pellet Form, I, II, III, Proc. 5th Intemat. Congr. on An. Reprod. Vol. IV, 410, 498, 503. 50. Nagase, H. and Graham, E. F. (1964) Pelleted Semen: Com- parison of Different Extenders and Processes on Fertility of Bo- vine Spermatozoa, Proc. 5th Intern. Congr. on An. Reprod., Trento, Italy, Vol. IV, 387. 51. Nelson, L. D., Pickett, B. W. and Seidel, G. E., Jr. (1975) Effect of Heterospermic Insemination on Fertility of Cattle. J. Anim. Sci. 40, 1124. 52. Olds, D. and Seath, D. M. (1954) Factors Affecting Repro- ductive Efficiency in Dairy Cattle, Ken. Agr. Exp. Stat. Bull 605. 53. Oltenacu, E. A. B., Foote, R. H. and Bean, B. (1980) Effects of Two Simulated Semen Culling Programs on Predicted Fer- tility in an Artificially Inseminated Cow Population. J. Dairy Sci. 63, 1351. 54. Pace, M. M. and Sullivan, J. J. (1978) A Biological Compar- ison of the .5 ml Ampule and .5 ml French Straw Systems for Packaging Bovine Spermatozoa, N.A.A.B. Proc. 7th Tech. Conf. Artif. Insem. Reprod. 22. 55. Pace, M. M., Sullivan, J. J., Elliott, F. I., Graham, E. J. and Coulter, G. H. (1981) Effects of Thawing Temperature, Num- ber of Spermatozoa and Spermatozoal Quality on Fertility of Bovine Spermatozoa Packaged in ,5-ml French Straws. J. Anim. Sci. 53, 693. 56. Park, Y. W. and Hunter, A. G. (1977) Effect of Repeated In- seminations with Egg Yolk Semen Extender on Fertility in Cat-ARTIFICIAL INSEMINATION 911 tie. J. Dairy Sci. 60, 1645. 57a. Pickett, R. W. (1969) A Symposium on Management of Beef Cattle for Reproductive Efficiency, Ft. Collins, Colo. 57b. Pickett, B. W. and Bemdtson, W. E. (1974) Preservation of Bovine Spermatozoa by Freezing in Straws: A Review, J. Dairy Sci. 57, 1287. 58. Pickett, B. W., Bemdtson, W. E. and Rugg, C. D. (1975) Se- men Handling in the Field. Proc. X Beef A.I. Conf., 54. 59. Pickett, B. W., Bemdtson, W. E. and Sullivan, J. J. (1976) Techniques for Processing and Packaging Bovine Semen. Proc. VI Tech. Conf. A.I. & Reprod. 60. Pickett, R. W., Hall, R. C., Jr., Lucas, J. J. and Gibson, E. W. (1964) Influence of Sperm Numbers on Fertility of Frozen Bovine Semen. J. Dairy Sci. 47, 8, 916. 61. Pickett, R. W., Martig, R. C. and Cowan, W. A. (1961) Pres- ervation of Bovine Spermatozoa at -790 and -196°C, J. Dairy Sci. 44, 11, 2089. 62. Polge, C., Smith, A. U. and Parkes, A. S. (1949) Revival of Spermatozoa After Vitrification and Dehydration at Low Tem- peratures, Nature 164, 666. 63. Randel, R. D., Short, R. E., Christensen, D. S. and Bellows, R. A. (1975) Effect of Clitoral Massage after Artificial Insem- ination on Conception in the Bovine. J. Anim. Sci. 40, 1119. 64. Rapatz, G. L. (1966) What Happens When Semen is Frozen, Proc. 1st Techn. Confer, on Art. Insem. and Bovine Reprod., Nat. Assoc, of Animal Breeders, 45. 65. Rasbeck, N. O. and Terpstra, J. I. (1962) Artificial Insemina- tion and Deep Frozen Semen; Danger of Dissemination of In- fections; Sanitary Measures; Livestock Infertility, Animal Health Monograph #5 F.A.O. 83. 66. Rendel, J., Bouw, J. and Schmid, D. O. (1962) Frequency of Cows Served Twice Which Remain Pregnant to First Service, An. Prod. 4, 359. 67. Robbins, R. K., Sullivan, J. J., Pace, M. M., Elliott, F. I., Bartlett, D. E. and Press, P. J. (1978) Timing of Insemination of Beef Cattle, Theriog. 10, 247. 68. Rugg, C. D., Bemdtson, W. E., Mortimer, R. G. and Pickett, B. W. (1977) Effect of Thawing Procedures on Fertility of Bo- vine Spermatozoa Frozen in .25-ml Straws. J. Anim. Sci. 44, 266. 69. Saacke, R. G. (1974) Follow A.I. Techniques Recommended by Suppliers. Hoard’s Dairymen March 25, 415. 70. Salisbury, G. W. (1969) Aging Phenomena in Spermatozoa, I, II, III. Fertility and Prenatal Losses, J. Dairy Sci. 50, 1675, 1679 and 1683. 71. Senger, P. L. (1980) A Simple Semen Inventory System. Hol- stein World, August 26, 1980, 181. 72. Senger, P. L., Becker, W. C. and Hillers, J. K. (1980) Quality of Semen Stored in On-the-Farm Semen Tanks. J. Dairy Sci. 63, 646. 73. Smith, R. L., Bemdtson, W. E., Unal, M. B. and Pickett, B. W. (1978) Influence of Percent Egg Yolk during Cooling and Freezing on Survival of Bovine Spermatozoa. J. Dairy Sci. 62, 1297. 74. Sturman, H. (1982) Personal Communication. 75. Tanabe, T. Y., Heist, C. E. and Almquist, J. O. (1955) Factors Affecting Pregnancy Interruption in Artificial Insemination in Dairy Cattle, J. Dairy Sci. 38, 6, 601. 76. Trimberger, G. W. and Davis, G. K. (1943) The Relationship Between Time of Insemination and Breeding Efficiency in Dairy Cattle, Nebr. Agric. Exper. Stat. Res. Bull No. 129. 77. Truscott, R. B. and Abreo, C. (1977) Antibiotics for Elimina- tion of Mycoplasma and Ureaplasma from Bovine Semen. J. Dairy Sci. 24, 905. 78. VanDemark, N. L. (1952) Time and Site of Insemination in Cattle, Cornell Vet. 42, 2, 215. 79. Webb, J. H. (1982) Should You Breed Your Own Cows? Hoard’s Dairyman 127, 16. 80. Wiltbank, J. N., Sturges, J. C., Wideman, D., LeFever, D. G. and Faulkner, L. C. (1971) Control of Estrus and Ovulation Us- ing Subcutaneous Implants and Estrogens in Beef Cattle. J. Anim. Sci. 33, 600. Artificial Insemination in the Horse Although the horse was one of the first animals suc- cessfully inseminated by Ivanov on Russian stud farms early in this century, the practice has not become wide- spread because of difficulties in storing and shipping liq- uid or frozen stallion sperm as compared to the sperm of bulls. Also freezing stallion semen reduces fertility considerably, and most importantly there is the problem of detecting and breeding the mare at the proper stage of estrum to obtain a high conception rate. Only a few of the purebred equine breed registries recognize artifi- cial insemination.1 The Thoroughbred association does not permit or recognize artificial insemination except as it immediately follows a natural service to the same stal- lion. The Standard Bred Association and American Quarter-Horse Association permit artificial insemination on a farm with fresh unfrozen semen but do not permit transport of semen. Much work over a number of years will be necessary to develop artificial insemination of horses to its full potential. It is not likely to reach the level practised in cattle because of the scattered small horse farms, and the difficulties posed by a long estrous period and in the detection of estrus. Mares do not ex- hibit homosexual activities during estrus as do cattle. Detection of estrus in mares is best and most easily ac- complished by teasing with a stallion. Artificial insemination has been used to control dis- eases such as dourine and equine infectious anemia. Other advantages include (1) reduced chance of injuring the mare, (2) correction of bad breeding habits in stallions, (3) the possibility of evaluating each ejaculate of semen, (4) preventing overuse of the stallion (5) aiding in iden- tification of reproductive problems, (6) permitting more mares to be bred to a particular stallion and (7) permit- ting use of valuable old stallions.18 If frozen semen can be improved, to have a good supply all the time, mares can be inseminated at the time to yield maximum fer- tility. Also, mares that have certain physical problems, and whose resistance to infection is low, may be insem- inated with semen containing added antibiotics. Semen collection has been described previously. Stai-912 VETERINARY OBSTETRICS lions can be trained to mount a phantom24 as well as a mare in estrum or one injected with estrogen. Thorough teasing of the stallion and scrubbing of the penis and sheath during the teasing period are important.26 This re- moves smegma and other debris. Any residual water and soap should be removed with a clean dry towel. The artificial vagina (A.V.)11'22 is the best device for semen collection. This equipment, its assembly and use has been described in a preceding chapter and in the general texts cited previously.-- — — Semen evaluation also was described previously. Care should be taken to protect the sperm from major changes in temperature or exposure to sunlight during examina- tion and while holding until it is used for insemination. The semen may be collected with a strainer or filter, nylon preferred,16 in the A.V. If this is not used the se- men should be strained and volume with and without gel recorded. Also, any gross contamination should be noted. In addition the percentage of motile spermatozoa and concentration of sperm per ml should be determined. This information is needed in calculating the volume of se- men required to provide sufficient sperm for insemina- tion. In addition, sperm morphology should be noted. However, in contrast to normal bull semen stallion se- men often contains more than 20 to 30 percent abnormal cells, even from fertile stallions. Handling, extending and storing semen should be done gently, avoiding shaking and rapid changes in tem- perature. Normally, if semen is collected for insemina- tion on the premises it should be collected just before the mares are ready for insemination. Fresh semen then can be used quickly without the necessity of preparing semen extenders and fertility is high.23 If the semen is to be stored for several hours it should be mixed with an extender and kept in the dark. Sperm in raw semen held at room temperature or higher for 8 hours loses its motility.15 By mixing semen with extenders at various rates and cooling slowly to 5° C sperm has been used for several days. It was reported that 67 percent of 218 mares inseminated with extended semen conceived while 79 percent of 199 mares handled similarly, but bred nat- urally, conceived.13 The composition of the extender as well as storage time markedly affect conception rates. The number of spermatozoa inseminated also is an im- portant factor. In one study96 the mares were inseminated with (1) “fresh semen” held less than 1 hour at 39° C in a cream-gel extender, (2) semen cooled to 5° C for 2 hours in cream-gel extender, (3) semen cooled as before, but with 7 percent glycerol added and (4) semen held at 5° for 24 hours in cream-gel extender. The pregnancy rates (18 mares per group) at the first cycle were 56, 39, 6 and 28 percent, respectively. After 3 cycles the cor- responding values were 94, 83, 44 and 56 percent, re- spectively. While the number of mares per group is too small to pinpoint accurately the conception rate due to each treatment, it is clear that both glycerol and storage for 24 hours were detrimental. Because cream-gel has been reported to be one of the better extenders for pre- serving unfrozen stallion sperm33 this decline in concep- tion rate emphasizes the desirability of using unfrozen semen in a relatively short period of time. There are many anecdotal accounts of using unfrozen semen after pro- longed storage, but these lack controls and sufficient numbers and information to verify the success rate. This emphasizes the need for substantial research on the pres- ervation of the fertilizing ability of stallion semen so that the most judicious use of desired stallions can be made to obtain maximum pregnancy rates in the mares. Stallion sperm are sensitive to centrifugation.7 9a 25 Un- der certain circumstances it may be desirable to concen- trate the sperm for storage or for freezing. Care should be taken to use low centrifugal forces and it was reported25 that 10% seminal plasma should be retained to preserve maximum motility and fertility. Also, care should be taken to avoid shaking and ag- itation of liquid semen that is to be transported or shipped. Tubes should be filled and sealed tightly to avoid agi- tation and leakage. Plastic bottles of ice in an insulated container should be provided to insure a temperature of approximately 5° C when extended semen is to be shipped long distances. Equine semen extender—Horse semen, as noted in the previous chapter, is high in electrolytes and low in sugar, and sperm cells survive only a relatively few hours in the seminal plasma. Most recommended extenders that have proven satisfactory have generally supplied sugar and other protective substances. Some recommended ex- tenders for equine liquid semen include:13 14 18 27 28 33 (1) Sterile skim milk or sterilized mare’s milk pre- pared in a manner similar to bovine sterilized skim milk extender by heating in a double boiler to 92° C for 10 minutes. This extender can be stored fro- zen. (2) Distilled water or sterilized skim milk, to which 7 gms of glucose and 0.8 gms of egg yolk have been added per 100 ml. (3) Homogenized sterilized, 9 percent, cream, 400 ml, to which one-half ounce of plain gelatin in 40 ml of water heated to 145° F is added with gentle stir- ring while both were warm to prevent the lumping of the gelatin. Penicillin (1000 I.U.) and 1000 mi- crograms of streptomycin per ml are added. This extender can be frozen and stored for several weeks or more.ARTIFICIAL INSEMINATION 913 (4) Hughes and Loy13 used a boiled skim milk diluter for extending semen and inseminating mares up to 24 hours after collection. For storing semen from 24 to 96 hours they used an extender in which “half and half” cream was heated to 95° C in a double boiler for 2 to 4 minutes. The scum was removed and the hot cream was added to 1.3 gm of Knox gelatin which had been autoclaved with 10 ml of distilled water, to a final volume of 100 ml. After cooling these two extenders, 1000 units of crystalline penicillin, 1 mg of dihydrostrepto- mycin and 200 units of Polymyxin B sulfate were added per ml of diluter. These diluters can be made up in advance and stored frozen in a freezer. (5) A dried skimmilk-glucose extender that is quite widely used for storage of stallion sperm for sev- eral hours consists of the following: 2.4 gm of “Sanalac” dried skimmilk, 4.9 gm. of glucose, 92 ml. of sterile distilled water, 2 ml. of 7.5% so- dium bicarbonate and 2 ml of gentamycin sulfate. (6) A cream-gel extender can be simply prepared18 by adding 1.3 gm. of Knox gelatin to 10 ml. of dis- tilled water, autoclaving and adding to 90 ml. of “half and half” cream which has been heated to 92° C. for 10 minutes in a double boiler. This can be frozen. (7) A Tris-egg yolk extender, modified from the bull semen extender, has been used, but fertility was lower than with cream gel.23 However, all of the Tris-egg yolk extenders contained glycerol, which in several other studies has been found to be det- rimental to stallion spermatozoa. Contrary to these earlier reports another study placed centrifuged stallion spermatozoa into a Tris-egg yolk-glycerol extender to remove the seminal plasma.10 Fertility of semen stored at 5° C was maintained for 2 to 6 days in a limited trial. (8) In Germany17 extensive use has been made of lac- tose extender modified from the Japanese lactose extender developed originally for pelleting bull semen.19 The extender has several modifications but consists basically of lactose, egg yolk, sodium citrate, EDTA, sodium bicarbonate, a detergent, glycerol, water and antibiotics (penicillin and streptomycin). It is used primarily for frozen se- men packaged as pellets or large volume (4 ml) straws. Best results were obtained when the se- men was centrifuged in extender, rediluted and frozen. Twelve of 19 mares conceived on a single insemination. (9) There have been many other extenders14'20,30 and references can be found listed in those cited. Many of the reports are based on preliminary laboratory studies without fertility information. Antibiotic additions to stallion semen have not been studied thoroughly. This is surprising in view of the po- tential contamination of stallion semen and the use of artificial insemination in mares which appear to be es- pecially susceptible to infection. Equine spermatozoa ap- pear to tolerate antibiotics commonly used for bull sper- matozoa,3 such as penicillin, streptomycin and polymyxin B. In addition gentamicin is used widely. Recently amikacin2 has been found to be innocuous to stallion spermatozoa. This antibiotic is especially effective against Pseudomonas and several other gram negative organ- isms. It can be combined with selected other antibiotics. It was used successfully to infuse mares before insemi- nation.5 Some clinicians report that they infuse mares with extender containing antibiotic a few hours before insemination. This treatment does not seem to have been tested experimentally, but likely has the same effect as other solutions of antibiotics. Freezing horse semen was first reported in 19574 when epididymal spermatozoa were frozen in sterilized milk containing with 10 percent glycerol. One mare, of seven bred, conceived with frozen semen stored for 30 days. In 19637 a technique of layering equine semen over an extender of sterilized skim milk containing glucose, fructose and egg yolk and centrifuging at 1200 rpm for 7 minutes at 30° C followed by and pouring off the su- pernatant seminal plasma after 95 percent of the sperm cells had been spun into the extender was reported. Fur- ther extender was added and the extended semen was cooled to 4°. Then equal parts of 20 percent glycerol in more extender was added slowly over a period of one hour. The semen was poured into 10 ml. vials, equili- brated for 5 hours and then frozen. Two of 11 mares inseminated with the frozen semen conceived. A similar technique resulted in about 70 percent recovery of sperm motility after freezing but no fertility trials were con- ducted.28 During the 1960’s experimental work with stallion se- men was in progress in Pennsylvania, New York, Wis- consin (American Breeders Service) and particularly at Colorado State University, along with studies in Ger- many. Support for this research has been surprisingly minimal, considering its importance. The importance of centrifugation is still controversial. If one wishes to store frozen semen in small volumes then concentration is important, and centrifugation is a convenient means of concentrating sperm. Low speed centrifugation is necessary, and possibly the retention of at least 10 percent seminal fluid during freezing is de- sirable. However, this may depend upon the extender914 VETERINARY OBSTETRICS and method of freezing.10,17 By freezing and storing in larger volumes one can avoid concentrating the sperm at all, or it can be partly concentrated by collecting only the sperm rich fraction.6 This procedure also has been used by others.29 The amount of cryoprotectant seems to be very im- portant as a detrimental effect occurred in cream-gel within 2 hours of storage.96 In another study10 7.5% glycerol did not reduce fertility with unfrozen semen stored in a Tris-fructose egg yolk extender. However, with frozen semen only 1 mare out of 16 conceived during the first cycle versus 70 percent for mares inseminated with un- frozen semen. Only 7 of 16 mares had conceived after 4 cycles when inseminated with the frozen semen. Per- haps glycerol in the freeze-thaw process was more dam- aging than it was protective. In other studies14,17 5 per- cent (v/v) of glycerol has been used. Recently14 stallion semen extended with a dried skim- milk based extender with 5 percent (w/v) glucose was used to extend stallion semen to 250 X 106 sperm per ml. A portion of the semen was frozen in the lactose- egg-yolk-glucose-ETDA formula.1' Over one hundred mares were inseminated daily starting at day 2 of estrus, assigned alternately to control or frozen semen. Only 29 percent of the mares inseminated with frozen semen con- ceived, compared with 66 percent for the controls. Sperm numbers may have been limiting in the trial just described, as frozen semen contained about half of the number of motile cells compared to the control. Many studies have been done to compare the number of motile sperm inseminated. 12,21,27,33 In some studies as few as 80 x 106 motile spermatozoa produced as high a pregnancy rate as more spermatozoa. However, with frozen semen 500 X 106 sperm per insemination usually produced a higher pregnancy rate than 50 to 100 X 106 sperm per insemination. Obviously the fertility of the mare and timing of insemination may alter the response obtained with different sperm numbers inseminated. Volume of semen inseminated is believed by some to be important and generally 5 to 10 ml of semen are inseminated. However, when smaller volumes containing adequate sperm numbers are inseminated, fertility is not affected. There is great variation in the fertility of sires14,31,32 with frozen semen. Thus, stallions used in fertility testing with frozen semen usually are selected for the freezing quality of their semen. At the present time 300 to 500 x 106 sperm are recommended as an optimal insemination dose. Earlier studies had indicated that a billion or more sperm cells were needed in a volume of 10 to 50 ml.---- — — With proper detection of estrum and multiple insemi- nations during estrus, 500 X 106 sperm cells appear to be satisfactory. With skilled management the optimal number of spermatozoa may be less. For convenience in insemination and to be sure sufficient volume is depos- ited in the uterus 5 to 20 ml is usually inseminated. With fresh undiluted semen, as is often used on Standardbred and Quarter horse farms, 5 ml of raw semen should have a sufficient number of sperm (> 500 x 106 sperm) to impregnate the mare. Insemination of mares. The mare should be in estrus. The characteristics of mares in estrus have been de- scribed many times and their quantification relative to the stage of estrus summarized.32 Winking of the vulva, crouching and urination in the presence of a teaser stal- lion all are positive signs of estrus. Because mares are not homosexual mares will not attempt to mount each other. Insemination is performed on the second to fourth day. If the mare is still in estrus on the fifth or sixth day, insemination should be performed again. If the stallion semen is of good quality and fertile, insemination need only be performed every 48 hours, because spermatozoa may retain their fertilizing capacity for up to 4 to 6 days in the mare.8 By careful teasing, speculum examination of the cervix or rectal palpation of the follicle on the ovary and the cervix, insemination may often be per- formed when ovulation is expected in 12 to 24 hours. Summarized data indicated that conception rates in- creased in mares bred from 48 hours to within 6 hours before ovulation but declined in mares during ovulation and decreased markedly in mares bred 2 to 10 hours after ovulation.13 A few mares may conceive if bred or in- seminated 6 to 14 hours after ovulation. There is less danger of introducing infection if insemination is per- formed only once, and at the most twice, during an es- trus. The administration of 2000 to 5000 I.U. of chorionic gonadotropin parenterally on day 2 of estrus usually re- sults in ovulation in the estrous mare within 48 hours and this shortens the estrus and reduces the need for mul- tiple inseminations. One insemination 24 hours after 3,300 I.U. of HCG gave 61 percent pregnancies in one study.33 Under field conditions insemination every second day is common. The mare should be suitably restrained. After band- aging the mare’s tail with sterile gauze or a bandage, the buttocks, perineal region, and external genitalia are thor- oughly scrubbed with mild soap and water, wiped and rinsed with clear water. Most mares are presently inseminated with a 14 to 16 inch or 35 to 40 cm bovine plastic disposable insemi- nation or uterine infusion pipette attached to a sterile 10 to 40 ml glass or plastic syringe. The tip of the pipette is guided alongside the index finger into and through theARTIFICIAL INSEMINATION 915 cervix of the mare, which is normally relaxed at estrus. The semen or extended semen is slowly deposited into the body of the uterus. A vaginal speculum and a syringe attached to a long catheter or plastic pipette may be used to inseminate mares but it is more difficult to pass the pipette through the cervix. The cervix and uterus may be injured if too much force is used to insert the pipette or if the mare suddenly moves. Because insemination takes place directly into the uterus, great care is essential to insure that a clean source of semen is used and that a sanitary technique of insemination is followed to pre- vent genital infections. In former times semen sometimes was placed in a gel- atin capsule. The capsule was held in the hand encased in a disposable glove and sleeve and inserted through the cervix. This is seldom done currently. Another proce- dure, called “impregnation” was the placement of fresh semen into the uterus of the mare by means of a capsule or inseminating pipette and syringe after its collection from a stallion as he dismounted from the same mare after a service.16 This has been a long-established cus- tom, done largely because of the wishes of the owners, and also to make certain that the stallion actually eja- culated as determined by microscopic examination of the dismount semen sample for the presence of spermato- zoa. There is no evidence that “impregnation” or “cap- suling” is of any value and there are several good rea- sons for not performing this operation. It is one of the most futile things done in the breeding of horses.15 The last portion of the ejaculate has relatively few sperma- tozoa; and there is a great risk of introducing infection. There might be a few occasions when “capsuling” or “impregnating” might be indicated, such as a small stal- lion on a large mare where a “good” cover was not pos- sible.16 References Artificial Insemination in Horses la. Amer. Assoc. Equine Practitioners (1968) Rules Relative to Reg- istering Foals Produced Artificially, A.A.E.P. Newsletter, 1, 10. lb. Amann, R. P., Loomis, P. R. and Pickett, B. W. (1983) Im- proved Filter System for an Equine Artificial Vagina, Eq. Vet. Sci., 3, 4, 120. 2. Arriola, J. and Foote, R. H. (1982) Effects of Amikacin Sulfate on the Motility of Stallion and Bull Spermatozoa at Different Temperatures and Storage Intervals. J. Anim. Sci., 54, 1105. 3. Back, D. G., Pickett, B. W., Voss, J. L. and Seidel, G. E., Jr. (1975) Effect of Antibacterial Agents on the Motility of Stallion Spermatozoa at Various Storage Times, Temperatures and Di- lution Ratios. J. Anim. Sci. 41, 137. 4. Barker, C. A. V. and Gandier, J. C. C. (1957) Pregnancy in a Mare Resulting from Frozen Epididymal Spermatozoa, Canad. J. Comp. Med. 21, 1, 47. 5. Blue, M. G. (1982) Conception in Mares Following Intrauterine Therapy with Amikacin. J. Equine Vet. Sci. 2, 200. 6. Blue, M. (1983). Personal Communication. 7. Buell, R. (1963) A Method of Freezing Stallion Semen and Tests of Its Fertility, Vet. Rec. 75, 36, 900. 8. Burkhardt, J. J. (1949) Sperm Survival in the Genital Tract of the Mare, J. of Agric. Sci. 39, 201. 9a. Cranwell, J. E., Roberts, A. D. and Pickett, B. W. (1969) Fac- tors Affecting Survival of Equine Spermatozoa, J. Anim. Sci. 29, 1, 186. 9b. Demick, D. S., Voss, J. L., Pickett, B. W. (1976) Effect of Cooling, Storage, Glycerolisation and Spermatozoal Number on Equine Fertility. J. Anim. Sci. 43, 633. 10. Guay, P., Rondeau, M. and Boucher, S. (1981) Effect of Glyc- erol on Motility, Viability, Extracellular Aspartate Aminotrans- ferase Release and Fertility of Stallion Semen Before and After Freezing. Equine Vet. J. 13, 177. 11. Hillman, R. B., Olar, T. T., Squires, E. L. and Pickett, B. W. (1980) Temperature of the Artificial Vagina and Its Effect on Seminal Quality and Behavioral Characteristics of Stallions. J. Am. Vet. Med. Assoc. 177, 720. 12. Householder, D. D., Pickett, B. W., Voss, J. L. and Olar, T. T. (1981) Effect of Extender, Number of Spermatozoa and HCG on Equine Fertility. J. Eq. Vet. Sci. Jan./Feb., 9. 13. Hughes, J. P. and Loy, R. G. (1970) Artificial Insemination in the Equine, A Comparison of Natural Breeding and Artificial In- semination of Mares Using Semen From Six Stallions, Cornell Vet. 60, 3, 463. 14. Loomis, P. R., Amann, R. P., Squires, E. L. and Pickett, B. W. (1983) Fertility of Unfrozen and Frozen Stallion Spermatozoa Extended in EDTA-Lactose-Egg Yolk and Packaged in Straws. J. Anim. Sci. 56, 687. 15. MacLeod, J. and McGee, W. R. (1950) The Semen of the Thor- oughbred, Cornell Vet. 40, 3, 233. 16. McGee, W. R. (1951) The Mechanics of Breeding, Blood Horse 61, 17, 808. 17. Martin, J. C., Klug, E. and Gunzel, A. R. (1979) Centrifugation of Stallion Semen and Its Storage in Large Volume Straws. J. Reprod. Fert. 27, 47. 18. Morrow, D. A., edit. (1980) Current Therapy in Theriogenology. W. B. Saunders Co., Philadelphia. 19. Nagase, H., Soejima, S., Niwa, T., Oshida, H., Sagara, Y., Ishizaki, N. and Hoshi, S. (1966) Studies on the Freezing of Stal- lion Semen. I. Fertility Results of Stallion Semen Frozen in Con- centrated Pellet Form. Jap. J. Anim. Reprod. 12, 48. 20. Nishikawa, Y., Iritani, A. and Shinomiya, S. (1972) Studies on the Protective Effects of Egg Yolk and Glycerol on the Freezabil- ity of Horse Spermatozoa, 7th Intemat. Congr. on Anim. Reprod. and Artif. Insem., Munich 2, 1545. 21. Pace, M. M. and Sullivan, J. J. (1975) Effect of Timing of In- semination, Numbers of Spermatozoa and Extender Components on the Pregnancy Rate in Mares Inseminated with Frozen Stallion Semen. J. Reprod. Fert. Suppl. 23, 115. 22. Pickett, B. W. and Back, D. G. (1973) Procedures for Prepa- ration, Collection, Evaluation and Insemination of Stallion Se- men. Colorado State Univ. Gen. Series 935. 26pp. 23. Pickett, B. W., Burwash, L. D., Voss, J. L. and Back, D. G. (1975) Effect of Seminal Extenders on Equine Fertility. J. Anim. Sci. 40, 1136. 24. Pickett, B. W., Squires, E. L. and Voss, J. L. (1982) Techniques916 VETERINARY OBSTETRICS for Training a Stallion to a Phantom for Seminal Collection. Equine Vet. Sci. Mar./Apr. 66. 25. Pickett, B. W., Sullivan, J. J., Byers, W. W., Pace, M. M. and Remmenga, E. E. (1975) Effect of Centrifugation and Seminal Plasma on Motility and Fertility of Stallion and Bull Spermato- zoa. Fertil. Steril. 26, 167. 26. Pickett, B. W. and Voss, J. L. (1973) Reproductive Management of the Stallion, Ft. Collins, Colo., Colorado State Univ., General Series 934. 27. Pickett, B. W. and Voss, J. L. (1975) The Effect of Semen Ex- tenders and Sperm Number on Mare Fertility. J. Reprod. Fert. Suppl. 23, 95. 28. Polge, C. and Minotakis, C. (1964) Deep Freezing of Jackass and Stallion Semen, 5th Intemat. Congr. on Anim. Reprod. and Art. Insem., Trento, Italy, VII, 545. 29. Rajamannan, A. H. J. (1968) Freezing and Fertility Studies with Stallion Semen, Proc. of Vlth Intemat. Congr. of Animal Re- prod. and A.I., Paris, France. 30. Rowlands, I. W. and Allen, W. R. (1979) Equine Reproduction II. J. Reprod. Fert. Suppl. 27. 31. Sullivan, J. J. (1978) Characteristics and Cryopreservation of Stallion Spermatozoa, Cryobiology 15, 355. 32. Sullivan, J. J., Parker, W. G., Larson, L. L. and Turner, P. C. (1972) Some Aspects of Reproduction in the Horse Including Stallion Semen. Symp. Reprod. in Cattle and Horses. Michigan State Univ. 33. Voss, J. L. and Pickett, B. W. (1976) Reproductive Management of the Broodmare. Colorado State University General Series 961. 29 pp. Artificial Insemination in Swine Application of artificial insemination in swine is highly variable in different regions of the world.3,4’20'25'30'32 Sub- stantial numbers of sows and gilts are inseminated in Russia, Hungary, Germany, France, Holland, Norway, Sweden and Denmark.- For example, in Holland and Denmark over 300,000 sows are inseminated (about 20%) and in East Germany 85% of the 1,200,000 sows are inseminated. Most of the semen used is unfrozen. In the United States there is one main supplier of boar semen for artificial insemination. About 20,000 sows are in- seminated annually with commercially available semen in addition to boars collected on farms and semen used directly for insemination. The main advantages of using artificial insemination in swine are similar to those in cattle. The first is the use of genetically superior boars that have been perfor- mance and progeny tested for such traits as rate of gain, efficiency of gain, litter size of female progeny, dressing percentage and carcass quality. One boar has the poten- tial of siring up to 1,500 litters per year or 15,000 prog- eny, although they seldom achieve this potential. The second advantage of A.I. in swine is disease con- trol. If the boar stud is carefully tested for diseases of importance the semen may be used to introduce new ge- netic material into specific pathogen-free herds. These include diseases such as virus pig pneumonia, leptospi- rosis, brucellosis, pseudorabies, tuberculosis, etc. An- other advantage of A.I. is the ease with which cross- breeding can be done. A three-breed rotational cross can be used and the owner need only to select females to inseminate with semen from a different breed. There are several disadvantages of A.I. The first is that the number of sperm cells required and volume of semen used for insemination requires that more boars be kept for the sow population than is necessary in cattle. Secondly, the price of a good boar usually is low enough that swine breeders may find it more economical to buy reasonably good boars and use natural service. Thirdly, as the value of each animal is not high, the cost of in- semination may be relatively high compared to the value of the animal. This is especially true where labor costs are high, making the cost per sow expensive. Therefore, most of the inseminations, excepting where the density of pigs is high, are done by farm personnel. It is very important that swine breeders be well trained in heat de- tection. Thorough training of personnel in detecting es- trus accurately is an essential component of a successful A.I. program in any species. With the present economic climate it is doubtful that A.I. in swine will increase substantially in the U.S., al- though the use of superior boars can be shown to be profitable. The largest application appears to be either in countries where labor is cheap or herd size is small. With the improvement of conception rates when frozen semen is used it is surprising that more advantage is not taken of the gene pool available through frozen semen. The actual insemination of a sow is easily done and se- men can be stored frozen in the same type of liquid ni- trogen tank used for bull semen. However, the cost of boar semen is high and fertility results tend to favor nat- ural service.7,11'34'38 Collection of semen from boars for artificial insemi- nation is done by the use of a simple artificial vagina or by the gloved hand grasping the penis'3 as described in the previous chapter. Young boars are the easiest of the farm animals to train to mount a dummy, especially if other boars have mounted the dummy previously and the urine, smegma and semen odor is present on the dummy. Occasionally young boars may require a gilt or sow in estrus for stimulation. Older boars that have been used in natural service are more difficult to train. Collections are made at 3 to 6 day intervals or 2 to 3 times per week for best results.9’20’24*39’40 Some boars can continue to produce satisfactory ejaculates when collected every 48 hours. Depending on his age and other factors39 a boar willARTIFICIAL INSEMINATION 917 ejaculate 125 to 500 ml of semen. The presperm frac- tion, which is usually heavily contaminated with bacteria due to preputial debris and fluid, should be discarded. The extirpation of the preputial diverticulum to reduce the bacterial contamination of semen at the time of col- lection has been recommended.2 This also reduces the boar odor. Douching the sheath and preputial divertic- ulum and washing the skin around the external preputial orifice will help in reducing the large number of bacterial contaminants in boar semen such as E. coil, Aerobacter sp., Proteus, Corynebacteria, Pseudomonas, Staph- ylococci, and Bordetella. The gelatinous fraction should be discarded during collection or removed by straining through sterile cheese cloth. Either the sperm-rich frac- tion or the entire ejaculate minus the presperm and gel fractions should be used for insemination. Using great care to prevent cold shock the semen is examined for concentration, motility and morphol- ogy.1218'34 Either a hemocytometer or the photoelectric method9 can be used to determine sperm cell concentra- tion in porcine semen. Most authors agree that the num- bers of actively motile spermatozoa should be about 65 to 80 percent for best fertility but the relationship be- tween fertility and motility is not high. Fertile boars, es- pecially those in heavy use, may have up to 20 percent or more proximal protoplasmic droplets, but a high per- centage of proximal protoplasmic droplets may be as- sociated with infertility. Occasional sterile boars may have a very high percentage of acrosomal defects. Although this defect is usually considered to be hereditary, it might be acquired.20 A typical ejaculate of boar semen would have 200 ml of gel-free volume, 250 X 106 sperm/ml, 70% motile sperm and 15% total sperm cell abnormal- ities. Extension of boar semen is based, as in cattle, on the number of actively motile spermatozoa required for optimum conception rates. According to a number of authors32 this varies from 1 to 10 billion actively motile spermatozoa per insemination. Most recommend 5 bil- lion or more. Fairly satisfactory conception rates oc- curred with 2 to 5 billion per insemination. Thus 10 to 20 sows may be inseminated per ejaculate. During the past several years International Boar Semen, in 10,000 semen collections, has averaged 120 billion sperm per week on a schedule of 2 ejaculates per week. With their recommended dose of 4 billion sperm per week one boar can produce enough semen to inseminate 30 sows per week. Conception rates including size of litters are also influenced by the volume of the extended semen insem- inated and the length of storage time before insemina- tion.6 Most authors recommend 50 to 100 ml of extended semen per insemination. Extending boar semen. Boar semen is usually ex- tended from 1 to 1 up to 1 to 8 times, depending on the concentration of motile spermatozoa and the volume of the ejaculate, with warm extender at 37° C immediately after collection. Slow cooling and the addition of phos- pholipids to the semen protects the sperm cell and aids survival. For use in a liquid semen program the extended semen is cooled gradually to 12 to 20° C (54° to 65° F), which is the optimal storage temperature for boar semen. This temperature requires special packaging for field use. Others cool the ejaculate slowly to 12° to 20° C and then add the extender at the same temperature. When boar semen is cooled to 4° to 5° C within 1 to 2 hours, many sperm cells lose their motility even if extenders have been added. In sperm-rich fractionated semen this harmful ef- fect of cooling is much less pronounced. The addition of egg yolk or milk to boar semen prevented injury to sperm cells at 5° C.4 Temperatures of 35° to 38° C are definitely unfavorable to porcine sperm cell survival. A variety of different types of egg yolk or heated milk extenders have been used to store boar sperm in the liq- uid state.- Because of the relative difficulty of freezing boar spermatozoa the majority of inseminations are with liquid semen. This semen is useful for up to 3 days of storage. Frozen boar semen for insemination was given con- siderable impetus in 1970 when it was reported33 that a high fertilization rate could be achieved by surgical in- semination into the oviducts. For freezing boar semen it is desirable to concentrate the semen by centrifugation in order to have enough sperm cells in a small volume. Several procedures were developed in the early 1970’s which produced moderately successful conception rates.7'10'15'22'24'26'34'42 In Minnesota10'34 the sperm rich fraction was collected and slowly cooled to 22° C. It was determined that exposure to seminal plasma was bene- ficial to the survival during freezing so the semen was held at 22° C for 1 hour. Thereafter an organic buffer, glucose, sodium citrate, egg yolk and 0.5% of a deter- gent were added. Semen was cooled to 5° C and pel- leted. Considerable attention also was given to thaw- ing.8'16'35’36 In the Minnesota studies pellets were initially thawed at 65° C. In Sweden a similar procedure was de- veloped. The final concentration of glycerol was 2.5% (v/v). Sperm were frozen in 0.1 ml pellets. Thawing is done with seminal plasma or other thawing extenders. Thawing media are at 65° C initially but the addition of many pellets results in a final temperature of thawed pel- lets of about 32 to 34° C. A series of Beltsville extenders has been developed. One tested widely in the field is BF5.11,34 This extender contains Tris, Tes, dextrose, 20% egg yolk and 0.5 per-918 VETERINARY OBSTETRICS cent Orvus Es Paste (a detergent). The semen is held at 22 to 24° C for two hours, centrifuged at 300 X g, ex- tended in BF5 to a sperm concentration of 1.2 x 109 sperm/ml. Semen is cooled to 5° C over a period of two hours. Then BF5 containing 2 percent (v/v) of glycerol is added in equal amounts, giving a final sperm concen- tration of 0.6 X 109/ml and 1 percent (v/v) glycerol. The semen is then frozen directly by placing 0.1 ml in predrilled dry ice to produce pellets. It is clear that there are many variations in freezing procedures. All involve certain principles.10 First, boar semen develops resistance to coldshock by being ex- posed to seminal plasma. Secondly, seminal plasma is removed before final cooling to concentrate the sperm and cooling must be done slowly. Third, the concentra- tion of electrolytes in the extender should be kept low. Fourth, low glycerol concentrations assist in protecting sperm during freezing, but the glycerol level must be kept low as it is harmful to boar sperm.23 Finally, by concentrating the sperm the number required for insem- ination can be frozen in small packages (pellets) for rapid thawing. Antibiotics should be used to control the large number of bacteria in boar semen stored at near room tempera- tures.29 37-41 Usually 500 to 1,000 I.U. of crystalline pen- icillin G and 500 to 1,000 micrograms of dihydrostrep- tomycin per ml of extended semen are recommended. Neomycin, polymyxin B and sulfadiazine are also of value. Improved conception rate and litter size was re- ported when antibiotics were added to extended boar se- men.12 Recently, several of the newer antibiotics such as amikacin and gentamicin have been reported to inhibit bacteria in semen stored at 15° C for many days.37 Detection of estrus and timing of insemination are of critical importance in obtaining good conception rates and litter size in artificial insemination of female swine. Gilts and sows should be observed for estrus twice a day separate from the time of feeding. In this regard the owner’s or herdman’s and inseminator’s judgement, and experience and skills of observation are highly impor- tant. Swelling and slight reddening of the vulva in sows and gilts persist for 2 to 3 days of proestrus, 2 to 3 days of estrus and for about 2 days of postestrus, with max- imum swelling generally seen at the onset of estrus. The degree of swelling of the vulva alone is unreliable. At the proper time for insemination the vulva is less swollen and more wrinkled and a clear or creamcolored flecked mucus is usually present in the lower vulvar commis- sure. The gilts and sows often become more restless and noisy during estrus. A method to aid in heat detection consists of approaching the female quietly, placing the flat of the hands on the loins and exerting moderate downward pressure.19 If the sow moves away the hands and arms are placed between the hind legs and the rear parts are lifted off the ground, simulating the action of a boar toward a sow in estrus. After a few minutes some sows will stand in a saw-horse attitude (lordosis) when back pressure is applied. If possible the owner, herds- man or technician should mount the female and sit astride the loins and remove the feet from the ground. Clawing the shoulders, digital manipulations of the clitoris or in- serting the insemination pipette into the vagina will in- duce the state of sexual receptivity if the sow is in estrus. At this time most sows will stand very quietly and may be nearly insensible to extraneous stimuli. If sows do not show the above signs of estrus, insemination should not be performed as conception rates are apt to be low and litter size reduced due to faulty timing in relation to ovu- lation. Sows and gilts inseminated during the period of standing reflex, indicating the peak period of estrum, had conception rates of 73 and 61 percent compared to 41 and 46 percent in those sows not showing a good stand- ing reflex.7 Sows and gilts should be bred without re- straint. The presence of a boar is very helpful in heat detec- tion. Both the preputial odor of the boar and his vocal- izations evoke external behavior signs of estrus in the sow that can be confirmed by hand pressure on the back. A vasectomized boar may be used as a aid in detection of estrus. Also, a boar in a pen adjacent to where the females are being checked for estrus will help evoke signs of estrous behavior. Lactating sows in good physical condition when weaning their pigs should be watched closely for estrus starting about the third day postweaning. Most sows come into estrum about four to seven days after their pigs are removed. Synchronization of breeding sows can be ac- complished by weaning a group of sows at the same time. For best results in insemination of gilts they should not be bred until they have been in estrus twice or more, weigh 280 pounds, or are 8 months of age. Reports,4-24 indicated that the duration of estrus proper averaged 55 hours for gilts and 70 hours for the sow. The time of ovulation was 25 to 36 hours after the onset of estrus. Spermatozoa in the sow retained their fertil- izing ability up to 25 to 30 hours. The best time for in- semination with unfrozen semen was about 12 hours after the onset of estrus with a second insemination 12 hours later, if the sow or gilt was still in estrus. With frozen semen, it is recommended that gilts be inseminated lb- 20 hours after onset of estrus and sows 22 to 26 hours after onset of estrus. A second insemination 12 hours later is recommended. Although under research condi- tions one well-timed insemination may be sufficient, 2ARTIFICIAL INSEMINATION 919 inseminations under field conditions improve conception rates 15 to 20 percent and litter size by one pig per lit- ter.7 This procedure is costly and not necessary if close careful observations and tests for estrus are made. Three types of insemination catheters and techniques used for inseminating swine have been described.- One type was designed to seal the sow’s cervix so no semen flows back into the vagina as the semen is infused. This type is made of rubber about 1.0 to 1.5 cm in diameter and 45 to 50 cm long. The anterior end may be tapered, end in a pear-shaped bulb, or have a corkscrew config- uration,21 that is pressed with gentle pressure or rotated or twisted counter-clockwise into the cervix. In the latter case the catheter is not easily dislodged. A 7 to 8 mm diameter catheter with an inflatable cuff about 4 to 5 cm posterior to the tip has been devised.1 The second type of pipette is designed to penetrate through the cervical canal and into the uterus. The diameter of this plastic or nylon tube with a bent tip is 4 mm. It is rotated with gentle pressure to negotiate the cervical canal. The third type is a combination of the two types, consisting of a double plastic tube. The outer tube is 1 cm in diameter and engages in the cervix while the smaller inner cather is rotated to the left as it is pressed forward from the larger tube. All types of insemination catheters should be inserted dorsal-cranially through the vulva to avoid entering the urethra. Presently most containers for holding and transporting extended boar semen are plastic bottles and bags that can be attached to the insemination pipette and used to expel the semen. The larger volume of extended semen is squeezed gently over a period of 3 to 5 minutes into the cervix and uterus of the sow. Most workers reported that after a minute or so the semen goes into the sow very rapidly without resistance. Miscellaneous factors. The results of artificial insem- ination in swine were more successful in sows than in gilts. Most workers presently report a 50 to 70 percent farrowing rate on first service using single inseminations of fertile semen inseminated correctly at the proper stage of estrus. Conception rates for a single natural services are 80 to 90 percent. With 2 inseminations in one estrus 70 to 80% will conceive. There are many factors affecting fertility in A.I. Dif- ferences among boars is one of the major ones. Frozen sperm are believed not to survive as long in the female reproductive tract. Therefore, timing of the insemination and expert detection of estrus are critical.14 Finally, the deposition of most sperm into the uterus with minimal loss also is important. Estrus and ovulation synchronization in swine has been the subject of much research in recent years be- cause of many desirable features in swine management possible if this could be successfully employed.5 The only natural synchronization observed and practiced in swine is that achieved by weaning pigs from sows. Estrus usu- ally follows weaning by 4 to 7 days. One study reported 2 percent of sows were in heat before the fourth day, 12 percent on the fourth day, 35 percent on the fifth day, 16 percent on the sixth day, 16 percent on the seventh day, 6 percent on the eighth day and 13 percent on the ninth to fourteenth day, or 79 percent from 4 to 7 days post-weaning.19 When young pubertal gilts are trans- ported and placed in a new environment, estrus may de- velop in up to 70 percent of the gilts within 5 to 10 days due to the induced stress. Early studies on hormonal con- trol of estrus in gilts and sows with gonadotropins, es- trogens and progesterone or progestational agents have not been very satisfactory, often because of the produc- tion of cystic ovaries. At one time an excellent synchronizing compound known as I.C.I. 33828 or “Aimax” was available and provided excellent synchronization. However, it was discovered that if this compound was inadvertently ad- ministered to pregnant sows early in gestation fetal anomalies were produced. Thus, this compound was hastily withdrawn from the market. Prostaglandins are not as useful in swine as most other species because the corpora lutea of sows seem only to be susceptible to luteolysis on days 11 to 12 or 14 to 15. One way to overcome this is to administer PMSG or HCG to induce accessory corpora lutea and postpone es- trus. Then 12 days later the administration of prostaglan- din often will cause regression of the corpora lutea and induce a fertile estrus. For sows nursing pigs, several can be weaned at the same time after about four weeks of age. Most sows will be in estrus within 2 to 3 days of each other. Then at the other end of pregnancy experimental work with pros- taglandin and relaxin may synchronize farrowing so that most pigs can be scheduled to be bom Monday through Friday. Further studies are indicated and if synchroniza- tion becomes feasible then practical management factors such as the number of boars available for A.I. or natural service, problems of heat detection if A.I. is to be used, the size of the farrowing house, and other factors must be considered. References Artificial Insemination in Swine 1. Aamdal, J. and Hogset, I. (1957) Artificial Insemination in Swine, JAVMA 31, 1, 59. 2. Aamdal, J., Hogset, I., Filseth, O. (1958) Extirpation of the Pre-920 VETERINARY OBSTETRICS putial Diverticulum of Boars Used for Artificial Insemination, JAVMA 132, 522. 3. Bennett, G. H. and O’Hagan, C. (1964) Factors Influencing the Success of Artificial Insemination of Pigs, Proc. V. Intemat. Congr. on An. Reprod., Trento, Italy. Vol. IV, 481. 4. Boender, J. (1966) The Development of A.I. in Pigs in the Neth- erlands and the Storage of Boar Semen, World Rev. of An. Prod. II Spec. Issue 29. 5. Day, B. N. (1967) Artificial Insemination in Swine and Estrus Synchronization, Ann. Meeting Amer. Soc. for Study of Breed- ing Soundness, Univ. of Mo., Columbia, Mo. 6. Dziuk, P. J. (1958) Effect of Artificial Insemination of Gilts with Semen Stored for 1 /2 Hour vs 72 Hours, J. An. Sci. 17, 4, 1214. 7. Einarsson, S. (1973) Deep Freezing of Boar Spermatozoa. World Rev. Anim. Prod. 9, 45. 8. Einarsson, S., Holtman, M., Soosalu, O., Swensson, T. and Vir- ing, S. (1974) Studies on the Fertility and Survival of Deep-Fro- zen Boar Spermatozoa Thawed in Four Different Diluents. Zuchthyg. 9, 40. 9. Foote, R. H., Young, D. C., Turkheimer, A. R. and Bratton, R. W. (1959) Collection, Preservation and Artificial Insemina- tion of Boar Semen. Ann. Zootech. 1959, 27. 10. Graham, E. F. and Crabo, B. G. (1972) Some Factors Influenc- ing the Freezing of Boar Spermatozoa 7th Int. Congress Anim. Reprod. Art. Insem. Munich II, 1627. 11. Johnson, L. A., Aalbers, J. G. and Arts, J. A. M. (1982) Use of Boar Spermatozoa for Artificial Insemination II. Fertilizing Capacity of Fresh and Frozen Spermatozoa in Gilts Inseminated Either at a Fixed Time or According to Walsmeta Readings. J. An. Sci. 54, 126. 12. King, G. J. and MacPherson, J. W. (1966) Boar Semen Studies: I. Laboratory Evaluation of Processing Phases, J. Comp. Med. and Vet. Sci. 71, 12, 227. 13. King, G. J. and MacPherson, J. W. (1973) Comparison of Two Methods for Boar Semen Collection, J. An. Sci. 36, 563. 14. Larsson, K. (1976) Fertility of Deep Frozen Boar Spermatozoa at Various Intervals Between Insemination and Induced Ovula- tion. Influence of Boars and Thawing Diluents. Acta. Vet. Scand. 17, 63. 15. Larsson, K. (1978) Deep-Freezing of Boar Semen, Cryobiology 15, 352. 16. Karsson, K. and Einarsson, S. (1976) Fertility of Deep Frozen Boar Spermatozoa. Influence of Thawing Diluents and of Boars. Acta. Vet. Scand. 17, 43. 17. Larsson, K., Einarsson, S. and Swensson, T. (1977) The De- velopment of a Practicable Method for Deepfreezing of Boar Spermatozoa. Nord. Vet. Med. 29, 113. 18. Larsson, K. and Ersmar, M. (1980) Laboratory Studies on Fro- zen-thawed Boar Semen in Relation to Contemporary Fertility with Liquid Semen of A.I. Boars. Zuchthg. 15, 111. 19. Madden, D. H. L. (1959) Progress in the Artificial Insemination of Swine. Some Factors Influencing Fertility Levels in its Field Application, Vet. Rec. 71, 12, 322. 20. Melrose, D. R. (1966) Artificial Insemination of Pigs—A Re- view of Progress and Possible Development. World Rev. of An. Prod. II, Spec. Issue, 15. 21. Melrose, D. R. and O’Hagan, C. (1969) Investigations into the Techniques of Insemination in the Pig, Proc. IV Intemat. Congr. on An. Reprod., The Hague, Vol. IV, 855. 22. Morrow, D. A. (1980) Current Therapy in Theriogenology. W. B. Saunders, Co., Philadelphia. 23. Neville, W. J., MacPherson, J. W. and King, G. K. (1970) The Contraceptive Action of Glycerol in Gilts, J. An. Sci. 31, 1, 227. 24. Niwa, T. (1961) Researches and Practices in the Artificial In- semination of Pigs, Proc. IV Intemat. Congr. on An. Reprod. The Hague, Vol. I, 83. 25. Paquignon, M., Bussiore, J., Bariteau, F. and Courot, M. (1980) Effectiveness of Frozen Boar Semen Under Practical Conditions of Artificial Insemination. Theriog. 14, 217. 26. Paquignon, M. and Courot, M. (1975) Fertilite et Prolificite de Truies Inseminees avec du Sperme Congele. Ann. Zootech. 24, 645. 27. Paquingnon, M. and Courot, M. (1975) Survie des Spermato- zoides de Verrat Apres Decongelation Effet du Rythme de Col- lectes, de la Concentration et du Taux de Glycerol. Ann. Biol. Anim. Bioch. Biophys. 15, 517. 28. Paredis, F. (1962) Fertility and Artificial Insemination in Pigs, Intemat. J. of Fert. 7, 3, 233. 29. Park, R. W. A., Melrose, D. R., Stewart, D. L. and O’Hagan, C. (1964) The Effects of Various Handling Methods and Anti- biotic Additions on the Numbers of Bacteria Present in Diluted Bull and Boar Semen after Storage, Brit. Vet. Jour. 120, 457. 30. Polge, C. (1956) The Development of an Artificial Insemination Service for Pigs. Anim. Breed. Abst. 24, 209. 31. Polge, C. (1978) Fertilization in the Pig and the Horse. J. Re- prod. Fert. 54, 461. 32. Polge, C. and Rowson, L. E. A. (1956) The Practical Applica- tion of Artificial Insemination in Pig Breeding, Vet. Res. 68, 952. 33. Polge, C., Salamon, S. and Wilmut, I. (1970) Fertilizing Ca- pacity of Frozen Boar Semen Following Surgical Insemination. Vet. Rec. 87, 424. 34. Pursel, V. G. (1979) Advances in Preservation of Swine Sper- matozoa. In: Animal Reproduction. Edit, by Hawk, H. W. BARC Symp. 3 Allanheld Osmum, Montclair, 145. 35. Pursel, V. G. and Johnson, L. A. (1975) Freezing of Boar Sper- matozoa: Fertilizing Capacity With Concentrated Semen and New Thawing Procedure, J. An. Sci. 40, 99. 36. Pursel, V. G. and Johnson, L. A. (1975) Frozen Boar Sperma- tozoa: Methods of Thawing Pellets. J. An. Sci. 42, 927. 37. Sone, M., Ohmura, K. and Bamba, K. (1982) Effects of Various Antibiotics on the Control of Bacteria in Boar Semen. Vet. Rec. Ill, 11. 38. Stratman, F. W. and Self, H. L. (1961) Comparison of Natural Mating with Artificial Insemination and Influence of Semen Vol- ume and Sperm Numbers on Conception, Embryo Survival and Litter Size in Sows, J. Anim. Sci. 20, 4, 708. 39. Swierstra, E. E. (1973) Influence of breed, Age and Ejaculation Frequency on Boar Semen Composition. Can. J. An. Sci. 53, 43. 40. Swierstra, E. E. (1974) A Comparison of Regular Ejaculation with Sexual Rest on Semen Characteristics and Reproductive Or- gan Weights in Young Boars. J. Anim. Sci. 39, 575. 41. Waltz, F. A., Foley, C. W., Herschler, R. C., Tiffany, L. W. and Liska, B. J. (1968) Bacteriological Studies of Boar Semen, J. An. Sci. 27, 5, 1357. 42. Wilmut, I. and Polge, C. (1977) The Low Temperature Preser- vation of Boar Spermatozoa. 3. The Fertilizing Capacity of Fro- zen and Thawed Semen, Cryobiology, 14, 483. Artificial Insemination in Sheep and Goats In the United States artificial insemination in sheep and goats has not generally passed from the experimental to the practical stage, although technically it has beenARTIFICIAL INSEMINATION 921 feasible for a long time.18,23'27,30 Artificial insemination with frozen goat semen has been used in a few goat dair- ies. In Russia, sheep have been artificially inseminated on a large scale for many years. In Australia, Argentina, Peru, France, East Germany and several countries it has been successfully practiced on a large scale. The advan- tages and the disadvantages of artificial insemination in sheep are much the same as in cattle. Probably the great- est disadvantages are its high cost when compared to nat- ural service and the difficulties associated with detecting and separating estrous ewes for insemination. With the current success in synchronizing ewes and the devel- opment of frozen semen, A.I. could make economical use of the best rams if sheep producers were properly trained to collect semen and inseminate ewes. It is very important that rams and bucks used for ar- tificial insemination be highly fertile in order to provide the maximum number of inseminations with a high con- ception rate. Collection of semen by means of an arti- ficial vagina is the preferred method. For rams not trained to the artificial vagina, electroejaculation can provide a satisfactory semen sample.3 Usually a fertile ram or buck can be collected 2 to 6 times or more daily to provide an adequate number of spermatozoa. There is only a moderate decrease in the number of sperm per ejaculate as the ram only ejaculates a limited volume of highly concentrated sperm. A typical ejaculate would contain 0.5 to 1.0 ml of semen with a sperm concentration of about 3 billion cells per ml. Much of the artificial insemination of ewes is done with freshly collected semen.23'25'27 30 Semen should not be chilled if it is to be used immediately. In warm weather (above 20° C) the semen can be allowed to cool to am- bient temperature or it can be maintained in warm water at 35° to 37° C. Excellent fertility can be obtained with ram semen used within a few hours as long as sufficient sperm (at least 100 x 106 sperm) are used in well-timed inseminations. This requires only 0.05 to 0.1 ml of nor- mal fresh ram semen to provide this many sperm cells.21 If unfrozen semen is to be held for several hours be- fore use,19’31 it can be extended at low rates of 1:1 up to 1:10 with heated skimmilk, heated homogenized milk or various combinations of 5 to 20 percent egg yolk with 2.9 percent sodium citrate dihydrate. Sometimes 0.5 to 1.0 percent glucose is added to this solution. Also Tris- yolk extenders, similar to those used for bull sperma- tozoa, have been used successfully. In glucose-saline buffers best results were obtained with only 1.5% egg yolk or less.32 Storage was at 5° C. When semen is to be stored for several hours it is especially important to use a large number of spermatozoa for insemination. In one study in which 25 x 106 versus 100 x 106 sperm cells were used for insemination fertility had declined after 5 hours of storage at 5° C, with the greatest decline when only 25 million sperm cells were used. Storage for 48 hours resulted in near zero fertility. However, Salamon23 compared the fertility of semen extended with a 300 mM Tris, 27.8 mM fructose, 95 mM citric acid plus 14 percent egg yolk when used fresh versus storage for up to 8 days. Then sperm were deposited surgically into the uterine horn. The inseminating dose was 200 x 106 sperm. The percentages of cleaved eggs when semen had been used after 0, 2, 4, 6 and 8 days of storage at 5° C were 95.5, 94.4, 91.3, 75.0 and 52.9. Correspond- ing samples inseminated normally (into the cervix) after 0, 2 and 4 days of storage at 5° C resulted in 62.5, 40.0 and 0% cleaved eggs. Thus, it is clear that the fertilizing ability of ram sperm can be maintained for many days at 5° C, but the ability for these sperm cells to pass the cervix and be transported to effect normal fertilization is lost rather rapidly during storage. There has been considerable success with frozen se- men.4,20'23 Again, part of the disappointing results with early frozen semen tests was the greater difficulty in fro- zen sperm passing the cervix as compared with unfrozen sperm cells. It has been recommended that ewes be tested for the possibility of intrauterine semen deposition via the cervical canal before expensive frozen semen is used. The repeatability of penetration was 0.745.13 The extenders used for frozen semen are similar to fresh semen with the addition by glycerol.8 Pellets have been found to give good results with raw sperm frozen in a lactose or raffinose extender (166 mM raffinose, 68 mM sodium citrate, 15 percent by volume egg yolk and 5 percent by volume glycerol). After five years of stor- age at -196° C the lambing rate was 53 percent com- pared with 54 percent for frozen semen stored for two weeks.28 Maxwell et al.20 used a triscitric acid-glucose- egg yolk extender with 6 percent glycerol. Lambing rate with unfrozen semen was 83 percent compared with 55 percent for semen frozen in pellets. In another experi- ment comparing semen frozen in pellets versus straws the lambing rates were 52 and 29 percent, respectively. It is apparent that the fertility obtained with A.I. de- pends upon the extenders used, whether semen is used fresh, cooled and stored or frozen, how it is frozen and thawed,4 the number of sperm cells inseminated and the season and fertility of the ewes. Optimal insemination time is 12 to 24 hours after the onset of estrus. With fresh semen 100 x 106 sperm are recommended. With stored or frozen sperm 300 X 106 motile sperm are rec- ommended. If the timing of the insemination is ideal one insemination is sufficient,24 but many studies,16 partic- ularly in the field result in marked increases in fertility with a double insemination. The most difficult problem to solve in artificial insem-922 VETERINARY OBSTETRICS ination of sheep is the handling of large numbers of ewes under flock conditions, while still detecting and sorting for breeding the ewes that come into estrum. Rams with aprons, or vasectomized teaser rams may be turned in with the flock of ewes or led through the flock once or twice daily. Vasectomized rams remaining with the ewes can be painted on the brisket or wear jackets holding different colors of paint or chalk to mark the rump of the ewes that are in estrum. Marked ewes are sorted from the flock daily for insemination. This latter procedure has proven most satisfactory for large flocks. Ewes and does in estrum will often bleat, switch their tails rapidly, have an edematous vulva, seek out the ram or buck and stand to be mounted. Does in estrum only occasionally mount each other. Normally estrum lasts about 30 to 36 hours in the ewe and possibly a little longer in the doe. Ovulation occurs late in estrum. Insemination should take place the last half of estrum. If insemination is to take place only once in a heat pe- riod, this should be about 12 to 18 hours after the onset of estrum. Spermatozoa survive about 30 hours in the ewe’s genital tract. For insemination the ewe should be placed in a crate that holds her securely and makes ex- amination and insemination easy for the operator. In- semination is accomplished by lubricating and inserting into the ewe’s vagina a pyrex glass speculum about 18 cm. (7 inches) long, and 2 cm. (7/8 inch) in diameter. By means of a head light, flashlight, or speculum light the cervix is located and a graduated pipette attached to a syringe is introduced into the cervix and the semen deposited. A speculum with a built in light source is very convenient. Plans and procedures for the artificial in- semination of large numbers of sheep have been outlined- - as management is highly important for sav- ing labor and for good conception rates. It has been dem- onstrated that if artificial insemination of sheep and goats is carefully conducted during the natural breeding season the results will compare favorably with those produced by natural mating. Synchronization of estrus has been discussed else- where and descriptions can be found.21 It is equally im- portant with synchronized ewes to have all conditions optimal, including insemination with at least 200 x 106 sperm.16 Under proper management conditions ewes can be synchronized and a large number inseminated suc- cessfully with semen from high quality rams. Under the usual conditions on farms, natural breeding with good quality rams has been more successful. Goat A.I. can be carried out in a manner almost iden- tical to sheep. It has one distinct advantage for the owner of a small flock of does with close neighbors. The strong buck odor can be eliminated if the owner desires to use A.I. to impregnate the does. There are many recent pub- lications on artificial insemination in goats.10,11,14’29’30 Results can be very successful. In Norway Fougner10,11 reported that buck sperm frozen in Tris-citric acid-yolk extender developed for cattle gave a 63.4 percent con- ception rate when 3,240 does were inseminated in utero with 75 X 106 sperm. A similar extender has been used in Australia.26 There is a lysolecithin compound in goat seminal plasma which may cause coagulation in egg yolk extenders containing sodium citrate, but this may not be a problem with Tris-buffered egg yolk. Corteel6 has eliminated this problem by centrifuging the semen and removing of the seminal plasma. This procedure is gen- erally recommended. He also used milk extender con- taining 100 gm of skimmed milk powder, 0.194 g. of glucose, antibiotics and 100 ml. of distilled water in the final extender. This extender is heated to 85° C for 10 minutes and cooled. Semen should be extended prior to centrifugation to remove the seminal plasma and then extended again so that there will be 100 million motile sperm per insemination dose. Convenient packages for freezing semen are the 0.5 ml or 0.25 ml French straws manufactured for freezing bull spermatozoa. For insemination the doe should have the hind quarters elevated over a bale of straw. Or one person can grasp the doe by the hind legs, hold the head down between ones legs and elevate the hind quarters. This provides an ideal position for a second person to insert the semen through the cervix, if possible. The use of a speculum and head lamp is useful in locating the cervix. Experi- enced inseminators achieve a higher penetration of the cervix and a higher kidding rate (Aamdal)..2 The insem- ination should be performed 12 to 24 hours after the on- set of estrus. Does can be synchronized when cycling during the breeding season with progestagens15 or prostaglandin. The most thoroughly tested method is to insert intravaginal sponges which release a progestagen for 16 days. Administration of 400-600 IU of PMSG at the time of sponge removal brings most animals into estrus within two or three days. A discussion of the various proce- dures for does both during and outside the breeding sea- son is given by Smith.296 References Artificial Insemination in Sheep and Goats 1. Ahmed, S., Phelps, D. A., Foote, W. D. and Foote, W. C. (1977) Out of Season Breeding in Dairy Goats. Proc. W. Sect. Amer. Soc. An. Sci. 28, 199. 2. Ayers, J. L. and Foote, W. C. Edit. (1982) Proceedings of theARTIFICIAL INSEMINATION 923 Third International Conference on Goat Production and Disease. Dairy Goat Journal Pub. Co., Scottsdale, Az. 3. Cameron, R. D. A. (1977) Semen Collection and Evaluation in the Ram. The Effect of Method of Stimulation on Response to Electroejaculation, Austral. Vet. J. 53, 380. 4. Colas, G. and Guerin, Y. (1981) A New Method for Thawing Frozen Ram Semen. Theriog. 16, 623. 5. Corteel, J. M. (1977) Production, Storage and Insemination of Goat Semen. Proc. Symposium Management of Reproduction in Sheep and Goats, Am. Soc. An. Sci. 41, 57. 6. Corteel, J. M. (1981) Collection, Processing and Artificial In- semination of Goat Semen. In: Goat Production, Gall, C. Edit., Academic Press, London. 7. FAO. (1979) Buffalo Reproduction and Artificial Insemination. FAO Animal Production and Health Paper #13. 8. First, N. L., Sevinge, A. and Henneman, H. A. (1961) Fertility of Frozen and Unfrozen Ram Semen, J. An. Sci. 20, 1, 79. 9. Foote, W. C. (1979) Breeding Without Checking Estrus: A/I on a Fixed Time Schedule. Buckshot, Spring, 73. 10. Fougner, V. J. A. (1976) Uterine Insemination with Frozen Se- men in Goats, VUIth Intemat. Congr. on Anim. Reprod. & Ar- tificial Insem., Krakow 4, 987. 11. Fougner, V. J. A. (1979) Die Intrauterine Besamung der Ziege mit Tiefgefrorenem Sperma. Drei Jahre Praktischer Einsatz. Zuchthyg. 14, 104. 12. Fraser, A. F. (1962) A Technique for Freezing Goat Semen and Results of a Small Breeding Trial, Canad. Vet. Jour. 3, 5, 133. 13. Fukui, Y. and Roberts, E. M. (1977) Repeatability of Non-sur- gical Intrauterine Technique for Artificial Insemination in the Ewe. Theriog. 8, 77. 14. Herman, H. A. (1982) Artificial Insemination and Genetic Im- provement of Dairy Goats. American Supply House, Columbia, Mo. 15. Hogue, D. E., Hansel, W., Bratton, R. W. (1962) Fertility in Ewes Bred Naturally and Artificially after Estrous Cycle Syn- chronization with an Oral Progestational Agent, J. An. Sci. 21, 3, 625. 16. Langford, G. A., Ainsworth, L. and Wolynetz, M. S. (1982) Reproductive Response of Progestagen-treated Sheep in Con- finement to a Single and Double Insemination. J. An. Sci. 54, 12. 17. Langford, G. A. and Marcus, G. J. (1982) Influence of Sperm Number and Seminal Plasma on Fertility of Progestagen-treated Sheep in Confinement. J. Reprod. Fert. 65, 325. 18. Lunca, N., Otel, V., Paraschievescu, M. and Seserman, O. (1961) Progress Realized by Artificial Insemination in Sheep with Di- luted Semen, Proc. 4th Intemat. Congr. on An. Reprod., the Hague. 19. Martin, I. C. A. and Watson, P. F. (1976) Artificial Insemi- nation of Sheep: Effects on Fertility of Number of Spermatozoa Inseminated and of Storage of Diluted Semen for up to 18 Hours at 5° C. Theriog. 5, 29. 20. Maxwell, W. M. C., Cumock, R. M., Logue, D. N. and Reed, H. C. B. (1980) Fertility of Ewes Following Artificial Insemi- nation with Semen Frozen in Pellets or Straws, A Preliminary Report. Theriog. 14, 83. 21. Morrow, D. A., ed. (1980) Current Therapy in Theriogenology. W. B. Saunders Co., Philadelphia. 22. Salamon, S. (1971) Fertility of Ram Spermatozoa Following Pellet Freezing on Dry Ice at -79 and -140°C. Austral. J. Biol. Sci. 24, 183. 23. Salamon, S. (1976) Artificial Insemination of Sheep, University of Sidney, N.S.W., Australia. 24. Salamon, S. (1977) Fertility Following Deposition of Equal Numbers of Frozen-Thawed Ram Spermatozoa by Single and Double Insemination. Austral. J. Agric. Res. 28, 477. 25. Salamon, S., Maxwell, W. M. C. and Firth, J. H. (1977) Fer- tilizing Capacity of Ram Spermatozoa Stored at 5° C. Theriog. 8, 200. 26. Salamon, S. and Ritar, A. J. (1982) Deep Freezing of Angora Goat Semen: Effects of Diluent Composition and Method and Rate of Dilution on Survival of Spermatozoa. Austral. J. Biol. Sci. 35, 295. 27. Salamon, S. and Robinson, T. J. (1962) Studies on the Artificial Insemination of Merino Sheep, Austral. J. of Agric. Res. 13, 1, 52. 28. Salamon, S. and Visser, D. (1974) Fertility of Ram Sperma- tozoa Frozen-Stored for 5 Years. J. Reprod. Fert. 37, 433. 29a. Shelton, M. (1978) Reproduction and Breeding of Goats. J. Dairy Sci. 61, 994. 29b. Smith, M. C. (1980) Caprine Reproduction, in Current Therapy in Theriogenology, Ed. D. A. Morrow, W. B. Saunders Co., Philadelphia, 971-995. 30. Terrill, C. E., edit. (1977) Proceedings. Management of Re- production in Sheep and Goats Symposium. Univ. of Wise., Madison, Wise. 31. Watson, P. F. and Martin, I. C. A. (1976) Artificial Insemi- nation of Sheep: The Effect of Semen Diluents Containing Egg Yolk on the Fertility of Ram Semen. Theriog. 6, 559. 32. Watson, P. F. and Martin, I. C. A. (1976) Artificial Insemi- nation of Sheep: The Fertility of Semen Extended in Diluents Containing Egg Yolk and Inseminated Soon After Dilution or Stored at 5° C for 24 or 48 Hours. Theriog. 6, 553. Artificial Insemination in Dogs Artificial insemination is performed most commonly in dogs for reasons that prevent or interfere with copu- lation.11 These include: shyness or fright on the part of either the male or female in the presence of their partner, lack of libido often associated with sexual inexperience in the male or for pathological reasons, including pre- mature erection preventing intromission, phimosis due to a small preputial orifice, painful lesions such as arthritis, spinal lesions, acute prostatitis, and exhaustion espe- cially in obese, young or old, inexperienced dogs on hot humid days. It may also be used for the control of in- fectious diseases such as caused by Brucella canis. The American Kennel Club has not encouraged the practice of artificial insemination, but will allow it to be per- formed under certain restrictions and stipulations, in- cluding the issuance of an affidavit by the sire’s owner certifying that he witnessed the collection of semen and the insemination by a licensed veterinarian, and another by the veterinarian certifying that he performed the col- lection and insemination in the presence of the sire’s owner. The male and female dogs are identified and the time and place of insemination is indicated. Relatively924 VETERINARY OBSTETRICS little controlled experimental work has been done with artificial insemination in the dog but the techniques of semen collection and insemination are fairly sim- pjei,6.9,10,12,13 an(j the proce(]ure js 0ften employed by vet- erinarians. The favored method of semen collection is by digital manipulation of the penis, with or without the presence of a teaser bitch, to produce ejaculation.6,1012 Semen may also be collected by means of the artificial vagina. A special vagina has been designed with a closed balloon in the space between the liner and casing attached to a bulb which, when squeezed, caused a pulsating pressure on the penis simulating the contractions of the vulva of the bitch.9 This artificial vagina could be used with or without a teaser bitch. In contrast to the good results reported with this A.V., another study1 reported poor motility in the semen collected with the artificial vagina possibly due to overheating of the spermatozoa in the vagina. Digital manipulation is simpler and requires less equipment and produces as good or better semen sam- ples. Dogs may be collected every other day without loss of semen quality. Good quality canine semen should have 70 to 90 percent actively motile sperm cells, less than 10 to 20 percent abnormal cells and a concentration of 90 to 300 million or more spermatozoa per ml, depend- ing upon the amount of prostatic fluid collected. Semen should be collected in a warm funnel and a 20 ml warmed test tube or a 20 to 30 ml warmed syringe from which the barrel has been removed. Immediately after collection the semen should be placed in warm water at 35° C. if it is not to be used promptly. Undiluted se- men, in vitro, usually survives about 20 hours. Sper- matozoa in extended semen remains viable and capable of fertilizing ova for 4 to 5 days if stored at 5° C. or 40° F.9,12 Harrop9 preferred heating pasteurized homog- enized milk to 92° C. for 10 minutes. The albuminous scum was removed and 500 |xg of streptomycin per ml was added. This extender was used at an extension rate of about 1 to 8, with the semen and extender both at either body temperatures, room temperature or refrig- erator temperature when added together to avoid cold shock. Foote4'7 reported that the best extender for canine semen was 20 percent egg yolk in a buffer solution com- posed of 1.45 gm of sodium citrate dihydrate, 0.93 gm of glycine, and 1.25 gm. of glucose per 100 ml of dis- tilled water. The extension rate was 1:10 to 1:20. Each ml of buffered-egg yolk extender contained 1000 units of crystalline penicillin G. and 1 mg of dihydrostrepto- mycin. This extended liquid semen could be stored at 40° F. or 5° C. for 24 hours before insemination. Good motility was still present after 4 days but no fertility trials were made. Subsequently,8 use of the same tris-buffered egg yolk with glycerol, as is used for cattle, resulted in high pregnancy rates when semen was stored for 24 hours at 5° C. From 100 to 200 X 106 motile sperm per in- semination were required. There were no pregnancies with frozen semen. It has been demonstrated that milk ex- tended liquid semen may be shipped over long distances and produce conceptions.9 The first successful pregnancies from frozen canine semen was 1969.17 There have been several reports since that time.1314 Some have used a lactose-egg yolk method devised for pelleting bull semen.17 Others have used the tris-fructose-citric acid egg yolk extender also developed for bull semen. Semen can be packaged in 0.25 or 0.5 ml straws. After cooling the semen, it can be frozen sim- ilar to bull semen. Considerable research still is needed because there is little quantitative evidence of the suc- cess rate with frozen canine semen. Insemination should be performed with undiluted or extended semen 24 to 48 hours after the onset of the estrus. That is the time when the bitch will accept coitus by the dog. A second insemination given one to two days after the first may increase conception rate. Usually at this stage the vulva is still swollen, the vulvar discharge is frequently clear instead of hemorrhagic as in proes- trum, and vaginal smears reveal many comified epithe- lial cells and few red blood cells. The bitch usually ovu- lates by the second or third day of estrus, but the ova require several days to mature and shed the polar bodies. Spermatozoa survive 4 to 6 days or more in the female genital tract.2 Conception is less likely late in estrus or early in postesrus when many leucocytes are present in the vaginal smear. Vaginal smears may be taken with a cotton swab on a six inch applicator stick, placed on a slide and stained with Wright’s or other stain. A sterile plastic inseminating tube, or pipette, about 20 cm. (8 inches) long and 6 mm. in diameter is fixed to a syringe and the semen is drawn into the syringe. A bovine plastic inseminating pipette broken in half makes a good canine inseminating tube. Most bitches in true estrum stand quietly to be inseminated even though pre- viously they may have resisted normal mating. They should be placed on a table of proper height and held by an assistant. The external genitals are washed and dried. Some veterinarians use a lubricated vaginal speculum and light to locate the cervix, and the insemination tube is placed at or into the cervix where 5 to 10 ml or more of undiluted or extended semen containing about 200 mil- lion actively motile spermatozoa should be deposited. Most operators insert the insemination tube without a speculum. In this technique the insemination tube is in- serted between the vulvar lips and directed in a dorsal direction until it passes into the vagina. It is then di-ARTIFICIAL INSEMINATION 925 rected horizontally and gently pushed to or into the cer- vix. It is desirable to elevate the rear parts of the bitch for 3 to 5 minutes after insemination to prevent the pos- sible loss of semen. A finger covered with a sterile fin- ger cot may be inserted into the vagina and the dorsal wall gently stroked or “feathered.” This appears to pro- mote the passage of the semen into the uterus. Usually 60 to 80 percent conception rates are realized by artifi- cial insemination with fertile dogs using unfrozen se- men. A technique for intrauterine insemination has been described.13 Artificial Insemination in Cats Studies on the reproductive physiology and insemi- nation of cats has been very limited because of their gen- eral economic value, and the belief that cats are difficult to handle, especially during mating. Sojka et al. 18 de- scribed successful procedures for the insemination of cats. Donor toms were selected on the basis of their libido and temperament when a “teaser” queen was placed in the tom’s cage. Teaser queens were either normal females in estrus or ovariectomized females that had been given 1.25 mg. Repositol diethlstilbesterol subcutaneously every 10 days to produce estrus and acceptance. The selected toms required about 2 weeks of training by a technician to get them to ejaculate routinely into an artificial va- gina. The artificial vagina was made by cutting off the bulb end of a 2 ml rubber bulb-pipet and fitting a 3 x 44 mm test tube into the cut end of the bulb to make a water tight system. The artificial vagina is then placed in a 35 x 75 mm (60 ml) polyethylene bottle filled with water at 52° C. to maintain a temperature of 44 to 46° C. at the time of collection. The rolled end of the rubber bulb- pipet is stretched over the rim of the bottle and the open- ing of the vagina is sparingly lubricated with K-Y jelly. The artificial vagina is slipped over the penis of the tom as he mounts the teaser female and develops an erection. The technicians other hand is used to steady the tom and queen. The volume of the ejaculate varied from 0.01 to 0.12 ml, with an average of 0.04 ml.18 The sperm cell num- bers per ml of ejaculate varied from 100 to 5,100 X 106 with an average of 1730 x 106. The total sperm numbers per ejaculate varied from 3 to 143 x 106 with an average of 57 x 106. The motility varied from 35 to 100 percent with an average of about 80 percent. Collection of the semen takes about 1 to 4 minutes with a trained tom. Toms could be collected 3 times a week on a regular basis or daily for short periods and maintain good semen quality. Methods of electroejactulation have been re- ported.15 The average volume for 303 ejaculates from 17 toms was 0.23 ml, with a mean of 28 X 106 sperm per ml ejaculate and 60 percent of the sperm being motile. The toms were anesthetized with ketamine hydrochloride (33 mg/kg of body weight). Thus, semen collected with the electroejaculator had a higher volume, much lower sperm concentration and fewer sperm per ejaculate, than semen collected with an artificial vagina. Females bred by artificial insemination can be checked for estrus daily by stroking them on the neck and down the back to the base of the tail and by gently rubbing the perineal region. A queen in estrus will crouch on its ster- num, elevate the pelvis, raise and laterally deflect the tail, extend the hind legs, tread with the hind feet and press against the hand when it is held over the pelvic region. Estrus can be confirmed by vaginal smears which contain only large, comified cells during the height of estrus. Queens are induced ovulators. Queens in full, natural estrus were stimulated to ovulate by the intra- muscular injection of 50 I.U. of HCG.18 The queen was also inseminated at this time by placing 0.1 ml of the saline-diluted semen containing 50 X 106 spermatozoa into the anterior portion of the vagina with a 20 gauge needle, 9 cm long, bulbed at the end with silver solder to make it blunt and attached to a 0.25 ml syringe. A second insemination 24 hours later increased the con- ception rate. These authors18 found that all queens in estrus would ovulate 26 to 27 hours after the injection of HCG. Suc- cessful matings occurred up to 49 hours after HCG in- jection. The queens would accept toms up to 55 hours after the injection. It was also reported that queens in full estrus could be stimulated to ovulate by probing the cervix with a glass rod. This, and the act of artificial insemination at the time the rod or pipette contacted the cervix, often resulted in a characteristic yowl followed immediately by an attempt to lick the perineal region. Thus, the spines on the penis are probably not the cause for this postcoital reaction in the female. Conception did not occur in queens inseminated with less than 1.25 million spermatozoa. The conception rate was 54 percent (14/26) with 5 to 50 million spermatozoa per insemination. In these insemination experiments18 the gestation periods ranged from 65 to 72 days, which is nearly a week longer than the 56 to 63 day period that follows natural matings. This should receive further study. Thus, by artificial insemination outstanding toms could be used to breed 12 to 15 queens per ejaculate, compared to natural mating conditions where one tom is usually kept per 15 to 30 females. There are limited data on freezing feline spermato- zoa.16 Semen was collected 6 months by electroejacu-926 VETERINARY OBSTETRICS lation followed by 6 months with an artificial vagina. The extender was composed of the one used frequently for pellets, containing 20 percent egg yolk by volume, 76 percent of a 11 percent (w/v) solution of lactose and 4 percent by volume of glycerol. Semen was pelleted. Subsequently 56 queens were inseminated in estrus with 50 x 106 or 100 x 106 motile sperm. Six became preg- nant, one from semen obtained by electroejaculation and 5 from semen collected with an artificial vagina. Preg- nancies lasted 65 to 71 days, with 1 to 4 kittens per litter. References Artificial Insemination in Dogs and Cats 1. Boucher, J. H., Foote, R. H. and Kirk, R. W. (1958) The Eval- uation of Semen Quality in the Dog and the Effects of Frequency of Ejaculation Upon Semen Quality, Libido and Depletion of Sperm Reserves, Cornell Vet. 48, 67. 2. Doak, R. L., Hall, A. and Dale, H. E. (1967) Longevity of Sper- matozoa in the Reproductive Tract of the Bitch, J. Reprod. and Fert., 13, 51. 3. Foote, R. H. (1964) The Effects of Electrolytes, Sugars, Glycerol and Catalase on Survival of Dog Sperm Stored in Buffered-Yolk Mediums, Am. J. Vet. Res. 25, 104, 32. 4. Foote, R. H. (1964) The Influence of Frequency of Semen Col- lection, Fractionation of the Ejaculate and Dilution Rate on the Survival of Stored Dog Semen, Cor. Vet. 54, 1, 89. 5. Foote, R. H. (1964) Extenders for Freezing Dog Semen, Am. J. Vet. Res. 25, 104, 37. 6. Foote, R. H. (1968) Current Veterinary Therapy, Edit, by Kirk, R. W., 3rd Ed. W. B. Saunders Co., Philadelphia, London and Toronto. 7. Foote, R. H. and Leonard, E. P. (1964) The Influence of pH, Osmotic Pressure, Glycine, and Glycerol on the Survival of Dog Sperm in Buffered-Yolk Extenders, Cor. Vet. 54, 1, 78. 8. Gill, H. P., Kaufman, C. F., Foote, R. H. and Kirk, R. W. (1970) Artificial Insemination of Beagle Bitches with Freshly Collected, Liquid-Stored and Frozen-stored Semen. Am. J. Vet. Res. 31, 1807. 9. Harrop, A. E. (1962) In: The Semen of Animals and Artificial Insemination, Edit, by Maule, J. P., Commonwealth Agric. Bur- eaux, Famham, Royal Bucks, England. 10. Kirk, R. W. (1959) Artificial Insemination in the Dog, Allied Vet. 30, 2, 38. 11. Kirk, R. W. (1968) Canine Medicine, Edit, by E. J. Catcott, Amer. Vet. Public, Inc. Wheaton, 111. 12. Leonard, E. P. (1968) In: The Artificial Insemination of Farm Animals, Edit, by Perry, E. J. 4th Ed., Rutgers Univ. Press, New Brunswick, N.J. 13. Morrow, D. A. (1980) Current Therapy in Theriogenology. W. B. Saunders Co., Philadelphia. 14. Platz, C. C., Jr. and Seager, S. W. J. (1977) Successful Preg- nancies with Concentrated Frozen Canine Semen. Lab. Anim. Sci. 27, 1013. 15. Platz, C. C., Jr. and Seager, S. W. J. (1978) Semen Collection by Electroejaculation in the Domestic Cat. JAVMA 173, 1353. 16. Platz, C. C., Jr., Wildt, D. E. and Seager, S. W. J. (1978) Preg- nancy in the Domestic Cat after Artificial Insemination with Pre- viously Frozen Spermatozoa, J. Reprod. Fert. 52, 279. 17. Seager, S. W. J. (1969) Successful Pregnancies Utilizing Frozen Dog Semen. A.I. Digest 17, 12, 26. 18. Sojka, N. J., Jennings, L. L. and Hamner, C. E. (1970) Artificial Insemination in the Cat (Fetus catus L.), Lab. Animal Care, 20, 2, 198. Other Species Semen collection and artificial insemination has been reported for many other species.2,3 One ruminant of con- siderable importance in many countries is the buffalo.1 Many of the techniques developed for cattle are useful in buffaloes. However, libido may be less and there are many problems associated with collection of semen from males and detection of estrus in females. Part of the lat- ter problem is associated with the small group of females and their general management in areas where buffaloes are kept. When A.I. is properly carried out, semen can be preserved and females impregnated successfully. Artificial insemination has been used by geneticists for multiplying stocks of chickens for decades. This tech- nique is standard practice in the turkey industry where selection for extensive breast meat has resulted in dif- ficulty in natural mating. There are hundreds of refer- ences in this field. To date most of the inseminations involve freshly collected semen as fertility declines rap- idly with storage. Fertility is reduced by freezing the sperm cells. Currently, the information on artificial insemination is very fragmentary for most non-domestic species. There is great interest in using this technique to perpetuate en- dangered species. It has been used quite successfully in several species. One of the problems in mammals, even when semen has been collected and apparently frozen successfully, is to be able to detect estrus in the female. One of the species of great interest which has been re- produced by artificial insemination in China is the great panda. Experiments with this species and many others have been initiated in recent years at several of the large zoos around the world and preliminary success has been reported in the popular press. References Artificial Insemination in Other Species 1. FAO. (1979) Buffalo Reproduction and Artificial Insemination. FAO, Rome. 2. Seager, S. W. J., Wildt, D. and Platz, C. (1980) Semen Collection by Electroejaculation and Artificial Vagina in over 100 Species of Zoo Mammals. 9th Intern. Congr. Anim. Reprod. & A.I., Madrid II, 571. 3. Watson, P. F., edit. (1978) Artificial Breeding of Nondomestic Animals. Symposia 43 of Zool. Soc. London, Academic Press, NY.Chapter XX EMBRYO TRANSFER By Maarten Drost, DVM* History Nearly a century has passed since Sir Walter Heape in 1890 successfully transferred the first fertilized ova between rabbits.22 A number of viable transfers were subsequently reported for laboratory animals such as guinea pigs, mice, rats and rabbits, but it was not until 1932 that Warwick, Berry and Horlacher made the first successful transfers in domestic sheep and goats in the United States.40 Then in 1951 Willett, Black, Casida, Stone and Buckner in Wisconsin reported the first suc- cessful ovum transfer in cattle using surgical technics.42 Rowson and coworkers firmly established the surgical technic as a research tool in cattle, sheep and goats dur- ing the 1960’s. Rowson and his colleagues were also the first to produce a calf after the 11-day blastocyst had been frozen prior to transfer.43 The introduction of “ex- otic” (European) breeds into North America in the early 1970’s precipitated a major impetus of the application of the technic. By the end of the decade the approach had shifted from surgical to nonsurgical technics in cattle. As with artificial insemination 25 years earlier, embryo transfer has found its widest application, for economic reasons, in cattle. In livestock the technic of embryo transfer permits the transfer of embryos from genetically superior animals in a population to the less desirable ones. In research, the application of embryo transfer is perhaps limited only by the imagination, and has already provided insight into the causes of early embryonic death, early maternal rec- ognition of pregnancy, maternal-fetal interrelationships and inter-species crosses. The process of embryo trans- fer is a factorial one whereby each step may limit the number of offspring bom, and whereby the end result is the product of the various probabilities involved. Embryo Transfer in Cattle Donor Selection The owner selects his donor animals on the basis of performance and genetic merit, criteria which are gen- *Professor of Reproduction, Department of Reproduction, College of Veterinary Medicine, University of Florida, Gainesville, Florida. erally more readily available for the older dairy cow than for the beef cow, and preferably would include data for a proven sire she produced. The role of embryo transfer in cattle improvement programs has been reviewed and placed in perspective elsewhere.9,24 Criteria applied by the owner do not automatically make the donor a good prospect for embryo transfer. The do- nor cow or heifer must be in good body condition and preferably gaining weight. She should be free from un- derlying disease, a minimum of 50-60 days postpartum and cycling regularly. Generally, cows with a history of reproductive problems do not make good donor animals. Donors are evaluated further by rectal and vaginoscopic examinations. Vaccinations should be current for infec- tious bovine rhinotracheitis, bovine viral diarrhea, lep- tospirosis (five types) and clostridial diseases. Brucellosis and tuberculosis tests should be performed and in the event of export, additional tests for blue tongue vims, leukemia and anaplasmosis. Bloodtyping of the donor for subsequent identification of offspring is re- quired by some breed associations and must be done be- fore embryo transfer. Accurate heat detection methods are also intensified. Donor Treatment Single embryos or multiple embryos may be collected from naturally ovulating or superovulated cows respec- tively. For optimal efficiency 2 to 4 donors should be treated and synchronized with their recipients for each attempt, this allows the sharing of the recommended po- tential 8 to 10 recipients per donor. Superovulation remains the least predictable step in the process of embryo production. Tremendous variation in response occurs with age, breed, lactational status, nutritional status, season and stage of the cycle at which treatment is initiated. The most commonly used super- ovulatory regime for cows in North America involves the use of follicle stimulating hormone (FSH). The short half-life of FSH necessitates twice-daily injections over a period of 4 to 5 days (Table 27). Treatment is begun during the mid-luteal (day 8 to 14) phase of the donor’s cycle and employs the use of prostaglandins (PGF2alpha)928 VETERINARY OBSTETRICS Table 27. Superovulation Treatments in the Cow Day Treatment I Treatment II -14 donors and recipients 25 mg PGF2alpha -5 am 5 mg FSH pm 5 mg FSH 7 mg FSH 7 mg FSH -4 am 5 mg FSH pm 5 mg FSH pm recipients 25 mg PGF2alpha 6 mg FSH 6 mg FSH recipients 25 mg PGF2alpha -3 am 5 mg FSH am donors 35 mg PGF2alpha pm 5 mg FSH 5 mg FSH donors 35 mg PGF2aIpha 5 mg FSH -2 am 5 mg FSH pm 5 mg FSH 4 mg FSH 4 mg FSH -1 am 5 mg FSH pm (5 mg FSH) 3 mg FSH (3 mg FSH) 0 Estrus, AI 8 hours after onset of estrus, repeated twice at 12-hour intervals. to synchronize the cycles of the donors and the recipi- ents. Alternately, treatment may be initiated on day 16 or 17 (day 0 = estrus) of the donor’s estrous cycle. Dose levels of FSH vary from decreasing levels of 7, 6, 5, 4, and 3 mg twice daily26 to increasing levels, or a uniform 5 mg twice daily 44 injection schedule. Colorado workers16 reported more ovulations, embryos recovered and preg- nancies after a superovulatory regimen with FSH and LH in a 5:1 ratio administered twice daily in decreasing doses for five days. Recent work29 has indicated that an im- proved response could be obtained when LH was not used. Consequently, two superovulatory regimens with only FSH are used today (Table 27).26 Prostaglandins (PG) (25-35 mg PGF2alpha or 500 meg PGF-analog (clopros- tenol) IM) are routinely given at the time of the fifth and sixth FSH injection which is then followed by estrus and ovulation in 2 and 3 days. This interval from PG to the onset of estrus is 12 to 24 hours shorter in superovulated animals than in naturally ovulating cows. Consequently, recipients should be injected with PGS 12 to 24 hours before the donors if this method of synchronization is used. The response to the foregoing FSH regimens ranges from zero to as many as 50-60 ovulations with an av- erage of 8 to 12. None of the specific dose levels cited has shown a consistent advantage. When a donor has failed to respond to the superovulatory treatment, the second attempt to superovulate her with the same or a similar regimen is also likely to result in failure. It is difficult to accurately assess the number of ovulations by palpation of the ovaries per rectum when the number exceeds 4 to 6 per ovary or when several anovulatory follicles are present. It is felt that an excessive number of anovulatory follicles in the presence of corpora lutea adversely influences the recovery percentage because of an unfavorable estrogen/progesterone ratio which alleg- edly affects gamete and embryo transport. Pregnant Mare Serum Gonadotropin (PMSG) has also been widely used for superovulation. Food and Drug Administration regulations have severely restricted its importation from the traditional South American sources for disease control reasons. While PMSG has the ad- vantage of requiring only a single injection, its half-life is perhaps too long as measurable levels could still be detected in the blood of cows 10 days after the admin- istration of 1500 to 3000 IU PMSG."8 The FSH/LH ratio of PMSG ranges from 1.9 to 95.5 and depends on the stage of gestation at which the serum was collected.23 PMSG is a crude product and as such is difficult to stan- dardize. It is a foreign protein that is antigenic, which may lead to a reduced response after repeated use5 38 PMSG may be injected SC or IM on day 16 or 17 of a normal estrous cycle. Doses range from 1500 to 3000 IU, but 2000 to 2500 IU are most commonly used. When used in conjunction with PG, PMSG is administered be- tween day 9 to 12 of an estrous cycle followed by PG 48 to 72 hours later. PMSG injections initially exert a luteotropic effect that has been related to its LH activity. LH is presumed to be responsible for the occasional pre- mature ovulation of a large follicle present at the time of the PMSG injection. The precocious CL is believed to inhibit further ovulations, perhaps because it is not old enough to be lysed by PG given 2 days later, yet secretes enough progesterone to block endogenous LH release. Equine Pituitary Extract and Human Menopausal Go- nadotropin are infrequently used. Equine pituitary ex- tract was used successfully to superovulate beef heif- ers.12 A single daily injection for three days appeared to be adequate with 75 percent of the cows responding with 5 or more ovulations. In a trial involving 20 cows, Hu- man Menopausal Gonadotropin (equal FSH and LH ac- tivities) when compared with FSH was found to be equally effective.11 There is no need to give the donor GnRH or LH at the onset of estrus in an attempt to precipitate or to group ovulations. There is also no benefit from the injection of a physiological dose of estradiol (500 meg) at the antic- ipated time of onset of estrus to intensify the expression of heat.10EMBRYO TRANSFER 929 Insemination of the Donor In the presence of hormonally stimulated ovulations, fresh semen gives higher fertilization rates than frozen semen.20 This probably reflects the number of viable spermatozoa in the inseminating dose. Donors should be artificially inseminated 2 to 3 times at 10 to 12 hour intervals beginning 8 to 10 hours after the onset of es- trus, to cover the range of time over which the ovula- tions may occur. Depending on the quality of the frozen semen, it is common practice to use a double insemi- nating dose at each insemination. Embryo Recovery Embryo recovery technics have evolved from slaugh- ter of the donor animals via surgical collection from the anesthetized live animal to nonsurgical embryo recovery from the standing animal. There are several detailed de- scriptions of the surgical procedures in the literature.13,14 The advantages of the surgical approach are that the pa- tient is immobolized, that sterile technic is possible, that the uterus can be manipulated directly, that the ovarian response can be accurately evaluated, that only 20 to 50 ml of recovery medium are needed and that the proce- dure can be carried out prior to the fifth day after estrus. However, the major disadvantage is the formation of adhesions which limits surgical collections to 1 or 2 op- erations without lowering reproductive efficiency. The midventral surgical approach further requires operating room facilities and brings with it the risks of general anesthesia. It is difficult in lactating animals with large udders. Nonsurgical embryo recovery on the other hand is re- peatable with relative impunity, it can be performed on the farm, neither fasting nor surgical risk are involved and probably fewer assistants are needed. However, nonsurgical recovery does require considerable manip- ulative skill and can only be performed in animals in which the cervical canal is passable, and must be done after day 5. Nonsurgical Embryo Recovery Bovine embryos descend into the uterus around day 4.5 to 5 (estrus = day 0) and shed their zona pellucida (“hatch”) around day 8.5 to 9. Consequently, most non- surgical recoveries are made between days 6 and 8. A 2-way or 3-way, roundtip Foley catheter (French size #12-20) with a 30 ml inflatable balloon is used. The 2-way catheter has one channel for inflation of the bal- loon plus a single channel for alternate inflow and out- flow of flushing medium. The 3-way catheter has sep- arate channels for inflow and return flow. A sterile stylet (such as the plunger of an insemination gun) is inserted the full length of the device to render it sufficiently rigid to allow introduction into the uterus under guidance per rectum. The donor is restrained in a squeeze chute or, in the case of a tractable dairy cow, in a stanchion. The feces are carefully removed from the rectum to avoid aspiration of air, and an estimate is made of the number of ovulations (CL). Inadvertent air can be removed from the rectum with a small stomach tube attached to a “wet- vac” vacuum cleaner. Epidural anesthesia is adminis- tered (4 to 6 ml 2 percent lidocaine) to prevent defeca- tion and straining. The vulva and perineal region are thoroughly washed and disinfected with 70 percent al- cohol, and the tail is tied out of the way. If the cervix feels small or tortuous, a cervical dilator14 may be used to gently expand and straighten the cervical canal. The rigid, relatively sharp-pointed dilator should be used with extreme caution as it can readily perforate the uterine wall as it is “forced” through the tight cervical canal. The lips of the vulva are again parted and the Foley cath- eter, with the stylet in place, is inserted into the vagina and on into the lumen of the expanded cervix. It is then manipulated into the appropriate horn until the inflatable balloon is situated at the base of the uterine horn. The balloon is slowly inflated with 15-25 ml of air in cows and 10-20 ml of air in heifers. The endometrium is eas- ily split by overdistension, resulting in hemorrhage and escape of the flushing solution into the mesometrium from which it cannot be recovered. After the catheter is in position, the stylet is removed and the inlet channel con- nected by sterile siliconized tubing to a 500 ml bottle of flushing solution. The outlet tubing channels the fluid directly through an embryo filter (75 um pore-Em-Con filter) placed well below the level of the uterus. When using the 3-way catheter, the flushing solution flows into the uterus by gravity with the bottle suspended one meter above the level of the uterus. The uterus is manipulated per rectum by alternately lifting and extending the tip of the horn and the intercomual ligament and by compress- ing the horn or pressing it against the pelvic wall. The out-flow tube may be clamped off periodically to allow build-up of the flushing medium in the uterus. In older cows with long pendulous tracts, manipulation of the cervix and uterus is facilitated by retracting the cervix into the vagina with cervical forceps. The flushing so- lution usually starts to flow back after 100 to 150 ml have entered the uterus of the cow, or 75 to 100 ml in the heifer. The filter should never be allowed to run completely dry leaving the embryos on the filter dish exposed to the air. A 1 cm layer of fluid can be main- tained by manipulation of a clamp on the tubing attached to the bottom of the filter unit. With the 2-way catheter a 60 ml catheter-tip syringe930 VETERINARY OBSTETRICS may be attached directly to the catheter. The medium is gently introduced and then allowed to flow back into the syringe, if necessary aided by gentle pull on the plunger. This process is repeated 6 to 7 times. Alternately, a Y- connector with inflow and outflow tubes is attached to the 2-way catheter and used in a manner similar to the 3-way catheter by alternately clamping off the outlet and inlet tubing. During the final collection of the flushing solution 50 IU oxytocin may be given IV to aid in the recovery of the last residual portion of the solution. In superovulated cows the procedure is repeated for the op- posite horn, using a separate sterile catheter. It is haz- ardous to re-insert the stylet into the Foley catheter while it is in the uterus because the sharp tip might come out one of the side openings. It is possible to pull the cath- eter back into the body of the uterus after partially de- flating the balloon, until the expanded balloon is held by the cervix. With the catheter stretched by pulling on the extended end, the stylet can be re-inserted until it reaches the tip where it can be palpated. Once the stylet is safely in place, the balloon is deflated and the Foley catheter once again placed one-third of the way into the selected horn. Some operators prefer placement of the catheter with the balloon in the cervix and the tip in the body of the uterus which enables them to flush the horns simul- taneously. Immediately after collection, dishes contain- ing media and embryos are placed in an incubator at 39C, but may be kept at 20C without loss of viability. How- ever, fluctuations in temperature must be avoided. Con- siderable dexterity, patience and practice are needed to achieve consistently satisfactory results. Flushing Media The most commonly used medium for nonsurgical embryo recovery is phosphate buffered saline (PBS). A modified solution is prepared by adding 1 percent heat- treated bovine serum'39 and 100 IU sodium penicillin G, 100 meg dihydrostreptomycin, 0.25 meg fungizone and 1 mg glucose per ml PBS and .33 mM sodium pyru- vate.2641 All culture media are passed through a dispos- able 0.22 micron millipore filter prior to use. Fetal bo- vine serum is added at a 20 percent concentration to the flushing medium to make a holding medium. It would seem that the glucose and pyruvate are only necessary for longer term culture of embryos, for “on-farm” use, media need only contain PBS, antibiotics and 1 to 2 per- cent bovine serum. Bovine serum contains a thermola- bile, embryotoxic factor which may be deactivated by heating to 56C for 30 minutes. The serum acts as a pro- tein source for embryo growth and membrane stabili- zation, and renders the embryos less sticky. Embryo Handling Identification and evaluation of embryos is one of the more difficult aspects and requires considerable experi- ence. The work area must be clean and free from dust. In- secticide sprays should be avoided; some sprays are ex- tremely toxic while the effect of others is unknown. Ex- treme temperatures are detrimental; stable temperatures are the key to success. The contents of the filter are poured into a (square 100 X 100 mm) grid searching dish and the filter disk is rinsed completely clean with plain PBS without serum by a forceful stream from a 35 ml syringe and a 22 ga needle. Then 5 to 7 ml of serum is added to the searching dish and stirred while clearing the bub- bles from the edge of the dish. After a brief settling period in the searching dish, the embryos are located as soon as possible so that they may be transferred to sterile holding medium containing 20 percent bovine serum. All dishes must be kept covered between searches to avoid contamination, and particu- larly evaporation, when placed in the incubator. Evap- oration of the small volume of medium in a flat dish rapidly leads to hypertonic solutions. Embryos are searched for and located at 10-15X mag- nification and evaluated at 70-100X using transmitting illumination (from below the stage). Embryos are picked up with a sterile, disposable Unipet attached with a short section of rubber tubing to a 0.5 ml syringe, or a short- ened sterile tomcat catheter attached to a small syringe, and deposited in a small sterile disposable petri dish (35x10 mm) containing fresh holding medium. In this way the embryos are rinsed and undesirable debris is re- moved. Formerly, recovery rates of embryos were improved by filtration after collection of the large volumes of non- surgical flushes.32 The technic used a nylon plankton mesh of 56-micron pore size. After filtration was complete, the sieve was backflushed with fresh medium which was subsequently allowed to settle for another 30 minutes be- fore examination. Morphologic evaluation of embryos is the only prac- tical method to determine the suitability for transfer. Such methods are subjective and depend very much on ex- perience.36 Diagrams of normal embryos at various stages of development are presented in Figure 206. The stage of development after fertilization must be appropriate for the day on which the embryo is collected. Embryos that are of doubtful quality can be cultured for a few hours. An improvement in appearance will suggest that the embryo is a candidate for transfer. A practical grading system based on morphology places embryos in good, fair and poor categories which pro-EMBRYO TRANSFER 1—cell Day 0-2 2—cell Day 1-3 931 4—cell Day 2-3 8—cell Day 3-5 16—cell Day 4-5 morula Day 5-6 tight morula Day 5-7 early blastocyst Day 7-8 blastocyst Day 7-9 expanded blastocyst Day 8-10 hatching blastocyst Day 9-11 Figure 206. Diagrams of Normal Bovine Embryos (adapted from Seidel, G. E. Jr., Seidel, S. M. and Bowen, R. A.35b).932 VETERINARY OBSTETRICS vides a basis for priority of transfer. A good embryo has a regular, round, symmetrical shape in contrast to a fair embryo which shows slight imperfections, an extraneous blastomere or has an odd shape, and a poor embryo which shows severe imperfections. Good embryos resulted in high pregnancy rates (65 percent) while fair and poor embryos resulted in a reduced number of pregnancies (45 and 33 percent respectively).44 It is of interest to note that good embryos were less sensitive to exact synchrony between the cycles of the donor and the recipient than fair and poor embryos. For optimal pregnancy rates, it is advisable to transfer embryos as soon as practical after collection. Enriched PBS allows embryo survival to remain constant for at least 7.5 hours. If embryos are not transferred within two hours from the initial rinse, they should be washed again by the same procedure. Short-term storage of bovine embryos is possible without significant adverse effects on embryo survival and pregnancy rates whether at 37C for 24 hours31 or at 4C for 48 hours.6 For long-term storage embryos are frozen to -196C in liquid nitrogen. Mammalian embryos must be stored in a quiescent state to retain viability for a long time. To freeze embryos, a cryoprotectant like dimethylsulfoxide or glycerol is required and slow cooling (0.1 to 2.0C/ min) and warming (1 to 50C/min) rates are used. Nu- cleation or seeding of the freezing medium is a neces- sity, and stepwise addition and removal of the cryopro- tectant at room temperature seems to be beneficial. Using the above parameters, embryos have been frozen and stored at - 196C for several years and upon thawing and transfer to a suitable recipient, viable offspring have de- veloped.27 Embryo morphology contributes to the success of the frozen-thawed technics: the presence of the zona pellu- cida protects37 and the presence of a blastocele appears to improve survival rates. Possibly each embryonic stage has its own optimal freezing and thawing requirements.19 Despite the losses, freezing is used commercially when recipients are not available. Frozen embryos offer a unique advantage for the marketing and distribution of embryos, be it for ex- port purposes or long distance transportation. Microsurgical technics applied to embryos include re- moving embryonic cells from, or transferring them into a zona pellucida, biopsy, dividing the embryo in half, aggregating them, injecting nuclei and removing mate- rial or structures such as pronuclei. Such manipulations make it possible to analyze chromosomes for sex deter- mination and to produce identical twins or multiplets. Eventually, it may be possible in livestock production to produce chimeras and homozygous diploid females, to clone by nuclear transplantation and to introduce exog- enous genes into pronuclei.35 Recipient Selection and Synchronization Recipients should be large-framed, healthy, mature heifers or young cows in good condition. A minimum of two normal cycles should have been recorded before use whether they are going to be synchronized with pros- taglandins or just selected from a pool of cycling ani- mals. It has been common in embryo transfer programs to overlook the quality of the recipients. Recipients and their maintenance represents the greatest single cost of running a commercial embryo transfer program. Culls from a breeding program, cattle in poor condition and early postpartum animals do not make suitable recipi- ents. Recipients should not be fat and should preferably be gaining 0.1 to 0.2 kg per day. They should be offi- cially calfhood vaccinated for brucellosis. Permanent (double) identification of each animal, me- ticulous record keeping, accurate heat detection, ample handling and quarantine facilities are all absolute essen- tials of reliable recipient management. Pregnancy rates are highest when the estrous cycles of the donor and the recipients are synchronized within 24 hours.44 Reason- able success can be achieved if they are out of phase by plus or minus one day, but results are too poor to be usable when they differ by two days. The availability of synchronous recipients can be achieved in three ways: 1) A pool of several hundred cycling females, which limits the number and times when donors can be collected. Five percent of the herd will be in heat on any given day. 2) Large commercial dairy farms can sometimes be persuaded to rent recipients which must of course not be inseminated. A fee will also need to be paid in the event a recipient is not used. 3) A rel- atively small number of recipients can be synchronized with PG to come in heat the same day as the donor. Animals with a palpable corpus luteum are injected with 25 mg PGF2alpha IM or 0.5 mg PG-analog and may be expected to come into estrus in 2 to 4 days with a peak on the third day. Alternately, all recipients may be in- jected with PG regardless of the presence or absence of a corpus luteum. The injection is repeated 11 days later and again estrus will peak on the third day after injec- tion. Those recipients which did not respond on the first occasion because they were in the first 5 days of the estrous cycle, respond the second time as they are then in the mid-to-late luteal phase; while the recipients that did respond are in the early-to-mid luteal phase at the time of the second prostaglandin injection.EMBRYO TRANSFER 933 The average donor yields 7 transferable embryos. Therefore, 8 recipients per donor is a reasonable number to prepare. When recipients are palpated for corpora lu- tea, about 20 are palpated in order to definitely identify 12 with corpora lutea on their ovaries. When 12 are in- jected with PG, 8 on the average will be suitably syn- chronized with the donor. Recipients must be injected with PG one day earlier than the donor. Due to prior gonadotropin treatment, the donor comes into estrus 48 hours after the PG, while the recipients which did not receive any gonadotropin treatment, will come into es- trus three days after PG. About 85 percent of fertile donors will respond to the superovulatory treatment on the first attempt. For opti- mal efficiency, 3 to 5 donors should be superovulated at the same time which permits the sharing of the prepared recipients and avoids the expensive failure encountered too frequently when only one donor is prepared at a time. Transfer Transfer of bovine embryos may be done either sur- gically or nonsurgically. The surgical approach seems to produce the most consistent results. Successful nonsur- gical transfer requires an even higher degree of dexterity and skill than does the nonsurgical recovery procedure. Surgical exposure of a uterine horn needs to be done via a midline incision if the recipient is a heifer with a short broad ligament or if she is to receive twin embryos. Halothane anesthesia provides excellent relaxation of the broad ligament. Single transfers are always made to the horn ipsilateral to the corpus luteum: twin embryos should be transferred to separate horns as uterine migration of embryos rarely if ever occurs in the cow. The horn is exteriorized by placing tension on the broad ligament over the distal portion of the horn. In cows, the incision may be made in the flank on the side of the corpus luteum as far caudally as possible with the animal in the standing position. In both approaches a small stab incision is made along the greater curvature about 7 cm from the tip of the exteriorized uterine horn with a small, closed mosquito forceps. The instrument characteristically “pops” through the endometrium. Care should be taken not to pass through the lumen into the endometrium and submucosa on the other side. The em- bryo is deposited in the lumen of the uterus via the stab incision with a fine, modified Pasteur pipet. Closure of the abdominal incision following either approach is by routine surgical methods. Nonsurgical transfers are made through the cervix similar to artificial insemination. It is important to min- imize contamination of the uterus because it is more sus- ceptible to infection during the luteal phase. Feces are evacuated from the rectum and the side of the corpus luteum is determined. Epidural anesthesia is induced to prevent defecation and to minimize straining. The per- ineal region is thoroughly washed and disinfected with 70 percent alcohol. The embryo is aspirated into a 0.25 ml French straw between two air pockets and two col- umns of culture medium. The straw is inserted into the AI gun and shortened to fit even with the end of the gun. A gas-sterilized 0.25 ml sheath is fitted over the AI gun and fixed in place. A second, sterile, large sheath which is closed at the distal end is fitted over the first to serve as a cannula and permits passage of the gun through the vagina without coming into contact with the vaginal flora. The tip is placed into the external os of the cervix and is then pushed through the sheath before it is guided as gently as possible through the remainder of the cervical canal and on into the uterine horn on the side of the corpus luteum. The embryo is deposited approximately one-third of the way up the uterine horn and the gun is withdrawn slowly. A negative correlation has been dem- onstrated between the time spent in the uterine horn and the pregnancy rate.33 Success is related to dexterity and practice. Pregnancy rates achieved by most operators improve with experience. The pregnancy rate after non- surgical transfer through the cervix is generally lower than that reported after surgical transfer. In the hands of some experienced embryo transfer practitioners, preg- nancy rates following nonsurgical transfer equal those after surgical methods. Pregnancy rates are higher (approximately 75 percent) after bilateral transfers to non-mated recipients or single transfers to mated recipients. The twinning rate of these recipients is 50 to 60 percent. As a consequence the em- bryo survival rate percent is not greater.2 Donor and Recipient Aftercare It is common practice to treat the donor with PG im- mediately after the collection of ova. At this time the ovaries are generally greatly enlarged by the excessive number of corpora lutea. Such treatment will not only rapidly reduce the size of the ovaries, but also terminate any unwanted pregnancies should an occasional embryo not have been flushed out. It is best not to breed the cow on this induced heat 2 to 4 days later. Furthermore, like a spontaneous heat, the induced heat will have a salutary effect on uterine health should any contamination have been introduced at the time of the collection. Cows can be superovulated at intervals of two months for three treatments without any appreciable decrease in re- sponse.18 Single embryo collections may be made be- tween these superovulatory treatments.934 VETERINARY OBSTETRICS Pregnant recipients should basically be managed like other pregnant cattle. Mature cows should be fed to gain 0.25 kg per day through the seventh month and 0.75 kg per day during the last 2 to 3 months. Heifer recipients should be fed to gain 0.5 to 1.0 kg per day depending on age, size and condition. Overly fat recipients are un- desirable. Pregnancy examinations are made at six weeks and confirmed at three months. Pregnancy loss after three months is less than 2 percent. Some recipients will be carrying large fetuses from breeds with a long gestation period and may—particularly when they are heifers— require delivery by cesarean section. Results Obtainable The following are average results for several large populations. Superovulation with FSH produces 8 to 12 ovulations per donor.18,34 Nonsurgical collections will yield 7 to 10 ova with 75 to 80 percent fertilization rates. Sin- gle embryos collected from nonsuperovulated cows tend to result in slightly higher pregnancy rates.18 34 Four to seven embryos are suitable for transfer.8,18,30 34 Surgical embryo transfer results in a 60 to 70 percent pregnancy rate, while nonsurgical pregnancy rates are 35 to 55 per- cent, a considerable attrition rate. The range of results varies a great deal from cow to cow; on the average, superovulation and embryo transfer results in four preg- nancies per attempt and can be repeated three times per year for an annual total of about 12 offspring. Cows With Reproductive Problems Valuable, infertile cows are often presented for em- bryo transfer. Many of these animals are classical repeat breeders with regular cycles and no palpable abnormal- ities of the reproductive organs. After a thorough phys- ical examination, nonsurgical embryo transfer technics may be used for examination of uterine contents and col- lection of ova. Cases of endometritis not diagnosed by rectal palpation may be obvious when excessive amounts of cellular debris are observed in the sediment of the flushing medium. If aseptic technics are used the sedi- ment may be submitted for bacterial culture. Cows with (a history of) cystic follicular degeneration must not be superovulated until after two normal estrous cycles have been observed. After the first observed es- trus each problem donor should be subjected to a single ovum recovery to determine: a) the condition of the uterus (nature of the flushing medium); b) if ovum transport is occurring; c) if the ovum was fertilized and d) the stage of development of the embryo.17 Cows with cystic fol- licles had fewer corpora lutea after superovulation than cows with uterine infections (4.1 vs 10.1). Furthermore, only 7 percent of the possible ova released (based on the number of corpora lutea) were fertilized, versus 60 per- cent in fertile donors. Also, significantly fewer ova and pregnancies per treatment were obtained from cows with cysts than from cows with adhesions. If an infertile donor does not respond with more than two corpora lutea to either of two superovulatory at- tempts, it is unlikely that a favorable response will be obtained. Embryo transfer can be used as a refined, so- phisticated technic for the diagnosis of infertility.3 21,25 Embryo Transfer in Horses Oguri and Tsutsumi in Japan reported the first suc- cessful nonsurgical recovery of equine eggs as early as 1972 and in 1974 the first successful nonsurgical transfer of 6 to 15 embryos.9 Allen and Rowson in England re- covered 11 embryos from 30 mares in 1975 and pro- duced 5 pregnancies after nonsurgically transferring 7 embryos.1 Donor Treatment The induction of superovulation in the mare has been very difficult. The mechanism of the marked resistance of the ovary of the mare to exogenous gonadotropic stimulation remains unknown. Prospects for induction of multiple ovulations and collection of multiple embryos in the mare have been reviewed.10 Pregnant mare serum gonadotropin, equine pituitary extracts with,3 and without, human chorionic gonadotro- pin (HCG)6 and porcine follicle stimulating hormone5 have all been tried with limited success. Single ovulations can be timed with HCG, 2000 to 3000 IU given intrave- nously on about the third day of estrus usually induces ovulation 24 to 72 hours later. Natural breeding or ar- tificial insemination are used when ovulation is antici- pated from palpation of follicles or following HCG in- jection. Embryo Recovery Surgical recovery technics were described by Allen and Rowson in 1975,1 and today are perhaps needed only for small ponies and experimental reasons. Nonsurgical technics have been adapted from those used for bovine embryos recovery. The easily dilatable cervix and straight uterine horns make the technic of embryo recovery rel- atively easier than in the cow. Although the embryo ar- rives in the uterus on day 6, most embryo recovery at- tempts are not made until 8 or 9 days after ovulation. The large size of the equine blastocyst on day 10 (5-7 mm diameter) precludes transfer of the blastocyst intact. An extended 2-way Foley catheter (French size 30) is used with simple in-out irrigation. The donor mare is confined in stocks and a thorough prebreeding prepara-EMBRYO TRANSFER 935 tion is done of the tail, perineum and vulva. The sterile catheter with a stylet in place is introduced per vaginam and passed through the cervix until it is approximately 5 cm into the uterine body. Its position is verified per rectum and the balloon is inflated with 75 ml air after which it is drawn back against the internal os of the cer- vix to form a seal preventing the escape of the flushing medium from the uterus. One liter of phosphate buffered saline containing 1 percent heat-treated bovine serum is infused into the uterus by gravity flow. Both uterine horns and the uterine body are flushed simultaneously. The re- turn fluid is collected in a prewarmed, sterile, one-liter graduated cylinder or embryo filter placed well below the level of the uterus. The procedure is repeated twice for a total of three liters per collection attempt. Mares predictably return to estrus 3 to 5 days after the flushing procedure in response to the endometrial stimulation.7 Synchronization of the Recipients Close synchrony of the times of ovulation of the donor mare and the recipient mare is desirable for maximal success.4 Synchronization of estrus in cycling mares may be achieved by a double prostaglandin treatment. All mares in a group are given a luteolytic dose of a prostaglandin (analog). Mares with a 4- to 13-day old corpus luteum will come into estrus on the third day after treatment and are given 2500 IU HCG IV on the sixth day. Those mares in estrus or with immature corpora lutea at the time of treatment will shortly become diestrous. Fourteen days after the initial injection of prostaglandin all mares are given a second luteolytic dose, and all mares are treated with 2500 IU HCG to synchronize ovulation. Identification of the Embryo The collection fluid is allowed to settle for 30 minutes before all but the bottom 100 ml are gently siphoned off, unless an embryo filter has been used. The day 8 post- ovulation blastocyst is 1 to 2 mm in diameter and can frequently be distinguished macroscopically. It can be readily transferred since it is not easily ruptured. Eval- uation of its suitability for transfer, like that of bovine embryos, is based on morphological appearance and stage of development in relation to the day of collection. After the embryo is located it is picked up with a fire-polished Pasteur pipet and passed through three consecutive small petri dishes (35 X10 mm) each containing a small amount of sterile phosphate buffered saline containing 20 per- cent heat-treated bovine serum. This procedure washes the embryo by the dilution of possible contaminants. The embryo is stored in a covered dish at 37C until transfer. Nonsurgical Transfer The recipient mare is prepared in a manner identical to the preparation of the donor. The embryo is aspirated into a sterile 55 cm insemination pipet in a 5 cm column of medium. The inseminator should wear a plastic pal- pation sleeve covered by a sterile surgical glove. The pipet is aligned with the index finger and a sec- ond, gas-sterilized sleeve is put on over the pipet. The lips of the vulva are parted and the hand is inserted into the vagina until the index finger has entered the cervix. At this time the pipet is pushed through the outer plastic sleeve and inserted 5 cm into the body of the uterus. Next the embryo is slowly discharged into the uterus. Upon withdrawal of the pipet and the hand from the va- gina, the lips of the vulva are held closed to prevent the aspiration of air into the vagina. The pipet is examined for the absence of the embryo by rinsing it with a small amount of medium into a petri dish.4 Although surgical transfer has been shown to yield higher pregnancy rates, practicality may dictate the use of nonsurgical technics. The surgical approaches are analogous to those used in other species and have been well described.4 In its research applications, the technic has already contributed much to our understanding of the reproduc- tive physiology and endocrinology of the estrous cycle, early development of the embryo and the early maternal recognition of pregnancy. The commercial application of embryo transfer will be limited to obtaining offspring from proven infertile mares and the management of older broodmares of the more enlightened breed associations, until the equine industry shows a genuine interest in the propagation of geneti- cally superior animals by relinquishing its restrictions on the use of artificial insemination and embryo transfer. The meager results obtained in the early 1980’s most likely relate to the ability to recover embryos from “problem” mares. At Colorado State University the re- covery rate from normal, fertile mares is 70 percent compared to only 26 percent from “problem” mares, mainly due to poor uterine environment or failure of un- fertilized ova to pass through the normal uterine tube. If 50 percent of these recovered embryos produce a preg- nancy after surgical transfer, the overall chance of suc- cess is one foal from eight problem donor mares. Embryo Transfer in Sheep and Goats Sheep and goats were the first species of large do- mestic animals to be used in embryo transfer experi- ments. Interestingly, the technic was employed to achieve intergeneric and interspecies transfers between goats and sheep.910 None of the pregnancies endured beyond 55936 VETERINARY OBSTETRICS days probably due to placental differences and diverging endocrine support of pregnancy. In the ewe the CL of pregnancy is no longer needed after 55 days of gestation7 while in the goat the CL is required throughout gesta- tion. Embryo transfer has remained an elegant research technic for the investigation of maternal-fetal interac- tions.2 There has been little if any commercial applica- tion in either sheep or goats. In many breeds embryo transfer is limited to the natural breeding season. Superovulation The induction of multiple ovulations is principally the same for the (domestic) ruminants. Follicles are stimu- lated near the end of the luteal phase and early part of the follicular phase of the estrous cycle, be it the natural end or the progestogen- or prostaglandin-manipulated end of the cycle. In the ewe, pregnant mare serum gonad- otropin (PMSG) is most commonly used. PMSG is ad- ministered IM in a single injection of 1200 IU (range 700-2000 IU) on day 12 or 13 of the cycle, and the ewes may be expected to come into estrus 2 to 4 days later. Alternately, horse anterior pituitary extracts may be given as three daily doses (total 60 mg) beginning on day 12.4 Optimum responses were obtained with horse anterior pituitary extracts in ewes coming into estrus 24 to 48 hours after the end of treatment. The estrous cycle and the time of ovulation can be controlled with the use of either progesterone or prostaglandins which is of value in scheduling the procedure and the recipients. Progesterone is administered daily by 12 mg per day IM injections or via progestogen-impregnated intrava- ginal pessaries. Progesterone treatment must be main- tained for at least the lifespan of the CL, or 14 days, in the ewe. Gonadotropin treatment is initiated on the day before the last progesterone injection is given or the day before pessary removal. The ewes generally come into estrus about 2 days after the cessation of progesterone treat- ment. Prostaglandins may be given in combination with go- nadotropin treatment when the latter has been initiated during the midluteal phase (day 5-10). Prostaglandin (10— 15 mg PGF2alpha or 100 meg PG-analog) is given 1 to 3 days after the PMSG injection. The majority of the ewes will come into estrus within 36 hours after the administration of prostaglandins. In the goat, 1000 IU PMSG are given IM on day 17 of the natural cycle. Intravaginal, progestogen sponges may be used to synchronize estrus. The sponges are left in place for 16 to 18 days, or the approximate lifespan of the CL in the doe. PMSG is administered two days before sponge withdrawal or cessation of daily (12 mg/ day) progesterone injections. Equally effective is a dose of prostaglandins (8 mg PGF2alpha or 50 meg PG-an- alog IM) administered between day 6 and 18 of the es- trous cycle, two days after PMSG. Porcine pituitary FSH (18 mg in 8 divided doses for 4 days) and horse anterior pituitary extract (40-60 mg in three equal SC injections on consecutive days) have also given satisfactory results of 10 to 16 ovulations.1 Insemination The donor animals should be handmated at 12-hour intervals until they no longer accept the male. This ap- proach aids in the timing of estrus and direct observation insures that actual mating took place. Alternately, arti- ficial insemination is also done at 12-hour intervals with the help of a teaser male. An inseminating dose of 400 million or more motile sperm is used at each insemi- nation. Fertilization failure is common in superovulated ewes, particularly in animals showing a high ovulatory response to treatment. This appears to be due to faulty transport of spermatozoa through the cervix and can be overcome by surgical insemination directly into the lu- men of the uterus.8 The uterine horns are exposed via a midline incision under local anesthesia. Manipulation of the reproductive tract should be kept to a minimum. Fer- tilization rates in excess of 90 percent of ova recovered, were achieved by injecting 0.02 ml of semen into the tip of each uterine horn around the time of onset of estrus, or on the second day after discontinuing progestogen treatment in synchronized ewes. In the doe fertilization failure following superovula- tion is not a severe problem, perhaps because the cervix is more patent in the doe than in the ewe, presenting less of a barrier to sperm transport.5 Embryo Recovery Nonsurgical embryo recovery as described for the cow and the mare is not possible because of the tortuous na- ture of the cervix and the inability to guide the catheter per rectum. Collections are generally carried out under general anesthesia. This provides maximal relaxation of the broad ligaments and precludes movement of the do- nor during the procedure. The uterine tubes are cannu- lated via the infundibulum. A portion or all of the horn and the uterine tube are flushed by gentle expression of the flushing medium from the base of the horns through the uterine tubes.3 Recovery rates of 80 percent can be achieved. Embryos enter the uterus around the third to the fourth day after estrus. Embryos collected on day 3 or earlier (embryos of 8 cells or less) should be trans- ferred to the uterine tubes and yield a 60 percent preg-EMBRYO TRANSFER 937 nancy rate. Embryos collected on or after day 4 must be transferred to the uterus and will have 70 to 75 percent survival rate.5 Luteal failure and early return to estrus occurred in the majority of superovulated does. This resulted in failure to recover embryos later than five days after estrus. By flushing uterine tubes and uteri between day 2 and 4, high embryo recovery rates could be achieved despite the premature luteal failure associated with superovu- lation in these does.1 Repeated collections from individ- ual animals have rarely been attempted and would be progressively hampered by the development of adhe- sions. As in cattle, phosphate buffered media are most commonly used and have the advantage over bicarbonate buffered media in that they do not have to be maintained under a gas phase to maintain pH. Procedures for embryo handling and evaluation are the same as those already described for cattle. Recipients The requirements for synchrony of the cycles of the donor and the recipients in sheep is less exacting than that in cattle. While close synchrony is optimal, a vari- ation of plus or minus two days is adequate in sheep. Critical data are not available for the doe, but there are indications that the doe may tolerate as much as 36 hours asynchrony. If a large pool of recipients is available, an- imals whose estrus occurs at the same time as that of the donor can be selected. About ten potential recipients should be available for each donor. Prostaglandins or progestogen administration may also be used. Proges- togen treatment of the recipients should be discontinued one day earlier than that of the donor. Aftercare of the recipients is the same as that of naturally pregnant fe- males. Nonreturns can be monitored with a teaser male. Transfer Transfer via the cervix is extremely difficult in small ruminants because of the tortuous nature of the cervix.6 Surgical transfer under local anesthesia via a midventral approach is rapid and economical. Each embryo is trans- ferred with a Pasteur pipet in 0.01 ml of medium to the uterine tube prior to day 4, or to the distal portion of the uterine horn after day 4. Single embryos are transferred to the horn ipsilateral to the CL, twin embryos one to each horn or uterine tube. Embryo Transfer in Pigs Genetic progress in the swine industry will require and rely on embryo transfer. There is also considerable in- terest in the use of embryo transfer to reduce the disease risk involved in the introduction of replacement herd sires.3,4 Embryo transfer has been a useful experimental technic for the study of uterine migration and the spacing of embryos,7 the local effect of the embryo on luteal function as well as the effect of a variable number of embryos on the maintenance of pregnancy and embry- onic survival rates. Descriptions of embryo recovery procedures have been available since 1962.10 Donor Selection and Treatment Sows should be reproductively sound and in good health for optimal results, especially since embryo recovery in- volves general anesthesia and surgery. Repeated embryo recovery is likely to be limited by adhesions of the uter- ine horns and ovaries which may have an adverse effect on egg transport and fertilization as well as on manip- ulation of the reproductive tract.12 Superovulation can be induced in sows at weaning by subcutaneous (SC) injection of 1200 IU pregnant mare serum gonadotropin (PMSG) on the day of removal of the pigs.14 Gilts can be superovulated by the SC injection of 1200 to 1500 IU PMSG on day 15 or 16 of the estrous cycle. Onset of estrus and the time of the LH peak are advanced by about one day, occurring 3.5 to 4.0 days after PMSG treatment in sows. As in other species tre- mendous variation in the ovulatory response occurs in sows and gilts of similar age, reproductive stage, breed- ing and management. An average of 20 to 30 ovulations may be expected with a range of 10 to 50.6 Donors are mated or inseminated every 12 hours after the onset of estrus. The most important single insemination is at 24 hours after the onset of heat. An inseminating dose of 100 ml diluted fresh semen containing at least 4 billion live spermatozoa is used. Embryo Recovery and Transfer Under general inhalation anesthesia, usually main- tained by a closed-circuit system,8 the reproductive tract is exposed via a midventral incision. Embryos can be collected from the uterine tubes by means of a flared glass cannula inserted at the infundibular end or through the uterotubal junction. Uterine embryos cannot be flushed back through the uterine tubes due to the valve-like na- ture of the uterotubal junction. Uterine embryos may be collected by first occluding the uterine hom 25 cm below the uterotubal junction with rubber-shod Doyen intestinal forceps, and then slowly introducing 25 ml of flushing medium into the uterine horn via the uterine tube. Next a cannula (e.g. a 12- French Foley catheter with 5 ml balloon or a flared glass cannula) is inserted through the uterine wall near the uterotubal junction while the fluid is trapped distally by digital pressure. The medium is then allowed to flow938 VETERINARY OBSTETRICS back toward the cannula and an additional 25 ml is in- fused into the uterus at a point adjacent to the intestinal forceps. Blastocysts, up to day 10 of pregnancy, may also be collected via a catheter inserted through an in- cision in the isthmus of the uterine tube, through the uterotubal junction and into the uterine lumen. The cath- eter (ID 1.25 mm) should have two to four sideholes cut in the last 3 cm of the catheter and is inserted into the uterus to facilitate blastocyst recovery.2 During the nor- mal rate of development of pig embryos following fer- tilization,11 cleavage from one to four cells takes place in the uterine tubes during the first 36 hours. They enter the uterus at this stage. Development is generally ar- rested at the 4-cell stage for up to 48 hours and 4-cell embryos are commonly still recovered as late as 70 to 80 hours after ovulation. When cleavage is resumed, there is roughly a 12-hour cell cycle. However, not all em- bryos resume cleavage at the same time, hence 4-cell embryos may be recovered in the presence of 8- to 16- cell embryos.16 Embryo transfer at the 4- to 8-cell stage is recom- mended primarily because embryos can be evaluated with less difficulty at this stage since normal cleavage is more apparent. A further reason for scheduling embryo trans- fer in the pig at the earlier stages of development is the sharply reduced embryonic survival rate and pregnancy rate obtained when the transfers are made more than 6 days after ovulation or 7 to 8 days after the onset of estrus.11 The length and tortuosity of the cervix and also of the uterine horns in the pig virtually preclude the possibility of nonsurgical recovery of embryos. Recipients Estrus in the recipients should occur within 24 hours of that of the donor, and preferably, the donor should exhibit estrus about 12 hours before the recipient. This may be especially important when sows are used as do- nors since they tend to ovulate 10 to 12 hours later after the onset of estrus than gilts.5 The survival of embryos transferred from sows to already pregnant gilts has been reported.1 Survival rates for transferred and native em- bryos were 51 and 35 percent (not significant), 56 and 20 percent (p < .01) and 72 and 3 percent (p < .01) when the sows were in estrus 12 hours before, at the same time or 12 hours after the recipient gilts. Weaning may be used to synchronize sows. Prepu- beral gilts may be injected SC with 750 IU PMSG fol- lowed 96 hours later by 500 IU HCG intramuscularly. The time of HCG injection is then considered as the on- set of estrus for the determination of synchrony. The ef- fective antigonadotropin, synchronizing agent methalli- bure is no longer available in the U.S.A. because of its teratogenic effects when fed to pregnant sows. Prostaglandins are impractical in the pig because they are only luteolytic between days 11 or 12 and 14 or 15 in normally cycling animals. Prostaglandins may be used in combination with gonadotropins. PMSG and HCG are used to prolong the luteal phase by inducing accessory corpora lutea (CL) which postpone estrus in all animals. Twelve days after the administration of HCG, prosta- glandins can cause all CL to regress resulting in a high degree of synchronization and normal fertility.9 A syn- thetic progestogen, allyl trenbolone or Regumate, shows great promise for estrus synchronization in swine. It is fed for 18 days and, upon withdrawal from feed, estrus occurs 4 to 7 days later with most gilts in estrus on days 5 and 6. Fertility of synchronized gilts was comparable to that for untreated gilts.13 Recipient gilts should be examined during surgery to determine that CL of normal appearance are present. Embryos are transferred with a fire-polished Pasteur pi- pet via a stab incision in the uterine wall about 10 to 15 mm from the tip of the horn. All embryos can be intro- duced at one site, since spacing within the uterus will occur by intrauterine migration. Aftercare is routine for a surgical patient. Pregnancy may be diagnosed at 30 to 60 days of gestation with ultrasonic technics. Embryo Transfer in Dogs and Cats The induction of estrus and ovulation in the bitch, and to a lesser extent in the queen, remains an obstacle to the ready application of embryo transfer in these species, although considerable information is available on the en- docrinology of the estrous cycle of the bitch410 and the queen.8,9 Preimplantation canine embryos have been described and illustrated.3 In addition to research applications, the technic of embryo transfer might be used for the genetic improvement of a breed or the preservation of an en- dangered species with the use of nonendangered and/or domestic canids or felids as recipients.2 The difficulty of synchronizing estrus and ovulation of the donor bitch and her recipient(s) might be circumvented by collecting the embryos and freezing them. The embryos could then be transferred to a suitable recipient during her respective natural cycle. However, neither dog nor cat embryos have been successfully frozen and thawed to date. The do- mestic cat ovulates in response to a coital or hormonal (LH, GnRH) stimulus. Ovulation may be induced by dailyEMBRYO TRANSFER 939 injections of 2.0 mg FSH until estrus is observed at which time she is mated.10 Embryo Recovery The donor bitch is anesthetized and the abdomen and perineal region are prepared for surgery. The ovaries, uterus and cervix are exposed via a mid-ventral abdom- inal incision. The corpora hemorrhagica cannot be ob- served directly without surgically opening the ovarian bursae, but an impression may be gained by the overall size of the ovary and by direct palpation of the ovary during surgery. A roundtip Foley catheter (8 or 10 French size) made rigid with a stylet is inserted into the vagina. The tip of the catheter is identified at the external cervi- cal os via the abdominal incision and manipulated through the cervix into the lumen of the uterus. The catheter is then directed into a uterine horn 2 cm cranial to the bi- furcation. After the stylet is removed, the balloon of the catheter is distended with 3 to 4 ml of flushing medium or air. The ipsilateral uterotubal junction is occluded by digital pressure and a blunt 18-gauge needle is inserted into the lumen of the uterus approximately 4 cm from the uterotubal junction. Next the lumen is flushed with 10 ml of warm phosphate buffered saline solution. The opposite horn is then flushed in a similar manner. Each horn is flushed three times with a total of 30 ml. The flushings are collected via the Foley catheter in sterile petri dishes for examination under a stereomicroscope as described for cattle embryos.1 In the queen, each horn is flushed separately by in- troducing recovery medium near the uterotubal junction with a blunt needle and a syringe, and collecting the phosphate buffered saline via a cannula inserted into the lumen near the bifurcation. Results Schriver and Kraemer5 recovered 47 feline embryos from 9 surgical collections 6 days after mating. Four pregnancies resulted from 9 transfers. Two litters of 3 and 1 males, respectively, were delivered naturally. A third pregnancy resulted in a stillborn male and the fourth pregnancy terminated in either an unobserved abortion or fetal resorption. A total of 72 canine embryos were obtained from 26 collections. Thirty seven of the em- bryos were transferred to 7 recipients. Three pregnancies were diagnosed and a total of 4 offspring was pro- duced.6'7 These studies show that embryo transfer is bi- ologically feasible in the dog and the cat. However, the efficiency must be markedly increased before embryo transfer will be useful in increasing the number of off- spring from genetically valuable females, for production of biomedical models, or for the presentation of endan- gered species. References Cattle 1. Allen, R. L., Bondioli, K. R. and Wright, R. W., Jr. (1982) The ability of fetal calf serum, newborn calf serum and normal steer serum to promote in vitro development of bovine morulae, Theriogenology, 17, 73. 2. Anderson, G. B., Cupps, P. T. and Drost, M. (1979) Induction of twins in cattle with bilateral and unilateral embryo transfer, J. An. Sci. 49, 1037-1042. 3. Barrios, D. R., Ramge, J. C., Harms, P. G., Blake, R. W. and Kraemer, D. C. (1982) Evaluation of embryo collection and transfer as diagnostic tools for bovine infertility, Theriogenol- ogy, 17, 77. 4. Boland, M. P., Kennedy, L. G., Crosby, T. F. and Gordon, I. (1981) Superovulation in the cow using PMSG or HAP, The- riogenology, 15, 110. 5. Bondiole, K. R. and Wright, R. W., Jr. (1980) Superovulation of progestogen synchronized ewes, Theriogenology, 13, 89. 6. BonDurant, R. H., Anderson, G. B., Boland, M., Cupps, P. T. and Hughes, M. A. (1982) Preliminary studies on bovine embryo survival following short-term storage at 4C, Theriogen- ology, 17, 223-230. 7. Bowen, R. A., Elsden, R. P. and Seidel, G. E., Jr. (1978) Em- bryo transfer for cows with reproductive problems, J. Am. Vet. Met. Assoc. 172, 1303-1306. 8. Brand, A., Trounson, A. O., Aarts, M. H., Drost, M. and Zaai- jer, D. (1978) Superovulation and non-surgical embryo recovery in the lactating dairy cow, An. Prod. 25, 55-60. 9. Church, A. B. and Shea, B. F. (1977) The role of embryo trans- fer in cattle improvement programs, Can. J. An. Sci. 57, 33- 39. 10. Cupps, P. T., Anderson, G. B. and Drost, M. (1977) Synchro- nization of estrus in cattle for embryo transfer, Theriogenology, 8, 111-118. 11. Critser, E. S., Critser, J. K., Winch, R. P. and Eilts, C. (1982) Efficacy of Pergonal as a superovulatory drug in cattle, Therio- genology, 17, 83. 12. Danner, M. L. and Oxender, W. D. (1980) Efficacy of an equine pituitary extract to superovulate cows, Theriogenology, 13, 94. 13. Drost, M. (1974) Embryo transfer in cattle. Bovine Practitioner 9, 18-26, 56. 14. Elsden, R. P., Hasler, J. F. and Seidel, G. E., Jr. (1976) Non- surgical recovery of bovine eggs, Theriogenology, 6, 523-532. 15. Elsden, R. P. (1977) Embryo collection by surgical methods In: Embryo Transfer in Farm Animals, Ed., K. J. Betteridge. Ag- riculture Canada, Monograph No. 16, pl0-13. 16. Elsden. R. P., Nelson, L. D. and Seidel, G. E., Jr. (1978) Su- perovulation of the cow with follicle stimulating hormone and pregnant mare’s serum gonadotropin, Theriogenology, 9, 17- 26. 17. Elsden, R. P., Nelson, L. D. and Seidel, G. E., Jr. (1979) Em- bryo transfer in fertile and infertile cows, Theriogenology 11, 17-25.940 VETERINARY OBSTETRICS 18. Elsden, R. P. (1980) Bovine embryo transfer, Proc. Ann. Mtg. Soc. Therio. 101-133. Omaha, Neb. 19. Farrand, G. D., Elsden, R. P. and Seidel, G. E., Jr. (1982) Effect of slow cooling prior to plunging into liquid nitrogen, Theriogenology, 17, 88. 20. Foote, R. H. and Onuma, H. (1970) Superovulation, ovum col- lection, culture and transfer, A review. J. Dairy. Sci. 53, 1681— 1692. 21. Greve, T. (1980) Embryo transplantation in cattle. Non-surgical recovery of embryos from repeat breeder cattle, Acta. Vet. Scand. 21, 26-33. 22. Heape, W. (1890) Preliminary note on the transplantation and growth of mammalian ova within a uterine foster-mother, Proc. Soc. (London) 48, 457-458. 23. Humphrey, W. D., Murphy, B. D., Rieger, R., Mapletoft, R. J., Manns, J. G. and Fretz, P. F. (1979) Effects of FSH/LH ratio of PMSG on ovulatory responses, Theriogenology, 11, 101. 24. Land, R. B. (1977) The genetics of breed improvement. In: Em- bryo Transfer in Farm Animals, ed. K. J. Betteridge. Mono- graph No. 16, 57-59. 25. Linares, T. (1981) A morphological study of the blastocysts col- lected from repeat breeder heifers, Theriogenology, 15, 116. 26. Mapletoft, R. J. (1980) Embryo transfer for the practitioner, The Bovine Proc. 13, 154-162. 27. Maurer, R. R. (1978) Freezing mammalian embryos: A review of the techniques, Theriogenology, 9, 45-68. 28. Menzer, C. H. and Schams, D. (1979) Radioimmunoassay for PMSG and its application to in vivo studies, J. Reprod. Fert. 55, 339-345. 29. Miller, D. M., Johnson, W. H., Cates, W. F. and Mapletoft, R. J. (1981) Superovulation studies in heifers to determine fer- tilization rates of bulls with high levels of certain sperm defects, Theriogenology, 15, 122. 30. Newcomb, R., Rowson, L. E. A. and Trounson, A. O. (1978) The Scarewell project: An on-farm demonstration of the poten- tial of egg transfer, Vet. Rec. 103, 415-418. 31. Peters, D. F., Anderson, G. B., BonDurant, R. H., Cupps, P. T. and Drost, M. (1978) Transfer of cultured bovine embryos, Theriogenology, 10, 337-342. 32. Pugh, A., Trounson, A. O., Aarts, M. H. and McPhee, S. (1980) Bovine embryo recovery by filtration of non-surgical flushes, Theriogenology, 13, 281-285. 33. Rowe, R. F., DelCampo, M. R., Critser, J. K. and Ginther, O. J. (1980) Embryo transfer in cattle: Non-surgical transfer, Am. J. Vet. Res. 41, 1024-1028. 34. Schneider, H. J., Jr., Castleberry, R. S. and Griffin, J. L. (1980) Commercial aspects of embryo transfer, Theriogenology, 13, 73-85. 35a. Seidel, G. E., Jr. (1982) Application of microsurgery of mam- malian embryos. Theriogenology, 17, 23-35. 35b. Seidel, G. E., Jr., Seidel, S. M. and Bowen, R. A. (1980) Bo- vine Embryo Transfer Procedures, General Series No 950, Col- orado State Univ., Ft. Collins, Colo. 36. Shea, B. F. (1981) Evaluating the bovine embryo, Theriogen- ology, 15, 31-42. 37. Tervit, H. R., Elsden, R. P. and Farrand, G. D. (1981) Deep freezing 7- to 8- and 10- to 11-day old cattle embryos, Therio- genology, 15, 114. 38. Turman, E. J. and Wettemann, R. P. (1978) Follicular growth and superovulation in beef cows following repeated treatments with PMSG, Amer. Soc. An. Sci. 70th Ann. Mtg., Abst. 451, p396. 39. Voelkel, S. A., Amtson-Morgan, K. C. and Godke, R. A. (1981) Heat inactivation of lamb, newborn calf and steer serum for po- tential use in embryo transplant procedures, Theriogenology, 15, 125. 40. Warwick, B. L., Berry, R. O. and Horlacher, W. R. (1934) Results of mating rams to Angora female goats, Proc. Am. Soc. An. Prod. 225-227. 41. Whittingham, D. G. (1971) Survival of mouse embryos after freezing and thawing, Nature (London) 233, 125. 42. Willett, E. L., Black, W. G., Casida, L. E., Stone, W. H. and Buckner, P. J. (1951) Successful transplantation of a fertilized bovine ovum, Science N.Y. 113, 247. 43. Wilmut, I. and Rowson, L. E. A. (1973) The successful low temperature preservation of mouse and cow embryos, J. Re- prod. Fertil. 33, 352-353. 44. Wright, J. M. (1981) Non-surgical embryo transfer in cattle. Embryo-recipient interactions, Theriogenology, 15, 43-56. NOTE: The Proceedings of the Annual Meeting of the Inter- national Embryo Transfer Society are published in the January issue of THERIOGENOLOGY/An Interna- tional Journal of Animal Reproduction. Horses 1. Allen, W. R. and Rowson, L. E. A. (1975) Surgical and non- surgical embryos transfer in horses, J. Reprod. Fertil. Suppl. 23, 525-530. 2. Day, F. T. (1940) Clinical and experimental observations on re- production in the mare, J. Agric. Sci. 30, 244. 3. Douglas, R. H., Nuti, L. and Ginther, O. J. (1974) Induction of ovulation and multiple ovulations in seasonally-anovulatory mares with equine pituitary fractions, Theriogenology, 2, 133-142. 4. Imel, J. K., Squires, E. L., Elsden, R. P. and Shideler, R. K. (1981) Collection and transfer of equine embryos, J. Am. Vet. Med. Assn. 179, 987-992. 5. Irvine, C. H. G. (1981) Endocrinology of the estrous cycle of the mare: Applications to embryo transfer, Theriogenology, 15, 85-104. 6. Lapin, D. R. (1977) Induction of ovulation and multiple ovula- tions in seasonally-anovulatory and ovulatory mares with an equine pituitary extract, J. An. Sci. 44, 834-842. 7. Neely, D. P., Hughes, J. P., Stabenfeldt, G. H. and Evans, J. W. (1974) The influence of intrauterine saline infusion on luteal function and cyclic ovarian activity in the mare, Equine Vet. J. 6, 150. 8. Oguri, N. and Tsutsumi, Y. (1972) Nonsurgical recovery of equine eggs, and an attempt at nonsurgical egg transfer in horses, J. Reprod. Fertil. 31, 187-195. 9. Oguri, N. and Tsutsumi, Y. (1974) Nonsurgical egg transfer in mares, J. Reprod. Fertil. 41, 313-320. 10. Woods, G. L., Scraba, S. T. and Ginther, O. J. (1982) Prospects for induction of multiple ovulations and collection of multiple embryos in the mare, Theriogenology, 17, 61-72. Sheep and Goats 1. Armstrong, D. T., Pfitzner, A. O. and Seamark, R. F. (1982) Ovarian responses and embryo survival in goats following su- perovulation and embryo transfer, Theriogenology, 17, 76. 2. Bradford, G. E., Taylor, St. C. S., Quirke, J. F. and Hart, R. (1974) An egg-transfer study of litter size, birth weight and lamb survival, Anim. Prod. 18, 249.EMBRYO TRANSFER 941 3. Hunter, G. L., Adams, C. E. and Rowson, L. E. A. (1955) In- terbreed ovum transfer in sheep, J. Agric. Sci. 46, 143-149. 4. Moore, N. W. and Shelton, J. N. (1964) Response of the ewe to a horse anterior pituitary extract, J. Reprod. Fertil. 7, 79-87. 5. Moore, N. W. (1980) Procedures and results obtainable in sheep and goats. In: Current Therapy in Theriogenology. Ed. D. A. Morrow. W.B. Saunders Co., Philadelphia. pp89-94. 6. Otsuki, K. and Soma, T. (1964) Transfer of fertilized ova through the cervix in the goat, Nat. Instit. Anim. Indust., Chiba, Japan. Bull. 6, 27-32. 7. Stabenfeldt, G. H., Drost, M. and Franti, C. E. (1972) Peripheral progesterone levels in the ewe during pregnancy and parturition, Endocrinology, 90, 144-150. 8. Trounson, A. O. and Moore, N. W. (1974) Fertilization in the ewe following multiple ovulation and uterine insemination, Aust. J. Biol. Sci. 27, 301-304. 9. Warwick, B. L., Berry, R. O. and Horlacher, W. R. (1934) Re- sults of mating rams to Angora female goats, Proc. 27th Ann. Mtg. Am. Soc. Anim. Prod. 225-227. 10. Warwick, B. L. and Berry, R. O. (1949) Inter-generic and intra- specific embryo transfers, J. Hered. 40, 297-303. 1. Bazer, F. W., Clawson, A. J., Robison, O. W. and Ulberg, L. C. (1969) Uterine capacity in gilts, J. Reprod. Fertil. 18, 121— 124. 2. Bazer, F. W., Roberts, R. M. and Sharp, D. C. (1978) Collec- tion and analysis of female genital tract secretions. In: Methods in Mammalian Reproduction, Ed. J.C. Daniel, Academic Press, New York. pp511-513. 3. Bolin, S. R., Runnels, S. J., Sawyer, C. A. and Gustafson, D. P. (1982) Experimental transmission of pseudorabies virus in swine, Am. J. Vet. Res. 43, 278-280. 4. Cumock, R. M., Day, B. N. and Dziuk, P. J. (1976) Embryo transfer in pigs: A method for inducing genetic material into pri- mary specific-pathogen-free herds, Am. J. Vet. Res. 37, 97-98. 5. Day, B. N. (1968) Reproduction in swine. In: Reproduction in Farm Animals, Ed. E.S.E. Hafez, Lea & Febiger, Philadelphia. pp255-265. 6. Day, B. N. (1980) Embryo transfer: Procedures and results ob- tainable in pigs. In: Current Therapy in Theriogenology, Ed. D.A. Morrow. W.B. Saunders Co., Philadelphia. p95. 7. Dziuk, P. J., Polge, C. and Rowson, L. E. A. (1964) Intrauterine migration and mixing of embryos in swine following embryo transfer, J. An. Sci. 23, 37-42. 8. Dziuk, P. J., Phillips, T. N. and Garber, J. W. (1965) Halothane closed-circuit anesthesia in the pig, Am. J. Vet. Res. 25, 1773- 1775. 9. Guthrie, H. D. and Polge, C. (1976) Control of oestrus and fer- tility in gilts with accessory corpora lutea by prostaglandin ana- logues ICI 79,939 and ICI 80,996, J. Reprod. Fertil. 48, 427- 430. 10. Hancock, J. L. and Hovell, G. J. R. (1962) Egg transfer in the sow, J. Reprod. Fertil. 4, 195-201. 11. Hunter, R. H. F., Polge, C. and Rowson, L. E. A. (1967) The recovery, transfer and survival of blastocysts in the pig, J. Re- prod. Fertil. 14, 501-502. 12. James, J. E. and Reeser, P. D. (1979) Embryo recovery in swine, Theriogenology, 11, 47-50. 13. Kraeling, R. R., Dziuk, P. J., Pursel, V. G., Rampacek, G. B. and Webel, S. K. (1981) Synchronization of estrus in swine with allyl trenbolone (RU-2267), J. An. Sci. 52, 831-835. 14. Longenecker, D. E. and Day, B. N. (1968) Fertility levels of sows superovulated at postweaning estrus, J. An. Sci. 27, 709- 711. 15. Oxenreider, S. L. and Day, B. N. (1965) Transport and cleavage of ova in swine, J. An. Sci. 24, 213-217. 16. Polge, C. (1977) Prediction of viability of embryos. In: Embryo transfer in farm animals, Ed. K. J. Betteridge. Canada Dept, of Agric. Monograph 16, p44. Dogs and Cats 1. Archbald, L. F., Baker, B. A., Clooney, L. L. and Godke, R. A. (1980) A surgical method for collecting canine embryos after induction of estrus and ovulation with exogenous gonadotropins, Vet. Med./Sm. An. Clin. 75, 228-238. 2. Durrant, B. and Benirschke, K. (1981) Embryo transfer in exotic animals, Theriogenology, 15, 77-82. 3. Holst, P. a. and Phemister, P. D. (1971) The prenatal develop- ment of the dog: Preimplantation events, Biol. Reprod. 5, 194- 206. 4. Joechle, W. and Anderson, A. C. (1977) The estrous cycle in the dog: a review, Theriogenology, 7, 113-140. 5. Schriver, M. D. and Kraemer, D. C. (1978) Embryo transfer in the domestic feline, Am. Assoc. Lab. An. Sci. Publ. 48-4, pl2. 6. Kinney, G. M. (1979) Embryo collection and transfer in the dog, M. S. Thesis, Texas A&M University, College Station, Texas. 7. Kinney, Gail M., Pennycook, John W., Schriver, Michael D., Templeton, Joe W. and Kraemer, Dwane C. (1979) Surgical col- lection and transfer of canine embryos, Biol. Reprod. Suppl. 1, 20, 96A. 8. Shille, V. M. and Stabenfeldt, G. H. (1980) Current concepts in reproduction of the dog and cat, In: Brandly, C. E., Cornelius, C. E. (eds). Adv. Vet. Sci. Comp. Med. 24, 211-243. 9. Wildt, D. E., Chakraborty, P. K., Panko, W. B. and Seager, S. W. J. (1978) Relationship of reproductive behavior, serum lu- teinizing hormone and time of ovulation in the bitch, Biol. Re- prod. 18, 561-570. 10. Wildt, D. E., Kinney, G. M. and Seager, S. W. J. (1978) Go- nadotropin-induced reproductive cyclity in the domestic cat, Lab. An. Sci. 28, 301-307.ADDENDUM—CURRENT SELECTED SUPPLEMENTAL REFERENCES (BY CHAPTER) Current, supplemental, selected, pertinent or review references from the literature on Theriogenology in 1983, 1984 and 1985 during the period of proof-reading and indexing of this Third Edition. S. J. Roberts General References 1. Arthur, G. H., Noakes, D. E. and Pearson, H. (1983) Veteri- nary Reproduction and Obstetrics, 5th Ed., (Baillier-Tindall), W. B. Saunders Co., Philadelphia, Pa. 19105. Chapter I—Female Anatomy 1. Ginther, O. J. and Pierson, R. A. (1984) Ultrasonic Anatomy of Equine Ovaries, Theriog. 21, 3, 471—483 (and Heifers Ova- ries)—Proc. 10th Intern. Congr. on An. Reprod. and AI, III, 496. 2. Pierson, R. A. and Ginther, O. J. (1985) Ultrasonic Evaluation of the Corpus Luteum of the Mare, Theriog. 23, 5, 795-806 (Corpus hemorrhagicum present in only 50% of luteal glands). 2a. Reeves, J. J., Rantanen, N. W. and Hauser, M. (1984) Trans- rectal Real-Time Ultrasound Scanning of the Cow Reproductive Tract, Theriog. 21, 3, 485-494. 3. Squires, E. L., Voss, J. L., Villahoz, M. D. and Shideler, R. K. (1983) Use of Utrasound in Broodmare Reproduction. (A Review), Proc. 29th Ann. Conv. AAEP., Las Vegas, 27-43. Chapter II—Examinations for Pregnancy 1. Taveme, M. A. M. and deBois, C. H. W. (1984) Linear-Array Real-Time Ultrasound Observations of the Pregnant Uterus in Domestic Animals, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., II, 113A. (Note diagnosis of hydrometra in does.) 2. van de Wiel, D. F. M. (1984) Evaluation of Pregnancy Status, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., IV, X26-33 (A Review). Cow 3. Booth, J. M. and Chaplin, V. M. (1984) Oestrone Sulphate in Bovine Milk as a Test for Pregnancy, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., II, 77 (after 112 days of pregnancy). 4. Shemesh, M., Ayalon, N., Lavi, S., Mileguir, F., Shore, L. S. and Toby, D. (1983) A New Approach to the Use of Pro- gesterone (PRID) for Pregnancy Diagnosis (and Conception), Brit. Vet. J. 139, 41-48. Mare 5. Chevalier, F. and Palmer, E. (1982) Ultrasonic Echography in the Mare, J. Reprod. Fert. Suppl. 32, 423. 6. Pierson, R. A. and Ginther, O. J. (1984) Ultrasonography for Detection of Pregnancy and Study of Embryonic Development in Heifers, Theriog. 22, 2, 225-233. 7a. Pipers, F. S. and Adams-Brendemuehl, C. S. (1984) Tech- niques and Applications of Transabdominal Ultrasonography in the Pregnant Mare, JAVMA, 185, 7, 766-771. 7b. Pipers, F. S., Zent, W., Holden, R. and Asbury, A. (1984) Ultrasonography as an Adjunct to Pregnancy Assessments in the Mare, JAVMA, 184, 3, 328. 8. Squires, E. L., Villahoz, M. and Voss, J. L. (1983) Ultrasound Scanning for Pregnancy in 250 Mares, Abstr., Eq. Vet. Data, 4, 17, 267. 9. Squires, E. L., Voss, J. L. and Villahoz, M. D. (1983) Im- munological Methods for Pregnancy Detection in Mares, (A Re- view), Proc. 29th Ann. Conv. AAEP, Las Vegas, 45-51. 10. Torbeck, R. L. (1983) The Application of Diagnostic Ultra- sound to Broodmare Practice, Proc. Ann. Mtg. Soc. for Ther- iog., Nashville, Tenn. 176-187 (Theoretical and Practical). 11. Villahoz, M. D., Iuliano, M. F. and Squires, E. L. (1983) The Use of Real-Time Ultrasound for Pregnancy Detection in Em- bryo Transfer Mares, Theriog. 19, 1, 149. 12. Zent, W. W. (1983) Pregnancy Diagnosis and Some of the Pit- falls of Ultrasonography in the Mare, Proc. Ann. Mtg. Soc. for Theriog., Nashville, Tenn. 189-193 (Practical!). Ewe and Doe 13. Pennington, J. A. (1982) Milk Progesterone for Pregnancy Di- agnosis in Goats, J. Dairy Sci. 65, 2011. 14. Rawlings, N. C., Jeffcoate, I. A., Savage, N. C., Stewart, D. M. K. and Steuart, L. H. M. (1983) Pregnancy Diagnosis and Assessment of Fetal Numbers in the Ewe in a Commercial Set- ting, Theriog. 19, 5, 655. 15. Refsal, K. R., Marteniuk, J. V. and Nachreiner, R. F. (1982) Elevation of Serum Estrone Sulfate in Pregnant Goats, Proc. Conf. of Res. Workers in An. Dis., Chicago, 111. 16. Trapp, M. J. and Slyter, A. L. (1983) Pregnancy Diagnosis in the Ewe, J. An. Sci. 57, 1, 1 (Comparison of 5 Methods). Sows 17. Almond, G. W., Bosa, W. T. K. and King, G. J. (1983) The “Not in Pig” Sow and Comparison of Amplitude-Depth and Doppler Pregnancy Detectors from 23 to 45 days of Gestation, Proc. Ann. Mtg. Soc. for Theriog., Nashville, Tenn., 242-247. 942ADDENDUM—CURRENT SELECTED SUPPLEMENTAL REFERENCES 943 Bitch and Queen 18. Cartee, R. E. and Rowles, T. (1984) Preliminary Study of the Ultrasonographic Diagnosis of Pregnancy and Fetal Develop- ment in the Dog, Am. J. Vet. Res. 45, 7, 1259. 19. Concannon, P. and Rendano, V. (1983) Radiographic Diagnosis of Canine Pregnancy: Onset of Fetal Skeletal Radiopacity in Re- lation to Times of Breeding, Preovulatory Luteinizing Hormone Release and Parturition, Amer. J. Vet. Res. 44, 8, 1506. 20. Vondruska, J. F. (1983) Diagnosis of Pregnancy in Cats, Vet. Med./Sm. An. Clin., 78, 8, 1225. Chapter III—Gestation Period—Embryology—Teratology Embryology 1. Allen, W. R. (1984) Aspects of Early Embryonic Development in Farm Animals, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111. IV, XII, 1—9 (A Review—Ovine, Porcine and Equine Embryos). 2. Flood, P. F., Betteridge, K. J. and Diocee, M. S. (1982) Trans- mission Electron Microscopy of Horse Embryos 3-16 Days af- ter Ovulation, J. Reprod. Fert. Suppl. 32, 319 (Capsule For- mation). Teratology 3. Bedford, P. G. C. (1982) Canine and Feline Breed Dispositions to Ocular Disease, Brit. Vet. J. 138, 2. 4. Denholm, L. J. and Cole, W. G. (1983) Heritable Bone Frag- ility, Joint Laxity and Dysplastic Dentin in Friesian Calves: a Bovine Syndrome of Osteogenesis Imperfecta, Austral. Vet J 60, 9. 5. DiBartola, S. P., Chew, D. J. and Boyce, J. T. (1983) Juvenile Renal Disease in Related Standard Poodles (A Review), JAVMA 183, 6, 693. 6. Eldridge, F., Leipold, H. W. and Harris, N. (1983) Goat x Sheep Hybrid: An Additional Case, J. Dairy Sci. 66, Suppl. 1, 253 (Abstr). 6a. Hamori, D. (1983) Constitutional Disorders and Hereditary Dis- eases in Domestic Animals, Elsevier Scientific Publ. Co. N.Y.C., 728 pages. 7. Hsu, F. S. and Du, S. J. (1982) Congenital Heart Disease in Swine, Vet. Path. 19, 676. 8. Johnston, S. D., Buoen, L. C., Madl, S. E., Weber, A. E., and Smith, F. O. (1983) X-chromosome Monosomy (37,XO) in a Burmese Cat with Gonadal Dysgenesis, JAVMA, 182, 986. 9. Jones, W. E. and Kent, M. (1983) Sex Reversal Syndrome (Ge- netic Gonadal Dysgenesis and Testicular Feminization in Ara- bian Horses), Eq. Vet. Data, 4, 23, 353. 10. Keeler, R. F. (1984) Teratogens in Plants, J. An. Sci. 58, 4, 1029. (A Review.) 11. Kingston, R. S. and Park, R. D. (1982) Atresia Ani with an Associated Urogenital Tract Anomaly in Foals, Eq. Pract 4, 1 33. 12. Leipold. H. W. (1983) Cause, Diagnosis and Control of Con- genital Defects in Cattle, Proc. Ann. Mtg. Soc. for Theriog., Nashville, Tenn., (Extensive Bibliography), 41-61. 13. Narfstrom, L. K. and Nilsson, S. E. G. (1983) Progressive Ret- inal Atrophy in the Abyssinian Cat; an Update, Vet. Rec 112, 525. 14. Osbum, B. I., MacLachlan, N. J., Anderson, G. A. and Scott, J. L. (1982) A Review of Bovine Bluetongue, Bovine Proc. (A.A.B.P.) 15, 23 (Nashville, Tn). 15. Owen, C. A. and McCall, J. T. (1983) Identification of the Carrier of the Bedlington Terrier Copper Disease, Am. J. Vet. Res. 44, 694. 15a. Panter, K. E., Keeler, R. F. and Buck, W. B. (1985) Induction of Cleft Palate in Newborn Pigs by Maternal Ingestion of Poison Hemlock (Conium maculatum), Am. J. Vet. Res. 46, 6, 1368- 1371. 16. Ralston, S. R. and Shideler, R. K. (1984) Inheritance of Um- bilical Hernias in Horses, Proc. 10th Intern. Congr. on An. Re- prod. and AI, Urbana, 111., Ill, 530 (8.6% incidence (17/198), a recessive, more common in females). 17. Reik, T. R., Rempel, W. E., McGrath, C. J. and Addis, P. B. (1983) Further Evidence on the Inheritance of Halothane Re- action (Porcine Stress Syndrome) in Pigs, J. An. Sci. 57, 4, 826. 18. Strasia, C. A., Johnson, J. L., Cole, D. and Leipold, H. W. (1983) Partial Albinism (Heterochromia irides) in Black Angus Cattle, Bov. Pract., 18, 147-149. 19. Stuart, L. D. and Leipold, H. W. (1983) Bovine Progressive Degenerative Myeloencephalopathy (“Weaver”) of Brown Swiss Cattle, Bov. Pract., 18, Nov., 129 and 133-146 (With Review of Other Nervous Diseases of Cattle). 20. Vonderfecht, S. L., Trommerhausen, B. A. and Cohen, M. (1983) Congenital Intestinal Aganglionosis in White Foals, Vet. Path , 20, 65. 21. Wiesner, E. and Wilier, S. (1981) Inheritance of Congenital Umbilical Hernias in Cattle, Monatshefte fur Veterinamedizin 36, 790. 22. Wilson, T. M., deLahunta, A. and Confer, L. (1983) Cerebellar Degeneration in Dairy Calves: Clinical, Pathologic and Serol- ogic Features of an Epizootic Caused by Bovine Viral Diarrhea Virus, JAVMA 183, 5, 544. Chapter IV—Physiology of the Gestation Period 1. Allen, W. R. (1982) Immunological Aspects of the Endometrial Cup Reaction and the Effect of Xenogeneic (Hybrid) Pregnancy in Horses and Donkeys, J. Reprod. Fert. Suppl. 31, 57-94. 2a. Bailey, E. (1984) Usefulness of Lymphocyte Typing to Exclude Incorrectly Assigned Paternity in Horses, Am. J. Vet. Res 45, 10, 1976-1978. 2b. Bazer, F. W. and First, N. L. (1983) Pregnancy and Parturition (A Review), J. An. Sci., 57, Suppl. 2, 425. 3. Bosu, W. T. K., Turner, L. and Franks, T. (1984) Estrone Sul- phate and Progesterone Concentrations in the Peripheral Blood of Pregnant Mares: Clinical Implications, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., II, 78. 4. Ginther, O. J. (1983) Mobility of the Early Equine Conceptus and Fixation and Orientation of the Early Equine Conceptus, Theriog. 19, 603 and 613. 5. Ginther, O. J. (1984) Mobility of Twin Embryonic Vesicles in Mares, Theriog. 22, 1, 83-95 (Cessation of intrauterine mo- bility occurs about 15-17 days postovulation). 6. Ginther, O. J. (1984) Ultrasonic Evaluation of the Reproduc- tive Tract of the Mare: The Single Embryo, Eq. Vet Sci 4 2 75-81. 7. Heap, R. B., Hamon, M. and Allen, W. R. (1982) Studies on Estrogen Synthesis by the Preimplantation Equine Conceptus, J. Reprod. Fert. Suppl. 32, 343. 8. Hogarth, P. J. (1982) Immunological Aspects of Mammalian944 VETERINARY OBSTETRICS Reproduction, Praeger Publ., N.Y.C. 9. Kindahl, H., Knudson, O., Madej, A. and Edqvist, L. E. (1982) Progesterone, Prostaglandin F2a, PMSG and Oestrone Sulphate during Early Pregnancy in the Mare, J. Reprod. Fert. Suppl. 32, 353. 10. Leith, G. S. and Ginther, O. J. (1984) Intrauterine Mobility of the Early Equine Conceptus, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., II, 118. (Fixation of embryo oc- curs on days 15 and 16 of gestation.) 10a. Muchmore, A. V. and Decker, J. M. (1985) Uromodulin: A Unique Immunosuppressive Glycoprotein Isolated from Urine of Pregnant Women, Science, 229, 479-481. 11. Neely, D. P., Liu, I. K. M., Hillman, R. B. and Hughes, J. P. (1983) Equine Reproduction, Hoffman-LaRoche, Inc., Nut- ley, New Jersey, 07110. (A Review for Equine Practitioners.) 12. Wachtel, S. S. (1984) H-Y Antigen in the Study of Sex Deter- mination and Control of Sex Ratio, Theriog. 21, 1, 18-28. Freemartins 13. Shore, L. and Shemesh, M. (1981) Altered Steroidogenesis by the Fetal Bovine Freemartin Ovary, J. Reprod. Fert. 63, 309. 14. Vale-Filho, V. R., Basrur, P. K., Pinheiro, L. E. L. and Wil- ton, J. W. (1984) Testicular Growth Characteristics and Cellular Constitution of Chimeric Bulls Produced by Embryo Transfer, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., Ill, 534. (Possible explanation for infertility in chimeric bulls.) 15. Van Haeringen, H. and Jacobs, W. (1983) Freemartins, Com- paring Three Methods for Diagnosis, J. Dairy Sci., 66, Suppl. 1, 247 (Abstr.). 16. White, K. L., Lindner, G. M. and Anderson, G. B. (1983) Cy- tolytic and Fluorescent Detection of H-Y Antigen on Preim- plantation Mouse Embryos, J. An. Sci. 55, Suppl. 1, 496 (Abstr). Twinning 17a. Ginther, O. J. (1983) The Twinning Problem: from Breeding to Day 16, Proc. 29th Ann. Conv. AAEP, Las Vegas, 11-26. 17b. Ginther, O. J. (1984) Transitory Nature of Twin Pregnancy in Mares, Proc. 10th Intern. Congr. on An. Reprod. and AI, Ur- bana, 111. II, 116. (Manual embryo reduction described.) 17c. Ginther, O. J. (1984) Postfixation Embryo Reduction in Uni- lateral and Bilateral Twins in Mares, Theriog. 22, 2, 213-223. (Greater reduction in unilateral (89%) than in bilateral (11%) average of all (64%). 18. Henry, M., Coryn, M. and Vandeplassche, M. (1982) Multiple Ovulation in the Mare, Zbl. Vet. Med. A 29, 170. 19. Pascoe, R. R. (1983) Methods for the Treatment of Twin Preg- nancy in the Mare, Eq. Vet. Jour. 15, 40. 20. Woods, G. L. and Ginther, O. J. (1983) Intrauterine Embryo Reduction in the Mare, Theriog. 20, 6, 699. 21. Woods, G. L., Sprinkle, T. A. and Ginther, O. J. (1983) Pre- vention of Twin Pregnancy in the Mare, Proc. Ann. Mtg. Soc. for Theriog., Nashville, Tenn., 194-202. Gestation Length 22. Concannon, P., Whaley, S., Lein, D. and Wissler, R. (1983) Canine Gestation Length: Variation Related to Time of Mating and Fertile Life of Sperm. Am. J. Vet. Res. 44, 10, 1819. Lactation 23. Adams, B. D., Smith, R. A., Wettemann, R. P. and Bush, L. J. (1981) Induced Lactation of Infertile Dairy Cows (Hormone Treatment, Subsequent Fertility). Oklahoma State Univ., Agric. Sci. Res. Rept. Miscellaneous Publication 112, 34. (Reserpine.) 24. Cowles, R. R. (1983) Lactation Failure in the Mare, Proc. Ann. Mtg. Soc. for Theriog., Nashville, Tenn, 222-233 (Practical). 25. Davis, S. R., Welch, R. A. S., Pearce, M. G. and Peterson, A. J. (1983) Induction of Lactation in Nonpregnant Cows by Estradiol-17b and Progesterone from an Intravaginal Sponge (A Review), J. Dairy Sci. 66, 450. 26. Frank, T. J., Peel, C. J., Bauman, D. E. and Gorwit, R. C. (1983) Comparison of Different Patterns of Exogenous Growth Hormone Administration on Milk Production in Holstein Cows, J. An. Sci., 57, 3, 699. 27. Gorewit, R. C., Wachs, E. A., Sagi, R. and Merrill, W. G. (1983) Current Concepts on the Role of Oxytocin in Milk Ejec- tion (A Review), J. Dairy Sci. 66, 2236. 28. Hemken, R. W., Jackson, J. A. Jr. and Boling, J. A. (1984) Toxic Factors in Tall Fescue (A Review), J. An. Sci. 58, 4, 1011. 29. Henton, J. E. Lathrop, C. D., Jr., Dean, D. and Waldrop, V. (1983) Agalactia in the Mare, A Review and Some New In- sights, Proc. Ann. Mtg. Soc. for Theriog., Nashville, Tenn., 203-221 (Fescue Poisoning!). 30. Lembowicz, K., Rabek, A. and Skrzeczkowsi, L. (1982) Hor- monal Induction of Lactation in the Cow, Brit. Vet. J. 138, 203 (Reserpine). 31. Peel, C. J., Frank, T. J., Bauman, D. E. and Gorewit, R. C. (1983) Effect of Exogenous Growth Hormone in Early and Late Lactation on Lactational Performance of Dairy Cows, J. Dairy Sci., 66, 776. 32. Smith, B. B. and Wagner, W. C. (1984) Suppression of Pro- lactin in Pigs by Escherichia coli Endotoxin, Science, 224, 605- 607. Chapter V—Diseases and Accidents During the Gestation Period Abortion Cattle 1. Boraker, D. K., Stinebring, W. R. and Kunkel, J. R. (1981) BrucELISA: an Enzyme-Antibody Immunoassay for Detection of Brucella abortus Antibodies in Milk: Correlation with the Brucella Ring Test and with Shedding Viable Organisms, J. of Clin. Microbiol., 14, 4, 396-403. 2a. Bulgin, M. S. (1983) Salmonella dublin: What Veterinarians Should Know, JAVMA, 182, 116. 2b. Butzler, J. P. (Editor) (1984) Campylobacter Infection in Man and Animals, CRC Press Inc., Boca Raton, Fla. 33431. 2c. Fitzpatrick, D. R. and Studdert, M. J. (1984) Immunologic Re- lationships between Equine Herpesvirus Type I (Equine Abor- tion Virus) and Type 4 (Equine Rhinopneumonitis Virus) Am. J. Vet. Res. 45, 10, 1947-1951. 2d. Grahn, T. C., Fahning, M. L. and Zemjanis, R. (1984) Nature of Early Reproductive Failure Caused by Bovine Viral Diarrhea Virus, JAVMA, 185, 4, 429-432 (A fertilization failure). 3. Hanson, L. E. (1984) Bovine Leptospirosis and Infertility, Proc. Ann. Mtg. AABP, 16, 159 (A Review).ADDENDUM—CURRENT SELECTED SUPPLEMENTAL REFERENCES 945 4. Idtse, F. S. (1984) Chalmydia and Chlamydial Diseases of Cat- tle: A Review of the Literature, Vet. Med. 79, 4, 543-550. 5. Jerrett, I. V., McOrist, S., Waddington, J., Browning, J. W., Malecki, J. C. and McCausland, I. P. (1984) Diagnostic Studies of the Fetus, Placenta and Maternal Blood from 265 Bovine Abortions, Cor. Vet. 74, 8-20. 6. Manns, J. G. (1983) The Use of Prostaglandins for Regulation of the Estrous Cycle and as an Abortifacient in Cattle, Vet. Clin, of N. Amer., Lg. An. Pract. 5, 1, 169. 7. McCausland, I. P., Badman, R. T., Hides, S. and Slee, K. J. (1984) Multiple Apparent Sarcocystis Abortion in Four Bovine Herds, Cor. Vet. 74, 146-154. 8. Meyer, M. E. and Vanderwagen, L. C. (1982) Comparison of Factors Influencing the Control and Eradication of Bovine Bru- cellosis in California during Two Ten-Year Periods, 1960-1970 and 1970-1980, Proc. 86th Ann. Mtg. U.S.A.H.A., 152. 9. Miller, R. B., Ruhnke, H. L., Doig, P. A., Poitras, B. J. and Palmer, N. C. (1983) The Effects of Ureaplasma diversum Inoculated into the Amniotic Cavity of Cows, Theriog 20, 3 767. 10. Nicoletti, P. and Milward, F. W. (1983) Protection by Oral Administration Brucella abortus Strain 19 against an Oral Challenge Exposure with a Pathogenic Strain of Brucella, Am. J. Vet. Res. 44, 9, 1641. 11. Reynolds, S. L. (1983) The Use of Elisa and Complement Fix- ation Tests in Managing Field Outbreaks of Brucella abortus, Proc. 87th Ann Mtg. U.S.A.H.A., Las Vegas, N. Mex., 129— 136. 12. Ruhnke, H. L., Palmer, N. C., Doig, P. A. and Miller, R. B. (1984) Bovine Abortion and Neonatal Death Associated with Ureaplasma diversum, Theriog. 21, 2, 295-301. 13. Stewart, M. (1984) Latent Brucellosis Infection, Soc. for Ther- iog. Newsletter, 7, 2, (Mar-Apr.). 14. Stringfellow, C. A., Scanlan, C. M., Hannon, S. S., Panan- gala, V. S., Gray, B. W. and Galik, P. A. (1983) Culture of Uterine Flushings, Cervical Mucus, and Udder Secretions Col- lected Post-Abortion from Heifers Artificially Exposed to Bru- cella abortus, Theriog. 20, 1, 77. 15. Thiermann, A. B. (1984) Leptospirosis: Current Developments and Trends, JAVMA, 184, 6, 722-726. 16. Thiermann, A. B. and Garrett, L. A. (1983) Enzyme-Linked Immunosorbent Assay for the Detection of Antibodies to Lep- tospira Interrogans serovars hardjo and pomona in Cattle, Am. J. Vet. Res. 44, 884. 17a. Tindall, W. (1983) Molds and Feeding Livestock (Mycotoxins), An. Nutr. and Health, 38, 4, 5. 17b. Welsch, R. D. (1984) Campylobacter jejuni Abortion in a Heifer, JAVMA, 185, 5, 549—551. (A Review on Terminol- ogy)- 18. Zaugg, J. L. and Kuttler, K. L. (1984) Bovine Anaplasmosis: In utero Transmission and the Immunologic Significance of In- gested Colostral Antibodies, Amer. J. Vet. Res. 45, 3 440- 443. Horses 19a. Anonymous (1984) Equine Viral Arteritis Outbreak in Ken- tucky, JAVMA, 185, 3, 256 and Chronicle of The Horse, 7/27/1984, 62. (Thirty-three farms affected.) 20. Morgenthal, J. C. and Van Nierkerk, C. H. (1984) Twinning, Infectious and Habitual Abortions as Related to Total Plasma Progestagens in the Thoroughbred Mare, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111. II, 92. (High, normal and low respectively.) 21. Saunders, J. R., Mathiesen, R. J. and Kaplan, W. (1983) Abor- tion due to Histoplasmosis in a Mare, JAVMA, 183, 10, 1097. 21a. Timoney, P. J. (1985) The 1984 Outbreak of Equine Viral Ar- teritis in the Thoroughbred Population in Central Kentucky, AAEP Newsletter #2, 4-6. 22. Welsh, R. D. (1983) Equine Abortion Caused by Listeria monocytogenes Serotype 4, JAVMA, 183, 291. Swine 23a. Culter, R. S., Molitor, T. W., Leman, A. D. and Werdin, R. E. (1983) Farm Studies of Porcine Parvovirus Infection, JAVMA 182, 6, 592. 23b. Diekman, M. A. and Long, G. G. (1984) Mycotoxins and Re- production in Swine, An. Nutr. and Health, 39, 4, 22-28. 24. Hathaway, S. C., Ellis, W. A., Little, T. W. A. and Ferguson, H. W. (1983) Leptospira interrogans serovar hardjo in Pigs, Vet. Rec. 113, 153. 25. Oirschot, J. T. and Gielkens, A. L. J. (1984) In vivo and in vitro Reactivation of Latent Pseudorabies Virus in Pigs Bom to Vaccinated Sows, Amer. J. Vet. Res. 45, 3, 567-575. 26. Schlafer, D. H. and Mebus, C. A. (1984) Abortion in Sows Experimentally Infected with African Swine Fever Virus: Clin- ical Features, Am. J. Vet. Res., 45, 7, 1353. 27. Thacker, B. J., Joo, H. S., Moliter, T. W. and Leman, A. D. (1983) Epidemiologic and Diagnostic Features of Porcine Par- vovirus (PPV), Proc. Ann. Mtg. Soc. for Theriog., Nashville, Tenn. 234-241. 28. Thawley, D. G., Solorzano, R. F. and Johnson, M. E. (1984) Confirmation of Pseudorabies Virus Infection, Using Virus Re- crudescence by Dexamethasone Treatment and in vitro Lym- phocyte Stimulation, Am. J. Vet. Res. 45, 981-983. 29. Waltman, W. D. and Dawe, D. L. (1983) Enzyme-Linked Im- munosorbent Assay for the Detection of Antileptospiral Anti- bodies in Swine Sera, Am. J. Vet. Res. 44, 6, 1120. Sheep and Goats 30. Appleyard, W. T. et al. (1983) Outbreak of Chlamydial Abor- tion in Goats, Vet. Rec. 113, 63. 31. Anderson, K. L., Hammond, M. M., Urbance, J. W., Rhoades, M. S. and Bryner, J. H. (1983) Isolation of Campylabacter jejuni from an Aborted Caprine Fetus, JAVMA, 183, 1, 90 (A Review). 32. Bagley, C. V. (1983) Prevention of Border Disease in Lambs, Vet. Med./Sm. An. Clin. 78, 426. 33. Ellis, W. A., Bryson, D. G., Neill, S. D., McParland, P. J. and Malone, F. E. (1983) Possible Involvement of Leptospires in Abortion, Stillbirths and Neonatal Deaths in Sheep Vet Rec 112, 291. 34. Fielden, E. D. (1984) Reproductive Diseases of Sheep and Goats, Proc. 10th Int. Congr. on An. Reprod. and AI, Urbana, 111.' IV, VII-39-46 (A Review) (Emphasis on abortion). 35. Groverman, F. A. and Salbury, D. L. (1983) Passive Antibody Response in Lambs After Vaccination of Pregnant Ewes with Modified Bovine Vims Diarrhea Vaccine (vs Border Disease), Vet. Med/Sm. An. Clin. 78, 9, 1445.946 VETERINARY OBSTETRICS 36. Libal, M. C. and Kirkbride, C. A. (1983) Brucella ovis-In- duced Abortion in Ewes, JAVMA, 183, 5, 553. 37. Linkater, K. A. (1983) Abortion in Sheep Associated with Sal- monella montevideo, Vet. Rec. 112, 372. 38a. Palmer, N. C., Kierstead, M., Key, D. W. and Williams, S. C., Peacock, M. G. and Velland, H. (1983) Placentitis and Abortion in Goats and Sheep in Ontario caused by Coxiella burnetii, Can. Vet. J. 24, 60. 38b. Rodolakis, A., Boullet, C. and Souriau, A. (1984) Chlamydia psittaci Experimental Abortion in Goats, Am. J. Vet. Res. 45, 10, 2086-2089. Dogs and Cats 39. Barlough, J. E. (1983) Feline Leukemia Virus, Cornell Feline Health Center Bull., 5, Sept. 1983 (Review). (Abortion, Infer- tility and Fading Kitten Syndrome.) 40. Bulgin, M. S., Ward, A. C. S., Sriranganathan, N. and Saras, P. (1984) Abortion in the Dog due to Campylobacter Species, Amer. J. Vet. Res. 45, 3, 555. 41. Conley, A. J. and Evans, L. E. (1984) Bromocryptine Induced Abortion in the Bitch, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., Ill, 504. (This drug given at dose levels of 20-30 meg/kg twice daily for 4 days was highly successful.) 42. Hashimoto, A., Hirai, K., Susuki, Y. and Fugimoto, Y. (1983) Experimental Transplacental Transmission of Canine Herpes- virus in Pregnant Bitches During the Second Trimester of Ges- tation, Am. J. Vet. Res. 44, 4, 610. 43. Paradis, M., Post, K. and Mapletoft, R. J. (1983) Effects of Prostaglandin F2a on Corpora Lutea Formation and Function in Mated Bitches. Can. Vet. Jour., 24, 239 (Abortion at midges- tation). 44. Shille, V. M., Dorsey, D. and Thatcher, M. J. (1984) Induction of Abortion in the Bitch with a Synthetic Prostaglandin Analog, Am. J. Vet. Res. 45, 7, 1295. Other Diseases 45. Narasimhan, K. S., Quayam, S. A. and Gera, K. L. (1975) A Method of Retention of Recurrent Prolapse of the Vagina of Cows, Indian Vet. J. 52, 311 (also see Sioss and Dufty). Chapter VI—Parturition 1. Armstrong-Backus, C. S., Hopkins, F. M. and Eiler, H. (1983) The Utero-tonic Effects of Prostaglandin F2a and Oxytocin on the Postpartum Cow. 64th Ann. Mt. of Conference of Res. Workers in An. Disease, Chicago, 111. (Abstract) (Former drug had no effect on uterine motility) (See Ref. 5, Chapter IX). 2. Bostedt, H. and Rudloff, P. R. (1983) Prophylactic Adminis- tration of the Beta-Blocker Carazolol to Influence the Duration of Parturition in Sows, Theriog., 20, 2, 191. 3. Burke, T. M. and Roberson, E. L. (1983) Fenbendazole Treat- ment of Pregnant Bitches to Reduce Prenatal and Lactogenic Infections of Toxocara canis and Ancylostoma caninum in Pups, JAVMA, 183, 9, 987. 4. First, N. L. and Lohse, J. K. (1984) Mechanisms Initiating and Controlling Parturition, Proc. 10th Int. Congr. on An. Reprod. and AI, Urbana, 111., IV, V-31-42 (A Review). 5. Gall, M. A. and Day, B. N. (1983) Effect of Estradiol Benzoate on the Synchrony of PGF2a and Oxytocin Inducted Parturition in Swine, J. An. Sci. 55, Suppl. 1, 77 (Abstr). 6. Kindahl, H., Fredriksson, G., Madej, A. and Edqvist, L-E. (1984) Role of Prostaglandins in Uterine Involution, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., IV, XI-9-16 (A Review). 7. Madej, A., Kindahl, H., Woyno, W., Edqvist, L-E and Stup- nicki, R. (1984) Blood levels of 15-Keto-13,14 Dihydro-Pros- taglandin F2a During the Postpartum Period in Primiparous Cows, Theriog., 21, 2, 279-287. 8. Neely, D. P., Liu, I. K. M., Hillman, R. B. and Hughes, J. P. (1983) Equine Reproduction, Hoffman-LaRoche, Inc., Nut- ley, New Jersey, 07110 (A Review). 9a. Price, E. O., Dunn, G. C., Talbot, J. A. and Dally, M. R. (1984) Fostering Lambs by Odor Transfer: The Substitution Ex- periment, J. An. Sci., 59, 2, 301-307 (Use of a stockinette). 9b. Putnam, M. R., Rice, L. E., Wetteman, R. P., Lusby, K. S. and Pratt, B. R. (1982) Planipart (Clenbuterol) for the Post- ponement of Parturition and the Alleviation of Dystocia, Proc. Am. Mtg. Soc. for Theriog., 176. 9c. Putnam, M. R. (1982) Bovine Parturition: A Mechanism Re- view: Induction, Intervention and Calf Viability, Bovine Proc. (of A.A.B.P.) 15, 122 (Nashville, Tn). 10. Rossdale, P. D. (and others) (1983) Panel: Management and Treatment of the Premature Foal, Proc. 29th Ann. Conv. AAEP, Las Vegas, 125-211. 11. Stanchev, Ph, Kunavongkrit, A., Edgvist, L. E. and Eriksson, H. (1984) Receptors for Estrogens and Progesterone in the Por- cine Cervix, Theriog., 21, 5, 757-766. 12. Wolfe, D. F. (1983) Manipulation of Cattle for Daylight Calv- ing, Mod. Vet. Pract. 64, 21-23. Chapter VII—Causes of Dystocia 1. Adams, N. R, and Naim, M. E. (1983) The Nature of Dystokia in Ewes after Grazing Oestrogenic Subterranean Clover, Aus- tral. Vet. Jour., 60, 124. Chapter VIII—Procedures Preliminary to the Handling of Dystocia Chapter IX—Obstetrical Operations for Relieving Dystocia 1. Blanchard, T. L., Bierschwal, C. J., Youngquist, R. S. and Elmore, R. G. (1983) Sequelae to Percutaneous Fetotomy in the Mare, JAVMA 182, 10, 1128 (21 cases). 2. Cochran, M. L. and Cochran, J. L. (1983) Ovariohysterectomy in Complicated Bovine Cesarean Sections, JAVMA 183, 1, 120. 3. Mortimer, R. G., Ball, L. and Olson, J. D. (1984) A Modified Method for Complete Bovine Fetotomy, JAVMA, 185, 5, 524- 526. Chapter X—Diagnosis and Treatment of the Various Types of Dystocia Chapter XI—Diseases of the Puerperium 1. Backstrom, L., Morkoc, A. C., Connor, J., Larson, R. and Price, W. (1984) Clinical Study of Mastitis-Agalactia in SowsADDENDUM—CURRENT SELECTED SUPPLEMENTAL REFERENCES 947 in Illinois, JAVMA, 185, 1, 70-73. 2. Bailey, E. (1983) Prevalence of Anti-Red Blood Cell Antibodies in the Serum and Colostrum of Mares and its Relationship to Neonatal Isoerythrolysis, Amer. J. Vet. Res. 43, 11, 1917. 3. Becht, J. L., Page, E. H., Morter, R. L., Boon, G. D. and Thacker, H. L. (1983) Experimental Producton of Neonatal Iso- erythrolysis in the Foal Including Detection Tests, Cor. Vet. 73, 380-401. 4. Curtis, C. R., Erb, H. N., Sniffen, C. J., Smith, R. D., Pow- ers, P. A., Smith, M. C., White, M. E., Hillman, R. B. and Pearson, E. J. (1983) Association of Parturient Hypocalcemia with Eight Periparturient Disorders in Holstein Cows, JAVMA 183, 5, 559. 5. Eiler, H., Hopkins, F. M., Armstrong-Backus, C. S. and Lyke, W. A. (1984) Uterotonic Effect of Prostaglandin in F2a and Ox- ytocin on the Postpartum Cow, Amer. J. Vet. Res. 45, 5, 1011- 1014 (See Ref 1, Chapter VI). 6. Haaland, M. A., Manspeaker, J. E. and Moreland, T. W. (1984) Antibiotic Residues in Milk after Intrauterine Infusion, Vet. Med. 79, 3, 382-386. 6a. Halpern, N. E., Erb, H. N. and Smith, R. D. (1985) Duration of Retained Fetal Membranes and Subsequent Fertility in Dairy Cows, Theriog. 23, 5, 807-813. 7. Johnston, S. D., Smith, F. O., Baillie, N. C., Johnston, G. R. and Feeney, D. A. (1983) Prenatal Indicators of Puppy Viability at Term, Comped, on Cont. Educ. 5, 12, 1013-1024. 8. Lawler, D. F. and Monti, K. L. (1984) Morbidity and Mortality in Neonatal Kittens, Am. J. Vet. Res., 45, 7, 1455. 9. Morkoc, A., Backstrom, L., Lund, L. and Smith, A. R. (1983) Bacterial Endotoxin in Blood of Dysgalactic (MMA) Sows in Relation to Microbial Status of Uterus, Milk and Intestine, JAVMA 183, 7, 786. 10a. Richardson, D. W. and Kohn, C. W. (1983) Uroperitoneum in the Foal. JAVMA 182, 267. 10b. Richardson, D. W. (1984) Paraovarian-omental Bands as a Cause of Small Intestinal Obstruction in Cows, JAVMA, 185, 5, 517— 519. 11. Silva, J. R. and Noakes, D. E. (1984) The Effect of Experi- mentally Induced Hypocalcemia on Uterine Activity at Partu- rition in the Ewe, Theriog. 21, 4, 607-623 (Similar to cow). 12. Thompson, J. R., Poliak, E. J. and Pelissier, C. L. (1983) In- terrelationships of Parturition Problems, Production at Subse- quent Lactation, Reproduction and Age at First Calving, J. Dairy Sci., 66, 1119. 13. Townsend, H. G. G., Tabel, H. and Bristol, F. M. (1983) In- duction of Parturition in Mares: Effect on Passive Transfer of Immunity to Foals, JAVMA 182, 3, 255. 14. Whitmore, H. L. (1982) (1983) Specific Infectious Diseases that Limit Bovine Reproduction, Proc. 15th Ann. Conv. A.A.B.P., 66. Chapter XII—Physiology of Reproduction la. Crighton, D. B. (1984) Immunological Aspects of Reproduction in Mammals, 80 Montvale Ave., Butterworth Publishers, Stone- ham, Mass., 02180. (See Reference above Chap. IV, 10a.) lb. Day, B. N. (1984) Estrous Cycle Regulation, Proc. 10th Int. Cong, on An. Reprod. and AI, Urbana, 111., IV, IV-1-8, (A Review). lc. Held, J. P. and Blackford, J. T. (1984) Vaginal Perforation after Coitus in Three Mares, JAVMA, 185, 5, 533-534. 2. Ireland, J. J., Curato, A. D. and Wilson, J. (1983) Effect of Charcoal-Treated Bovine Follicular Fluid on Secretion of LH and FSH in Ovariectomized Heifers, J. An. Sci., 57, 6, 1512 (Inhibin, Folliculostatin). 3. Jainudeen, M. R. (1983) The Water Buffalo (A Review), Per- tanika 6 (Rev. Suppl.), 133-151. 4. Ramasharma, K., Sairam, M. R., Seidah, N. G., Chretien, M., Manjunath, P. and Schiller, P. W. (1984) Isolation, Structure and Synthesis of a Human Seminal Plasma Peptide with Inhibin- Like Activity, Science, 223, 1199 (See Ref. 3, Chap. XIV). Chapter XIII—Infertility in the Cow 1. Whitmore, H. L. (1984) Bovine Reproductive Problems; Di- agnosis and Treatment, N.Y.S. College Veterinary Conference Proc., Jan., Ithaca, NY. Reproductive Physiology 2. Cavestany, D., El-Wishy, A. B. and Foote, R. H. (1985) Effect of Season and High Environmental Temperature on Fertility of Holstein Cattle, J. Dairy Sci. 68, 1471-1478. 2a. Folman, Y., McPhee, S. R., Cumming, I. A., Davis, I. F. and Chamley, W. A. (1983) Conception Rates in Cows after Var- ious Synchronization Techniques Using Progesterone Releasing Intravaginal Devices (PRID), Austral. Vet. J. 60, 44. 2b. Gwazdauskas, F. C. (1985) Effects of Climate on Reproduction in Cattle, J. Dairy Sci. 68, 1568-1578. 3. Hansel, W. and Convey, E. M. (1983) Physiology of the Es- trous Cycle (A Review), J. An. Sci. 57, Suppl. 2, 404. 3a. Helmer, S. D. and Britt, J. H. (1985) Mounting Behavior as Affected by Stage of Estrous Cycle in Holstein Heifers, J. Dairy Sci. 68, 1290-1296. 4a. Hunter, R. H. F. and Wilmot, I. (1982-83) The Rate of Func- tional Sperm Transport into the Oviducts of Mated Cows, An. Reprod. Sci. 5, 167. 4b. Ireland, J. J., Fogwell, R. L., Oxender, W. D., Ames, K. and Cowley, J. L. (1984) Production of Estradiol by Each Ovary during the Estrous Cycle of Cows, J. An. Sci. 59, 3, 764-771 (Nearly continuous). 5. Jochle, W. (1983) Review; Releaser Hormones (GnRH), Uses in Therapy, 6, 33, An. Reprod. Rept. an Animal & Health Newsletter, 10 Old Boonton Rd., Denville, N.J. 07834. 6. Momont, H. and Sequin, B. (1982) Temporal Factors Affecting the Response to Prostaglandin F,a Products in Dairy Cattle, Proc. Ann. Mtg. Soc. for Theriog., Milwaukee, Wise., 166. 7. Randel, R. D. (1984) Seasonal Effects on Female Reproductive Functions in the Bovine (Indian Breeds) (A Review), Theriog. 21, 1, 170-185. 8. Smith, R. D., Pomerantz, A. J., Beal, W. E. McCann, J. P., Pilbeam, T. E. and Hansel, W. (1984) Insemination of Heifers at a Preset Time after Estrous Cycle Synchronization Using Pro- gesterone (PRID) and Prostaglandin, J. An. Sci. 58, 4, 792. 9. Tanabe, T. Y. and Hann, R. C. (1984) Synchronized Estrus and Subsequent Conception in Dairy Heifers Treated with Prosta- glandin F2a. I. Influence of Stage of Cycle at Treatment, J. An. Sci. 58, 4, 805. 9a. Watts, T. L. and Fuquay, J. W. (1985) Response and Fertility of Dairy Heifers Following Injection with Prostaglandin F2a During Early, Middle and Late Diestrus, Theriog. 23, 4, 655- 661.948 VETERINARY OBSTETRICS Infectious Diseases 10. Ball, L., Cheney, J. M., Mortimer, R. G. and Olson, J. D. (1983) Diagnosis and Control of Herd Infertility in Beef Cattle (Campylobacteriosis and Trichomoniasis), Proc. Ann. Mtg., Soc. for Theriog., Nashville, Tenn., 22-31. 11. Ball, L., Mortimer, R. G., Cheney, J. M. and Olsen, J. D. (1984) Trichomoniasis: Diagnosis, Pathogenesis, Treatment and Control, Proc. Ann. Mtg. AABP, 16, Oklahoma City, 163 (A Review). 12. Clark, B. L. (1983) The Effect of Tritrichomonas foetus In- fection on Calving Rates in Beef Cattle, Austral. Vet. Jour. 60, 71. 13. Corbeil, L. B. (1984) Bovine Respiratory and Reproductive In- fections: Pasteurella, Haemophilus and Campylobacter, N.Y.S. College of Veterinary Medicine Conference Proc., Jan., Ithaca, NY. 14. Doig, P. A., Ruhnke, H. L. and Miller, R. B. (1984) Bovine Reproductive Failure Associated with Ureaplasma diversum, Proc. Ann. Mtg., AABP, 16, 155 (Oklahoma City) (A Review). 15. Lein, D. H. (1982) Bovine Reproductive Disorders Associated with Ureaplasma, Mycoplasma, Hemophilus somnus and Chla- mydia, Proc. Ann. Mtg. Soc. for Theriog., Milwaukee, Wise., 118. 16. Mickelsen, W. Duane (1982) Diagnosis of Trichomoniasis: Herd History and Culture Techniques, Bovine Proc. (A.A.B.P.) 15, 134 (Nashville, Tn). 17. Miller, R. B., Lein, D. H., McEntee, K. E., Hall, C. E. and Shin, S. (1983) Haemophilus somnus Infection of the Repro- ductive Tract of Cattle: A Review, JAVMA 182, 12, 1390. 18. Olson, J. D., Ball, L., Mortimer, R. G., Farin, P. W., Adney, W. S. and Huffman, E. M. (1984) Bacteriology of Pyometra in the Dairy Cow, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., IV, XI-25-32. 19. Richards, M. W., Spitzer, J. C., Newman, S. K. and Thomp- son, C. E. (1984) Bovine Pregnancy and Nonreturn Rates Fol- lowing Artificial Insemination Using a Covered Sheath. Ther- iog. 21, 6, 949-957 (Routine use of no value). 19a. Shin, S., Kaproth, M., Lein, D., Arlitsch, H. and Howe, B. (1985) Whole Milk Extender with Antibiotics to Eliminate Campylobacter fetus from Frozen Bovine Semen, J. Dairy Sci. 68, 1280-1285. 20. Vahdat, F., Bey, R. F., Williamson, N. B., Whitmore, H. L., Zemjanis, R. and Robinson, R. A. (1983) Effects of Intrauterine Challenge with Leptospira interrogans Serovar hardjo on Fer- tility in Cattle, Theriog. 20, 5, 549. 21. Vasquez, L. A., Ball, L., Bennet, B. W., Rupp, G. P., Ellis, R., Olson, J. D. and Huffman, M. H. (1983) Bovine Genital Campylobacteriosis (Vibriosis): Vaccination of Experimentally Infected Bulls, Am. J. Vet. Res. 44, 8, 1553. Hormonal Disturbances—Cystic Ovaries and Anestrus 22a. Aanes, W. A. and Rupp, G. (1984) Iatrogenic Preputial Ste- nosis for Preparation of Teaser Bulls, JAVMA, 184, 12, 1474- 1476. 22b. Ball, P. J. H. et al. (1983) Treatment of Ovarian Acyclicity in Lactating Cows (Use of PRID and GnRH), Brit. Vet. J. 139, 6. 23. Elmarimi, A. A., Gibson, C. D., Morrow, D., Marteniuk, J. Gerloff, B. and Melancon, J. (1983) Use of Prostaglandin F2a in the Treatment of Unobserved Estrus in Lactating Dairy Cat- tle, Amer. J. Vet. Res. 44, 6, 1081. 24a. Eyestone, W. H. and Ax, R. L. (1984) A Review of Ovarian Follicular Cysts in Cows, with Comparisons to the Condition in Women, Rats and Rabbits, Theriog. 22, 2, 109-125. 24b. Flanagan, D., Oltenacu, P. A., Smith, R. D. and Milligan, R. A. (1984) Control of Reproductive Performance in Dairy Herds Through Management: Evaluation of Heat Detection Level (Economics), Proc. Ann. Mtg., Abstr., J. Dairy Sci. 68, 251. 25. Foulkes, J. A., Cookson, A. D., Sauer, M. J. and Stimpson, P. M. (1984) Insemination Without Observation, Proc. 10th In- tern. Congr. on An. Reprod. and AI, Urbana, 111. (Field study of daily milk progesterone assay). 26. Pedersen, K. M. (1983) Treatment of Cystic Ovarian Disease in the Dairy Cow with 50, 100 or 250 ug of Gonadopin-Re- leasing Hormone (GnRH, LHRH), Nord. Vet. Med. 35, 18. 27. Pilbeam, T. E., Smith, R. D. and LaFaunce, N. A. (1983) Pros- taglandin Treatment of Lactating Dairy Cows not Detected in Estrus, J. Dairy Sci. 66, Suppl. 1, 229 (Abstr). 28. Sequin, B. E., Tate, D. J. and Otterby, D. E. (1983) Use of Cloprostenol in a Reproductive Management System for Dairy Cattle, JAVMA 183, 5, 533. 29. Vasquez, L., Whitmore, H., Rodrian, J., Puckett, H., McCoy, G., Lodge, R. and Ott, R. (1984) Use of Electronic Pedometers to Measure Hourly Activity Before and After Conception (Es- trus) in Dairy Cows, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., Ill, 298. Nutritional Causes 30. Bindas, E. M., Gwazdauskas, R., Aiello, R. J., Herbein, J. H., McGilliard, M. L. and Polan, C. E. (1984) Reproductive and Metabolic Characteristics of Dairy Cattle Supplemented with Beta- Carotene, J. Dairy Sci. 67, 1249-1255 (No value). 31. Cates, W. F. and Christensen, D. A. (1983) The Effect of Nu- trition on Conception Rate in Beef Cows at Cumberland House, Saskatchewan, Can. Vet. J. 24, 145. (Phosphorus and energy.) 32. Larson, L. L., Wang, J. W., Owen, F. G. and Meader, J. E. (1983) Effect of Beta-carotene Supplementation During Early Lactation on Reproduction, J. Dairy Sci. 66, Suppl. 1, 240 (Abstr). Pathological Causes 33. Al-Guedawy, S. A., Vasquez, L., Neff-Davis, C. A., Davis, E. D., Whitmore, H. L. and Gustafson, B. K. (1983) Effect of Vehicle (Saline or Water) on Intrauterine Absorption of Gen- tamicin in Cattle, Theriog. 19, 6, 771. 34. Mortimer, R. G., Olson, J. D., Huffman, E. M., Farin, P. W., Ball, L. and Abbitt, B. (1983). Serum Progesterone Concentra- tion in Pyometritic and Normal Postpartum Cows, Theriog. 19, 5, 647. Repeat Breeders 35. Almeida, A. P., Ayalon, N., Faingold, D., Marcus, S. and Lewis, I. (1984) The Relationship between Uterine Environment and Early Embryonic Mortality in Normal and Repeat-Breeder Frie- sian Cows, Proc. 10th Intern. Congr. on An. Reprod. and AI,ADDENDUM—CURRENT SELECTED SUPPLEMENTAL REFERENCES 949 Urbana, 111., Ill, 438 (See IV; 14-41). 36. Ayalon, N. (1984) The Repeat Breeder Problem, Proc. 10th Int. Cong, on An. Reprod. and AI, Urbana, 111., IV, III-41 -50 (A Review). 37. Berepubo, N. A. and Long, S. E. (1983) A Study of the Re- lationship Between Chromosome Anomalies and Reproductive Wastage in Domestic Animals, Theriog. 20, 2, 177. 38. Bosu, W. T. K. and Leslie, K. E. (1984) The Effects of GNRH Administration Four Days After Insemination on First-Service Conception Rates and Corpus Luteum Function in Dairy Cows, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., 111, 309 (No improvement). 39. Echtemkamp, S. E., Mauer, R. R. and Kile, D. L. (1983) Con- ception, Embryonic Development and Corpus Luteum Function in Beef Cows Open for Two Consecutive Breeding Seasons, Theriog. 19, 1, 125 and 20, 6, 627. 40. Gustavsson, I. (1984) Chromosome Evaluation and Fertility, Proc. 10th Int. Congr. on An. Reprod. and AI, Urbana, 111., IV, VI- 1-8 (A Review). 41. King, W. A. and Linares, T. (1983) A Cytogenetic Study of Repeat-Breeder Heifers and their Embryos, Can. Vet. J., 24, 112. 42. Lauritsen, J. G. (1982) The Cytogenetics of Spontaneous Abor- tion, Res. in Reprod. 14, 33 (Human). 43. Lee, C. N., Maurice, E., Ax, R. L., Pennington, J. A., Hoff- man, W. F. and Brown, M. D. (1983) Efficacy of Gonadotro- pin-Releasing Hormone Administered at the Time of Insemi- nation of Heifers and Postpartum and Repeat Breeder Cows, Am. J. Vet. Res. 44, 11, 2160. 44. Linares, T., Ploen, L. and King, W. A. (1984) Zona Pellucida Defects in Eggs/Embryos from Repeat Breeder Heifers, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., Ill 457. 45. Manspeaker, J. E., Haaland, M. A., Robl, M. G., Edwards, G. E. and Russek, E. (1984) Relationship of the Degree of Per- iglandular Fibrosis in the Bovine Endometrium with Conception Rate, Proc. 10th Intern. Cong, on An. Reprod. and AI, Urbana, 111., Ill, 460 (Minimal effect on fertility). 46. Maurer, R. R. and Chenault, J. R. (1983) Fertilization Failure and Embryonic Mortality in Parous and Nonparous Beef Cattle, J. An. Sci. 56, 5, 1186. 47. Maurer, R. R. and Echtemkamp, S. E. (1984) Factors Causing Repeat-Breeder Females in Beef Cattle, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., Ill, 461. 48. Salgado, R. and Donaldson, L. E. (1984) The Effect of Intra- vaginal Progesterone on Pregnancy Rates in Cows Receiving Embryo Transfers, Tehriog. 21, 1, 258. 49. Shemesh, M., Ayalon, N., Lavi, S., Mileguir, F., Shore, L. S. and Toby, D. (1983) A New Approach to the Use of Pro- gesterone (PRID) for Pregnancy Diagnosis (and Conception), Brit. Vet. J. 139, 41-48. 50. Stevenson, J. S., Schmidt, M. K. and Call, E. P. (1984) Go- nadotropin-Releasing Hormone and Conception of Holsteins, J. Dairy Sci. 67, 1, 140-145. 50a. Tanabe, T. Y., Hawk, H. W. and Hasler, J. F. (1985) Com- parative Fertility of Normal and Repeat-Breeding Cows as Em- bryo Recipients, Theriog. 23, 4, 687-696. Postpartum Period 51. Etherington, W. G., Bosu, W. T. K., Martin, S. W., Cote, J. F. and Leslie, K. E. (1984) Reproductive Performance in Dairy Cows Following Postpartum Treatment with GNRH and/or Prostaglandin: A Field Trial, Proc. 10th Intern. Cong, on An. Reprod. and AI, Urbana, 111., Ill, 317 (Increased pyometra and anestrus after GnRH at 15 day pp). 52. Jochle, W. (1983) Review: The Critical Postpartum Period, An. Reprod. Rept., An. Health Newsletter, 6, 32, 21-39. 53. Karg, H. and Schallenberger, E. (1982) Factors Influencing Fer- tility in the Postpartum Cow, Current Topics in Veterinary Med- icine and Animal Science, 20, Martinus Nijhoff Publ., The Hague. 54. Lee, C. N. and Ax, R. L. (1984) Milk Progesterone of Dairy Cows Injected with GnRH at the First Postpartum Breeding, Proc. 10th Intern. Cong, on An. Reprod. and AI, Urbana, 111., Ill, 401. 55. Lee, C. N., Critser, J. K. and Ax, R. L. (1984) Endocrine Changes in Cows Injected with Gonadotropin-releasing Hor- mone at First Service, Proc. Ann. Mtg. Abstr., J. Dairy Sci. 68, 149. 56. Leslie, K. E. (1983) The Effects of Gonadotrophin-releasing Hormone Administration in Early Postpartum Dairy Cows on Hormone Concentrations, Ovarian Activity and Reproductive Performance: A Review. Can. Vet. J. 24, 116. 57. Oltenacu, P. A., Britt, J. H., Braun, R. K. and Mellenberger, R. W. (1983) Relationship Among Type of Parturition, Type of Discharge from Genital Tract, Involution of Cervix and Sub- sequent Reproductive Performance in Holstein Cows, J. Dairy Sci. 66, 612. 58. Rutter, L. M. and Randel, R. D. (1984) Luteal Competency During the Resumption of Ovarian Cyclicity in Postpartum (Brahman) Cows, Theriog. 21, 5, 713-723. Management Problems 59. Bourdon, R. M. and Brinks, J. S. (1983) Calving Date Versus Calving Interval as a Reproductive Measure in Beef Cattle, J. An. Sci., 57, 6, 1412. 59a. Britt, 1. H. (1985) Enhanced Reproduction and Its Economic Implications, J. Dairy Sci. 68, 1585-1592. 60. Fonseca, F. A., Britt, J. H., McDaniel, B. T., Wilk, J. C. and Rakes, A. H. (1983) Reproductive Traits of Holsteins and Jer- seys. Effects of Age, Milk Yield, and Clinical Abnormalities on Involution of Cervix and Uterus, Ovulation, Estrous Cycles, Detection of Estrus, Conception Rate and Days Open, J. Dairy Sci. 66, 1128. 61. Foote, R. H., El-Wishy, A. B. and Cavestany, D. (1984) Cli- matic Effects on Fertility of Holsteins Inseminated Artificially, Proc. 10th Intern. Congr. on An. Reprod. and AI, II, 138 (Low fertility May-Oct, 7-17% in S. Florida). 62. Francos, G. and Mayer, E. (1983) Observations on Some En- vironmental Factors Connected with Fertility in Heat-Stressed Cows, Theriog. 19, 5, 625. 63. Gwazdauskas, F. C., Lineweaver, J. A. and McGilliard, M. L. (1982) Environmental and Management Factors Affecting Es- trous Cycle Activity in Dairy Cattle, J. Dairy Sci. 66, 1510. 64. Schultz, R. H., Editor (1984) Reproductive Management in Food Animals (A Symposium Proceedings on Applied Uses of Pros- taglandin Compounds in Cattle and Swine), Spec. Edit. Comped, on Contin. Educat. (Fall Conference, Univ. of Minn.), pp 1- 63. 65. Turner, H. G. (1982) Genetic Variation of Rectal Temperature in Cows and Its Relationship to Fertility, Anim. Prod. 35, 401. 66. Wiltbank, J. N. (1983) Maintenance of a High Level of Repro-950 VETERINARY OBSTETRICS ductive Performance in the Beef Cow Herd. Vet. Clin, of N. Amer., Lg. An. Pract. 5, 1, 41. Chapter XIV—Infertility in the Mare General 1. Rowlands, I. W., Allen, W. R. and Rossdale, P. D. (1982) Proc. 3rd International Symposium on Equine Reproduction, Sydney, Australia, J. Reprod. & Fert., Suppl. 32, P. O. Box 32, Commerce Way, Colchester, C02 8HP, Essex, UK. 2. Neely, D. P., Liu, I. K. M., Hillman, R. B. and Hughes, J. P. (1983) Equine Reproduction, Hoffman LaRoche Inc., Nut- ley, NJ 07110, (A Review). Physiology, Estrous Cycle and Nutrition 3. Belling, T. H. Jr. (1983) Reproduction in the Mare: A Com- pedium of Published Normal Data, Eq. Pract. 5, 9, 13. 4. Bergfelt, D. R. and Ginther, O. J. (1984) Follicle Suppression by a Proteinaceous Fraction of Follicular Fluid in Mares, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., Ill, 491 (“Inhibin”?). 5. Bristol, F. (1982) Breeding Behaviour of a Stallion at Pasture with 20 Mares in Synchronized Oestrus, J. Reprod. and Fert. Suppl. 32, 71-77. 6. Bristol, F., Jacobs, K. A. and Pawlyshyn, V. (1983) Synchro- nization of Estrus in Post-Partum Mares with Progesterone and Estradiol, Theriog. 19, 6, 779. 7. Draincourt, M. A. and Palmer, E. (1984) Time of Ovarian Fol- licular Recruitment in Cyclic Pony Mares, Theriog. 21, 4, 591 — 600. 8. Ginther, O. J. (1983) Sexual Behavior Following Introduction of a Stallion into a Group of Mares, Theriog. 19, 6, 877. 9. Ginther, O. J., Scraba, S. T. and Nuti, L. C. (1983) Pregnancy Rates and Sexual Behavior under Pasture Breeding Conditions in Mares, Theriog. 20, 3, 333. 10. Henneke, D. R., Potter, G. D. and Kreider, J. L. (1984) Body Condition During Pregnancy and Lactation and Reproductive Efficiency of Mares, Theriog. 21, 6, 897-909 (Similar to cat- tle). 11. Hintz, H. F. and Squires, E. L. (1983) Equine Reproduction and Nutrition (A Reveiw), J. An. Sci. 57, Suppl. 2, 58. 11a. Hughes, J. P., Couto, M. A. and Stabenfeldt, G. H. (1985) Fertility of Ovulations Occurring During the Luteal Phase of the Estrous Cycle (Abstr.), JAVMA, 187, 3, 292. 12. Irvine, C. H. G. (1984) Pituitary Hormones: Basic Aspects, Eq. Vet. Sci. 3, 6, 203-207. (Review inch “Folliculostatin”.) 13. Maker, J. M., Squires, E. L., Voss, J. L. and Shideler, R. K. (1983) Effect of Anabolic Steroids on Reproductive Function of Young Mares, JAVMA 183, 5, 519. 14. Okolski, A. (1984) Mares’ Ovarian Function and Unfertilized Egg Retention, Proc. 10th Intern. Congr. on A. Reprod. and AI, Urbana, 111., Ill, 484 (Equal numbers of ova from each ovary of 1163 mares and average of 3.7 (0-24) unfertilized oviductal eggs/mare). 15. Palmer, E., Draincourt, A. and Ortavant, R. J. (1982) Photo- periodic Stimulation of the Mare during Winter Anoestrus, J. Reprod. Fert., Suppl. 32, 275, 282. 16. Scraba, S. T. and Ginther, O. J. (1984) Lighting Programs to Stimulate Onset of the Ovulatory Season in Pony Mares, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., II, 150 (15 hrs. light, 9 hrs. dark was best). 17. Squires, E. L., Pickett, B. W. and Voss, J. L. (1984) Repro- ductive Performance of Horses During and After Anabolic Ste- roid Treatment, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., IV, XII-28-38. 18. Withrow, J. M., Sargent, G. F., Scheffrahn, N. S. and Kessler, D. J. (1983) Induction of Male Sex Behavior in Pony Mares with Testosterone Propionate, Theriog. 20, 4, 485. Genital Infection and Pathology 19. Acland, H. M., Allen, P. Z. and Kenney, R. M. (1983) Con- tagious Equine Metritis: Distribution of Organisms in Experi- mental Infection of Mares, Amer. J. Vet. Res. 44, 7, 1197 (A Review) (F. A. Staining). 20. Allen, W. E. and Newcombe, J. R. (1979) Aspects of Genital Infection and Swabbing Techniques in the Mare, Vet. Rec., 104, 228. 21. Asbury, A. C. (1982) Some Observations on the Relationship of Histologic Inflammation in the Endometrium of Mares to Fer- tililty, Proc. 28th Ann. Mtg., A.A.E.P., Atlanta, Ga. 22. Asbury, A. C. (1984) Uterine Defense Mechanisms in the Mare: The Use of Intrauterine Plasma in the Management of Endome- tritis, Theriog. 21, 387-393. 23. Asbury, A. C., Gorman, N. T. and Foster, G. W. (1984) Uter- ine Defense Mechanisms in the Mare: Serum Opsonins Affect- ing Phagocytosis of Streptococcus zooepidemicus by Equine Neutrophils, Theriog. 21, 2, 375-385. 24. Belling, T. H., Jr. (1983) Surgery of the Vulva (of Mares), Modification of the Caslick Operation, Eq. Pract. 5, 6, 870. 25. Belling, T. H., Jr. (1984) Clinical Observations of Post-Ovu- lation Breeding and Related Phenomena in the Mare, Eq. Pract. 6, 6. 26. Blue, M. G. and Oriol, J. G. (1982) Conception in Mares Fol- lowing Intrauterine Therapy with Amikacin, J. Eq. Vet. Sci. 2, 200. 27. Bosu, W. T. K., Raeside, J. I. and Franks, T. (1984) Plasma Steroid Concentrations in Mares with Ovarian Problems, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., Ill, 445 (High plasma testosterone levels in mares showing virilism due to granulosa cell tumors). 28. Gingerich, D. A., Rourke, J. E., Chatfield, R. C. and Strom, P. W. (1983) Amikacin: A New Aminoglycoside for Treating Equine Metritis, Vet. Med/Sm. An. Clin., 78, 787. 29. Ginther, O. J. and Pierson, R. A. (1984) Ultrasonic Anatomy and Pathology of the Equine Uterus, Theriog. 21, 3, 505-516. 30. Gross, T. L. and LeBlanc, M. M. (1984) Seasonal Variation of Histomorphologic Features of Equine Endometrium, JAVMA, 184, 11, 1379-1382. 31. Jones, E. and Kent, M. (1983) Sex Reversal Syndrome (Genetic Gonadal Dysgenesis and Testicular Feminization in Arabian Horses), Eq. Vet. Data, 4, 23, 353. 32. King, S. S. and Evans, J. W. (1984) Equine Endometrial PGF2a Production in Response to Oxytocin and Arachidonic Acid Dur- ing the Normal Estrous Cycle and the Spontaneously Prolonged Corpus Luteum Syndrome, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana. 111., Ill, 483. (Block of PGF2asynthesis during latter syndrome.) 33. Knudsen, Odd (1982) A Combined Cytologic and BacteriologicADDENDUM—CURRENT SELECTED SUPPLEMENTAL REFERENCES 951 Endometrial Examination in the Mare, Proc. 28th Ann. Mtg., A.A.E.P., Atlanta, Ga. 34. LeBlanc, M. M. and Gross, T. L. (1982) Seasonal Variation in Uterine Morphology of Mares: A Clinical and Histopathologic Study, Proc. Ann. Mtg. Soc. for Theriog., Milwaukee, Wis. 168. 35. Sahu, S. P., Rommel, F. A., Fales, W. H., Hamdy, F. M., Swerczek, T. W., Youngquist, R. S. and Bryans, J. T. (1983) Evaluaton of Various Serotests to Detect Antibodies in Ponies and Horses Infected with Contagious Equine Metritis Bacteria, Am. J. Vet. Res., 44, 8, 1405. 36. Shideler, R. K., Voss, J. L. and Squires, E. L. (1984) Treat- ment of Endometritis in Mares, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., Ill, 470 (Excellent results with 2% betadine alone or with serum or systemic antibiotics plus good management). 36a. Villahoz, M. D., Squires, E. L., Voss, J. L. and Shideler, R. K. (1985) Some Observations on Early Embryonic Death in Mares, Theriog. 23, 6, 915-924. 37. Wingfield, Digby, N. J. (1978) The Technique and Clinical Ap- plication of Endometrial Cytology in Mares, Eq. Vet. J., 10, 167. Chapter XV—Infertility in Sows la. Cantley, T. C., Redmer, D. A., Osweiler, G. D. and Day, B. N. (1983) Effect of Zearalenone Mycotoxin on Prolonging Lu- teal Function in Gilts, J. An. Sci. 55, Suppl. 1, 17 (Abstr.). lb. Christenson, R. K. (1984) Influence of Number of Gilts per Pen on Estrous Traits in Confinement-Reared Gilts, Theriog. 22, 3, 313-319. lc. Cole, D. J. A. and Foxworth, G. R. (1982) Control of Pig Re- production, Butterworth Publishers, 80 Montvale Ave., Stone- ham, Mass. 02180. ld. Dial, G. D., BeVier, G. W., Hixon, J. E. and Gustafson, B. K. (1984) Endocrine Pathogenesis of Postweaning Anestrus in Swine: Response of the Persistently Anestrous Sow to Hormonal Stimuli, Am. J. Vet. Res. 45, 9, 1737-1742 (PMSG only hor- mone capable of inducing a fertile estrus). 2. Hurtgen, J. (1983). Slaughterhouse Evaluation of Swine Repro- ductive Organs, Proc. Ann. Mtg. Soc. for Theriog., Milwau- kee, Wise., 9. 3. Hurtgen, J. P. and Johnston, S. D. (1983) Response of Gilts with Delayed Puberty to Pregnant Mare Serum Gonadotropin or Estrogen, Am. J. Vet. Res. 44, 10, 1943. 4. Stephens, D. B. and Close, W. H. (1984) The Influence of Transportation, Proximity of Adults and Other Stimuli on the Age of Onset of First Puberty in the Gilt, Cor. Vet. 74, 187— 197. Chapter XVI—Infertility in Ewes and Does Ewes 1. Ainsworth, L. and Shrestha, J. N. B. (1983) Effect of Type of Intravaginal Progestogen Treatment on Estrous Response and Reproductive Performance of Ewes, Theriog. 19, 869. 2. Langford, G. A., Marcus, G. J. and Batra, T. R. (1983) Sea- sonal Effects of PMSG and Number of Inseminations on Fer- tility of Progestogen-Treated Sheep, J. An. Sci. 57, 2, 307. 3. Riera, G. S. (1984) Some Similarities and Differences in Fe- male Sheep and Goat Reproduction, Proc. 10th Int. Congr. on An. Reprod. and AI, Urbana, 111., IV, VII-1-7 (A Review). 4. Woody, C. O., Beauchene, S. L., Feccia, R. C., Sepe, P. A., Higgins, F. M., Cowan, W. A. and Riesen, J. W. (1983) Reg- ulation of the Estrous Cycle in Ewes with Progestin Containing Implants (“Norgestomet”), Theriog. 19, 5, 677. Does 5. Bretzlaff, K. N., Hill, A. and Ott, R. S. (1983) Induction of Luteolysis in Goats with Prostaglandin F2s, Amer. J. Vet. Res. 44, 6, 1162. 6. Corteel, J. M., Baril, G., Leboeuf, B. and Boue, P. (1984) A Comparison of Two Hormonal Treatments to Provoke Oestrus and Ovulation in the Anoestrus Dairy Goat, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., Ill, 313. 7. Homer, G. W., Hunter, R. and Day, A. M. (1982) An Outbreak of Vulvovaginitis in Goats Caused by a Caprine Herpesvirus, N. Z. Vet. J. 30, 150. 8. Lawson, J. L., Forrest, D. W. and Shelton, M. (1984) Repro- ductive Response to Suckling Manipulation in Spanish Goats, Theriog. 21, 5, 247. 9. Mizinga, K. M. and Verma, O. P. (1984) LHRH—Induced Ovulation and Fertility of Anestrous Goats (including persistent C.L., pseudopregnancy and mucometra), Theriog. 21, 3, 435- 445 (see 444). Chapter XVII—Infertility in the Bitch and Queen Chapter XVIII—Infertility in the Male Anatomy and Physiology 1. Amann, R. P. and Shanbacher, B. O. (1983) Physiology of Male Reproduction (A Review), J. An. Sci., 57, Suppl. 2, 380. 2. Bartels, J. E., Beckett, S. D. and Brown, B. G. (1984) An- giography of the Corpus Cavemosum Penis in the Pony Stallion During Erection and Quiescence, Am. J. Vet. Res. 45, 7, 1464. 3. Foote, R. H. (1984) General Evaluation of Male Reproductive Capacity, Proc. 10th Intn. Congr. on An. Reprod. and AI, Ur- bana, 111., IV, C-l-8 (A Review). Bulls 4. Alanko, M. and Virula, M. (1984) Tail Stump Sperm Defect in Ayrshire Bulls, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., Ill, 522. (Probably due to a single recessive autosomal gene causing a complete lack of motility.) 5. Ball, L., Ott, R. S., Mortimer, R. G. and Simons, J. C. (1983) Manual for Breeding Soundness Examination of Bulls, J. Soc. for Theriog., XII, Assoc. Bldg. 9th and Minnesota, Hastings, Nebr. 68901. 6. Blom, E. (1979) Studies on Seminal Vesiculitis in the Bull, Nord. Vet. Med. 31, 193-205 and 241-250. 7. Blom, E. (1982) Aplasia of the Ductuli Efferentes—a New Ster- ilizing Congenital Syndrome in the Bull, Nord. Vet. Med 34, 431.952 VETERINARY OBSTETRICS 8. Blom, E. (1983) The Spermiogram of the Bull, Nord. Vet. Med. 35, 105-130. (A Review). 9. Bowen, R. A., Howard, T. H., Entwistle, K. W. and Pickett, B. W. (1983) Seminal Shedding of Bluetongue Virus in Ex- perimentally Infected Mature Bulls, Amer. J. Vet. Res. 44, 12, 2268. 10. Cates, W. F. (1983) Examination of the Bull for Breeding Soundness, Vet. Clin, of N. Amer., Lg. An. Pract., 5, 1, 157. 11. Chenoweth, P. J. (1983) Examination of Bulls for Libido and Breeding Ability, Vet. Clin, of N. Am., Lg. An. Pract. 5, 1, 59. 12. Hrodecky, P., Sis, R. F. and Klemm, W. R. (1983) Distribution of Flehmen Reactions of the Bull Throughout the Bovine Es- trous Cycle, Theriog. 20, 2, 197. 13. Hudson, R. S. and Wolfe, D. F. (1984) Physical Defects Which Limit Breeding Soundness of Bulls (A Review), Proc. Ann. Mtg. AABP, 16, 144-146. 14. Humphrey, J. D., Little, P. B., Barnum, D. A., Doig, P. A., Stephens, L. A. and Thorsen, S. (1982) Occurrence of “Hae- mophilus somnus” in Bovine Semen and in the Prepuce of Bulls and Steers, Can. J. Comp. Med. 46, 215. 15a. Mader, D. R. and Price, E. O. (1984) The Effects of Sexual Stimulation on the Sexual Performance of Hereford Bulls, J. An. Sci., 59, 2, 294-300. 15b. Metz, A. L., Haggard, D. L. and Hakomaki, M. R. (1984) Chronic Suppurative Orchiepididymitis Associated with Hae- mophilus somnus in a Calf, JAVMA, 184, 12, 1507. 16. Wiltbank, J. A. (1982) Evaluation of Bulls for Potential Fertil- ity, Proc. Ann. Mtg. Soc. for Theriog., Milwaukee, Wise., 141. 17. Wolfe, D. F., Hudson, R. S., and Walker, D. F. (1983) Com- mon Penile and Preputial Problems of Bulls, Comped, on Cont. Educ. 5, 8. Stallions 18. Arighi, M., Bosu, W. T. K., Raeside, J. I. and Singh, A. (1984) A Hormonal Technique for the Detection of Retained Testes in Horses, Proc. 10th Intern. Congr. on An. Reprod. and AI, Ur- bana, 111., II, 265. 19. Bristol, F. (1982) Breeding Behaviour of a Stallion at Pasture with 20 Mares in Synchronized Estrus, J. Reprod. Fert. Suppl. 32, 71-77. 20. Hughes, J. P. (1983) Significance of Fertility Evaluation of the Stallion, Proc. Ann. Mtg. Soc. for Theriog., Nashville, Tenn., 167-175. 20a. Irvine, C. H. G., Alexander, S. L. and Hughes, J. P. (1985) Sexual Behavior and Serum Concentrations of Reproductive Hormones in Normal Stallions, Theriog. 23, 4, 607-617 (Re- view). 21. Kenney, R. M., Hurtgen, J., Pierson, R., Witherspoon, D. and Simmons, J. (1983) Theriogenology and the Equine, Part II, The Stallion, J. of the Soc. for Theriog., Hastings, Nebr. 68901. 22. Neely, D. P. (1983) Stallion Reproductive Physiology, Proc. Ann. Mtg. Soc. for Theriog., Nashville, Tenn., 137-147. 23. Peterson, D. E. (1984) Equine Testicular Tumors, Eq. Vet. Sci. 4, 1, 25 (A Review). 24. Rich, G. A., McGlothlin, D. E., Lewis, L. D., Squire, E. L. and Pickett, B. W. (1984) Effect of Vitamin E. Supplementation on Stallion Seminal Characteristics and Sexual Behavior, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., II, 163. (No effect.) 25. Wallach, S. J. R., Pickett, B. W. and Nett, T. M. (1983) Sexual Behavior and Serum Concentrations of Reproductive Hormones in Impotent Stallions. Theriog. 19, 6, 833. Boars 26. Alanko, M. (1984) The Knobbed Sperm Defect in Boars: Fer- tility and Inheritance of the Defect, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., Ill, 521. (This defect due to a single recessive autosomal gene with incomplete penetrance causing altered sperm transport and early embryonic deaths.) 27. Blom, E. and Jensen, P. T. (1984) Studies on Boar Semen: III Sperm Concentration and Seminal Plasma Total Solids, Acta Vet. Scand. 25, 1-6. 28. Hurtgen, J. P. (1984) Reproductive Examination of the Boar, Jour, of The Soc. for Theriog., Vol. XIII, 1-48 (A Review). 29a. Juniewicz, P. E., Toelle, V. D., Robison, O. W. and Johnson, B. H. (1984) Variation in Testosterone Production Among Boars and Its Relationship to Sexual Interest and Breeding Perfor- mance, Theriog. 22, 3, 259-268 (No relation!). 29b. Paquignon, M., Nowak, R., Kuo, Y. H. and Signoret, J. P. (1984) Sperm Production in the Boar under Intensive Ejacula- tion Rhythm, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., II, 61. (Over 2 ejaculations/day = lowered fertil- ity). Rams and Bucks 30a. Healey, Mark (Editor) (1984) Ram Epididymitis Control, Proc. Western Regional Coordinating Comm. Mtg., Grand Junct., Colo., Dept, of Animal, Dairy and Vet. Sci., Utah State Univ., Logan, Ut., 84322. 30b. Memon, M. A. (1983) Male Infertility, from Symposium on Sheep and Goat Medicine, Edit, by Smith, M. C., Vet. Clinics of North Amer. 5, 3, 619-635, W. B. Saunders Co., Phila- delphia. Dogs and Toms 31. Dooley, M. P., Murase, K. and Pineda, M. H. (1983) An Elec- troejaculator for the Collection of Semen from the Domestic Cat. Theriog. 20, 3, 297. 32. Dooley, M. P., Pineda, M. H., Hopper, J. G. and Hsu, W. H. (1984) Retrograde Flow of Semen Caused by Electroejaculation in the Domestic Cat, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., Ill, 363. (Semen going into bladder may be normal during ejaculation in some animals.) 33. Hart, B. L. and Cooper, L. (1984) Factors Relating to Urine Spraying and Fighting in Prepubertally Gonadectomized Cats, JAVMA, 184, 10, 1255-1258. 34. Howard, J. G., Bush, M., Hall, L. L. and Wildt, D. E. (1984) Morphological Abnormalities in Spermatozoa of 28 Species of Non-Domestic Felids, Proc. 10th Intn. Congr. on An. Reprod. and AI, Urbana, 111., II, 57 (19 of 28 toms had over 45% ab- normal (spermatozoa). (No effect on fertility.) 35. Klausner, J. S. and Osborne, C. A. (1983) Management of Ca- nine Bacterial Prostatitis, JAVMA 182, 292. 36. Laing, E. J., Harari, J. and Smith, C. W. (1983) Spermatic Cord Torsion and Sertoli Cell Tumor in the Dog, JAVMA, 183, 8, 879.ADDENDUM—CURRENT SEUECTED SUPPLEMENTAL REFERENCES 953 37. Larsen, R. E. (1983) Breeding Soundness and Semen Handling in the Stud Dog, Proc. Ann. Mtg. Soc. for Theriog., Nashville, Tenn. 129-135. 38. Morgan, R. V. (1982) Blood Dyscrasias Associated with Tes- ticular Tumors in the Dog, JAAHA 18, 970. 39. Pineda, M. H. and Dooley, M. P. (1984) Surgical and Chemical Vasectomy in the Cat. (Population Control), Am. J. Vet. Res. 45, 2, 291-299. Chapter XIX—Artificial Insemination 1. Amann, A. P. (1984) Preservation of the Male Gamete (Bull, Stallion, Dog), Proc. 10th Int. Cong, on An. Reprod. and AL, Urbana, 111., IV, 11-28-36, (A Review). 2. Amann, R. P. and Pickett, B. W. (1984) An Overview of Fro- zen Equine Semen: Procedures for Thawing and Insemination of Frozen Equine Spermatozoa, Special Series 33, Colo. State Univ. Exper. Stat. Ft. Collins, Colo. 80523, 1-30. 3. Bowen, R. A. and Howard, T. H. (1984) Transmission of Blue- tongue Vims by Intrauterine Inoculation or Insemination of Vi- rus-Containing Bovine Semen, Am. J. Vet. Res., 45, 7, 1386. 4. Cochran, J. D., Amann, R. P., Squires, E. L. and Pickett, B. W. (1983) Fertility of Frozen-Thawed Stallion Semen Extended in Lactose-EDTA-Egg-Yolk Extender and Packaged in 1.0-ML Straws, Theriog. 20, 6, 735. 5. Corteel, J. M. and Pauignon, M. (1984) Preservation of the Male Gamete (Ram, Buck, Boar), Proc. 10th Int. Congr. on An. Re- prod. and AI, Urbana, 111., IV, 11-20-27. (A Review). 6. Cristanelli, M. J., Squires, E. L., Amann, R. P. and Pickett, B. W. (1984) Fertility of Stallion Semen Processed, Frozen and Thawed by a New Procedure, Theriog. 22, 1, 39-45. (Preg- nancy rate with frozen semen 86% of the rate with fresh semen.) 7. Douglas-Hamilton, D. H., Osol, R., Olsol, G., Driscoll, D. and Noble, H. (1984) A Field Study of the Fertility of Transported (Liquid) Semen, Theriog. 22, 3, 291-304 (Good results from slow cooling for over 36 hours). 8. Froman, D. P. and Amann, R. P. (1983) Inhibition of Motility of Bovine, Canine and Equine Spermatozoa by Artificial Vagina Lubricants. Theriog. 20, 3, 357. 9. Gledhill, B. L. (1983) Cytometry of Deoxyribonucleic Acid Content and Morphology of Mammalian Sperm, J. Dairy Sci. 66, 2623-2634. (Sexing of Mammalian Sperm, A Review). 10. Lunstra, D. D., Hays, W. G., Bellows, R. A., Laster, D. B. and Hruska, L. (1983) Clitoral Stimulation and the Effect of Age, Breed, Technician and Postpartum Interval on Pregnancy Rate to Artificial Insemination in Beef Cattle, Theriog. 19, 555. 11. Newman, S. K. (1983) Do We Need More A.l. Sanitary Pre- cautions? (Use of “Protected” or “Double” Sheath for Pipette), Hoards Dairymen, Feb. 10th, 172 and Richards, M., (1984) Ef- fect of a Covered Sheath on A.L in Bovine Females, Theriog., 1985. 11a. Province, C. A., Squires, E. L., Pickett, B. W. and Amann, R. P. (1985) Cooling Rates, Storage Temperatures and Fertility of Extended Equine Spermatozoa, Theriog. 23, 6, 925-934. 12. Sullivan, J. J. (1982) Semen Handling—A Factor Which Af- fects Fertility, Proc. Ann. Mtg. Soc. for Theriog., Milwaukee, Wise., 81. 13. Thacker, B. J., Larsen, R. E., Joo, H. S. and Leman, A. D. (1984) Swine Diseases Transmissible with Artificial Insemina- tion, JAVMA, 185, 5, 511-516 (A Review). Chapter XX—Embryo Transfer 1. Allen, W. R. and Antczak, D. F. (Editors) (1985) Equine Em- bryo Transfer, Eq. Vet. Jour., Suppl. 3, Mar. pp. 1-114. la. Armstrong, D. T. and Evans, G. (1983) Factors Influencing Success of Embryo Transfer in Sheep and Goats, Theriog. 19, 1, 31. 2. Bolin, S. R. and Bolin, C. A. (1984) Pseudorabies Virus In- fection of Six- and Ten-Day-Old Porcine Embryos, Theriog. 22, 1, 101-108. 3. Bolin, S. R., Runnels, L. J., Turek, J. I. and Gustafson, D. P. (1982) Observations on Pseudorabies Virus, Porcine Parvovirus and Porcine Enterovirus in Porcine Embryo Transfer, Proc. 86th Ann. Mtg., U.S.A.H.A., Nashville, Tn., 391. 4. Bowen, R. A. (1984) Viral Agents and Embryo Loss, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., IV, XIII-16-21. 5. Bowen, R. A., Howard, T. H., Elsden, R. P. and Seidel, G. E., Jr. (1983) Embryo Transfer from Cattle Infected with Blue- tongue Virus, Amer. J. Vet. Res. 44, 9, 1625. 6. Brackett, B. G., Seidel, G. E. Jr. and Seidel, S. M. (1982) New Technologies in Animal Breeding, Academic Press Inc., P. O. Box 733, Old Chelsea Station, N.Y., N.Y. 10113. 7. Donaldson, L. E. (1984) Embryo Production in Superovulated Cows: Transferrable Embryos Correlated with Total Embryos, Theriog. 21, 4, 517-524. 8a. Donaldson, L. E. (1984) The Day of Estrous Cycle that FSH is Started and Superovulation in Cattle, Theriog. 22, 1, 97-99. (Equal number of embryos obtained when FSH treatment started on days 9 through 13 of the estrous cycle.). 8b. Donaldson, L. E. (1984) Dose of FSH-P as Source of Variation in Embryo Production from Superovulated Cows, Theriog. 22, 2, 205-212. (Recommended 4 day treatment with 28 mg or less per dose of FSH-P) 9. Drost, M., Wright, J. M., Jr., Cripe, W. S. and Richter, A. R. (1983) Embryo Transfer in Water Buffalo (Bubalus bubalis), Theriog. 20, 5, 579. 10. Hare, W. C. D. (1983) Embryo Transfer and Disease Trans- mission in Farm Animals, Proc. 87th Ann. Mtg. USAHA, Las Vegas (A Review). 11. Hare, W. C. D. (1984) Embryo Transfer and Disease Trans- mission (An Overview), Proc. 10th Into. Congr. on An. Re- prod. and AI, Urbana, 111. IV, IX-1-8. 12. Hasler, J. F., McCauley, A. D., Schermerhom, E. C. and Foote, R. H. (1983) Superovulatory Responses of Holstein Cows, Theriog. 19, 1, 83. 13. Iuliano, M. F. and Squires, E. L. (1983) Pregnancy Rates after Transfer of 7 or 8-day-old Equine Embryos either Surgically or Non-Surgically, Theriog. 19, 1, 134. 14. James, J. E., James, D. M., Martin, P. A., Reed, D. E. and Davis, D. L. (1983) Embryo Transfer for Conserving Valuable Genetic Material from Swine Herds with Pseudorabies, JAVMA 183, 5, 525. 15. James, D. M., Martin, P. A. and Davis, D. L. (1983) Repopu- lation of Pseudorabies-Infected Swine Herds by Embryo Trans- fers, J. An. Sci. 55, Suppl. 1, 188 (Abstr.). 16. Lehn-Jensen, H. (1984) Deep Freezing of Cattle Embryos, Proc. 10th Int. Congr. on An. Reprod. and AI, Urbana, 111., IV, 1-1- 12, (A Review). 17. Leibo, S. P. (1984) A One-Step Method for Direct Nonsurgical Transfer of Frozen-Thawed Bovine Embryos, Theriog. 21, 5, 767-789.954 VETERINARY OBSTETRICS 18. Lindner, G. M., Anderson, G. B., BonDurant, R. H. and Cupps, P. T. (1983) Survival of Bovine Embryos Stored at 4° C, Ther- iog. 20, 3, 311. 19. Lindner, G. M. and Wright, R. W., Jr. (1983) Bovine Embryo Morphology and Evaluation, Theriog. 20, 4, 407. 20. Markert, C. L. (1984) Genetic Manipulation of Mammalian Embryos: Current Techniques and Their Potential Usefulness in Livestock Improvement, 10th Int. Congr. on An. Reprod. and AI, Urbana, 111., IV, 11-13-19. 21. Shea, B. F., Janzen, R. E., McAlister, R. J. and McDermand, D. P. (1983) Freezing of Bovine Embryos: Effects of Embryo Qualilty, Time from Thawing to Transfer and Number Frozen per Vied, Theriog. 20, 2, 205. 22. Singh, E. L., Hare, W. C. D., Thomas, F. C., Eaglesome, M. D. and Bielanski, A. (1983) Embryo Transfer as a Means of Controlling the Transmission of Viral Infections. IV Non-Trans- mission of IBR/IPV Following Trypsin Treatment of Exposed Embryos, Theriog. 20, 2, 169. 23. Slade, N. P., Williams, T. J., Squires, E. L. and Seidel, G. E., Jr. (1984) Production of Identical Twin Pregnancies by Mi- crosurgical Bisection of Equine Embryos, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., II, 241. (Difficult in mare due to early capsule development (day 6) of embryo.) 24. Takeda, T., Elsden, R. P. and Squires, E. L. (1984) In vitro and in vivo Development of Frozen-Thawed Equine Embryos, Proc. 10th Intern. Congr. on An. Reprod. and AI, Urbana, 111., II, 246. (Must freeze before blastocyst stage, before day 7.) 25. Woods, G. L. and Ginther, O. J. (1983) Induction of Multiple Ovulations During the Ovulatory Season in Mares, Theriog. 20, 3, 347. 26. Woods, G. L. and Ginther, O. J. (1983) Recent Studies Relat- ing to the Collection of Multiple Embryos in Mares, Theriog. 19, 1, 101. 27. Woods, G. L. and Ginther, O. J. (1984) Collection and Transfer of Multiple Embryos in the Mare, Theriog. 21, 3, 461-469.INDEX Abnormalities (see anomalies) Abortion (also see mummification), 123-222, 705, 728-741 causes of, 123, 127, 162, 163, 180, 193, 207, 211, 705, 728- 741 definition of, 38, 123 diagnosis of (causes of) 123-125, 153, 162, 180, 192, 208, 211, 212 due to abscesses and adhesions of uterus, 153 allergies or anaphylaxis, 153 anomalies of the fetus, 126, 152, 173, 201 arsenic, 148 campylobacteriosis (vibriosis), 134, 193, 194 chemicals, 147-149, 170, 188 chlamydiosis, 137 chlorinated napthalenes, 148 chromosomal defects, 126, 152, 173, 174, 189, 202, 209, 213 douching of the pregnant uterus, 151, 173 drugs, 147-149, 170, 201, 209 endocrine deficiencies (mainly progesterone), 150, 171, 172, 201,209, 212, 406, 438, 561-565, 673, 692, 715 endotoxins, 136 ergot, 148, 188, 201 estrogens, 149, 170, 188, 201, 209, 213, 404, 692 glucocorticoids, 149, 172, 173, 188, 201, 209, 408 hereditary or congenital disease of fetus, 123-222 hormones, 149, 150, 170-173, 201, 209, 213, 220-222, 248-251, 404, 407, 408, 691-694, 705, 707 inanition, 151, 201, 202, 213 insemination during pregnancy, 151 ketosis in ewes, 202 lack of uterine caruncles and placenta, 153, 173 lack of progesterone (see due to endocrine deficiencies) lead, 148, 201 manual trauma to amniotic vesicle, embryo or fetus, 151 miscellaneous bacteria: cows, 135-137 mares, 162-165 sows, 183, 184 ewes, 197 bitches, 207, 208, 732, 735, 738 queens, 735, 738 mycotic or fungal agents, 145, 148, 170, 188, 199 nitrates, 147 nutritional deficiencies, 150, 151, 173, 188, 202 pediculosis, 146, 153 phenothiazine, 170, 201 physical causes, 125, 151, 152, 173, 188, 209 plant poisons, 147-149, 188, 201 poisons, 147-149, 170, 201 prostaglandins, 150, 171, 188, 201, 407, 438, 691-699, 707 protozoa, 146, 170, 188, 200 purgatives, 170 removal of corpus luteum, 151, 171, 172, 201, 209, 212 rickettsia, 136, 137 septic processes, 152, 188 shipping (stress), 136, 172, 188, 202 sodium iodide, 148 starvation, 157, 172, 201, 202 strangulation of uterus, 173 stress, 152, 172, 173, 188, 201, 202 surgical operations, 152 torsion of the umbilical cord, 152, 173 torsion of the uterus, 152, 173 trauma, 125, 151, 152, 173, 209 twinning, 99, 100, 152, 174, 175 vaccination, 187, 199 violence, 125, 152 viruses, 138-145, 165-170, 184-188, 197-199, 209, 211, 212, 729 yeasts, 170 enzootic in sheep, 138, 197, 198 epizootic in cattle (EBA), 137, 138 importance of, 123 in anaplasmosis, 146 animals, infectious for humans, 147 bovine virus diarrhea (BVD-MD) 142, 143. 199 brucellosis—of cattle, 126-131, 374 of horses, 163, 165 of sheep, 195, 196 of swine, 182, 183 of dogs, 206-208, 728, 729 cats, 210-213, 705, 741 cattle, 125-162 distemper (dogs), 209 dogs, 206-210, 728-740 dourine, 170 eperythrozoonosis, 188 hog cholera, 187 horses, 162-180 IBR-IPV, 138-142 ketosis in ewes, 202 leptospirosis: of cattle, 131-134 of horses, 165 of sheep and goats, 197 of swine, 180-182 listeriosis, 134, 135, 163, 165, 194, 195 panleukopenia in queens, 211 pasteurellosis in sheep, 197 pseudorabies, 144, 185, 186 salmonellosis, 135, 164, 196, 208, 210 sarcocystosis, 146 sheep and goats, 192-206, 673 shipping fever, 136 streptococcal infections in mares, 163, 164 955956 INDEX swine, 180-192 swine erysipelas, 184 tick-borne fever, 136, 137, 198 toxoplasmosis, 146 trichomoniasis, 146, 450 tuberculosis, 135, 136, 184 viral diseases: in cats, 211, 212, 705, 741 in cattle, 138-145 in dogs, 209, 729 in horses, 165-170 in sheep, 197-199 in swine, 184-188 virus diarrhea (BVD), 142, 143 incidence of, 124-127, 162, 165, 175, 180, 184, 192 induced, 149-151, 170, 172, 173, 188, 201, 209, 212, 220- 222, 691-694, 705 mycotic, 145, 148, 170, 188, 199, 374 paratyphoid, in sheep, 196 repeated in dogs and cats, 728, 729, 741 salmonella, in horses, 163, 164 trichomonad, 146, 450 vibrionic (see campylobacteriosis), in cattle, 134, 374, 460 in sheep, 193, 194 Abscess of uterine wall, 153, 549 of uterus, 550, 608, 609 perimetrial, (see septic metritis), 384-386, 388, 394 perivaginal, 359, 361 preputial, 797-799 “Absorption” of the embryo or early fetus, 14, 17, 23, 25, 26, 31, 38, 77, 99, 100, 152, 175, 182, 184, 186, 188, 189, 207, 209, 210, 625, 626, 640 Accessory glands, male, 755, 756, 762, 763, 769 Acetonemia (see ketosis), 202, 240, 370, 394 Achalasia, esophageal, 64, 67 Achondroplasia, 53, 54, 57, 62, 65, 66, 78, 278, 336, 344 Acromegaly, dog, 717 Acrosome, 426, 763, 765, 766, 813, 814 Acroteriasis, 54, 60, 61 ACTH, 201, 247 Actinobacillosis, 58 Actinomycosis, 58, of sheath and penis, 803 Adenocarcinoma of the ovary, 722 Adenohypophysis (see anterior pituitary gland) Adenomyosis, 720, 737, 740, 845 Adhesions, of ovarian bursa and uterus, 354, 535, 538, 609, 611, 642, 643 of prepuce, 796-799, 806, 807 of sigmoid flexure of penis, 794, 796 Adjustment of extremities of the fetus, 298-301, 326-333 Adrenal gland, 201, 408 Adrenal virilism, 483 Aftercare of dam following parturition or dystocia, 272, 273 Agalactia, 116, 148, 273, 387, 388 due to failure of milk “let down,” 116, 401—403 Ageing of ovum or spermatozoa, 562, 563, 829 Agenesia of the Mullerian ducts, 12, 13, 41, 277, 346, 522-528, 535, 550, 622, 623, 642, 643, 710 Agnathia, 62 Albinism, 57 Allantoic fluid, 18, 27, 223-228 amount of the, 18, 27, 43, 223—228 source of the, 43 Allantois, 43, 44 blood supply of the, 43 calcification of the, 43 dropsy of the, 43, 223-228 embryology of the, 43, 44 Allantois chorion, 42-44, 223-228, 251, 253 necrotic tips of the, 43 Alopecia, partial (see hypotrichosis), 56 Amaurotic idiocy, 63 Amelia, 82 Amniocentesis, 75 Amnion, 41-43, 253 dropsy of, 43, 223-228 embryology of, 41-43 Amniotic cavity, 42, 43 Amniotic chorion, 42 Amniotic fluid, 18, 27, 42, 43, 224, 225 amounts of the, 18, 27, 42, 224, 225 function of the, 42, 43 properties of the, 42 sources of the, 42, 43, 224, 225 swallowing of by the fetus, 41, 43, 224, 225 Amniotic plaques, 42 Amniotic vesicle, 18 rupture of the, 18, 173-175, 222 Ampullae of the vas deferens, 755 Ampullitis, 845, 846 Amputation of the ectopic cervical folds, 553 forelimb, 309, 310 head and neck, 308, 309 penis, 800, 802, 803, 807 prepuce, 801 prolapsed uterus, 365, 366 rear limbs, 311, 312 Amorphus globosus, 79-81 Anasarca, fetal, 55, 63, 226, 278, 334, 335 Anastomosis of placental vessels, 97, 98 Anatomy of the female reproductive organs, 2-11 of the male reproductive organs, 752-758 Androgens (see testosterone) Anencephaly (see cerebral hernia) Anemia, during pregnancy in dogs, 109, 685 hemolytic in Basenji dogs, 71 Anesthetics, obstetrical, 294-297 duration of anesthesia with, 295 for epidural anesthesia, 294-296, 299, 361, 363 general, 296, 297 local, 295, 296 technique of administration of, 294-296 Anestrum (see failure of estrum) 412, 413, 415, 478-491, 495-512, 574, 677, 699-702, 712, 714 in cows, 478-491, 495-512 in does, 672 in dogs, 677, 712, 713 in ewes, 654-656 in mares, 583, 591-597 in queens, 699, 701, 702, 712, 714 in sows, 645, 646 lactational, 413, 438-440, 595, 646 Aneurism, middle uterine artery, 354 Ankyloses, 54, 58, 60, 61, 76—78, 278, 335—337 Anomalies (see teratology), 51-82, 266, 709-711, 718-721INDEX 957 causing dystocia, 75 due to ageing of ova and spermatozoa, 70 due to duplication of the fetus or its parts, 79-82, 313, 335- 337 hormones, 69, 709, 710 nutritional causes, 69 physical causes, 69 plants and chemicals, 69, 70 in cattle, 53-58, 521-530 dogs and cats, 62-67, 709-711, 718-721 horses, 58-60, 623 sheep and goats, 61, 62 swine, 60, 61 incidence of, 53, 58, 60, 61 inherited, 53-68, 266, 278 noninherited, 68-82 causes of, 68-70 of the cervix and vagina, 526-530 digestive system, 39, 55, 59, 64, 67, 72 epididymis, 843-845 eyes, 57-59, 61-63, 66 genital organs, 72-76, 97-99, 521-530, 562, 622, 623, 642, 643, 660, 672, 709-711, 718-721, 793-795, 815- 818, 820-822 head and central nervous system, 39, 61, 63, 65, 66, 76- 78 heart and blood vessels, 39-41, 64, 66, 67, 71 mammary glands, 58, 61, 72, 673 penis, 893-895 respiratory system, 60, 64 scrotum, 822, 823 skeleton, 53-56, 58, 59-61, 64-66, 77-79 skin, 53, 59, 61, 64 spermatozoa, 814, 818-820 testes, 819-822 trunk, 78, 79 urinary organs, 41, 63, 66 uterine tubes, 523, 643, 709-711, 718-721 parasitic, 82 progeny testing for, 67, 68 Aorta, 38, 39 dextro-position of the, 40 persistence of the right, 40 Anovestibular stenosis (see rectal vaginal constriction) in Jerseys, Anovulation, cows, 410, mares, 588 Anoxia, fetal, 72 Anterior pituitary gland, 39, 106, 107, 399-402, 620 Antibiotics in semen extenders, 615, 856, 897-899, 900-904, 912- 914, 917, 921, 922, 924-926 Anury, 62, 64, 66, 78 Aplasia, of the adrenal gland, 106, 333 endometrium, 525 mesonephric duct (see Wolffian duct) 529, 535, 556, 621, 622, 709-711, 843-846 paramesonephric ducts (Mullerian ducts) 12, 13, 41, 277, 346, 522-529, 535, 550, 642, 643, 660, 672, 710 segmental, 622, 642, 660, 672, 721 Appendix testis, 759 Amold-Chiari malformation, 55 Arrests in development (see aplasia) Arteritis virus, equine, 169 Artery, pudendal, male, 770 spermatic, 753 umbilical, 40 uterine, 8, 20, 21 Arthritis, males, 792, 793 Arthrogryposis, 54, 60, 61, 335-337 Articulation, coxofemoral, 4 dislocation of the, 5, 34, 241, 271, 304, 394 Artificial insemination, 894-926 advantages and disadvantages of, 895, 896, 900, 901, 916, 921, 923, 926 history of, 894, 901 in bitches, 924 beef cows, 907 dairy cows, 896-909 does and ewes, 660, 920-922 mares, 614, 615, 911-915 other animals, 926 queens, 925, 926 organizations, 895, 898, 903, 904, 908, 909, 911 Artificial vagina, 789-791, 861-870, 897, 912, 916, 921, 924, 925 for boars, 868, 916 bulls, 789-791, 864-866, 897 dogs, 870, 924 rams and bucks, 867, 868, 921 stallions, 789-791, 866, 867, 912 toms, 870, 925 washing and sterilizing of the, 865 Ascheim Zondek test, 31 Ascites, fetal, 226, 334, 335 maternal, 533, 534 Asphyxiation, of the newborn, 259, 263, 291, 303 Assistance in normal parturition, 259 Ataxia, 54, 59, 63, 66 Atresia ani, 39, 55, 60, 62, 72 coli, 39, 55, 59, 61 of follicles, 418-421, 585, 587 of the vagina, 54, 277, 346, 528, 529 Attachment of the embryo, 39, 683 Attraction of males by spayed females, 715 Aujezsky’s disease (see pseudorabies) Auscultation of the fetal heart, 15 Autoimmunization causing sterility in males, 845 Autolysis of the fetus, 123 Autosite, 82 Azoospermia, 816-818, 833, 841, 843-846, 889 Bacterial causes of abortion in: cows, 126-138 dogs and cats, 206-210, 728, 729 ewes, 192-200 mares, 162-165 sows, 180-186 Bacterial “flora” of the uterus, 103, 104 Balanitis, 618, 775, 803-807, 855, 856 Balanoposthitis, 468-471, 474, 618, 661, 794, 800, 801, 803-807, 855, 856, due to screw worms, 801, 806 trauma in young bulls, 794 in boars, 806 bulls, 468-471, 474958 INDEX dogs, 806 rams and bucks, 661, 805 stallions, 618, 805, 806 noninfectious, 805 Ballottement of the fetus, 15, 18, 24 Bandl’s ring as a cause for dystocia, 281, 316, 327, 348, 349 Bang’s disease (see brucellosis) “Barking” foals and piglets (respiratory distress), 270 Barr body, 74 Bartholin’s glands (see vestibular glands), 11 cysts of, 235, 557 Beefalo cattle, 76 Behavior, sexual (see estrum) in females: abnormalities of, 63 bitches, 680, 681 cows, 435-442, 500-504 does and ewes, 656, 669, 670 mares, 588-590 queens, 699-701 sows, 637 Behavior, sexual in males, 762, 773, 774, 776, 785, 786, 787-790 effect of progesterone on, 785 inhibition of, 788 Bicomual pregnancy in the mare, 93, 331, 332 Biologic tests for pregnancy in the mare, 30, 31 Ascheim Zondek, 31 Cuboni, 31 Friedman’s modification of the A.Z. test, 31 M.I.P. test, 30 Biopsy of the testis, 828 uterus, 540, 541, 591, 616-618, 624 vagina, 31, 32, 637 Birth (see parturition) multiple (see twinning), 104 of “overtime” fetuses, 104, 106, 107 of premature fetuses, 38, 104, 123 Bisection of the fetal pelvis (see fetotomy), 311, 312 Bladder, 39, 41 eversion of the, 233-236, 361 prolapse of the, 233-236, 314, 346, 360, 361 rupture of the, in foals, 265 Blastodermic vesicle, 38, 42 Blastocyst (blastula), 38, 426, 640, 931 Bleeding from vulva postestrus in cows, 15 Blood coagulation defect, 58, 63, 64, 67 Blood typing in bulls, 96, 97, 909 in dogs, 97, 269 in freemartins, 97-99 in horses, 97, 267-269 with histocompatibility or lymphocyte antigens, 97 Blood vessels in the placenta, 39, 43 thromboses of the, 48 Bluetongue, 70, 144, 199, 887 Body temperature decline, at parturition, 109, 247, 252, 686 near ovulation, 436, 503 Bonding, neonate and dam, 259, 271 Border disease, sheep, 199 Bovine virus diarrhea (BVD-MD), 142, 143 Brachygnathism, 54, 55, 59, 62, 65 Breakdown of ribs after evisceration of fetus (see fetotomy), 310, 312 Breeding history, 858 hygiene, minimal contamination technique for AI, 615, 856 natural service, 616, 856 season, in bitches, 676 in ewes and does, 654-656 in mares, 582-584 in queens, 699 soundness examination, 857-870, 872-890 time after parturition, in the bitch, 676 cow, 438, 439, 567, 572-574 ewe and doe, 655-657, 669-670 mare, 584 queen, 701, 702 sow, 638 Bromoergocryptine, 682, 691, 692 Brucellosis in cattle, 126-131, 374, 467, 468, 544, 545, 813, 841, 848, 850 dogs, 206-208, 228, 729, 813, 842, 851 sheep and goats, 195, 196, 841, 842 swine, 182, 183, 643, 647, 813, 898 Buhner’s vulvar suture technique, 237 Bulbocavernosus muscle, 758, 770 Bulbo-urethral glands, 755, 756, 769, 770, 852 squamous metaplasia of the, 852 Bulbus glandis, 757, 771 Bull, blood typing of, 96, 97, 909 physical examination of, 857-870, 872-890 preparation of a teaser (“gomer”), 502, 503, (stallion) 589 “Bullers,” see nymphomania in cows, 484 Bulling syndrome in steers (in feedlots), 785 Bursa ovarii, 6, 8 Bursatte, genital (see habronemiasis), 805 Bursitis, 535-538, 609, 642, 643, 661 Cadaver, static fetal, 214 Calcification of the fetal membranes, 43 retractor penis muscle, 794 testis, 815, 826-838 Calculi, urethral, 776, 808 Calving interval, 439, 440, 572-575 Campylobacteriosis (see vibriosis), 134, 193, 194, 374, 456-465, 539, 563, 564, 813 Campylorrhacis scoliosa, 78, 335, 336 Canine herpesvirus infection, 729, 730 Canine transmissible venereal tumor, 724 Cannibalism in animals, 271, 272 Capacitation of spermatozoa, 426, 566, 767 Carbonic anhydrase inhibitors, 114 Carcinoma, ocular, 57 Cardiac defects or anomalies, 55 Care of the dam, 272, 273 newborn, 262-272 orphan newborn, 264, 265 Caruncles, uterine, 44, 45, 257, 373 dissolution of after parturition, 257, 373 Casein, iodinated, 115 Caslick’s vulva-suturing operation, 238, 346, 347, 354, 355, 556, 581, 599, 600, 609-611 Castration, 761, 762, 777, 785 Cataract, congenital, 58, 62, 66 Catlin mark (see cerebral hernia) Cats, tortoise-shell, 711, 815, 820 (CEM) Contagious equine metritis, 163, 175, 599-613 (603-605),INDEX 959 complement-fixation test for, 605 culture of mare for, 606, 607 stallion for, 607 treatment for, 613, 614 Cephalotomy (see fetotomy), 308, 336 Cerebellar abiotrophy, 54, 63 Cerebellar hypoplasia, in cats, 211 in cattle, 54 in dogs, 63 in horses, 59 in sheep, 62 Cerebral hernia, 55, 56, 60, 333 Cervical “star,” 44 Cervicitis, in cows, 309, 475, 551-553 in mares, 609 post puerperal, 390, 551-553 Cervicotomy, 343, 345 Cervix, amputation of the ectopic folds of the in cows (trachelo- plasty), 553 anatomy of the, 9, 10 anomalies of the, 526-528, 554, 622, 623 atresia or obstruction of the, 526, 527, 553, 554 culture of the, 603, 607, 738 cysts of the, 553, 554 dilation (relaxation) of the, at parturition, 247, 248, 251, 252, 345, 346 double, 526-528, 622 ectropion of the, 390, 553 embryology of the, 12, 13 excessive mucus in the, 487, 526, 554 failure to dilate or relax at parturition, 344-346, fixation of the, in prolapse of the vagina (cervopexy) (trachelo- pexy), 238, 239 hypertrophy of the, 527, 552, 555 hypoplasia of the, 326-328, 622 induration or fibrosis of the, 344 inflammation of the, 551-553 involution of the, after parturition, 258, 345 laceration or rupture of the, 314, 354, 357, 359 prolapse of the, 233-240, 343, 527 stenosis of the, 343-346, 526, 527, 552, 737, 738 tumors of the, 554, 621 Cesarean operation, 314-323, 331-336, 343-351 anesthesia for the, 315, 318-322 in bitches and queens, 321-323 in cows, 316—320, 333—336, 343—351 in does and ewes, 320, 343-351, 371 in fetal maceration, 219 in hydrops of the fetal membranes, 227, 228, 335 in mares, 230, 314-316, 332 in rupture of the prepubic tendon, 230 in sows, 320-321, 343-351 in torsion of the uterus, 233, 314, 343 indications for the, 314, 316, 321, 322, 333—336, 343—351,360 postoperative care in, 315, 316, 320-323 Chains, obstetrical, 291, 292 Chediak-Higashi syndrome, 55, 66 Cheiloschisis, 71, 72 Chilling causing losses in newborn, 270 Chimerism, 97-99, 820 Chisel, obstetrical, 292 Chlamydiosis, 138, 197, 198, 841, 848 Chlorinated napthalones (hyperkeratosis), 147-150, 852 Chondrodystrophy (see achondroplasia) “Chorioepithelioma,” 48, 724 Chorion, 41-44 Chorionic vesicle, 24, 25, 27, 28, 43, 173-175, 222 Chromosomes, 51, 52, 640, 711, 815, 819, 820 Circulatory system, embryology of the, 39-41 Circumcision, 801 Clamps, vulvar, 238-240 Claw defects, 58 Cleft lip and palate, 39, 55, 60 Clenbuterol, 248, 296 Clitoridectomy, 612, 613 Clitoris, anatomy of the, 11 embryology of the, 12 hyperplasia of the, 709, 710, 716, 734 sinuses of the, in mares, 11, 604, 605 culture of the, 604, 605, 612, 613 Clitoritis, 734 Cloaca, 39, 72 Clover, subterranean, 201, 662, 663, 852 Cochliomyiasis of the penis and prepuce, 806 Coital vesicular exanthema, 474, 618, 644, 805 Coition (see copulation) 415-417, 700, 771, 774-776, 786, 787 duration of, 416, 700, 771 false entry in, 416, 417 frequency of, 700, 774, 775 inability to complete, in male, 762, 786-808 infection in, 600, 601 injuries from, in the female, 416, 417, 644 in the male, 774-776 Colic, due to retained meconium in foal, 265 Collection of semen, 861-870 Colliculus seminalis, 755 Collie eye anomaly, 62 Coloboma, ocular, 57 Color and infertility, 815-818 Color of semen, 769, 774, 776, 873, 874 Colostrum, 47, 113, 263, 264 Concentration of spermatozoa in semen, 769 determination of the, 874, 875 in testicular pathology, 816, 817, 836 Conception (see fertilization) males as a cause of lower rates of, 561, 562, 857, 885-890 number of spermatozoa required for, 425, 894-926 prevention of, after service, 220-222, 404, 688-692, 707 Conception rate in mares, 581, 584, 627 Conception, spurious, in mares and bitches (see pseudopregnancy) Condom, for collection of equine semen, 866, 867 Contractions of the abdominal muscles during labor, 253-255 uterus during parturition, 251-259 causing “ring” dystocia, 281, 316, 327, 348, 349, 351 Control of the pet population, 687-694, 706, 707, 715 Contusions of the birth canal, 354-356 pelvic nerves, 355-357 Copulation (see coition) Cord, spermatic, 753 umbilical, 48, 49 Corpus albicans (ovary), 6, 258, 436 cavernosum penis, 756, 770960 INDEX hemorrhagicum (ovary), 420, 436, 585 luteum (ovary) anatomy of the, 6 cysts of the, 436, 479, 480 involution of the (luteolysis), 404, 406-408, 436 505-507 586 of pregnancy, 21, 108, 109, 111 of the estrous cycle, 405, 406, 436, 585, 586 persistence of the, 24, 214, 217, 407, 496, 497, 546, 587, 594 removal of, 107-110, 222, 504, 505, 547 spongiosum urethrae, 756, 770 Cortisone, effect on spermatogenesis, 829 for arthritis in males, 793 Cotwin to freemartin, 97-99, 820 Cotyledons (see placentome), 21, 44, 45, 48, 373 Cow, infertility in the, 398-579 reproductive cycle of the, 434-442 Cowper’s gland (see bulbourethral gland) Coxitis, in the male, 792 Coxofemoral articulation, 5 dislocation of the, 5, 34, 240-242, 271, 304, 394, 792 Cremaster muscle, 753 Crutch repellers, Kuhn’s, 293 Williams’, 293 Cryptorchidism, 61, 62, 65, 784, 821, 822, 826 incidence of, 821, 822 inheritance of, 62, 821 treatment of with hormones, 784, 822 tumors of the retained testis, 821, 822 Cuboni test, for estrogens, 31 Cul-de-sac of vulva, rupture of in sows, 644 Culture of the cervix and uterus, in the bitch and queen, 733, 741 in the cow, 540, 541 in the mare, 606-608 Cyclopia, 76 Cystadenomas of the bitch and queen, 723 Cysts Bartholin’s or vestibular gland, 235, 557, 710 branchial, 72 bursal, or Morgagni, of oviducts, 536, 643, 720 cervical, or Nabothian, 553, 554, dermoid, 79 endometrial, 25, 720 follicular, of ovary, in cows, 102, 402, 404-406, 415, 478-491 estrogen content of the, 483 etiology of, 480-484 incidence of, 478-481 in postpartum vaginal prolapse, 234, 240 pathology of, 479, 480, 483-486 symptoms of, 484-487 types of, 479, 480 treatment of, 487-491 in dogs and cats, 712, 714, 718-720 in mares, 587 in sows, 644, 645 luteal, 479, 480, 644, 645, 737 of the liver, 72 of the mesonephric, paramesonephric ducts (Gartner’s, Muller- ian and Wolffian), 11-13, 529, 556, 586, 622, 710 of the ovarian fossa in the mare (paramesonephric and germinal inclusion), 586, 620 parovarian, 12, 535, 621, 645, 661, 712, 719 pharyngeal, 39 renal. 60, 72 serosal, 741 Cytogenetics, 51-53, 70, 73-76, 97-99, 529, 621, 709 814 815 820 Cytology, vaginal smears, bitch, 677-679, 712, 736 queen, 702 Cytoplasmic droplet on sperm cells (see protoplasmic droplet) Dam, care of the, after obstetrical operations, 272, 273, 313, 314, 343, 346, 348, 350 care of the postpartum, 272, 273 nutrition of the, 245 splitting of the pelvis of the (symphysiotomy), 313 viciousness of the, killing of the newborn, 259, 271, 272 Dartos muscle, 753, 764 Deafness, 63, 66 Death and postmortem changes of the fetus, 38, 213-220, 232, 685 Debility (see inanition) Decapitation of the fetus (see fetotomy), 308 Defects (see anomalies) Deficiencies, nutritional as a cause of abortion, 150, 151, 173, 188, 202 infertility, 413,515-519, 647, 657,662, 782, 783, 788 paraplegia of pregnancy, 240-242 in the newborn, 269 Degeneration of the testes, 815, 818, 826-838 diagnosis of, 836, 837 etiology of, 826-836 semen characteristics in, 836, 837 Density of the spermatozoa in semen, 772, 874, 875 Deoxyribonucleic acid (DNA), 51, 766, 814 Dermatitis, scrotal, 826, 827 vulvar, 710, 734 Dermatosis, ulcerative of sheep (lip and leg ulceration), 661 vegetans, 61 Dermoids, 58, 79 Detorsion rods, obstetrical, 294, 300 Detruncation of the fetus (see fetotomy), 310, 311, 330 Diagnosis of pregnancy, 14-33, 683-686, 705 Diestrum, 412, 591, 677 Differentiation, sexual, 417 Digestive system, embryology of the, 39 Diluters of semen (see extenders) Diseases, metabolic of the puerperal period (see metabolic diseases) Disinfection of the navel of the newborn, 255, 263, 265, 269 Dislocation of the hip, 34, 241, 271, 304, 394 occipital joint, 271, 304 Displacement of the fetus(es) (see extrauterine “pregnancy”), 218, 219, 222, 223, 338, 741 Distichiasis, 62 Diuretics, 114 Diverticulum of the prepuce in boars, 758, 806 extirpation of the, 806 of the urethra in stallions, 757 Dog-sitting posture of the fetus, 253, 329 Double muscling (see muscular hypertrophy) Dourine, 170, 618, 619, 805, 886 “Downer-cow” syndrome, 240-242, 393-396INDEX 961 Drive, sex (see libido, impotency) Droplets, protoplasmic on spermatozoa, 763, 765, 768 Dropsy, congenital, 54, 223-228, 278 of the allantois, 43, 76, 225-228 amnion, 43, 224-228, 278 fetal membranes and fetus, 43, 223-228, 240, 278 fetus, 54-56, 63, 226, 278 Ductus arteriosus, 40, 41, 55 Ductus deferens (see vas deferens) Ductus venosus, 40, 41 Duration of coitus, 416, 700 of pregnancy, 104-107, 684, 701 of reproductive ability, 110 Dwarfism, 53, 54, 64, 78, 717 Dysgenesis, gonadal, 596 Dystocia adjustment of the fetal extremities (mutation) in, 298-301, 326- 331 aftercare of dam with, 313-315, 320, 321, 323 basic causes of, 277-285 maternal, 282 fetal, 283 cesarean operation in, 314-323, 331, 333, 334, 336 in bitches and queens, 321-323, 331 cows, 316-320, 331 ewes and does, 320 mares, 230, 314-316, 331 sows, 320, 321 common forms of, in the various animals, 283-285 definition of, 277 due to abdominal hernias, 277, 280, 283, 343 abnormal fetal postures, 280, 283, 300, 301, 326-332 positions, 280, 283, 299, 300, 326, 330 Bandl’s uterine contraction rings, 281, 316, 327, 348, 349, 357 breech presentation, 283-285, 300-302, 330 fetal ascites, 334, 335 death, 280 dropsy or anasarca, 278, 335 emphysema, 283, 305, 316, 317, 328-332, 338, 348-351 gentoype of sire or dam, 281, 282 gestation length, 281, 282 giantism, 278, 283, 333, 334 maceration, 218-220, 232, 283, 340, 349, 351 monsters, 278, 281, 283, 335-337 hereditary causes, 277, 278, 283, 329 hiplock, in anterior presentation, 255, 300, 303, 304 in posterior presentation, 305, 331 infectious causes, 280, 283 lack of observation, 279 large fetuses in multipara, 280 mummification of fetus, 278 nutritional causes, 278-282 obesity, 279, 282 over-sized fetuses, 278, 301-307, 335-337 pathological presentations, positions and postures of the fetus, 282-285, 288, 289, 298-301, 326-332 postmortem changes in the fetus, 278, 283, 289, 328- 332 stenosis (failure to relax) of the cervix, 282, 283, 343, 344 stenosis (small size) of the pelvis, 278-280, 282, 334 stenosis of the vagina, 277, 282 stenosis of the vulva, 277, 282, 304 transverse presentation, 283, 331, 332, 357 traumatic causes, 280, 285 twinning, 100, 277, 282, 335 the umbilical cord, 333 uterine inertia, 279-281, 283, 285 torsion, 230-233, 280, 282, 283, 337-343 vaginal-cervical prolapse, 343, 344 wedging of the fetuses in the pelvis, 99-102, 277, 282, 335 wry neck, 283, 327, 328 equipment used for the relief of, 290-294 examination of the dam and fetus in, 287-290, 333-337 extension of the fetal extremities in, 300-302, 326-331 fetal causes of, 282, 283 fetotomy operations in, 307-313, 326-332, 333-337 advantages and disadvantages of, 307 in anterior presentation, 308-311, 326-330 in posterior presentation, 311-313, 330, 331 forced extraction in, 301-307, 333, 334 dangers of, 303-306 manner of application of, 303-305 handling of, preliminary procedures for, 287-297 immediate causes, 282, 283 incidence of, 100, 277, 278, 281-283 injuries due to, 301-307 lubricants used in, 294, 305, 326 management as a cause for, 278-280, 333, 334 maternal causes for, 282, 283 mutation operations for relief of, 298-301, 326-332 obstetrical operations for the relief of, 298-324, 326-351 pelvis-splitting (symphysiotomy) operation for the relief of, 313 prognosis in, 290, 307, 315-317, 320, 322-324 repulsion of the fetus in, 298, 299, 326-332 restraint in, 287, 288 rotation of the fetus in, 299-301 signs of, 253-255 size of the sire as a cause of, 281, 282, 334 symphysiotomy for the relief of, 313 version of the fetus in, 300, 331, 332 Dystrophia adiposogenitalis syndrome, 717, 829 Ear, defects of, 63, 66 Eclampsia, 241, 371, 372 Ectopia cordis, 40 ureteral, 63 Ectropion of the external os of the cervix, 551-553 eyelids, 62 Edema, of the abdominal floor, 229, 230 allantois chorion, 43, 226 fetus, 54, 63, 226, 271 head, tongue and limbs of fetus in dystocia, 271 udder, 14, 24, 114 vagina and vulva, 15, 24, 246, 679 Efferent tubules of testis, 753, 768 Ehlers-Danlos syndrome, 53, 59, 61, 64, 67 Ejaculate, of semen, 771 Ejaculation, effect of excessive frequency on semen and libido, 772-775962 INDEX optimum frequency of, 772-775 phases of in the boar, dog and stallion, 774 physiology of, 771-774 stimuli for, 771 Ejection or “let-down” of milk, 116, 402, 403 Electroejaculation, in boars, 869 bulls, 862-864 dogs and cats, 869, 870 rams, 868 stallions, 866 Embryo diagrams of (1-16 cells, morulas, blastocysts), 931 filter, 929 migration of, 111, 428, 588 microsurgical techniques applied to, 932 rate of transport to uterus, 422-424, 586 spacing of in uterus of multipara, 38, 111, 641, 642, 657 transfer, 422, 568, 927-939 donor selection and treatment and aftercare in, 927-929, 933-937 examination of donor before, 930, 931 handling of, 930 history of, 927 in cattle, 927-934 in dogs and cats, 938, 939 in horses, 934, 935 in sheep and goats, 935-937 in swine, 937, 938 recipient, selection, synchronization and aftercare, 932, 933, 937, 938 recovery of embryos, 929, 930, 934-937, 939 results of, 934 superovulation treatments of donors, 928, 936, 937 techniques, surgical and nonsurgical, 933, 935, 937, 939 storage of, 932, 938 Embryonic deaths, 23-25, 38, 77, 218, 423, 425-427 in the bitch, 728, 730, 735, 738 cow, 14, 17, 152, 447-455, 456-465, 467, 471, 476, 497, 498, 500, 568 ewe and doe, 31, 201, 202, 657, 658, 663, 664 mare, 25, 26, 175, 625-627 queen, 210 sow, 182-189, 639, 640, 647 twinning, in unipara, 99, 100, 657 Embryonic duplications, 79-82 “Embryotomy” operations (see fetotomy operations) Emphysema of the fetus, 218-220, 348-351, 357 in torsion of the uterus, 230-233, 338 pulmonary, 60 time of development after onset of labor, 349, 350 Encapsulatum genitalium (see Klebsiella) Endocrine glands, 399-409 adrenal, 408, 409 anterior pituitary, 399-402 ovary, 403-406 pineal, 409 placenta (temporary), 107-110, 247, 402, 405 posterior pituitary, 402-403 testicle, 760-763 thyroid, 408 Endocrines (see hormones) Endometrial cups (mare), 29, 30, 402 Endometritis, in the bitch and queen, 734-740 cow, 218-220, 346, 348-350, 377, 378, 449, 468, 469-472, 474, 538-546, 563, 564 mare, 595, 600-608, 612 sow, 643, 644 Endometrium, aplasia of, 496, 525 cysts of, (cystic hyperplasia) bitches and queens, 712, 734-740 cows, 405 mares, 617, 622, 736 ewes and goats, 663 lymphangiectasis of, 622 Endotoxin abortion, 136 Enucleation (removal) of the corpus luteum, 107-110, 222, 504, 505 Enzootic abortion of ewes, 138, 197, 198 Enzyme immunoassays, 14 Epididymis, anatomy of the, 753, 768 anomalies of the, 843-845 inflammation of the, 841-843 obstruction of the, 841-845 physiology of the, 753, 768 sperm granulomas of the, 842, 843, 845 tumors of the, 845 Epididymitis, 841-843 in brucellosis (in dogs and rams) 841, 842 in specific bovine venereal, (Epivag), 474, 475, 841 Epidural anesthesia, 294-296, 299, 357, 363, 378 Epilepsy, 57, 63 Episiotomy, 347, 355, 360 Epitheliogenesis imperfecta, 53, 58, 60, 62, 67 Epivag, specific bovine venereal epididymitis and vaginitis, 474, 475 Epizootic bovine abortion, 137, 138 Epoophoron (see parovarian cysts), 12, 535, 621 Equine arteritis virus, 169 Equine chorionic gonadotropin (ECG or PMSG), 401, 402 Equine herpes virus (see abortion), 165-170, 618 Equipment, obstetrical, 290-294 sterility, 371 Erection, of the penis, 762, 770, 771, 807, 808 premature, 795, 807, 895 vascular shunts causing failure of, 807, 808 Ergot poisoning, 147, 148, 188, 273 Erhlichiosis in stallions, 832 Esophagus, stenosis or obstruction of the, 64, 67 Estradiol (see estrogens) Estrogenic hormones, 104, 149, 170, 188, 201, 209, 213, 247-251, 403-405, 505-507, 852 adverse effects of, 209, 405, 440, 482, 483 amounts of in mare’s urine, 107-110, 404 in cystic ovarian follicles (bovine), 483 causing cystic endometrial hyperplasia, endometritis and pyom- etra, 734-740 cystic ovaries, 440 porcine vulvovaginitis, 644 vagino-cervical prolapse, 234, 484 during gestation, 107-110, 685 feeding of the, 182-189, 852 for incontinence in bitches, 716 forms of, 404 in anestrus, 403-405INDEX 963 in involution of the corpus luteum (see abortion), 441, 500 in mismating (preventing conception) in bitches and queens, 691, 694, 707 in pregnancy, 32, 106-110, 685 in the induction of abortion and parturition, 149, 170, 188, 201, 209, 213, 247-251, 692 in the treatment of pyometra, 505, 506 physiology of the, 104, 107-110, 247, 403-405 presence of the, in subterranean clover, 201, 483, 662, 663, 852 sources of the, 404 toxic effect of the, in dogs and cats, 209, 405, 692, 829, 833- 835 uses of the, 149, 170, 188, 201, 209, 213, 404, 405, 505, 506 Estrous cycle, 411-415, 427, 434-442, 676, 699 body temperature during the, 436, 437 classification of animals by the frequency of their, 413 factors affecting the, 413-415 in bitches, 676-682 cows, 434-442 does, 669, 670 ewes, 654-657 mares, 582-597 abnormalities of the, 591-597 queens, 699-704, 714 sows, 636-639 induction of the, in bitches, 694, 695, 713 queens, 705, 706 length of the, 412, 413, 415, 434, 435, 565, 566, 584, 637, 656, 669, 700, 701, 713 onset of the, after parturition in the cow, 258, 438-440 stages of the, 411-413, 676, 699-701 Estrum, 411, 412 aids for detection of, 501-503 control of, or prevention of, in bitches and queens, 500-504, 582-586, 637-639, 680, 681 detection of, 500-504, 565, 566 by teaser (“gomer”) bulls, 502, 503 during the gestation period, 14, 24, 31, 435, 714 failure of (see anestrum) in cows, 412-415, 478-491, 495-512 574 accompanied by a corpus luteum, 495-507 due to cystic ovaries, 478-491, 507, 712, 718-720 debility, 508, 509 luteal cysts, 478-491, 509, 737 miscellaneous causes, 509, 510, 712, 713 “retained” or persistent corpora lutea, 495-497 “silent” or subestrum, 497, 498, 499, 500-508, 530 unobserved estrum, 499-507 etiology of, 495-500, 507-510 treatment of, 500-507, 510-512 with no corpora lutea, 507-511 failure of in mares, 594-597 foal (heat), 584 in bitches, 676-682, irregularities of, 713 in cows, 435-442, 501-504 in does, 669, 670, 672, 706, 922 in ewes, 654-658 , 921 in mares, 582-586, 588-597 examination for, 588-591 irregularities of, 581, 586, 591-597 teasing to detect, 588-590 in mules, 584 in sows, 637, 645, 646, 918, 919 onset of in days after weaning, 638, 918, 919 the production of, during lactation, 638, 919 prediction of time of in cows, 503, 504 signs of in cows, 435-437, 501, 503, 504 suppression of in bitches, 687-690, 706 synchronization of in cows, 405-408, 441, 442, 507, 908 does, 670, 671 ewes, 402, 405, 406, 655, 659, 660 mares, 593, 597, 598 sows, 638, 918, 919, 921, 922 Eunuchoidism, 817 Eutocia, 277 Eversion of the bladder, 361 uterine horn, 361-371 uterus, 361-367 Evisceration of the fetus (see fetotomy), 310, 312 Examination for breeding soundness, 745 pregnancy, 14-33 of the bull, 857-861, 862-870 of the semen (see semen examination) Exanthema, coital vesicular in cattle (see IBR-IPV), 138-142, 474, 555, 556, 804 in horses, 618, 805 Exercise for males, 788, 790 Exostoses of the vertebrae in bulls, 792 multiple, 60, 65 pelvic, 344 Expulsion of the conceptus (see abortion) fetal membranes, 255, 256 fetus (see parturition) Extenders for semen of the boar, 912-918 bull, 897-899, 900-904, antibiotics in, 898, 903 dog and cat, 923-926 ram and buck, 921, 922 stallion, 615, 912-914 Extractor, fetal, 291, 292 Eye, defects of, 57-59, 61-63, 66 “Fading pup” syndrome, 732 Failure of estrum (see estrum, failure of) Fallopian tubes (see uterine tube or oviducts) False entry (see coition), 416, 417 “Fat cow” syndrome, 393-396 Fat necrosis, 346 Fat, perivaginal, prolapse of, 233-236, 344, 346, 361 removal of, 236, 361 “Feathering” of the vagina, 348 Feeding of orphan newborn, 264, 265 Feline panleukopenia, 66, 211 Fertility evaluation of the bitch and queen, 745 of males, 786-890, 906 of mares, 623, 624 Fertilization, 422-424, 426, 559-569, 587, 639, 640, 658, 683, 704 failure of, in repeat breeders, 559-569, 647 due to abnormalities of ovulation 423, 564, 568 due to the inability of the ova or spermatozoa to fertilize, 422-428, 559-569964 INDEX due to failure of sperm transport in the female, 660 due to obstructions in the genital tract, 562, 841-845 number of spermatozoa required for, 425, 426, 587, 639 Fetal electrocardiography, 15, 25, 31 Fetal membranes, 41-44 dropsy of the, 43, 223-228, 240 eating of the, by the dam, 256 examination of the, 48 retention of the, 256, 373-384 separation and expulsion of the, from the uterus after parturition, 255, 256 slipping of the, in bovine pregnancy diagnosis, 18, 20 tumors of the, 48 weight of the, 48 Fetal monsters, 335-337 incidence, 80, 81, 335 methods of handling, 335-337 Fetatomes, obstetrical, 293 uses of, 309-337 Fetotomy operations, 307-313, 327-332 advantages and disadvantages of, 307 Feto-pelvic disproportion, 278, 279, 281, 305, 335, 344 Fetus adjustment of the extremities of the, 300, 301, 326-332 amputation of the forelimbs of the, 309, 310, 327-332 head and neck of the, 309, 327, 328 rear limbs of the, 311, 312, 330 anasarca of the, 55, 63, 226, 278 anomalies of the, 51-82 antibodies in the, 124 ascites of the, 226 autolysis of the, 123 ballottement of the, 15, 18, 24 bisection of the pelvis of the, 311, 312, 329, 331 bovine, 19, 20, 39 breakdown of the ribs of the, 310 breech presentation of the, 253, 312, 330, 331 cephalotomy of the, 308 changes in the size of the, during gestation, 19, 20, 27, 37 characteristics of the, during the stages of gestation, 19, 27 circulation of the, 39-41 craniotomy of the, 308, 336 death and postmortem changes of the, 38, 218-220, 337-343, 346, 348-351, 685 decapitation of the, 308, 328 detruncation of the, 310, 311, 330 displacement of the, or extrauterine, 218, 219, 222, 223, 741 dropsy of the, 43, 226, 278 edema of the, 43, 226, 271 embryotomy of the (see fetotomy) emphysema of the, 218—220, 328, 330—332, 346, 348—351 equine, 27, 28 evisceration of the, 310, 312, 328 excessive size of the, 106, 107, 278, 329, 331, 333-337, 349, 350 expulsion of the, during parturition (see abortion) 252-255 extractor for the, 291, 303-305 extrauterine, 218, 219, 222, 223 fetotomy of the, 307—314, 326—337, 344, 349, 350 forced extraction of the, 259, 301—307, 328, 329, 331, 343— 350 fractures in the, 271, 303-307 fructose in the, 41 giantism of the, 106, 107, 278, 333, 334 growth of the, 20, 27, 39 injuries to the, at parturition, 271, 272, 303-307 killing of the, before fetotomy, 307 maceration of the, 23, 218-220, 283, 338, 340, 349, 350 methods of handling abnormal presentations, positions and pos- tures of the, 298-303, 326-332 methods of handling excessive size of the, 301-323 methods of handling the severely deformed, 307-323, 335-337 movements of the, 41, 113 mummification of the, 22, 143, 153, 123-222, (213-218), 232, 346, 349, 351, 404, 407, 415, 496, 500, 642 mutation of the, 298-301, 326-332 number of, in the uterus, 94, 95, 110 nutrition of the, 39-44, 45 nutritional deficiencies in the, 150, 151, 173, 188, 202, 269 ovine, 39 period of the, 39 physiology of the, 41, 113 position of the, in the uterus, 94, 252, 253; 299, 300, 326-332 postures of the, 252, 253, 300, 301, 326-332 presentations of the, 94, 252, 253, 300, 326-332, 687 protection of the intrauterine, 42 repulsion of the, 298-301, 326-332, 335, 350 respiration of the, 41, 262, 263 rotation of the, 94, 252, 299-304, 326, 330, 341, 342 size of the, as regulated by the sire and dam, 281, 282 bovine, 20; canine, 33; equine, 27; ovine, 32; porcine, 32, 39 time of intrauterine death of the, after the onset of parturition, 289, 290 traction on the, 301—307, 326—331, 333—337, 344—350 transverse presentation of the, 252, 300-332 tumors of the, 334 version of the, 300-332 weight of the, at term, 19, 27, 106, 107 withdrawal of the, 304-307, 326-331, 333-337, 344-350 wryneck of the, 41, 280, 283, 327 Fibroelastosis of the heart, 270 Fibromas, vaginal, 723 Fibropapillomas, infectious, on the vulva, 476, 557 on the penis and prepuce, 557 Fibrosis of the testes (see testicular degeneration) Fistula, recto-vaginal, 359, 614 Flehmen stance or reaction, 409, 670, 787 “Flora,” bacterial of the uterus, 103, 104, 538, 539, 602, 728-739 Flushing of ewes, 657 Follicle, ovarian (see Graafian follicle), primordial, 417-419, 676 Follicle-stimulating hormone (FSH), 399, 400, 420, 422, 584, 586, 694, 713 Follicular atresia, 418, 421, 585, 645, 703 Folliculogenesis, 419 Foramen ovale, 40, 41, 55 Forced extraction, 301-307, 326-337, 344-350 Forceps, obstetrical, 291, 292 Fracture of the fetal jaw, 271, 303, 347 limbs, 271, 303 ribs, 271 pelvis, 241, 344, 394 rear limbs, 241, 303, 304, 394 spine, 241, 304, 394INDEX 965 Freemartins, 75, 97-99, 529, 660, 672, 673, 820 Fremitus, in the middle uterine artery, 21 Frenulum, persistence of, 758, 763, 795 Frohlich’s syndrome (see dystrophia adiposogenitalis) Frozen semen, 900-922 Fructolysis in semen, 769-773 Fructose, 41, 769, 772, 773 Galea capitis, 767 Gangliosidosis, 61, 63, 66 Gangrene of the uterus, 230-233, 337, 338, 343 Gartner’s ducts, 11, 13 abnormalities of the, 529 cysts of the, 11, 529, 556, 586, 622 embryology of, 12, 13 Genes, 51, 52 sex-limited, 52 sex-linked, 52 Genetic profile of sires, 890 Genetics, 51-68 of twinning, 101, 102 Genistein, in subterranean clover, (see estrogens), 201,483, 663, 852 Genital horse pox (see coital exanthema), 474, 618, 644, 805 Genital tract anatomy of female, 2-11 male, 752-758 embryology of the female, 12, 13 male, 12, 759, 760 injuries to the, 353-368 with lacerations and rupture, 353-355 segmental aplasia of the, 622, 721 Gestation period (see pregnancy), 38, 104-107 duration of the, in animals, 104-107, 684, 701 factors influencing the duration of the, 104-107 hormonal control of the, 107-110, 399-409, 685, 704 periods of the embryo and fetus in the, 38, 39 physiology of the, 41, 107-110, 685, 701 prolonged, 43, 104, 106, 107, 278, 333 Giantism, fetal, 43, 104, 106, 107, 333, 334 “Gillflirter,” 347, 359, 360 Glandulae vesiculares (see seminal vesicles) Glaucoma, 62, 66 Globoid, leukodystrophy, 63, 66 Glucocorticoids, 108-110, 149, 247-251, 408, 829 Gluteal nerves, paralysis of the, 355 Golgi apparatus, 765 “Gomer” animals (see teaser bulls, stallions), 502, 503, 589 Gonadal dysgenesis, 596, 621 Gonadal hormones (see estrogenic, androgenic and progestational hormones), 403-406, 762 Gonadotropic hormones, 30, 31, 108, 109, 399-402, 488-491, 512, 515, 575, 584-586, 593, 597, 646, 658, 671, 760-763 influence of high blood levels of on pregnant mares’ ovaries, 107-110 levels of, in the blood of pregnant mares, 29-31, 401, 402 physiology of the, 399-402, 761-763 sources of the, 30, 401, 402 uses of the, 402, 597 Gonads, embryology of the, 12, 759 in hermaphrodites, 72-75, 709 size of, in the equine fetus, 108, 109 undifferentiated, 460 Gonitis, in males, 792 Graafian follicle, 6, 29, 418—422, 584—586, 680, 704 manual rupture of, 567, 568 polyovular, in queens, 96 Granular venereal disease, 468-471, 803, 806 Granulosa-cell tumor, 533, 534, 620, 673, 722, 723 Granulomas (sperm) in testes and epididymides, 842, 843 Grass tetany, 240-242 Growth hormone, 114, 399 effect of the, on lactation, 114 Gubemaculum, testis, 759 Habronemiasis, genital, 805 Hair, defects of the, 53, 56, 57, 61, 62, 64, 67 Hairballs, in the amniotic cavity, 43, 333 Hair “rings” around the penis of young range bulls, 803 Handles, obstetrical, 291, 292 “Heat” (see estrum) Heat excess, causing testicular degeneration, 815, 818, 826-838 embryonic deaths, 640, 641, 664 Heaves, 60 Hematocolpos, 710 Hematomas, of the vagina, 346, 353-355 vulva, 233, 355 placenta, 45 Hematoporphyrinuria, 58, 61, 67 Hemeralopia, 62 Hemicardius monster, 79 Hemimelia, 54, 66, 79 Hemiplegia, laryngeal, 60 Hemivertebrae, 63, 78 Hemoglobin, fetal, 40 Hemoglobinuria, postpartum, 372 Hemophilia, 58, 59, 60, 63, 64, 67 Hemophilus equigenitalis, 599-613, 603-605 Hemophilus somnus, 469-471, 848 Hemorrhage, interplacental, in mummification of the bovine fetus; 214-217 intrapelvic or perivaginal, 346, 353 intraperitoneal, 242, 337, 338, 353, 354, 362 intrauterine, 214-217, 353, 354, 362, 720, 740 in uterine torsion, 232, 337, 338 of pregnancy, 242 ovarian, after CL removal, 504, 505, 534, 535 postpartum, from genital tract, 346, 353, 354, 362, 394, 742- 745 preputial, 770, 775, 794, 797, 799, 800 subconjunctival, in newborn, 271 umbilical, 232, 337, 338 urethral, male, 775, 776 Hemospermia, 776 Hepatitis, infectious in horses (see Theiler’s disease), 401, 402 Hereditary infertility in cows, 481, 482, 521-531 in males, 752-890 Hermaphroditism, 61, 62, 72-75, 709, 820, 821 in dogs and cats, 72, 73, 75, 709, 820 in horses, 74, 75, 623, 820 in sheep and goats, 62, 65, 671-673, 820, 821 in swine, 61, 75, 643, 645, 821 Hernias, abdominal, 72, 228, 229, 343 causing dystocia, 343 causing inability to copulate in male, 807966 INDEX cerebral, 55, 60 diaphragmatic, 67, 72, 228, 343 inguinal (scrotal), 59, 61, 65, 228, 343, 822, 826 perineal, 228, 343, 346 umbilical, 57, 59, 61, 65, 67, 72, 228, 343, 807 ventral, due to rupture of prepubic tendon, 229, 230, 343 Herpes viruses, in abortion, 138-142, 165, 209, 211, 729 genital infections, 474, 555, 556, 618 Hip joint, 5, 792 dislocation of the, 3, 4, 34, 226, 241, 271, 356 dysplasia of the, 57, 65 Hiplock (see dystocia), 255, 300, 329, 331 causing obturator paralysis, 329, 356 Hippomanes, 43 Hooks, obstetrical, 291, 292 Hormones, 398-409, 680-683, 700, 701 abortions due to, 149, 150 adrenal, cortisone (glucocorticoids), 106, 107, 149, 247-251, 408 epinephrine (adrenaline), 408 adenohypophysial, 399-402 adrenocorticotropic (ACTH), 106, 247-251, 399, 408, 409, 481, 763, 784 anabolic steroids, 784 androgenic (testosterone), 709, 760-762, 784, 785, 829, 851, 852, 936-938 anterior pituitary (see adenohypophysial), 106, 107, 399-402, 488-491, 583-585, 784 antihormones, 401, 422, 585 anti-Mullerian duct, 709 controlling the estrous cycle, 399-409 of the bitch, 678-683 cow, 399-409, 437, 438, 478-491, 495-512 ewe, 655-658 mare, 584, 585 queen, 700, 701 sow, 637, 638 controlling the gestation period, 106-110, 149, 247-251, 399- 409, 683-686, 704 controlling lactation, 114-116, 399, 401 corpus luteal, progesterone, 107-110, 405, 406, 437, 438, 491, 507, 585, 734, 740 relaxin, 247-251, 406, 687 deficiency as a cause of abortion, 150, 171, 172, 201, 209, 212, 406 as a cause of impotency, 784, 785 as a cause of reduced spermatogenesis, 764 as a cause of skin and hair lesions, 115, 408, 512, 599, 763, 784, 790 equine gonadotropin (see PMSG), 401, 402, 694, 705, 706, 760, 928 estrogenic, 403-405, 438, 482, 547, 564, 585, 658, 692, 709, 710, 761, 762, 784, 785, 829 feeding of, 404, 483, 564, 644, 662, 663, 852 follicle stimulating (FSH), 399, 437, 584, 593, 598, 658, 694, 760, 928, 938 glucocorticoids (see cortisone) gonadal, 403-406, 593, 708-711, 734-740, 760, 761 gonadotropic, 30, 31, 108, 109, 399-402, 488-491, 512, 515, 584-586, 593, 597, 646, 658, 671, 677-683, 694, 760, 761, 762-764, 784, 785, 928, 934-938 human chorionic gonadotropic, (HCG), 760 releasing (GnRH), 399, 489-491, 500, 564, 586, 593, 760- 764, 785, 938 growth (somatotropic) 114, 399, 717, 763 hypothalamic (see gonadotropic releasing, GnRH) inhibin, 5, 947, 950 in the female, 104-107, 247-251, 399-409 in the male, 760-764 in the therapy for impotency and infertility in the male, 691 — 694, 704, 784, 785 initiating parturition and abortion, 248-251, 404, 407, 408 lactogenic (prolactin), 108, 109, 114, 115, 399, 401, 691, 763 levels in the plasma in pregnant mares, 30, 584-586 luteinizing (LH or ICSH), 400-402, 405, 437, 438, 480, 482, 483, 488-491, 585, 658, 677-682, 703, 713, 760 Mullerian-inhibiting substance, 760 posterior pituitary, 116,401-403 oxytocin (pitocin), 116, 150, 248, 249, 253, 345, 348, 349, 401-403, 763 pitressin (vasopressin), (antidiuretic, ADH), 401-403 progestational (progestogens), 405, 406, 438, 491, 507, 585, 593, 594, 597, 598, 658, 688-690, 706, 709, 734-740, 936, 938 prostaglandins, 438, 490, 491, 507, 547, 585, 594, 597, 614, 638, 659, 671, 672, 691-694, 928, 936, 938 pulsatile release of GnRH, LH and FSH, 400, 437, 438 relaxin, 247-251, 345, 406, 687 “repositol,” preparations, 404, 406 somatotropic (see growth), 114, 399, 712, 763 testosterone (see androgenic) therapy in “repeat breeders,” 564, 565, 569 thyroid, 115, 408, 512, 599, 763, 784, 790 thyrotropic, 399 Hyaluronidase, 426, 767 H-Y antigen, 75 Hybrids, 75, 76, 820 Hydatid cysts of Morgagni, 621 Hydrallantois (see hydrops of allantois) Hydramnios (see hydrops of amnion) Hydrocephalus, 54, 60, 62, 63, 65, 77, 278, 285, 308, 336 Hydrocortisone, 149, 172, 173, 188, 201, 209, 247-251, 408 Hydrometra (see mucometra) Hydrops allantois, 43, 76, 223-228, 334, 335, 395 Hydrops amnii, 43, 77, 223-228, 334, 335, 395 Hydrosalpinx, 535-538, 609, 621, 642, 643, 661 Hymen, 10 embryology of the, 12, 13 imperforate (persistent) 346, 522, 528, 622, 623 Hyperadrenocorticism, 716 Hyperbilirubinemia, 62 Hyperestrinism, in the dog and cat, 405, 714, 717, 718 Hyperkeratosis, 551, 661, 845 Hyperplasia, of the prostate gland, 785 Hypertrophy of muscle (“double” muscle), 56, 61, 278 Hypocalcemia, 241, 346, 348, 353, 357, 361, 362, 368-370, 372, 374, 380, 394 Hypoestrinism, and incontinence in dogs, 716-718 Hypomagnesemia, 241, 371, 394 Hypophysis (see pituitary gland) Hypophosphatemia, 372 Hypoplasia of the adrenal gland, 106, 107, 333, 334 cerebellum, 54, 63 ovaries, 521, 522, 621INDEX 967 pituitary gland, 55, 106, 107, 333, 334 testes, 763, semen characteristics of, 815-818 Hypothalamus, relation to pituitary gland, (releaser substances from), 399, 489-491, 500, 564 Hypothyroidism, 712, 717, 718 Hypotrichosis congenita (see alopecia), 53, 57, 61, 62, 64, 67 Hypoxia, 270 Hysterectomy, 596 causing persistence of CL, 496 in dystocia, 323, 324, 331, 348-351 fetal emphysema and maceration, 218-220, 232, 324, 331, 348-351 uterine prolapse, 363, 365 rupture, 359 torsion, 32, 233, 340, 343, 359 infections, 387 IBR-IPV infection, in females, 138-142, 474, 555, 556 in males, 139, 775, 803-805, 813 Icthyosis congenita, 53, 64 Icterus of the newborn (see neonatal isoerythrolysis), 267-269 Idiogram (see Karyotype) Iliocolonic aganglionosis, 59 Ilium, 3 Immunity, transfer of from the dam to the newborn, 47, 263, 264 Immunodeficiency, combined and other, 59 Immunogenetics, 96, 97 Immunologic pregnancy tests, 30 Implantation or attachment of the embryo, 39, 560, 561, 563-565, 683 Impotency in males (see libido), 762, 772—774, 782—785, 786—808 acquired factors, 786-789, 792-808 due to cardiac disease, 808 due to pain (in peritonitis, orchitis, balanitis, prostatitis, arthritis and etc.) 792-808 due to respiratory disease, 792-808 environmental factors, 788, 789 hormones in, 787, 790, 791 inheritance of, 787, 807 psychic, 789, 790, 794 tests for, 790 “Impregnation” of mares, 866 Inanition, as a cause of infertility, 515, 516, 596, 598, 782 Inbreeding, 52, 67, 68, 278, 530, 819, 820 Incontinence, in dogs, 716 Induction of estrum in ewes during anestrum, 402, 659, 660 in mares during anestrum, 583-592 Inertia, uterine, 225-227, 278-281, 305, 306, 344, 345-349. causing dystocia, 347-349 Infections of the genital organs, in bitches and queens, 728-740 cows, 374, 447—476 ewes and does, 660, 661, 672 males, 803-806, 841-843, 886, 887 mares, 599-619 sows, 643, 644 of the navel, 263 of the newborn, contracted in-utero, 266, 267 Infertility, 398-870 associated with, “repeat breeders,” 559-569, 575-579, 625-627, 646, 647 caused by stress, 566, 567, 645, 646, 663, 664 caused by cytogenetic defects, 819, 820 incidence of, 434, 581, 582, 636, 654, 673 induction of, to control pet populations, 687-694, 706, 707 instruments for the treatment of, 540 in the bitch and queen, 675-745 due to anatomic or congenital factors, 709-711 genital infections, 728-740 hormonal factors, 712-718 nutritional factors, 711 pathological factors and tumors, 718-728, 734-745 in the cow, 434-579 due to anatomical or congenital factors, 521-530, 709-711 genital infections, 447-476 hereditary factors, 481, 482, 521-531 high ambient temperatures, 566, 567 hormonal factors, 478-491 management factors, 481, 496-512, 514-519, 530, 57 579 nutritional factors, 481, 514-519 pathological factors, 533—557, 814 twinning, 100, 481, 482 economic importance of, 434 in the ewe and doe, 654-664 due to anatomic and congenital factors, 660 genital infections, 660-662 nutritional factors, 657, 662 pathologic factors, 660-662 in the hybrids, 820 in the male animal, 752-870, 872-890 breeding soundness evaluation (BSE) (or diagnosis of), 857- 870, 872-886, (see 885) due to age, 789 anatomic, congenital and hereditary factors, 787 hormonal factors, 784, 785, 787, 790, 791 impotency or lack of libido, 784-792 inability or difficulty in copulating, 786-808 inability or reduced ability to fertilize, 813-815, 857- 890 management factors, 789, 790 nutritional factors, 782, 783, 788 in the males twin to freemartins, 820 in the mare, 581, 582, 588-628 due to early embryonic or fetal death, 600-606 genital infections, 599-619 hereditary or congenital factors, 621-623 hormonal factors and irregularities of the estrous cycle, 591-597 management factors, 588-590 nutritional factors, 598 in the sow, 636-648, 814 due to anatomic or congenital factors, 642, 643 genital infections, 643, 644, 647 hormonal factors, 644-646 nutritional factors, 647, 648 Infusions, intrauterine, 538-547, 612, 615, 616 Inguinal canal, 754, 755 hernia, 59, 61, 65, 760, 822 Inhibin, 5, 947, 950 Injuries, at coitus (copulation), 416, 417, 644, 700, 711, 774-776 to the female during dystocia or parturition, 240-242 fetus and newborn, 271, 272, 303-307968 INDEX joints, tendons, muscles of the dam, 240-242 of the male preventing cop- ulation, 792 penis and prepuce preventing copulation, 794, 796- 799 spine of the male, 792, 793 Insemination, artificial, 894-926 advantages and disadvantages, 895, 896, 900, 901, 911, 916, 922, 923 as a cause of abortion, 151, 906 blood-typing of bulls for parentage tests, 96, 97, 909 history of, 894, 901 “impregnation” in mares, 915 in bitches, 923-925 cows, 896-909 ewes and does, 920-922 others, 926 mares, 911-915 queens, 925, 926 sows, 916-919 organizations and health standards in, 895, 898, 903, 904, 908, 909, 911, 923 site of, in bitches, 924 cows, 567, 905-907 ewes and does, 921, 922 mares, 914, 915 queens, 925 sows, 919 time of, in bitches, 924 cows, 437,-566, 905 ewes and does, 921, 922 mares, 914 sows, 639, 918 Intrauterine devices, (I.U.D.), 221, 407, 659 Instruments, used in obstetrics and sterility therapy, 290-294 Interestrous interval in bitches, 676 Intersexes (see hermaphrodites), 72-75, 97-99, 671, 672, 673, 709- 711, 715, 820 Interstitial cells, 753, 760, 764, 769 hypoplasia of the, 817, 818 tumors of the, 833-835 Intestines, prolapse of, 360, 362 Intrauterine migration of embryos, 38, 111, 588, 641, 642, 657 Intromission (see coition) Invagination of the uterine horn, 353, 362, 366, 367, 382 Involution of the uterus, 256-259, 438-440, 544, 545 corpus luteum, 406, 407, 411, 436, 440, 441, 742 Iodinated casein, 115, 408 Irradiation, effect on testes, 828, 829 Ischiocavemosus muscle, 757, 770 Ischium, 3 Isoerythrolysis, neonatal, 267-269 Isoxsuprine, a tocolytic agent, 248, 296 Isthmus, of uterine tube, 8, 423, 424, 427 Joints, lesions of, 60, 65, 792, 793 malformations of, 57, 59, 60, 61, 64, 65, 69, 70, 78 Kartagener’s syndrome, 819 Karyotype, 51, 70, 73-76, 96, 97, 529, 621, 709, 814, 815, 820 Ketosis, in cattle, 240, 370 ewes and does, 202, 240, 370, 371, 394 Kidneys, anomalies of the, 63, 66, 72 fetal, 41 Klebsiella pneumoniae genitalium infection in the mare, 165, 602, 605 Klinefelters’ syndrome (XXY), 585, 815, 817, 820 Labor, 251-255 Laceration of the cervix, 314, 354 uterus, 354 vagina, 314, 344, 353, 354, 416 vulva, 259, 314, 354 Lactation, 113-117, 686, 704 artificial induction of, 115, 405 hormonal control of, 113-116, 401, 404-406, 686, 704 of milk “letdown,” 116, 402, 403 suppression of, 116, 405 Lacuna, lymphatic, 25 Laminitis, puerperal. 389, 390, 394 Laparohysterotomy (see cesarean operation) Laparoscopy, 681, 704 Laparotomy, for extrauterine fetuses, 222, 223, 359 rupture of the uterus, 359, 360 uterine infections, 387 prolapse, 363, 365 torsion, 233, 341 Leiomyomas, 723 Leptospirosis, as a cause of abortions, 131-134, 165, 180-182, 197 in relation to infertility, 471 Leydig cells (see interstitial cells) Libido (see impotency), 762, 772-774, 782, 784, 785, 786-792 effect of frequency of service on, 772, 773 lack of, in males, 777, 782, 784-808 effect of hormones on, 762, 784, 785, 787, 791 Ligaments, accessory, 3, 4 broad, of the uterus (see mesometrium), 9 cotyloid, transverse, 5 dorsal apical, of penis, 795 dorsal and lateral sacroiliac, 3 pelvic, 3, 246, 484, 485 relaxation of, at parturition, 5, 246 round, of the bladder, 41 hip, 4 liver, 41 sacrosciatic, 3, 484-486 Ligamentum arteriosum, 41 venosum, 41 Light, effect of on breeding season in ewes, does, males, queens and sows, 583, 592, 654-656, 669, 699 “Limber legs,” in Jersey calves, 54 Lip and leg ulceration, in sheep, 661 Lipoma, strangulation of uterus by, 173 Lipomatosis, 58 Listeriosis, causing bovine abortion, 134, 135 ovine abortion, 194, 195 Lithopedion, 223 Litter size, 95, 101, 640, 641, 699 Liver, 40 Liveability or longevity tests for spermatozoa, 587, 877 Lochia, 257, 258 infection of the, 257 Losses of newborn, 270 Lubricants, obstetrical, 294, 299, 304, 305, 326, 334, 344-346, 349, 350INDEX 969 Luteinizing hormone (LH), 400, 401,402, 404, 437, 438, 593, 677- 682, 703, 763 Luteolysin or luteolytic factors (see prostaglandins and estrogens), 440, 594, 595 Maceration of the fetus, 218-220, 232, 283, 338, 340, 349, 351, 415, 496, 500 Major histocompatibility complex (MHC), 97 Malformations (see anomalies, teratology) Malingerers, 395 Malpractice, in relief of dystocia, 306 Mammary gland, 14, 113-117, 402, 404, 405 anatomy of the, 113 artificial involution of the, 273 ectopic, 673 tumors of the, in the bitch and queen, 725-728 Management, as a cause of dystocia, 278-280 infertily in cows, 481, 496-512, 514- 519, 530, 575-579, 813 mares, 581, 582, 625-628 sows, 648, 814 diseases of the newborn, 269-272 Mannosidosis, 54, 62 Mastitis, 387, 388, 726 Masturbation, 769, 776 Meconium, 43, 72 retained, 265 “Medusa heads,” 768, 882, 884 Melanoma, 620, 621 Melatonin, 409 Menopause, 110, 419 “Menstruation,” metrorrhagia in the bitch, 677-699, 742-745 in the cow, 15, 437 Mesometrium, 7, 8, 9 Mesonephric duct (see Wolffian duct), 11-13, 529, 535, 556, 621, 622, 709, 759, 843-846 Mesorchium, 753 Mesosalpinx, 8 Mesovarium, 6 Metabolic disease of the puerperal period, 240-242, 368-372 eclampsia, 240-242, 368-370, 372 grass tetany (hypocalcemia), 240-242, 368-372 ketosis, 240-242, 370, 371 parturient paresis (milk fever), 240-242, 346, 348, 368-370 Metestrum, 412, 677 Metritis, endo- in the bitch and queen, 734-740 cow, 218-220, 346, 348, 349, 350 mare, 382, 383, 538-546, 600, 601, 608 laminitis from, 382, 389, 390 metritis-mastitis-agalactia (MMA) syndrome in sows, 387, 388 peri- and para-, 219, 223, 351, 359, 535-538, 548, 549, 643 postpartum, 272, 353, 376-389, 538-550 sclerotic, 219, 550 septic, 384-386, 389, 394 of pregnancy, 218-220, 227, 228, 241 Microphthalmia, 55, 62, 66 Milk, composition of, in animals, 117 production of, 117 stimulation of the “let-down” of, 116, 402, 403 suppression of the let-down of, 116, 402, 403 uterine, (“milk”), 39, 42, 405 Milk fever (parturient paresis) in the cow, 240-242, 346, 348, 368- 370, 374 syndrome in the cow, 387, 388 Minchev’s operation of vaginal fixation, 238 Mineral deficiencies, 150, 151, 173, 188, 202, 518, 519 M.I.P. test for pregnancy in the mare, 30 Mismating, prevention of conception and abortion, 687-694, 705- 707, 715 Mitochondria of spermatozoa, 767, 768 “Moles,” hydatiform of the fetal membranes, 48, 551 “Monorchidism” (see cryptorchidism) Monotocous animals, 94 Monsters, fetal (see anomalies and teratology), 69, 76-82, 278, 313, 335-337 campylorrhacis scoliosa, 78, 313, 335, 336 causing dystocia, 278, 313, 335-337 double, 81, 82, 313, 336 conjoined twins (diplopagus), 81, 82 dicephalus, 82 dipygus, 82 perosomus elumbis, 78, 335, 336 perosomus horridus, 78, 336, 337 schistosomus reflexus, 78, 313, 335, 336 Morphology of spermatozoa, 763, 766-768, 814-819, 837, 877-885 in testicular pathology, 836, 837 primary abnormalities, 763, 814, 837, 879-882 secondary abnormalities, 818, 837, 879-882 Morula, 38 Mosaicism, 52 Motility of spermatozoa, 768, 813-815, 818, 819, 836, 875-877 degree of, 875-877 determination of, 875-877 in testicular or genital pathology, 815-838, 874 percentage of, 875-877 rate of, 424, 425 Mucocervix, 487, 554 Mucometra, 23, 486, 487, 496, 500, 546, 550, 551, 642, 672, 720, 734 associated with cystic ovaries, 486, 487, 720 in white heifer disease, (segmental aplasia of the paramesoneph- ric ducts), 41, 277, 346, 522-528, 642 Mucus, from nose and mouth of newborn, 263 from vulva in estrum, 435, 436 pregnancy and cervical, 22 Mules, 75, 76 Mules’ operation on ewes, 661, 662 Mullerian duct (see paramesonephric duct), 12, 13 agenesia of the, in the cow, 277, 346, 522-528 in the sow, 642, 643 persistence of the median wall of the, 277, 346, 526-528, 622, 642 , 643 segmental aplasia of the, 522-528, 622, 642, 643, 660, 710, 721, 845 Multipara, 94 Multiple births, in unipara (see twinning), 95, 96, 335 incidence of in cows, 96 Mummification, fetal (see abortion), 123-222, 213-218, 232, 346, 349, 351, 415, 496, 500, 642 hematic in cows, 214-217, 407, 496 papyraceous, in the mare and multipara, 214, 217, 218, 741 static fetal cadaver, 214 Muscle, corpus spongiosum, 770 external cremaster, 764 hypertrophy (“double”-muscling), 56, 61, 278 relaxants for uterine, 248, 296, 299, 349970 INDEX rupture of the gastronemius, 357, 394 Mutation of the fetus, 298-301, 326-333 Mycoplasmas (see ureaplasma or T mycoplasma), in females, 135, 136, 164, 165, 184, 199, 469-471, 538, 539, 661, 672, 730, 813 in males, 469-471, 848, 849 Mycotic abortion, 145, 148, 170, 188, 199 Mycotoxins, 148, 188, 519, 644 Myiasis, 661, 662 Myoclonia congenita, 61 Myositis, Zenker’s, 241, 357, 394 Myotonia congenita, 62 Navel, care and disinfection, 255, 263, 265, 269 infection of the, due to a persistent urachus, 265 Necrosis, of the skin of the udder associated with edema, 114 Necrospermia, 889 Necrotic tips of the allantochorion in the cow, 44 Necrotic vaginitis and vulvitis, 355, 379, 390, 391, 555 Neonatal isoerythrolysis, 267-269 Neoplasms (see tumors) Nerve, hemorrhoidal, 236-238 gluteal, 355, 394 obturator, 279, 306, 329 pudendal, 236-240 nerve block of the, 236-240 Nervous system, embryology of the, 39 in the physiology of reproduction, 398, 399, 400, 401,403, 421, 422 Neurohypophysis, 402, 403 Newborn anomalies of the, 51-82, 335-337 antibiotics in diseases of the, 263, 265 care and feeding of the, 262-265 orphan, 264, 265 infection of the, contracted in-utero, 266 injuries of the, 259, 271, 272, 303—307 due to a vicious dam, 259, 271, 272 killing of the, due to avicious dam, 259, 271, 272 losses due to chilling of the, 270 need of the, for colostrum, 263, 264 neonatal isoerythrolysis of the, 267-269 neoplasms of the, 269 nutritional diseases of the, 269 parasitisms of the, contracted in-utero, 267 stimulation of respiration in the, 262, 263 Nitrate poisoning, as cause for abortion, 147-149 Nodular venereal disease (see granular venereal disease) Nonreturn rates in AI of cattle, 560, 888, 906, 907 Nullipara, 95 Nutrition, deficiencies of causing abortion, 150, 171, 173, 188, 202 causing dystocia, 278-280 causing infertility in females, 508, 509, 514— 519, 566, 598, 599, 647, 648, 657, 662, 711 causing paraplegia of pregnancy, 240-242 of the dam, 240-242, 245, 711, 712 of the orphan newborn, 264, 265 overfeeding and obesity, 279, 882, 888 Nyctalopia, 59 Nymphomania (see cysts, ovarian) in the bitch and queen, 714, 715 cow, 478-491 mare, 593, 596 Obesity, as a cause of dystocia, 279 infertility in females, 516, 599 males, 782, 788 Obstetrical operations (see operations, obstetrical) Obstetrics, definition of, 1 Obturator nerve, paralysis of the, 279, 306, 329, 355, 356 Occipital joint, dislocation of the, 304 Odor, male (see pheromones), 398, 409, 410 Onanism (see masturbation) Oocytes, 417-419, 676 number of, 418, 419, 676 Oogenesis (see ovogenesis) Oogonia, 417, 418 Operations, obstetrical, 298-324 cesarean section, 314-323 in bitches and queens, 321-323 in cows, 316-320 in ewes and does, 320 in mares, 314-316 in sows, 320-321 episiotomy, 347 fetotomy, 307-314, 327-332 advantages and disadvantages, 307-317 amputation, of the forelimb, 309, 310 of the head and neck, 309 of the rear limbs, 311, 312 bisection of the fetal pelvis, 311, 312 breakdown of the ribs, 310, 312 cephalotomy, 308 decapitation, 308 detruncation, 310, 312 evisceration, 310, 312 on monsters, 333-337 forced extraction, 259, 301-307, 326-337, 343-350 hysterectomy, 323, 324 incidence of, 298 mutation, 298-301 extension and adjustments of the fetal extremities, 300, 301 repulsion, 298, 299, 301 rotation, 299, 300, 301, 303, 304 traction, 301-307 version, 300 splitting of the pelvis of the dam (see symphysiotomy), 313, 344 vulva-suturing (see Caslick’s operation), 237—240, 346, 347, 355, 556 Orchitis (see testis, degeneration of the), 776, 829-832, 837, 838, 841, 842 in brucellosis, 829 treatment of, 837, 838 Orphans, adoption of by other dams, 264, 265 feeding and care of, 264, 265, 323 Os coxae, 3 Os penis, dog, 757 Osteoarthritis, 57 Osteochondrosis dissecans, 60, 65 Osteogenesis imperfecta, 53, 65 Osteopetrosis, 53 Ovariectomy, 400, 596, 713 during pregnancy, 104-108INDEX 971 Ovaritis, 504, 505, 534, 535, 610, 734 Ovary, agenesia of the, 522 anatomy of the, 5-8 cysts of the, in bitches and queens, 712, 714 in cows, 402, 404-406, 415, 478-491 in sows, 644, 645 during pregnancy, 21, 22, 29, 93 dysgenesis of the, 621 effects of removal of the, on pregnancy, 104-108 hematoma of the, 620, 621 hormones of the (see estrogenic, progestational, relaxin, and in- hibin), 403-406 hypoplasia of the, 419, 521, 522, 621 palpation of the, at estrum in the cow, 567, 568 in the mare, 587, 588, 591, 592 parovarian cysts of the, 535, 621, 645, 661 “smooth,” nonfunctional, 507-511 tumors of the, 533, 534, 620, 647, 661, 673, 722, 723 Ovigenesis, 417-419, 676 Oviducts (see uterine tubes), anatomy of the, 8 anomalies of the, 535, 643 embryology of the, 12, 13 pathology or disease of the, 535-538, 609, 610, 643 tests for patency of the, 537, 610 transport of ova and embryos through the, 422, 424, 586, 639, 640, 658, 670, 683, 704 transport of spermatozoa through the, 424-428, 587, 639, 658, 670, 680- 683, 700-704 Ovulation, 419-422, 565, 566, 584-588, 591, 637, 655-658 double in mares, 95, 585, 586, 588 endocrine control of, 399-401, 420-422, 584-586, 637, 639, 681-683, 694, 700-704 failure of, or delayed, 491, 492, 588, 645, 646, 670 follicular atresia, after or before, 418-420, 584, 586, 645, 703 fossa, in the mare, 6, 420, 585, 586 in bitches, 681-683 cows, 96, 432, 437, 565, 566 does, 670 ewes, 655-659 mares, 584-586 queens, 700-704 sows, 637, 639 induction of, in bitches, 694, in queens 703, 704 influence of the nervous system on, 421, 422 multiple, in unipara associated with infertility, 95, 96, 588 species with spontaneous and nonspontaneous, 421, 422, 585 super-, 101, 422, 492, 597, 598, 928, 936, 937 time of, 422, 435, 437, 491, 492, 566, 586, 639, 657, 669, 681-683, 700-704 Ovum or early embryo, 36, 417-419 abnormal or defective, 562, 563 migration of the, 38, 111, 428, 588, 640-642, 657, 683 rate of transport of the, to uterus, 422-424, 586, 640, 658, 670, 683, 704 size of, 423 spacing of the, in the uterus of multipara. 111, 428, 588, 640- 642 viability of, after ovulation, 423, 587, 639 Oxygen, for the stimulation of respiration in the newborn, 263 Oxytocin, 116, 150, 248, 249, 253, 345, 348, 349, 358, 364, 365, 383, 401-403, 440, 670, 686 in the male, 763, 768, 771, 772 Palatoschisis, 39, 55, 60, 61, 67 Pampiniform plexus, 753, 764 Panleucopenia abortion in queens, 211 Paradidymides, 759 Paralysis, of the gluteal nerve, 355, 394 obturator nerve, 279, 306, 329, 355, 356, 394 penis, 802 peroneal nerve, 356, 357, 394 Paramesonephric duct (see Mullerian duct), 12, 13, 41, 277, 346, 522-529, 535, 550, 621, 622, 709-711 Paraphimosis, 619, 775, 800, 801, 802, 805 Paraplegia, of pregnancy, 240-242, 353 postpartum, 353, 355-357, 393-396 Parasite, 82, 267 Paratyphoid (see salmonella) abortion in ewes, 196 Parentage testing (blood), 96, 97, 909 Paresis (see paraplegia) Paresis, spastic in cattle, 240-242, 346, 348, 368-370, 374, 394 Parturition, 107-110, 245-276, 686, 704, 705 artificial interference in normal, 248-251, 259 cervical dilation in, 247, 248, 251, 252 double, 112 duration of stages of, 251-259, 687, 705 expulsion of the fetal membranes in, 255, 256, 687, 705 expulsion of the fetus in, 253, 255, 687 induction of, 248-251 initiation of, 108-110, 247-251, 333, 345, 686-687, 705 involution of the uterus after, 256-259, 742 lowering of the body temperature during the early stages of in the bitch, 109, 247, 252, 686, 705 nutrition of the fetus in relation to, 247 placental changes prior to, 255, 256 placental separation from uterus after, 255, 256, 687 postponement of, by tocolytic agents, 248 presentation, position and posture of the fetus at, 252, 253, 687 stages of, 251-259, 687 symptoms of, 245-247, 251-259, 687 time of day as related to, 246, 247 uterine contractions in, 251-259 Parvovirus abortion in sows, 186, 187 Patella, subluxation of, 59, 65 Pavilionitis (see oviduct), Pederasty, 111 Pelvis, bisection of the fetal, 311, 312 comparative anatomy of the, 3-5 diameters of the, 4, 5 disproportion of fetal and maternal, 278, 279 ligaments of, 3-5 relaxation of the, 4, 107-110, 245-276 splitting of the, in the dam (see symphysiotomy), 313, 344 stenosis of the, causing dystocia, 278, 279, 344 withdrawal of the fetus through the, 303-307 Penis, adhesions of, 763, 796-799, 803, 806, 807 amputation of the, 800, 802, 803, 807 anomalies of, 793-795972 INDEX anatomy, comparative of the, 756, 757, 771 arrested development of the, 793, 794, 807 broken (see rupture of the) bulbus glandis of the, in the dog, 757 chronic protrusion of the, in dogs, 802 coiled or “corkscrewed,” 771, 795, 807 congenitally short, 793, 794, 807 corpora cavernosa of the, 756, 770, 795, 799 deviated, curved, bent or spiralled, 771, 795, 796 double, 793 edema of the, 802 embryology, 12, 759 erection of the, 756, 770, 771, 799, 807, 808 excessive size of the, 807 fibropapillomas of the, in the bull, 799, 800 fistula of the, 776 glans of the, 756, 757, 770, 771 “belling” of the, in stallions, 770 hematoma of the, 770, 775, 776, 796-799 hemorrhage from the, 770, 775 hypospadias of the, 793, 794 inability to protrude the, 793-798 infections of the, 468-471, 474, 618, 661, 775, 794-807 injuries and diseases of the, preventing copulation, 793-807 injuries to the, at coitus, 775, 797 loss of sensation to the glans, 771, 798, 807 muscles of the, 757, 794 os of, 757, 776, 795, 807 fracture of the, 776 papillae or spines of the, in the cat, 758 paralysis of the, 757, 802, 806 persistent frenulum of the, 758, 763, 795 prolapse and paralysis of the, 757, 802, 806 rupture of the, 770, 775, 796-799 sarcoma, infectious venereal, of the dog, 799, 800 sigmoid flexure of the, 757, 763, 794, 796 tumors of the, 775, 799, 800 twisting of glans at ejaculation, 771, 795 Perianal gland neoplasia, 854 Perimetritis, 219, 223, 351, 359, 535-538, 547, 549 Perineum, anatomy of, 11 rupture of, 259, 347, 359, 360 Periods or stages of gestation, 38, 39, 104-107 Peritonitis, 333, 338, 340, 343, 354, 357-359, 385, 547-549, 743 Perivaginal fat, prolapse of the, 233, 236, 346, 361 removal of the, 235-240, 361 Peroneal nerve paralysis, 356, 394 Perosomus elumbis, 61, 78, 79, 329, 330, 335, 336 horridus, 78, 79, 336 Persistence of the corpus luteum, in cows, 24, 214, 217, 407, 496, 497, 546 in does, 672 in mares, 587 ductus arteriosus, 40, 64, 67 urachus, 59, 265 Pessaries, 237, 365, 597, 608 pH of semen, 772, 874 Phallocampsis, 795 Phenocopies, 69 Pheromones, 398, 409, 410, 680, 699, 761, 762, 785, 787 Phimosis, 793, 794, 796, 800, 801, 802, 805 Photoperiodism and the breeding season, 413, 582, 583, 656, 669- 671, 699 Physiology of coition, 415-417, 700 fertilization, 422-426, 586, 587 gestation, 41, 104-110, 149, 247-251, 399-409 ovulation, 419-422, 565, 566, 584-588, 591,637, 655-658, 681-683, 700-704 puberty, 409-411, 438, 582, 675, 698, 762-764 in males, 763 semen, 764-774 the estrous cycle, 411-415, 427, 434-442, 582-585, 588- 597, 676-683, 702-704 the female, 398-428 bitch, 475-495 cow, 434-442 doe, 669-671 ewe, 654-660 mare, 582-588 queen, 698-707 sow, 636-642 the fetus, 41 the male, 760-777 the nervous system as it affects reproduction, 398-403, 421, 422, 484-491, 500, 564, 595 the reproductive hormones, 398-409, 760-763 Picomaviruses (see SMEDI viruses), 184 Pineal gland, 409 Pitocin (see oxytocin), 116, 150, 248, 249, 253, 345, 348, 349, 402, 403, 440, 670, 686, 763, 768, 771, 772 Pitressin (see vasopressin), 402, 403 Pituitary gland, anterior, 399-402, 717, 760, 761 cysts of the, 717 embryology of the, 39 hormones of the, 399-402, 717, 760, 761 posterior, 39, 402, 403 relation of the adrenal gland to the, 106, 399-402 hypothalamus to the, 598-602, 760, 761 Pizzle rot (see balanoposthitis) of sheep Placenta, 39, 41, 44-48 adventitious, 45, 46, 48, 376 anastomosis of the, in twinning, 97-99 attachment of the, to the endometrium, 39 changes in the, prior to parturition, 255, 256 choking on the, 256 chorioepithelioma of the, 48, 724 classification of the, 44-47 eating of the, by the dam, 256 examination of the, 48 expulsion of the, after birth of fetus, 255, 256 fetal, 44-47 fluids of the, 19, 27 hematomas of the, 45 maternal, 44-47 retained, 255, 256, 373-384 separation of the from endometrium at parturition, 255, 256 subinvolution of placental sites in the bitch, 354, 742-745 transfer of immunity through the, 47 tumors of the, 48, 724 types of the, 44-47 villi of the, 39, 44, 45 Placentation, 44-47 Placentitis, 374-384 Placentome, 21, 45, 373, 376 Plaques, “dollar,” in dourine, 619INDEX 973 Pleiotropism, 68 Plexus, pampiniform, 753, 764 Pluripara, 95 Pneumoperitoneum, to control straining, 236-240 Pneumovagina, 355, 360, 392, 484, 536, 544, 555, 581, 599, 600, 610-612 Pneumovestibule, 600 Poisons causing testicular degeneration, 832, 833 Polycythemia, 58 Polydactyly, 56, 61, 66 Polygyny, 427 Polyps, endometrial, 720, 740 vaginal, 720 Polyspermy, 423, 427, 639 Polytocous animals, 94 Population control, of pets, 687-694, 706, 707 Porcine stress syndrome, 60 Porphyria, congenital, 58, 61, 67 Positions of the fetus at parturition, 94, 252, 253, 326-333 in the uterus during pregnancy, 94 Posterior pituitary gland (see neurohypophysis), 39, 402, 403 Postestrum (see metestrum), 412 Posthitis (see balanoposthitis), 618, 661, 775, 800, 803-807 Postpartum period, 438, 439, 567, 572-574, 584 time to breed in, 572 diseases of and their effect on conception rate, 572- 574 effect of suckling the dam on the, 574, 595 Postures of the fetus at parturition, 252, 253, 326-331 Potency (see libido, sex drive) Pregnant mare serum gonadotropin (PMSG), 401, 402, 422, 646, 659, 660, 671, 694, 760 Pregnancy (see gestation) amounts of fetal fluid at various stages of, 18, 19, 27 auscultation of the fetal heart during, 15 ballottement of the fetus during, 15, 24, 28, 31 bicomual and rotated bicomual, in the mare, 93, 357 diagnosis of, 14-23, 683-686, 705 by abdominal palpation, 31, 32, 33, 683, 705 biologic tests for, 30, 31, 32 laparotomy, 31, 32, 33 radiography, 31, 33, 683-685, 705 rectal palpation of the, amniotic vesicle, 18 changes in fetal size, 19, 20, 27 changes in the size and location of the middle uter- ine artery, 21, 29, 32 changes in the size and location of the uterus, 20, 28, 32 fetal fluids, 18, 20 placentomes, 21 slipping of the fetal membranes, 18, 20 by ultrasonography, 15, 24, 25, 31, 32, 33, 683, 705 vaginal biopsy, 31, 32 vaginal changes, 22, 28, 31, 32 differential diagnosis, 22-24, 28, 29 in the bitch, 32, 33, 683-686 cow, 14-24 ewe and doe, 31 mare, 24-31 queen, 32, 33, 701-705 sow, 32 disease, in ewes, 202, 240, 370, 371, 394 duration of in animals, 104-107, 684, 701 factors influencing the, 104-107 effects of delayed conception on, 70 estrum during, 14, 24, 31, 657, 701 external indications of, 14, 15, 24, 31, 32 extrauterine (see displaced fetus or extrauterine fetus), 218, 219, 222, 223, 338, 741 false, 24, 107, 109, 596, 597, 682, 701-704, 715 hemorrhage of, 242 hormonal control of, 107—110, 399—409, 683—686, 704 incidence of right and left horn, in cows, 24 length of, in animals 104-107, 684 maintenance of, 106-110, 641, 642 maternal recognition of, 38, 107, 407, 428, 440 paraplegia of, 240-242 prepubic desmorrhexis of, 229, 230 prevention of, after mismating, 220-222 pseudo-, 24, 112, 682, 701-704 septic metritis of, 218, 219, 349 twin-, 24, 29, 30, 31, 95-102, 585-588 vaginal examination for, 22, 29 Prepubic tendon, 5 rupture of the, 229, 230, 343 Prepuce (see sheath) abscess of the, 797-799 adhesions of the, 796-799, 806, 807 amputation of the, 801 anatomy of the, 12, 756, 758, 762, 801 diverticulum of the, in boars, 758, 806 extirpation of the, 806 embryology of the, 12, 758, 762 fornix of the, 758, 797 hemorrhage from the, 770, 775, 794, 797, 800 glands of the, 762 infections of the, in bulls, 471, 474, 794, 855, 856 in stallions, 614, 855 inflammation of the (see posthitis), 618, 661, 775, 794, 801, 803-807 injuries to the, preventing copulation, 793-807 orifice of the, 758, 800 persistence of the frenulum of the, 795 prolapse of the, 757, 800-802 ring of the, in stallions, 758, 800 separation of the, from the glans penis at puberty (see persistence of the frenulum), 758, 763, 795 smegma in the, 758, 799 stenosis of the, 794, 800-802 trauma to the, 794, 800 tumors of the, 794, 799, 800 venereal and other infections of the, 855, 856 Preputial orifice, stenosis of the, 794 Presentation of fetus, at parturition, 94, 252, 253, 283, 284, 328- 332, 687 breech, 27, 253, 283, 284, 330, 331 incidence of anterior and posterior, 94, 253, 254 poll, 253, 328 transverse ventral or dorsal and rotated, 331, 332 Primipara, 95 Productivity, 110, 111, 572-575, 640, 641, 648, 655, 657, 664, 673 Progeny testing, in bulls and boars, 67, 68, 895, 916 Progesterone, 103, 104, 107-110, 113, 114, 405, 406, 688-690, 706 abortion due to deficiency of, 150, 171, 172, 209, 212, 406, 438, 561, 565974 INDEX assays for, 14, 24, 31 in estrus synchronization, 406, 441, 507, 593, 597, 598, 637, 641, 645, 658-660 in the maintenance of pregnancy, 107-110, 150, 171, 172,209, 212, 405, 406, 561, 564, 565, 686 in the treatment of vaginal prolapse, 233-240 physiology of, 107-110, 171, 247, 405, 406, 785 sources of, 406 supplementation with, 108, 150, 171, 172 uses of, 405, 406, 785 Progesterone releasing intravaginal device (PRID), 441, 597, 659 Progestogens, 108 , 247 , 405 , 406, 438 , 491, 507 , 585 , 593 , 594, 658, 688-690, 706, 709, 734-740, 936, 938 in dogs, 670 in males, 785 in mares, 597, 598 in sheep, 658-660 in swine, 637, 641, 645 Programs, for herd health (cattle), 575-579 Prolactin, 108, 109, 114, 401, 686, 704 Prolapse, of the bladder, 233-236, 314, 346, 357, 360, 361 cervix, 233-240, 343, 527 intestines, through ruptured genital tract, 359, 360 into the everted bladder or uterus, 361, 362 penis, 757, 802, 806 perivaginal fat, 236, 357, 361 prepuce, 757, 800-802 rectum, 234, 235, 360 uterus, 354, 361-367 vagina, 233-240, 343, 484, 679 as a cause for dystocia, 343 Pronephros, 41, 759 Prostaglandins, 150, 171, 188, 247-251, 258, 406-408, 438, 440, 441, 500, 507, 594, 597, 614, 641, 642, 646, 659, 671, 672, 686, 691-694, 705, 707, 739, 769, 774, 919, 928, 936, 938 Prostate anatomy of the, 755, 756 cysts of the, 851, 852 effects of castration on the, 762, 852 effects of estrogens on the, 785, 852 effects of testosterone on the, 762, 851 embryology of the, 12, 759 hyperplasia of the, in the dog, 785, 851 inflammation of the, 806, 851, 852 pars disseminata of the, 755, 756, 770 pathology of the, 851, 852 physiology of the, 762, 770, 785 squamous metaplasia of the, 852 tumors of the, 852 Prostatectomy, 852 Prostatitis, 851, 852 Protoplasmic droplets, on the spermatozoa, 763, 765, 768 Pseudocyesis (see pseudopregnancy) Pseudohermaphrodites, 61, 62, 72-75, 623, 643, 645, 671-673, 709- 711, 793, 820 Pseudomonas aeruginosa, 606 Pseudopregnancy, 24, 112, 596, 597, 682, 701-704, 715, 738 Pseudorabies, 144, 185, 186 Puberty, 409-411, 438, 582, 636, 637, 654, 669, 675, 698 age and size to breed females after, 279 , 409 , 410, 582, 636, 654, 669 physiology of, 409-411, 438 in the male, 763 separation of the glans penis from the prepuce during, 758, 763, 795 time of onset of, 279, 409-411, 438, 582, 636, 654, 669, 675, 698, 699 in the male, 763, 764, 782, 817 Pubis, 3 Pudendal arteries, 753, 757 Pudendal nerves, 11, 113 nerve block of the, 236-240 neurectomy, unilateral of the, 236-240 Puerperium cervicitis of the, 390, 478 hemorrhages in the, 353, 354 incidence of diseases of the, 353 infections of the, 373-393, 600 injuries and diseases of the, 353-396 laminitis during the, 389, 390 metabolic diseases of the, 240-242, 368-372 metritis or pyometritis during the, 272, 600, 601, 736 septic, 384-386, 600 milk fever syndrome in the sow, during the, 387, 388 paraplegia of the, 240-242, 353, 355-357, 393-396 placental retention during the, 373-384 tetanus, during the, 390 Pyometra (animal exhibits anestrus), Pyometritis (animal, exhibits es- trous cycling) differential diagnosis of, 23, 736 definition of, 546, 736 in bitches and queens, 734-740 in cows, 23, 380, 381, 390, 407, 415, 449, 450, 496, 500 in mares, 596, 608, 609 in sows, 643 trichomonad, in cows, 449, 450 Pyosalpinx, 536-538, 642, 643, 734 Queen, physiology of reproduction 698-707, infertility in, 708-745 Radiography of the fetus, 31, 33 Radioimmunoassays (RIA), 14, 22, 24, 31, 32 Ram epididymitis organism (see brucellosis, ovine) Rate of movement of spermatozoa, 424, 425 reproduction (see productivity), 110, 111, 640, 641, 648, 655, 657, 664, 673 transport of spermatozoa in the genital tract, 422-424, 425-428, 587, 639, 658, 670, 680, 683, 704 of ova through the oviducts, 423, 424, 586, 640, 658, 670, 683, 704 Recessive defects, 52-68, 333, 346 Rectal examination for the diagnosis of pregnancy in the cow, 15-24 mare, 25-29 sow, 32 restraint during the, 15, 16, 25 rupture of the rectum during the, 16, 25 Rectal vaginal constriction in Jerseys, 54, 277, 529 Rectogenital pouch, 236-240 Rectovaginal fistula, 357-360, 614INDEX 975 Rectum, prolapse of the , 234, 235 rupture of the, 16, 25, 360 Red factor in Holstein cattle, 58 Relaxation of pelvic structures and vulva prior to parturition, 246 Relaxin, 247, 406, 687 Releasing factors from the hypothalamus, 399, 489-491, 500, 564, 586, 593, 760-764, 785, 938 “Repeat breeders”, 497, 498, 538-546, 559-569, 625-627, 662, 663, 738-740 early embryonic death in, 497, 498, 559-569, 625-627, 662, 663, 738-740 failure of fertilization in, 497, 498, 538-546, 559-569, 626, 662, 663 hormonal therapy for, 564, 565, 569, 738-740 in cows, 538-546, 559-569 in dogs and cats, 738-740 in ewes, 663, 664 in mares, 625-627 in sows, 644, 646, 647 incidence of, 559-562, 565 Repellers, obstetrical, 293, 299 Repulsion of the fetus, 298, 299, 301, 326-333, 349 Reproduction cycle of, 411-415, 427, 434-442 duration of the ability for, 110, 699 hormones in, 398-409, 680-683, 700, 701 nervous system influence on, 398-403, 421, 422, 489-491, 500, 564 physiology of, in bitches, 475-495 in cows, 434-442, 572-574 in ewes and does, 654-660 in males, 760-777 in mares, 582-588 in queens, 698-707 in sows, 636-642 rate of, 110, 111, 648 table of, in animals, 427 Resection, submucous, of the prolapsed vagina, 237-240 Respiration, stimulation of in the newborn, 262, 263 distress in foals and piglets, 270 Restraint for dystocia examinations and operations, 287, 288 pregnancy examinations, 16, 25 Rete ovarii, 535 Rete testis, 753, 759 Retention of the fetal membranes, 100, 256, 272, 273, 343, 346, 348, 349, 350, 362, 373-384, 385 due to hormonal and nutritional deficiencies, 374, 375 infections with, 374-376, 377, 382 in the bitch and queen, 256, 272, 347, 348, 384 in the cow, 100, 256, 272, 347, 348, 350, 353, 362, 373-384, 385 in the ewe and doe, 256, 272, 362, 383, 660, 672 in the mare, 256, 272, 382, 383 in the sow, 256, 272, 384 in twinning, dystocia and abortion, 373-384 Retention of the meconium by the fetus, 265 Retinal, atrophy and dysplasia, 63, 66 Retraction of the uterus, 16 Retraction ring dystocia (see Bandl’s or contraction ring) 281, 316, 327, 348, 349, 357 Retractor penis muscle, anatomy of the, 757 calcification of the, 794 congenital, short, 794 myectomy of the, 794 Rhinopneumonitis due to equine herpesvirus, 165-169 Ribs, breakdown of the fetal, 310, 312 Rickettsia, abortion due to, 136, 137 "Ring-womb,” 283, 344-346 Robertsonian, chromosomal translocation, 820 Rolling of the cow and mare for relief of uterine torsion, 230-233, 339, 340 Schaffer method of, 340, 341 Rotators, obstetrical, 293, 294, 299-301 Rotation of the fetus and uterus for the correction of uterine torsion, 230-233, 339-342 Rubin’s insufflation apparatus for oviducts, 537, 538 Rupture of the allantois and amnion at parturition, 251-254 bladder, 265, 360, 417 in foals, 265 cecum, 360 cervix, 357-360 diaphragm, 360 follicle on ovarian palpation, 567, 568 gastrocnemius muscle, 357, 394 genital organs (tract) 353-355, 357-359 liver, 271 penis, 770, 775, 796-799 perineum, 357-360 prepubic tendon, 226, 227, 343 rectum, 16, 25, 360 uterine vessels, 242, 338, 340, 353, 354 uterus, 218, 219, 222, 223, 226, 232, 333, 338, 340, 343, 354, 357-359 vagina, 314, 344, 346, 353, 354, 357-360, 416 vulva, 259, 314, 346, 347, 359, 360, 644 "Rut,” 764 Sacrum, 3 Sadism, 417 Salmonella abortion, in cattle, 135 in mares, 164, 165 in sheep, 196 Salpingitis (see inflammation of the oviducts) 535-538, 609, 643, 734 Sarcosporidiosis, 146, 170, 188, 200 Saws, obstetrical, 293 Schistosomus reflexus, 72, 78, 278, 283, 335, 336 “Scotty cramp,” 63 Screwworms (cochliomyiasis) in the sheath, 806 Scrotum, abnormalities of the, causing infertility, 822-828, 835 anatomy of the, 752, 753, 759 circumference of, to estimate fertility, 763, 766, 860, 885 dartos muscle of the, 753, 764 dermatitis of the, causing infertility, 826, 827 freezing of the, 827 heat regulation of the, 764, 827 hernia of the, 822, 826 physiology of the, 764, 827 suspensory for the, in shipping, dangers of, 828 tumors of the, 835 width of the, in stallions to assess fertility, 766976 INDEX Segmental aplasia of the mesonephric duct (Wolffian), 843-846 paramesonephric duct (Mullerian), 12, 13, 41, 227, 346, 522-529, 535, 550, 642, 643, 660, 672, 710, 721, 845 Semen amount of (see volume of), 772, 873 antibiotics in extenders of the, 898, 903, 913, 918, 924 artificial coloring of the, 899 bacteriological and virological examination of the, 855, 856, 885- 887, 898 buffers in the, 769, 772-774 cells, other than spermatozoa, in the, 882, 884 characteristics of, during phases of ejaculation, 772-774 in the boar, 774 dog, 771, 774 stallion, 774 citric acid in the, 769, 772 collection of the, 861-870, 896, 911, 912 as male dismounts, 774, 866 by electroejaculation, 862-864, 868-870 by masturbation or penile manipulation in the dog, 869, 870 by the artificial vagina, 864-866, 867-870 by the condom, 866 by the gloved hand from boars, 868 from boars, 868-870, 916 bulls, 861-866, 896 dogs and toms, 869, 870 rams and bucks, 867, 868 stallions, 866, 867, 911, 912 from the vagina and uterus, 866, 867 sanitation and cleanliness in the, 865, 866, 872,873 color of the, 769, 774, 776, 873, 874 composition of the, 772-774 concentration of spermatozoa in, 772, 874, 875 consistency of, 770, 774 constituents of, 772-774 definition of, 771 depletion trial, for reserves of, 772, 773, 874 diluters of (see extenders of) dismount sample of, 774, 866 effect of frequency of service upon, 772-775 enzymes in, 887 evaluation of, 872-890, 896, 897, 912 examination of, 872-890, 896, 912 extenders and techniques for liquid, 856, 897-899 from boars, 917, 918 bulls, 897-899 dogs and toms, 924 rams and bucks, 921, 922 stallions, 615, 912, 913, 914 extenders and techniques for frozen, 900-926 from boars, 917 bulls, 900-904 dogs and toms, 924 rams and bucks, 921, 922 stallions, 913, 914 fructose in, 769, 772, 773 gel fraction of, 770, 774 handling of, after collection, 872, 873, 897, 901, 912, 917 “impregnation” of mares with, 915 insemination of, 567, 568, 615, 905, 906, 914, 915 miscellaneous tests on, 887 morphology of spermatozoa in, 763, 766-768, 818, 819, 878- 885 motility of spermatozoa in, 768, 818, 819, 875-877 organisms, infectious, in, 855-856, 898, 903, 904, 908, 917 percentage of abnormal spermatozoa in, 818, 819, 879-885 pH of, 772, 874 physiology of, 764-774 quality of, 872, 873-890 at different times and seasons, 873 ratio of volume of spermatozoa to plasma in, 772 riboflavin in or yellow color of, 769 shipping of, 904, 905 site of deposition of, 415—417, 424, 434, 437, 567, 773, 905, 906, 919, 921, 922, 924, 925 staining of spermatozoa in, 877, 878 storage of, 768, 769, 899, 901, 904, 912-914, 917, 921, 922, 924, 925 from boars, 917 bulls, 899, 901, 904 dogs and cats, 924, 925 rams and bucks, 921, 922 stallions, 912-914 tests on (see examination of) 872-890, 896, 912 total solids in, 887 transport in female genital tract of, 424-428, 587, 639, 658, 670, 921 urine in, 791 viability or longevity of spermatozoa in, 587, 877 volume of, 772,873 Seminal fluid or plasma, 772-774 Seminal vesicles (see vesicular glands) 755, 769, 770, 847-851 anatomy of the, 755 anomalies of the, 846, 850 effect of testosterone on, 763, 769 embryology of the, 759 extirpation of the, 850, 851 inflammation of the, 847-851 secretion of the, 769, 770 Seminiferous tubules, 753, 764 Seminoma, 833-835 Semino-vesiculitis, 847-851 Septal defect, subaortic, 71 Serosa (see blastodermic vesicle or trophoblast) Sertoli cells, 761, 765 tumor of the, 710, 761, 784, 829, 833-835 Service, frequency of, in males, 774, 775 “poor,” in mares, 417 time during estrus, 437, 566, 657 during postpartum period, 567 Sex chromatin, 74, 97 Sex drive (see libido and impotency) Sexing, kittens, 705 Sex parity, 102, 103 Sex ratio (see sex parity) Sexual behavior, female (see estrum) male, 763, 770, 771 Sexual differentiation, 75, 98, 762 Sheath (see prepuce) Shipping as a cause for abortion, 136, 172, 188, 202, 566 of males, 828, 829 of semen, 899 , 901, 904 , 905 , 912-914 , 917 , 921, 922, 924, 925INDEX 977 Shock, due to rupture of prepubic tendon, 226, 227, 343 of uterus, 218, 219, 222, 223, 337, 338, 343 sudden release of excessive uterine fluids, 223-228 Sigmoid flexure of penis, 757, 794 adhesions of the, 794-796 anomalies of the, 794 Sinusectomy, clitoral, 612, 613 Sinuses, clitoral, 612, 613 Sire, genetic profile of, 890 Sire, size of, as a cause of dystocia, 281, 282, 334 Site of deposition of semen, 415, 416, 417, 437, 567, 773, 905, 906, 919, 921, 922, 924, 925 Smears, vaginal, 591, 677-679, 702 SMEDI viruses in swine, (see entero and picomaviruses), 184 Smegma, preputial, 758, 799, 806 Snares, obstetrical, 291, 292 Sodomy, 417 Somatotropic (see growth) hormone, 114, 399, 717, 763 Spacing of embryos in the uterus of multipara, 38, 111, 588, 640, 642, 647 Spastic paresis, cattle, 55, 57, 792, 793 Spastic syndrome, cattle, 55, 57, 395, 793 Sperm (see semen and spermatozoa) Sperm granuloma, 62, 842, 843, 845 Sperm reserves, 769 Spermatic artery and veins, 753 Spermatic cord, 753 varicocele of the, 828 Spermatids, 763, 764, 765 Spermatocytes, 760,764 Spermatogenic wave, 764 Spermatogenesis, 760-766, 878 Spermatogonia, 760, 764 Spermatozoa, abnormal acrosomes of, 763, 813, 814, 819, 879 anomalies of (inherited), 814, 818-820 capacitation of, 426 concentration or density of, in semen, 769, 772, 836, 873-875 determination of, 874, 875 in testicular pathology, 815-838, 874 cytogenetic defects of, 819 daily production of, per gram of testis, 765, 766 Kartagener’s syndrome, 819 maturation of, 768 morphology of in testicular pathology, 763, 766-768, 814-819, 837, 877-885 normal, 763, 766-768, 879-882 primary abnormalities of, 763, 814, 818, 819, 837, 877- 882 secondary abnormalities of, 818, 837, 879-882 motility of, 768, 813-815, 818, 819, 836, 875-877 determination of the degree and percentage, 875-877 in testicular or genital pathology, 815-838, 849, 875, 876 rate of, 768 number of, required for conception, 425 protoplasmic (cytoplasmic) droplet on, 763, 765, 768, 881-884 rate of movement of, 424, 425, 765, 875, 876 rate of transport of, in the female genital tract, 424, 425, 426, 587, 639, 658, 670, 683, 704 in the male genital tract, 764, 765, 768 site of deposition at coitus, 415-417, 424, 437 at insemination, 434, 567, 773, 905, 906, 919, 921, 922, 924, 925 staining of, 768, 769, 813, 814, 877, 878 storage of, 768, 769, 899, 901, 904, 912-914, 917, 921, 924, 925 survival time of, in the female genital tract, 425, 426, 587, 639, 670, 683, 704 unejaculated, fate of, 769 viability or longevity of, 587, 877 determination of, 877 Spermiogenesis, 760-766, 814, 818, 819, 878 Spermiostasis, 843-845 Spina bifida, 65, 66, 78 Spinal cord, compression of, in males, 792 Spine, injuries of, in males, 792, 793 Splitting of the maternal pelvis to relieve dystocia in heifers (see sym- physiotomy) 313, 344 Spondylosis, in males, 792 Spraying of urine by cats, 699 Staining of vaginal smears, 678 Stallion, ring or shield, to prevent masturbation, 776, 771 roll to control penetration of the penis into the vagina, 416, 611 Starvation, 151, 172, 201, 202, 240, 515, 516 Static fetal cadaver (see mummification), 214 Stenosis of the cervix, 343-346, 526, 527, 554, 608, 622, 737, 738 esophagus, 64, 67 pelvis, 278, 279, 344 rectum, 529 vagina, 277, 346, 528, 555, 720, 721 vulva, 54, 277, 304, 314, 346, 347, 529, 710 Sterility (see infertility) “Sterility” hump, 485, 486 Steroids, anabolic, 597, 784-791 effect on mares, 597 stallions, 784-791, 829 Stilbestrol (see estrogens) Stillbirths (see abortions, dystocia), 38, 123, 180, 189, 277-285 Storage of semen (see semen and spermatozoa) Strabismus 58, 59, 66 Straining (labor)(abdominal contractions) at parturition, 253-255 control of, 233-240 due to rabies, in cattle, 345 in prolapse of the rectum, 233-240 prolapse of the uterus, 354, 361-367 prolapse of the vagina, 235, 343, 484, 679 in vaginitis and vulvitis, 390-392, 468-472, 474, 475, 554- 556, 672 with retained meconium in foal, 265 Strangulation of the colon by the uterus, 242 of the uterus by a lipoma, 173, 242 Streptococcus (genitalium) zooepidemicus, 163, 164, 600-606 Stunting as a cause of dystocia, 278-282 Stress, causing infertility, 566, 567 inducing the estrous cycle, 646, 658 in males, affecting fertility, 829 Subaortic septal defect, 71 Subinvolution of placental sites in bitches, 354, 742-745 Subterranean clover, estrogenic effect on ewes, 201, 234, 662, 663 Suckling, effect on milk “let down,” 114 effect on release of gonadotropic hormones, 114, 115 Superfecundation, 111 Superovulation, 101, 422, 492, 597, 598, 928, 936, 937 Suspensory for the scrotum during shipping, danger of, 828 Sutures of the vulva, for the correction of vaginal prolapse, 236-240, 347, 354, 355, 556978 INDEX Swine, abortion in, 180-192 Sympathomimetic (tocolytic) agents, 248, 296 Symphysiotomy, ischiopubic, 313, 344 Symphysis of pelvis, 2, 586 Synchronization of estrus, in cows, 402, 405-408, 441, 442, 507 in does, 670, 671 in ewes, 402, 659, 660 in mares, 584-586, 597, 598 in sows, 638 Syndactyly, 55, 56, 61 Tail, defects of, 58, 62, 64, 66, 78, 82 Tarsitis, in bulls, 792 Teaser or “gomer” males, preparation of, 502, 503, 589, 907 handling of, 502, 503, 907, 908 Teasing of bulls, 789, 865 of mares, 588-590 Teats, supernumerary, 72 Teats, “waxing” of the in mares near parturition, 24, 246, Telegony, 111 Temperature of body, lowered prior to parturition in bitches, 109, 252, 686, 705 effects of elevated, on early embryonic deaths, 640, 641, 664 Tendon, contractures of the, 54, 60, 61, 76-78, 278, 335-337 prepubic, 5 Tenesmus (see straining) Teratogenic mechanisms, 68 Teratogens, 51, 52, 68, 69, 70 Teratology (see anomalies) 39, 51-82, 333, 335—337 Teratoma, 79, 533, 723, 821, 834 Tetany, grass, 240-242 puerpural (see eclampsia) 241, 371, 372 Testes anatomy of the, 753 appendix of the, 754, 759 biopsy of the, 828 consistency of the, 836, 860, use of tonometer, 836, 860 cryptorchid or undescended, 760, 821, 826 degeneration of the, 815, 818, 826-838 due to acute infectious diseases, 829-832 auto-immunization, 833 chronic, wasting diseases, 832 hormonal causes, 829 irradiation of the, 828, 829 imperfect descent of the, 822 inflammation of the, 776, 829-832, 837, 838, 841, 842 neoplasms of the, 833-836 nutritional factors, 832 poisons or toxins, 832, 833 scrotal dermatitis, 826, 827 torsion of the, 822 trauma of the, 829 tumors of the, 821, 822, 828, 833-836 varicocele of the cord, 828 prognosis of, 837 signs or symptoms of, 836, 837 treatment of, 837, 838 descent of the, 760, 762 embryology of the, 759, 760 fibrosis of the, 815, 826-838 gubernaculum of the, 759 hypertrophy of the, 763, 766 hypoplasia of the, 763, 815-818 semen characteristics in, 816-818 influence of size of the, on semen production, 753, 754, 763, 766 palpation of the, 766, 816 physiology of the, 763, 764 temperature of the, 753, 764, 827 time of descent of the, 760 tumors of the undescended, 821, 822, 829, 834, 835 tunica albuginea of the, 753, 764 tunica vaginalis of the, 753 twisting of the, to castrate lambs, 822 width of stallion testes as an indication of fertility, 766 Testosterone, 690, 706, 760-762, 764, 768, 769, 784, 851, 852 effect on sex drive or libido, 762, 784 in production of testicular degeneration, and the rebound phe- nomena, 761, 764, 784 physiologic actions of, 760-762, 768, 784 sources of, 760, 762, 784 uses of, 784 Tetanus, puerperal, 390 Tetany, puerperal (see eclampsia), 241, 371, 372 Theilers’ disease (hepatitis), 401, 402 Thyroid gland, 408 Thyroxine, 115, 408 potency of, in iodinated casein, 115, 408 use of, to promote lactation, 115, 408 in the impotent, obese male, 784, 790, 791 in the infertile female, 717 Tickbome fever, a cause of abortion, 136, 137, 198 Time of service related to onset of estrus, in the, bitch, 675-695 cow, 437 doe, 669 ewe, 656 mare, 582-585 sow, 639 Tocolytic agents, or smooth muscle relaxants, 248, 296, 299 Tongs, obstetrical (Krey’s) 291, 292 Torsion of the testis, 822, 828 umbilical cord of fetus, 49, 152, 173, 216 uterus, 93, 230-233, 314, 337-343, 351, 354, 738, 740, 741 as a cause of dystocia, 283, 314, 337-343 prepartum, 230-233 Toxoplasmosis, in abortion and disease of the newborn, 146, 170, 188, 200, 209, 212 Trachelectomy, 553 Trachelorrhapy, 553 Traction (see forced extraction) Transfer of the embryo (see embryo transfer) Translocation of chromsomes, causing infertility in cattle, 820 Transport of ova in the uterine tube, 442-424, 586, 639, 640, 658, 670, 683, 704 of spermatozoa in the female genital tract, 424-428, 587, 639, 658, 670 Transportation of males or semen (see shipping) Trichomoniasis, 146, 218, 447-455, 544, 545, 803, 813, 887 Triiodothyronine, 408, 718 Triplets, 95, 96 Trophoblast (see blastodermic vesicle) 38, 41-43 Truss, vulvar, for prolapse of vagina, 237INDEX 979 Trypanosome equiperdum, 170, 618, 619, 805 Tubal locking of ova, 404, 424, 564 Tuberculosis, avian, 135, 136, 184, 473 bovine, 135, 136, 473, 535, 548, 803, 829 humans, 135, 136 Tubules, efferent, 753 seminiferous, 753 Tumors of the cervix, 554 epididymis, 845 genital organs of the cow, 22, 346, 533, 534, 550, 554, 556, 557 bitch and queen, 721-728 ewe and doe, 661 mare, 620, 621 sow, 647 mammary gland of the bitch and queen, 725-728 ovary, 533, 534, 619, 620, 647, 661, 673, 722, 723 penis and prepuce, 799-800 perianal adenomas, 854 pituitary gland, 510, 620, 784, 829 placenta, 48 prostate, 852 scrotum, 835 testes, 710, 761, 784, 833-836 undescended, 710, 761, 784, 821, 822, 829, 834, 835 transmissible venereal in the dog, 724, 799 uterus, 550, 621,647, 673, 723, 724 vagina, 346, 556, 621, 723 vulva, 557, 621, 661, 673, 724 Turner’s (XO) syndrome, 75 Twins, 23, 25, 30, 79, 81, 82, 95, 96, 99-102, 335, 585, 586, 588 causes of, 101, 102 conjoined, 81, 82, 335 differential diagnosis in pregnancy examinations, 24, 25, 30, 335 dizygotic, 75, 95, 96 “double” parturitions in, 112 double (twin) ovulation in mares, 558 dystocia due to, 95, 96, 100, 335 incidence of, 95, 96, 585-588 influence of nutrition on, 95, 101 monozygotic, 79, 95, 96 prevention of, 99-102, 173-175 monsters, conjoined, “Siamese”, 81, 82, 335, 336 undesirability of, in unipara, 99-101, 335 unicornual, 93 Udder, (see mammary gland), 15, 113-117 Ulcerative dermatosis of sheep, 661, 662, 805 Ultrasonography, for pregnancy diagnosis, 15, 24, 25, 31, 683, 741 Umbilical arteries, 40, 41, 49, 255 cord, 40, 48, 49 dangers of ligation of the, 263 disinfection of the, 263 dystocia due to the, 333 pulsations in, in foal at birth, 254 rupture of the, at parturition, 49, 255 torsion of the, 49, 152, 174, 271 hernia, 49, 57, 67, 343 vein, 40, 49, 255 Umbilicus, 49, 255, 259 care of, after birth, 255, 259, 263 Underfeeding (see inanition), 151, 172, 201, 202, 278-282, 515, 516, 782 Unipara, 94 multiple births in, 95 Urachus, 41, 43, 49, 255, 265 persistence of the, 59, 265 Ureaplasmas (see T-mycoplasmas), 469-471, 538, 539, 661, 672, 730, 731, 813, 841, 848 Ureters, 39, 63 ectopic, 63, 72, 622 Urethra, 11, 41, 755, 756, 757 calculi in the, 776, 808 diverticulum of the, in boars, 11, 607, 756, 757 fossa of the, in stallions, 607 embryology of the, 41 process (filiform or vermiform) in stallion and ram, 757, 771 Urethral glands, 756, 770 muscle, 757 Urethritis, 776 Urinary calculi, 808 Urine, in continence of bitch, 716 pooling, in vagina (see urovagina), 440, 539, 555, 556, 609, 641, 642, 659 Uro-genital system, embryology of, 12, 13, 39, 709 Urovagina, 539, 555, 556, 609, 641, 642, 659 Urticaria, 272 Uterine artery, 8, 20, 21, 29 lochia, 257 “milk”, 34, 405 “sand” (inspissated plasma) 48, 376 tube, (see oviduct) anatomy of the, 8 embryology of the, 12 incidence of diseases of the, 536, 621, 643 pathology of the, 535-538, 621, 643 vessels, rupture of, 353, 354 Utero-ovarian pathway (see prostaglandins) Uteroverdin, 258 Uterus abscess of the, 390, 549, 550, 608, 609 adhesions of, 358 amputation of the prolapsed, 363-365 anatomy of the, 9 anomalies of the, 522-525, 622, 660, 718, 719 “bacterial flora” of the, 103, 104 biopsy of the (see biopsy, endometrial), 540, 541, 591, 616- 618, 624 blood flow to, during pregnancy, 112, 113 collagen increases in the, with aging and disease, 568 contractions of the, during and after parturition, 251-259, 296, 299 culture of the, 599-613, 616-618, 624 evaluation of the, 602, 617, 624 curetting of the, in the mare, 595 cytology (smear) in the mare, 616-618, 624 “degeneration” of the endometrium of the, 478-491, 616-618, 734-740 didelphys, 526, 527, 642 douching of the, to cause abortion, 151, 173, 221 to cause luteolysis in the mare, 594 embryology of the, 12, 13 enlargement of the, localized in mare, 621, 622 hemorrhage into the, 214, 216, 257, 353, 354, 720, 740980 INDEX inertia of the, or failure of uterine contractions, 225, 226, 227, 278-281, 305, 306, 344, 345-349, 599-613 infections or inflammation of the, (see endometritis, metritis, pyometritis, pyometra and retained placenta), 23, 257, 374- 388, 538-550, 734-740 influence of hormones on the, 103, 734-740 infusion of the, 542, 544, 569, 614, 616 invagination of the apex of the horn of the, 353, 366, 367 involution of the, 256-259, 439, 544, 545, 584 laceration of the, 353-355 masculinus, 12, 13, 756, 759 number of fetuses in the, 94, 95 position of the fetus in the, 94, 252, 253 prolapse of the, 361-367 retraction of the, to assist palpation of the, 16, 17, 26 rotation of the, in uterine torsion, 93 rupture of the, 218, 219, 222, 223, 233, 242, 314, 345, 353- 355, 357-360, 737, 743 size and location of the pregnant, 8, 20, 28, 93 torsion of the, 93, 230-233, 337-343, 351,354, 357, 738, 740, 741 incidence of, 337 tumors of the, 550-557, 620, 621, 647, 661, 673, 723 unicornis, 524, 525, 622, 710 Vagina, anatomy of the, 10 anomalies of the, 346, 528, 529, 720, 721 atresia of the, 346, 528, 529, 720, 721 biopsy of the, for pregnancy diagnosis, sows, 31, 32 cysts of the, 529, 556, 622, 710 cytology of the (see smears), 591, 677-679, 702, 712, 741 during pregnancy, 22, 29 edema of the, during estrus in the bitch, 679 embryology of the, 12, 13, 709 examination of the, 22, 29, 679, 721, 741 “feathering” of the, to promote oxytocin release, 348 Gartner’s ducts in the, 11-13, 529, 556, 622, 710 hematoma of the, 346, 353, 354, 355, 361 hymen of the, 10, 12, 13, 346, 622 hyperplasia (edema) and prolapse of the, 240, 679 inflammation of the, (see vaginitis) lacerations of the, 314, 344, 416 prolapse of the, 233-240, 343, 344, 354, 355, 484, 679 reefing operation on the, 239 rupture of the, 314, 344, 346, 353-355, 357-359, 361, 416 septate, 278, 346, 526, 528, 622 smear of the, for cytology, 591, 677-679, 712, 702, 736, 741 stenosis or constriction of the, 277, 346, 529, 609, 741 tumors of the, 346, 361, 556, 621, 723 Vaginal hysterotomy (trachelotomy), 345 smear in the bitch, 677-679 queen, 702 Vaginitis, 343, 468-472, 474, 475, 554-556, 672 due to C. pyogenes, 472 due to IBR-IPV (infectious pustular vulvo-vaginitis) 138, 142, 474, 555, 556 in “epivag,” 474, 475, 555 in granular venereal disease, 468-471, 555, 729 in prolapse of the vagina, 233-240, 343, 679 in the bitch and queen, 33, 741 in the cow, 468-471, 475, 554-556 in the mare, 599, 600, 609, 614 in trichomoniasis, 449 necrotic, 355, 379, 390, 391, 556, 557 Vaginoscopy, 501-504, 582-591, 679, 733 Varicocele, 828 Vas deferens, 755, 759, 769 ampullae of the, 755, 769 anatomy of the, 753, 755 anomalies of the, 843-845 inflammation and pathology of the, 845, 846 Vasectomy, 502 Vasopressin (antidiuretic hormone, ADH) 401-403 Vein, umbilical, 40, 41, 255 Ventricle, ovarian (see bursa) Version of the fetus, 300, 331, 332 Vertebrae, pathology of, in the male, 792, 793 Vesicle, amniotic, 18 blastodermic, 26-28 chorionic, 26-28 Vesicular coital exanthema (see IBR-IPV), 138-142, 165, 474, 555, 556 Vesicular gland (see seminal vesicle) Vestibular gland (see Bartholin’s gland), 11 Vestibule, (see vulva) anatomy of the, 11 inflammation of the, (see vulvitis, vestibulitis) pneumovestibule, 600 stenosis or constriction of the, 54, 277, 529 vestibulitis (see vulvitis), 554-557, 600, 609 Viability, of ova, after ovulation, 423, 587 of spermatozoa in the female genital tract, 425, 426, 437, 565, 566, 587 tests on spermatozoa, 872-887 Vibriosis, abortion in (see campylobacteriosis), 134, 460, 462, 539, 813 in cattle, 134, 456-465 in sheep, 193, 194 Vices, in male animals, 776, 777 Viciousness in female animals, after parturition, 271, 272 in males, 777 Villi, of the fetal placenta, 39, 44, 45, 48 Viruses, as a cause of abortion in bitches, 209, 729 cows, 138-145 ewes and does, 197-199 mares, 165-170 queens, 211, 212 sows, 184-188 as a cause of anomalies, 70 as a cause of infertility in cows, 474-476 Viscid rod infection (see Klebsiella), 162-165 Vitamin deficiencies, contributing to abortion, 150, 151, 173, 188, 202, 374 causing infertility, 517, 783 Vitelline sac (see yolk sac) Volume of semen at ejaculation, 873 Vomemasal organ (see pheromones), 409, 699 Vulva (vestibule) anatomy of the, 11 Bartholin’s (vestibular) gland, 11 cysts of the, 235, 557, 710 clitoris in the, 11, 604, 612, 709, 716 contusions and edema of the, 346, 347, 354, 355, 484INDEX 981 depigmentation of the, 618, 619 discharge (type of) from the, in dystocia, 350 edema of the, 645, 646, 679 embryology of the, 13 episiotomy of the, 347, 355, 529 “fish-hook”, in hermaphrodite swine, 73, 643, 645, 821 granular venereal disease of the, 468-471 hematomas of the, 355, 361 hemorrhage from the, 353, 354, 623, 742-745 immature or juvenile, 346, 347, 529, 710, 721, 734 infantile, 346, 347, 529, 710, 721, 734 inflammation of the, (see vulvitis or vestibulitis) lacerations of the, 259, 303-306, 314, 346, 347, 354, 355 rupture of the, 259, 303-306, 314, 346, 347, 354, 355 stenosis of the, 304, 314, 346, 347, 529, 710 suturing of the, in the cow, 237, 238, 347, 355, 365, 556 in the mare, 347, 609-612 tumors of the, 361, 557, 621, 661 Vulva-suturing operations, in the cow, 236—240, 347, 355, 556 in the mare, 347, 609-612 Vulvitis catarrhal, 556, 609, 661, 672 due to C. pyogenes, 472 in dourine, 618, 619 in granular venereal disease, 468—471, in bitches, 729, 734 in the bitch, 734 in the cow, 556, 557 in the mare, 609 postpuerperal, 390, 391, 392, 609 necrotic, 390-392, 473, 556 ulcerative, in bitches, 734 in ewes, 661, 662 Vulvo-vaginitis in swine caused by moldy, estrogenic grain, 188, 234, 644 Wattles, in swine, 60 in sheep and goats, 62 on the vulva, 557 “Waxing” of the teats in mares, close to parturition, 24, 246 Wharton’s jelly, in the umbilical cord, 49, 255 Wheat poisoning (hypocalcemia, hypomagnesemia), 371, 394 Whipple’s operation, for vaginal prolapse in the bitch, 238-240 White heifer disease (see arrests in development of the Mullerian ducts), 522-529 Windsucking, genital (see pneumovagina and pneumovestibule) Wobbles, genetic, in horses, 59 Wolffian body (see mesonephric ducts), 12, 41 ducts, 12, 13, 41, 709 anomalies of the, 529, 535, 556, 621, 622, 709-711,843- 846 Wry neck, of fetus, 41, 280, 283, 327 Xxy or Klinefelter’s syndrome, 815 Yolk sac, 26, 42, 80 Zearalenone, an estrogenic mycotoxin, 644, 785 Zenker’s degeneration (myositis) of the gastrocnemius muscle, 357, 394 Zona pellucida, sperm cell penetration of, 426