v^^ "'^^ ■XlO^ or ,0 o. !> -U. 'i^ -^ ' » ^ "* .^^^- -,r. .\\ . ^ - .-^^ ,0 c> ^0 x^<=^^ "/• ^ .\^- ^•^' ,<^^ %. *'"^'' \> •A^^^ .-^^ •^^. 'b 0^ \ f , " A o - • ., V .A O % " ''%: /^'..X'--rr;-v -^'^o;^7':f'^/'''^%. -'S^y^W'-r^/': \y .'•^ > ( 1 » • -^ \\ s , '7' " * -N 1 1 e -^, '_^ . '^0^ ' - ^ ■'^- <^ \V '^0^ V^ "^ ^ " x^^ "%. ■ ' ^^V x^ ■^. ^^ , ^^ ^^^'-^ ^ ' ^'^'>- ^"^ .<'^'' .«,. ^^^^' '*;, ^^^- x^"^'..,,'^^-/*'-"^^'' ,., ■"^-^-'*. - ' ', y .0" '^^ ^ O- ,^ •< * ^ *^. / J*-' :^>^%^)^//% ^ ■ ^^'^ ^/ '-^^ "^A / % , " ^^' -^ ^. ; ,.^^ '^ ' y ■ . s " .0 1 1 f , •x'^ ^ K ^ ' ^ ,- ' -. cP- ^^ ■ x^" ^--'.^^■-\<^#>.0,\.'' , iX- -■ ■> A^ ~ " ^. -^^ ^^" ^'^^. .^\^^ \ ' ^0 O ' J -y A Textbook of Veterinary Pathology Copyrighted at Washington, D. C, by ALEXANDER EGER 1915 ^vy^ SEP -7 1915 'CI,A410677 PREFACE TO THE SECOND EDITION. This second edition of Veterinary Pathology has been care- fully revised and it is hoped that no errors have crept in. The subject matter has been elongated where it was deemed advis- able. The chapter on Immunity was revised by Dr. J. \\\ Kal- kus, Pathologist of the Washington State College. New illus- trations have been substituted wherever the subject could be more clearly demonstrated by so doing. To his publisher, Alex. Eger, the author desires to express his appreciation. A. T. Kinsley. Kansas City. Mo., September. 1915. PREFACE. A knowledge of pathology is essential to practitioners and to students of medicine. The general considerations of pathol- ogy, whether in reference to diseases of the human or diseases of domestic animals, are practically identical. Many textbooks on this subject are available, but they are especially written for the practitioner and student of human medicine, and the illus- trations and examples are all in reference to diseases of the human. Such textbooks have been used by the author for sev- eral years in veterinary classes and it was thought that if the same general pathological principles could be exemplified by cases and illustrations in veterinary medicine, the subject mat- ter would be more readily understood by the veterinary student. This explains the issuance of the present volume. The writer has endeavored to place every phase of pathol- ogy from the veterinarian's point of view\ The entire subject matter has been expressed as far as possible in common every day language, with the hope that all readers will have no trou- ble in grasping the pathologic facts. An extensive glossary has been appended and will be of considerable aid because practi- cally every technical term, with its analysis and definition, will be found therein. The author is greatly indebted to Dr. S. Stewart, Dean of the Kansas City Veterinary College ; Dr. D. M. Campbell, edi- tor of The American Journal of Veterinary Medicine ; Prof. W. E. King. Bacteriologist of the Kansas State Agricultural College ; Dr. F. J. Hall, Chief of the Food Inspection Department Kan- sas City, Mo., and formerly pathologist of the Medical Depart- ment University of Kansas ; Dr. L. Rosenwald, formerly patholo- gist of the Kansas City Veterinary College ; Dr. Geo. F. Babb, Milk Inspector of the city of Topeka, Kansas ; Dr. D. Cham- plain, editor of The Milk-Man, for suggestions made by them concerning the text matter. Also Dr. R. F. Bourne, physiologist of the Kansas City Veterinary College ; Dr. C. D. Folse, City Milk and Meat Inspector of Marshall, Texas, and Mr. Chas. Sals- bery, microscopic laboratory assistant in the Kansas City Vet- erinary College, for their assistance in the preparation of the illustrations. The author consulted various text-books, journals and other publications while preparing the text for which acknowledge- ment is hereby made. If this book supplies the practitioner and the student of veter- inary medicine with clear, concise statements of veterinary pathology, the purpose of the book has been fulfilled. A. T. K. CONTENTS. PAGE Preface to The Second Edition 5 Preface 6 CHAPTER I. Definitions 19 The Cell 20 CHAPTER H. General Consideration of Disease .' 34 Inherited Diseases 35 Acquired Diseases 38 Table of Vegetable Parasites 49 Hypnomycetes 50 Saccharomyces 53 Schizomycetes 54 Animal Parasites 64 Protozoa 64 Helminthes 65 Arthropoda 66 CHAPTER HI. Immunity 75 CHAPTER IV. Malformations 90 CHAPTER V. Circulatory Disturbances 109 Hemorrhage Ill Lymphorrhagia 117 Oedema, Dropsy or Hydrops 118 Thrombosis 122 Embolism 138 Ischemia 132 Hyperemia (Passive) 133 Hyperemia (Active 135 CHAPTER VI. Inflammation 138 CHAPTER VII. Progressive Tissue Changes 177 Regeneration 177 i CONTENTS PAG£ Wound Healing 184 Hypertrophy 189 Hyperplasia 192 Metaplasia 194 CHAPTER Vni. Retrogressive Tissue Changes 196 Atrophy 197 Cloudy Swelling 201 Fatty Changes 204 Fatty Infiltration 206 Fatty Degeneration 208 Amyloid Changes 211 Hyaline Changes 213 Mucoid Changes 215 Colloid Changes 218 Serous Infiltration 221 Glycogenic Infiltration 222 Uratic Infiltration 224 Keratosis 225 Ossification 227 Calcareous Infiltration 228 Calculi 231 Concrements 239 Pigmentary Changes 242 Excessive Pigmentation 244 Absence of, or Diminished Pigmentation 250 CHAPTER IX. Necrosis and Death 251-262 Physiologic Death 263 Pathologic Death 264 CHAPTER X. Tumors 268 Fibroma 279 Myxoma 284 Chondroma 285 Lipoma 287 Osteoma 290 Glioma 291 Odontoma 291 Neuroma 295 Angioma 295 Myoma 298 CONTENTS 111 Sarcoma 300 Papilloma 321 Embryonic Kpithelial Tumors 324 Placentoma 334 Teratoma 335 Cysts 338 CHAPTER XI. Fever 342 CHAPTER XII. Infective Granulomata 347 Tuberculosis 347 Actinomycosis 358 Glanders 364 Epithelioma Contagiosum 373 Glossary 376 LIST OF INSERTS. Insert I — Botanical Names Next to page 45 Insert II — Bacteria Next to page 62 Insert III — Protozoa Next to page 63 Insert IV — Helminthes Next to page 66 Insert V — Arthropoda Next to page 71 Insert VT — Explanatory to Plate I Next to page 86 PLATE I. Immunity 87 A LIST OF THE ILLUSTRATIONS FIGURE PAGE I — Diagram of a Typical Cell 21 2, 3— Amitosis 25-26 4 — Division of Nucleus 26 5 — Division of Cell 27 6 — Cell in Resting Stage 27 7 — Prophase, Showing Division of Centrosome 27 8 — Prophase, Shovtring Separation of Centrosomes 28 9 — Metaphase 28 10, II, 12, 13 — Indirect Cell Division — Metaphase, Anaphase, Telophase 28-29 14 — Ciliated Epithelium, Trachea 30 15 — Spermatozoa 31 16 — Red Buckeye 47 17 — Astragalus Molissimus (Loco) 48 18 — Trichophyton Tonsurans So 19 — Aspergillus Fumigatus 51 20 — Saccharomyces Farcimosus 53 21 — Various Forms of Cocci 54 22 — Various Forms of Bacilli 54 23 — Various Forms of Spirilla 55 24 — Flagellate Bacteria 55 25 — Capsulated Bacteria 56 26 — Bacterial Fission 58 27 — Sporulation 59 28 — Bacterium Anthracis 60 29 — Bacillus Tetanus 61 30 — Piroplasma Bigeminum 64 31 — Trypanosoma Evansi 65 S2 — Sarcocystis Miescheri 66 33 — Taenia Echinococcus 67 34 — Oxyuris Curvula 68 35 — Trichocephalus Depressiusculus 69 36 — Melophagus Ovinus 70 27 — 'Gastrophilus Equi 71 38 — Oestrus Ovis 71 39 — Culex Pungens 72 40 — Distoma Hepaticum 73 41 — Echinorhynchus Gigas 73 42 — Hematopinus Phalanges Ovis 7^ 43 — Pulex Serraticeps 76 44 — Margarapus Annulatus, Female 77 iv LIST Ul ILLLSTKATlUiNS FIGURE PAGE 44 — Margarapus Annulatus, Male yy 46 — Margarapus Annulatus, Female laying eggs yy 47 — Margarapus Annulatus Larva yy 48 — Psoroptes Communis Ovis 79 49> 50 — Demodex Folliculorum Canis (From Kaupp Parasites) 80 51 — Dithoracisamclus 92 52 — Cranio Schisis 94 53 — Chelo Schisis 95 54 — Palato Schisis 96 55 — Abdomino Schisis 96 56 — Synophthalmia 97 57 — Solipedia 98 58 — Polydactilism 99 59 — Prognathism 100 60 — Schistosis, Melus Anticus loi 61 — Pseudo-hermaphrodite 104 62 — Dicephalic, Calf 106 63 — Dicephalic, Calf 107 64 — Petechial Hemorrhage 113 65 — Hematoma 114 66 — Ascites, Dog 119 67 — Subcutaneous Oedema, Horse 120 68 — Thrombus in Aorta of Horse 125 69 — Thrombus, Red 126 70 — Embolism 129 71 — Infarction, Anemic-splccn 130 72 — Hyperemia Hemorrhage and Oedema Intestine 135 yi — Hyperemia Kidney 136 74. 75> 76, 77 — Vascular Variations in Inflammation T47-148-149-150 78 — Types of Cells in Inflammatory Exudates 151 79 — Gastritis 153 80 — Acute Pleurisy 154 81 — Acute Meningitis 156 82 — Gray Hepatization 157 83 — Fibrinous Pleurisy 158 84 — Myositis, Acute 160 85 — Chronic Pneumonia 162 86 — Chronic Hepatitis 165 87 — Pus, from a case of Strangles 168 88 — Suppurative Nephritis 170 89 — Red Hepatization 172 90 — Vascular Regeneration 178 91 — Fibrous Regeneration 179 92 — Wound Healing by first Intention 187 93 — Exulierant Granulation 188 VI LIST OF ILLUSTRATIONS FIGURE PAGE 94 — Hyperplasia Interstitial Testicular Cells 192 95 — Hyperplastic Ureter 193 96 — Fibrous Tissue Ossification 194 97 — Cloudy Swelling 202 98 — Fatty Infiltration, Liver 207 99 — Fatty Degeneration, Liver 210 100 — Amyloid Degeneration, Liver 213 loi — Hyaline Degeneration, Vessels 214 102 — Mucoid Degeneration 217 103 — Colloid Degeneration 219 104 — Colloid Degeneration 220 105 — Keratotic Growth 226 106 — Atheromatous Degeneration 230 107 — Group Calculi 233 108 — Cystic Calculus 234 109 — Urinary Calculi 235 no — Salivary Calculus 236 III — Inteestinal Calculus 237 112 — Biliary Calculi 238 113 — Hair Balls 240 114 — Inspissated Pus 241 115 — Hemosidern Pigmentation 245 1 16 — Icterus 247 1 17 — Necrosis 254 118 — Bacillus Necrophorus 255 119 — Ergot of Rye 256 120 — Ergot Poisoning in Cattle 257 121 — Fatty Necrosis 259 122 — Necrotic Center of Tubercle 260 1231 — Sarcoma 271 124 — Metastatic Sarcomata 274 125 — Epithelioma 277 126 — Hard Fibroma 281 127 — Soft Fibroma 282 128 — Myxoma 284 129 — Chondroma 286 130 — Lipoma, Horse 288 131 — Lipoma, Ox 289 132 — Osseous Tumor, Maxilla 290 133 — Odontoma, Horse 292 134 — Odontoma, Epithelial 294 135 — Hemangioma, Simplex 296 136 — Hemangioma Cavernosum 297 137 — Hemangioma Hypertrophicum 298 138 — ^Leiomyoma, Small Intestine 299 LIST UK ILLUSTRATIONS VU FIGURE PAGE 139 — Leiomyoma, Microscopic 300 140 — Sarcoma, Horse 301 141 — Sarcoma Mediastinum (Sections of Tumor) 302 142 — Sarcoma, Round Cell 303 143 — Lympho-Sarcoma Heart 304 144 — Lympho-Sarcoma 3^5 145 — Spindle Cell Sarcoma, Mule 306 146 — Spindle Cell Sarcoma 307 147 — Myeloid or Giant Cell Sarcoma 308 148 — Mixed Cell Sarcoma, Horse 309 149 — Mixed Cell Sarcoma, Jaw 310 150 — Mixed Cell Sarcoma, Maxilla 31 ^ 151 — Alveolar Sarcoma 312 152 — Endothelioma 3^3 153 — Endothelioma-Mediastinal 3^4 154 — Tumor in Ventricle 315 155, 156 — Nature of Connective Tissue, Leucocytes, Neoplasm Cells, Etc. 316 157 — Grape-Sarcoma, Uterus of Cow 3'^^? 158 — Melano-Sarcoma, Hog Skin 3^8 159 — Melano-Sarcoma, Microscopic, of Horse's Liver 319 160 — Myxo-Sarcoma 3^0 161 — Papillomatosis, Horse 322 162 — Papilloma, Microscopic 3^3 163 — Carcinoma-Encephaloid 325 164 — Epithelioma, Microscopic 326 165 — Epithelioma. Microscopic 3^7 166 — Epithelioma, Pearl Cell 328 167 — Adenoma, Mammary 329 168 — Adenoma, Microscopic 33*^ 169 — Adeno-Sarcoma, Microscopic 331 170 — Cystadenoma 332 171 — Hypernephroma 333 172, 173 — Dermoid Cysts 335 174 — Dermoid Cyst, Eye of Steer 336 175 — Dentigerous Cyst 337 176 — Cyst, Abdomen of Mule 339 177— Uterine Cyst 340 178 — Fever — Crisis and Lysis 343 179 — Continuous Fever 345 180 — Remittent Fever, Curve 345 181— Intermittent Fever, Curve 346 182 — Bacterium Tuberculosis, Bovine 348 183— Small Cellular Tubercular Liver 35i LIST OF ILLUSTRATIONS FIGURE PAGE 184 — Tuberculosis Lesion 353 185 — Tuberculosis ?\Iammary Gland 354 186 — Ray Fungus (Actinomyces) 359 187 — Actinomycotic Tongue 362 188— Bacterium Mallei 365 189 — 'Glanders, Nasal Septa 368 190 — ^Glanders, Cutaneous 369 191 — Glanders, Microscopic 370 192 — Epithelioma, Contagiosum 373 193 — Epithelioma, Contagiosum 374 194 — Epithelioma, Contagiosum, Microscopic 375 CHAPTER I. DEFINITIONS. Pathology is tlie science nf disease. It is the science which treats of tlie nature, causes, progress, symptoms and termina- tion or result of disease. It includes etiology, i. e., the study of the causes of disease, and pathogenesis, that is, the study of tlie course, abnormal functions and lesions produced in disease. General Pathology is confined to the explanation of the sum- mary of tlie facts obtained in the study of special pathology. It is concerned essentially in the solution of general principles of those morbid conditions that are common to the entire organism, as malformation, degeneration, regeneration, inHamniation. neo- formation and feyer. Special Pathology deals with all the abnormalities or diseased conditions of one part or organ as the diseases of the ear, skin, etc., and consequently special pathology is further subdi\-idc(l into otologic pathology, dermatologic pathology, etc. Pathologic Physiology, is that part of pathology which has to do with the inyestigation and description of abnormal functions of a diseased organ or animal. The pathologic physiology is, in many cases, the principle symptom of a disease, e. g., paraly- sis of the radial nerye. Abnormal function is frequently the only eyidence discernible in a disease, e. g.. epilepsy. Pathologic Anatomy, or morbid anatomy, is concerned in the structural changes in a diseased tissue or organ. Pathologic changes that haye occurred in the structure of a living tissue or organ are coUectiyely termed lesions. Lesions may be suiliciently gross that they are readily observed with the unaided eye or they may be so minute that the microscope is necessary for their detection. The inyestigation and the recording of facts obserycd in the study of gross and minute lesions are included in gross, or macroscopic pathologic anatomy and minute, or microscopic pathologic anatomy respecti\el\-. Human Pathology has to do with the facts observed in the study of the diseases of the human. Comparative Pathology, is the name applied to the study of the diseases of all animals in which the diseases of one genus, (group of animals) is taken as a standard and the diseases of all other animals are di.scussed in comparison with the type selected. Veterinary Pathology, is a discourse on the disease? of domestic animals. 19 20 \liTERINARY PATHOLOGY. THE CELL. ANATOMIC. Structure. Body. Nucleus. Ceiitrosoiiic. Membrane. Shape. Sice. PHYSIOLOGIC. Grozvth. Reproduction. Motion. Metabolism. Anabolisni. Katabolism. Irritability. Structurally, an animal body is composed of definitely ar- ranged parts, called organs. An organ is a portion of the body having a particular function and is, structurally, a tissue-complex in which each tissue has a certain definite proportion and relation. A tissue is composed of like or similar cells with more or less intercellular substance interposed. The intercellular substance is usually a product of the cells. A cell has been defined as a microscopic mass of protoplasm containing sufficient individ- uality to possess a life history. The function of an animal body is the sum total of the corre- lated functions of its component tissues. The function of a tissue is the sum total of the function of its cells. Thus a cell represents the anatomical or structural unit and the physiologic or functional unit of all animal bodies. In ancient times disease was thought to be the result of the entrance into the body of some "evil spirit," and the symp- toms presented during disease was evidence of the struggle beween the body and the "evil spirit." During the middle ages, Hippocrates, "The Father of Medicine," established the Hippo- cratic Theory of disease. Hippocrates taught, 1st, that the body was composed of four humors, viz., blood, phlegm, yellow bile and black bile ; 2nd, that health consisted of the proper balance of the humors ; and 3d, that disturbed proportions of the hum- ors resulted in disease. Modern pathologv is based upon the knowledge of cell activi- ties. Virchow was the father of cellular pathology. He first taught the cellular theory to students of pathology and he first advocated it in published articles. Cellular physiology was really fin outgrowth of cellubr pathology. A knowledge of cells is THK CPAA. 21 indispcnsal)lc in the study of patholo£vy and a l)ricf description is here appended. Structure — Cells are variable in structure. The active consti- tuent of all animal cells is protoplasmic in nature. The essen- tial parts of animal cells are the cell-bod\-, nucleus and centro- some. The ccU-bddy is present in praticall\- all cells. It is com- posed of semisolid protoplasm a portion of which is of a stringy Fip. 1 — Uiagrani dI a '!'.« pi<-al Oil, alli r Hiihin DaAidnff-IIiibor. I. Vacuoles. 8. Centrosome. 2. Cell-membrane. 9. Foreign inclosuii s. 3. Exoiilasni. 10. Hyaloplasm. 4. Xuoliar nicmbranc. 11. SpoiiKiiiplasm. 5. Nucleolus. 12. riironiatin ml work t;. ("linimatin inl-kiiot. :3. I..lnin network. 7. Ceiitrosi)here. :4. •Nucleoplasm. consistency and is termed sponirioplasm. In the meshes of the spongioplasm tliere is found a fluid protoplasm, designated hya- loplasm. The relative proportion of spongioplasm and Inalo- 22 VETERINARY PATHOLOGY. plasm varies in different cells and even in different parts of the same cell. Particles of food and various other insoluble sub- stances are not uncommon in the cell body. Coagulation of portions of the cell protoplasm characterize the pathologic condition known as cloudy swelling. Vacuoles are frequently observed, especially in wandering cells. The nucleus is constant in all functioning or active cells except the mammalian red blood corpuscles, and some of the pulmonary alveolar epithelial cells. The nucleus appears as a dense body and is usually centrally located in the cell body. The relative proportion of nucleus to cell body is inconstant, e. g., the lymphocyte is practically all nucleus ; some epithelial cells have a very small nucleus and a very large cell body. The nucleus varies in shape from a sphere to an irregular mass, and is surrounded by an incomplete membrane. It has been held that the essential structure of the nucleus is a chromatin net- work, but according to Ross the nuclear chromatin, at least in leucocytes, is distributed throughout the cell body in the form of granules. The spongioplasm and hyaloplasm of the cell body are continuous through the incomplete nuclear membrane into the nucleus where they are designated linin and nucleoplasm respectively. The nucleus may also contain a nucleolus which is a knot in the chromatin network and probably represents the centrosome in a dormant state. Nuclear fragmentation (kary- olysis) is a common pathologic condition. The centrosome is a dense refractile body found in the nuc- leus or in the cell body just outside the nuclear membrane. Many fine radiating fibres may extend outward from the centro- some. A cell membrane may or may not be present. This mem- brane is formed by a condensation of the substance of the cell body. The sarcolemma of a muscle fibre is perhaps the most typical cell membrane found in animal cells, the red corpuscle has a modified cell membrane. A nerve cell possesses a neuri- lemma, although it is probably not a true cell membrane. Shape. — Embryonic cells are usually spherical in shape and it is probable that sphericity is a primitive quality of cells. The shape of matured cells is determined by their function and loca- tion. External surface cells are usually flat and when subject to pressure and friction they are arranged in strata, i. e., they are stratified. The cells lining the air vesicles are flat because of the necessity of the exchange of gases through them. Muscle cells are elongated to allow of contraction to produce motion. THE CELL. 23 Goblet cells are large and more or less spherical because of the elaboration of mucus in them. Accommodation to space pro- duces variation in the shape of cells, thus ; fat cells are originally spherical, but because of pressure, they become polyhedral. Cells vary from the flat pavemental cells to those spherical in shape. Pressure is probably the most important factor in the produc- tion of pathologic variation in cell morphology. Thus paren- chymatous cells, as hepatic and renal cells, frequently become compressed by hyperplastic interstitial tissue sufficiently to change their shape from polygonal or cuboidal to irregularly flattened or fusiform. Columns of tumor cells may become pressed sufficiently by the invaded tissue to produce scale like cells or the so-called pearl cells. On the other hand, the same variety of tumor cells developed in tissue in which mutual pressure is limited, assume sphericity. Size. — Cells vary in size from the lymphoid cells that are from 4 to 8 microns in diameter to the marrow cells that are from 30 to 60 microns in diameter. The size of the cell is characteristic of the tissue they compose. Equalization of the surface and mass is a factor in the determination of the size of cells. Function of cells also has some bearing upon their size ; thus, cells that have the power of independent motion and rap- idly acting cells are usually small. Food is no doubt a deter- mining factor in the size of cells. Ova are large because of the storage of food. Pathologic variation in the size of cells is of common occur- rence. Hypertrophy is the abnormal enlargement of individual cells. The size of red blood cells is variable in pernicious ane- mia (swamp fever), of the horse. Several cells may fuse, form- ing a cell-complex, syncytium, or giant cell in and around foreign bodies, and in tubercular and actinomycotic lesions. Growth. — Growth in cells is the exercise of that property or function which results in their enlargement or it is the process by which they are increased in size. That cells do grow is self- evident and is common knowledge. A central, polymeric protein- molecule is supposed to be the essential structure of all active cells. This central, polymeric molecule is probably unsaturated and new simple molecules may be serially combined with it and then the cell becomes larger and grows. This property of cells is especially evident during the embryonic period but gradually diminishes to the time of maturity, when it is largely supplanted by other functons. The growth of cells is accompanied by the accumulation of energ}\ The larger a cell, other things being 24 VETERINARY PATHOLOGY. equal, the greater the potential energy. All functioning of cells, except growth, is accompanied by the liberation of energy. Growth results in accummulation of potential energy and other functions convert potential into kinetic energy, though both types of energy may be produced simultaneously and may be interdependent ; thus the growth of muscle is dependent upon frequent and appropriate exercise (liberation of kinetic energy). Growth within the normal cell is dependent upon inherited tendencies and a sufficient supply of nutrition. Other functions, as motion, are apparently entirely governed by environmental stimuli plus the required nutrition. The growth of cells con- tinues until they, and the part they compose, become of such a size that the economic relation of surface and mass becomes disproportionate. The disproportionate relation of surface to mass is corrected by rapid cell division or cell dissociation. In either case the total cell surface is increased. According to Harris, "Physiologic inertia'' is of considerable importance in growth of cells. When a cell is stimulated to action, the action does not cease immediately when the stimulus is removed or suspended. Thus when a cell starts to grow, it tends to grow continually because of the "physiologic inertia." Abnormal var- iation in cell growth is characteristic of hypertrophy and tumors. Reproduction. — The present knowledge of cell reproduction is based almost entirely on the observation of reproduction of plant cells, and the investigations thus far have been almost entirely of dead fixed specimens, and therefore it is possible that a marked difference may be noted when methods are devised for observing cell reproduction in living animal tissues. Cell repro- duction is the process by which the number of cells is increased. The ultimate outcome of cell reproduction and cell growth, is to increase the mass or volume. Cell reproduction is not distinct and separable from cell groM^th, in fact growth always precedes division. The cause of cell reproduction is probably due to chemic substances derived from dead cells and destructive meta- bolism. At least katabolic products, as kreatin, xanthin, choline and globin, are auxetic in action, for by experiment they have been found to increase cell multiplication. Reproduction is one means of regulating the relation of surface to mass. Two types of normal cell reproduction have been described by cytologists. These methods are amitosis, (direct cell division), and mitosis, (indirect cell division). 1. DIRECT CELL DIVISION, AMITOSIS, as usually described, is simple cell division in which the entire cell body divides without Tin: cKi.L. 25 any previous intracellular changes. This type of cell reproduc- tion or division is nornial in some lower forms of life and pos- sibly in some embryonic tissues of higher animals. However, it is not very common in normal adult tissues of higher animals. The polynuclear leucocytes are thought to occasionally repro- duce by amitosis ; endothelial cells are also thought to reproduce in the same way. it is possible that cells of any tissue may multiply by amitosis. Cells reproduced by amitotic division are considered abnormal by most investigators. Direct cell division is especially evidenced in rapidly growing tumors, chronic inflam- matory areas, leukemic tissue and many other pathologic condi- tions. The process is briefly as follows : There are one or more depressions in the nucleus which gradually extend until the nucleus is divided into two or more parts, (this is the origin of polynuclear cells ; possibly it may also account for the giant cells). After, the nucleus has divided, each part migrates to a Fig 2. — Amitosis, showing division of tho nuclpolua different part of the cell l)ody and the cell body is so divided that one or more nuclei are found in each segment. Thus the process is completed. In some instances, one or even two centrosomes may be present. 2. INDIRECT CELL DIVISION, MITOSIS, OR K.VRVOKINESIS, is tllC usual mode of cell reproduction. The frequency and intricacy of this complicated process is indicative of the exactness of nature's methods. .\n equal division of the nucleus, or more specifically of the nuclear chromatin (Altman's granules), is apparently the object of this type of reproduction. It is more delicate and exact than direct cell division. The following four stages, according to most cytologists, are recognized in indirect cell division, but these stages are not separate and distinct. 26 VETERINARY PATHOLOGY. A. Prophase. This is the preparatory stage. The nuclear chromatin which, in the resting cell, is an irregularly arranged network, becomes a continuous single thread, forming the so- -Amitosis, shnw ins. migration of the miclruH to ojiposite poles ot the nucleus. called spirem or loose skein. The chromatin thread divides into a definite and even number of segments, (the number varying in different animals, but always constant in the same species) known as chromosomes. These chromosomes are equal in length and are usually bent like the letter "u." The chromosomes are radially assembled around the central point in the nucleus, thus Fig. 4 — Division n£ nucleus forming the monaster or single star. The nuclear membrane becomes less and less distinct as the spirem is forming and fin- ally disappears. As the nuclear changes are progressing, a centrosome becomes prominent either within the nucleus or in the cell body just outside the nuclear membrane. The centro- TIIF, CELL. 27 some divides, the tlaughter centrosomes separate and wander to opposite sides of tlic nucleus. Radiating lines, known as mantle fibres, appear and e.xtend from each centrosomc to the chromo- somes. Fig. 5. — Division of cell. B. Mctaphasc. During this stage the chromosomes are split or cleaved longitudinally into daughter chromosomes apparently by the traction of the mantle fibres of the centrosomes. C. .liiapJiase. The daughter chromosomes are attracted along the mantle fibres until they reach the centrosomes around wdiich they are ultimately assembled, forming an aster or star at either pole. This particular portion of the anaphase is de- I'ig. C. Fie. T. Fig. 6. — Cell in rest In c stapre. I'ip. 7. — Prophase showing division of c>ntrosomp. signated the diaster or double star. There is also evidence o.i transverse indentation of the cell body near the median line. 28 VETERINARY PATHOLOGY. D. Telophase. The nuclear changes during this phase afC practically the reverse of those occurring in the prophase, i. e., the chromosomes fuse forming a chromatin thread which later forms the chromatin network. The nuclear membrane appears and the centrosome loses its mantle fibres and may even entirely Fig 8. ¥ig. S. — Prophase showing Fig. 9. — Metaphase. Fig. 9. separation of centrosomes. disappear. The cell body is completely divided by invagination from the margins, and then the daughter cells are completed and assume the appearance of their ancestors. Fig. 10. Fig. 11. Fig. 10. — Metaphase. Fig. 11. — Anaphase. MAiOTic cell division is characterized by a reduced number of chromosomes. This type of reproduction may occur physio- logically in the production of spermatozoa, and it is rather TIIR CEI.L, 29 common in pathologic processes. This type of reproduction characterizes tumor formation, particularly malignant tumors. Indirect division is probably of most frequent occurrence in hyperplasia, the rapidity of multiplication being materially in- creased. All variations of division occur in tumors. Motion. — Motility is that property of a cell which refers either to the intracellular movement of its parts, the i)osition of the cell as a whole remaining fixed, or it signifies the indepen- dent movement of the cell. All movement is dependent upon activity of the cell protoplasm. The cells of specialized tissues, except blood, are fixed, i. e., not motile. Intracellular movement is due to the circulation or stream- ing of the protoplasm from one portion of the cell to another. 'Jliis type of movement may become so extensive that the shai)e of the cell will be changed. It is common in the cells of lower forms of life as well as in some of the cells of higher animals. Fig. 12. Fig 12. — Anaphase. Fif . 13. — Telophase. Fig. 13. The specific cause of the intracellular j^rotojdasmic circulation has never been positively determined but it is probably the result of a disturbed chemic equilibrium of the cell margins and their surroundings. Leucocytic amoeboid movement is due to intra- cellular protoplasmic circulation. Leucocytic immigration jirob- ably is the result of chemic attraction, (positive chemotaxis), which stimulates the circulating protoplasm within the cell to constanty flow toward the point of greatest chemical afifinity and finally the cell reaches that point. Leucocytic emigration is based upon the same principal, except that the chemic influence is negative, (negative chemotaxis). and the cell is forced away from the center of the disturbed chemic equilibrium. 30 VETERINARY PATHOLOGY, Ciliary movement is the wave like motion of small hair like protoplasmic projections of cells known as cilia. Ciliary motion occurring in migrating or wandering cells produces movement of the entire cell and in stationary cells, produces movement of fluids or semifluids that contact the cilia. In higher animals motion of entire cells as a result of ciliary movement is observed only in spermatozoa. The normal function of ciliary movement is to aid in propelling mucus in the respiratory tract, ova in the Fig. H. — Ciliated Kpitlieliuui, Trachea, Fallopian tubes, spermatozoa in the vas deferens, etc. Ciliary movement is due to intracellular protoplasmic disturbances, at least it is the result of chemic influences. Over stimulation or disease may produce increased action and finally fatigue or par- alysis of the cilia, or they may produce cessation of their action. The most extensive and important cell movement is noted in the highly specialized muscular cell. As the muscle cell maintains its relative position when contraction takes place, the movement is principally evident in the structures to which the muscle fibre is attached. The rate and extent of contraction vary in the different varieties of muscles. The spongioplasm is the active portion of the cell in contraction, the hyaloplasm being passive THE CELL. 31 only in function. Xcrve fibres terminate in end-organs, i. c., muscle plates, through which are transmitted impulses that pro- duce muscular movement. Muscular movement is an indis- 1 Rat. 2 Horse. Fig. 15. — Spermatozoa. pensable function, as circulation and respiration are absolutel\- dependent upon it. Digestion and urination would also be suspended if muscular action were curtailed. Immobility may 32 VETERINARY PATHOLOGY. be the result of muscular fatigue or dissociation of motor nerves and muscle fibres, or it may be due to neuroses. Muscular spasms are usually the result of violent stimulation of the motor nerves, although it may result from excessive stimulation of the muscle fibres themselves. Metabolism, — Metabolism is a term used to designate the processes included in nutrition or digestion, absorption, assimila- tion, katabolism, and excretion. These processes are the results of cell action. Metabolism includes two general processes, i. e., constructive metabolism or anabolism and destructive metabol- ism or katabolism. Active cells are constantly consuming foods and eliminating waste material. The quantity, quality and pre- vious preparation of the nutritive substances required, varies according to the specialization and degree of action of cells. The leucocyte is relatively simple, i. e., it is a primitive type of cell. A leucocyte is not very selective in its food requirements. It produces ferments that digest food substances, as well as necro- tic tissue as inflammatory exudate. The phagocytic action of leucocytes is largely dependent upon the fact that the substances phagocytized have been previously rendered inert. Connective tissue cells are closely related to leucocytes in their power of producing digestive ferments. Endothelial cells produce fer- ments vv^hich aided by the leucocyte ferment, dissolve and devour thrombi and emboli. On the other hand nerve cells are quite selective in their food requirem,ents and they have practically no power of producing digestive ferments. The foods required by cells are nitrogenous and non-nitro- genous. Nitrogenous nutrients are used in the construction and maintainance of the cell protoplasm. The non-nitrogenous foods are essentially carbohydrates and fats which are consumed when energy, in the form of either heat or motion, is liberated. When non-nitrogenous foods are consumed in excess, some of them may be stored as glycogen in the liver, or as fat in the various parts of the body, thus producing glycogenic or fatty infiltration. The consumption of nitrogenous food in excess may resvdt in overwork of nitrogenous excretory organs as in induced albu- minuria. Insufficient supply of carbonaceous food produces disturbed metabolism, because of the necessary conversion of nitrogenous food or nitrogenous cell constituents into carbon- aceous substances, in order that the body energy may be main- tained. Diminished supply of nitrogenous foods is temporarily compensated for by consumption of the protoplasm of the body cells. If the nitrogenous food supply is materially diminished Tin-: ci:ll. 33 for a long lime or entirely withheld, the body cells atrophy, degenerate, and ultimately die. The waste products are also divisible into two classes, nitro- genous and non-nitrogenous. The nitrogenous waste substances are urea, or some allied product. They represent katabolic pro- ducts, i. e., the results of destructive changes in the cell proto- plasm. The carbohydrates and fats are almost entirely converted into energy; carbon dioxide and water being the chief katabolic l)ro<:iucts. Irritability. — Irritability is the property of certain cells which enables lliem to respond to stimuli. Stimuli may be chemic. thermic, electric or mechanic. The property of irritabilitv is \ested especially in nerve cells, although other cells are slightly irritable, e. g., muscle cells. The degree of sensitiveness varies greatly in different species of animals and to a less extent in different individuals of the same species. Thus, horses are more sensitive than cattle and the thoroughbred horse has a more sensitive skin than the draft horse. Irritability is a very import- ant property because it is the means through which the nature of environments is recognized. Many of the activities of the body are responses to impulses resulting from stimulation of irritable cells. Irritability is the propertv of cells which enables an animal to communicate with its environments as. sight, hear- ing, smell, etc. Irritability may be intensified or diminished by pathological processes. Thus chemic Aariations. resulting from katabolism in tissues affected with inflammation, produce in- creased irritability or intensify stimulation of nerves, and is manifested by hyperasthesia or by pain. Anemic and venous hyperemic tissues are usually less sensitive than normal tissues l>ecause of the accumulation of waste product that tends to inhibit impulses or diminish irritability. Correlation of the cell to the entire organ is of considerable moment, and is dej)endcnt upon irritability and response to stimuli. CHAPTER II. GENERAL CONSIDERATION OF DISEASE. DEFINITION. CLASSIFICATION as to, Time affected. Inherited. Definition. Predisposition. Tumors. Neuroses. Malformations — not rare. Infections — rarely if ever. Acquired. Definition. Antenatal — (congoiital) — Contagious abortion. Post-natal — Spavin. Extent in affected animals. Local — inflammation. General — anthrax. Etiology. Infectious. Non-infections. ETIOLOGY. Predisposing. Heredity — Epiplepsy. Inbreeding — General debility. Age — Canine and colt distemper, blackleg. Sex — Males urethral calculi; females, peritonitis. Genus — Hogs, cholera; cattle, blackleg. Breed — Clydesdale, laminitis; Jersey tuberculosis. Color — JVhife ajiiinals, sunburn. Location — Pica, catarrh. Climate — Contracted hoofs, :scratchcs. Season— Pneumonia , insolation. Food and JJ^ater — Indigestion. Occupation — City horses, foot disease; dairy coiu, udder disease. Effects of previous disease — Purpura hemorrhagica. Exciting. Mechanic — Fractures, dislocations, sprained tendons. Physic. Electric; Lightning stroke, electric zvires. Thermic; Burns, overheat, freezing. Photic; Dermatitis. Chemic. Inorganic — Saturnism. Organic — Sorghum poisoning. Poisonous plants — Loco, hemlock, larkspur. Poisons secreted by snakes, bees, etc. Parasitic. Bacteria — Glanders, tuberculosis. Yeast — Epizootic lymphangitis. Moulds — Pulmonary mycosis. Protozoa — Tick fever. Vermes — Trichinosis. Arthropods — Lousiness. EXTENSION. Natural channels — Digestive, urinary, etc. Continuity — Along a muscle, etc. Contiguity — From muscular to connective tissues, etc. Blood — In plasma, leucocytes or red cells. Lymph — In plasma or leucocytes. Nerve fibres — Along axone. TERMINATION. «4. GENERAL CONSIDERATION OF DISEASE. 35 Health has been defined as that condition in which the normal structure and functions of all the component parts of an organized being arc maintained. Disease is a functional or structural deviation from the nor- mal. It is that C(.)n(lition in which an organism cannot accustom itself to its environments. He^ilth and disease are, however, only relative terms, because of the difficulty of determining a normal standard. The two conditions necessarily overlap. Diseases may be classified in many w^ays, as local and gen- eral, infectious and non-infectious, inherited and acquired, etc. INHERITED DISEASES. A detailed discussion of heredity is not deemed advisable in a text of general pathology. A knowledge of inheritance is of importance to the veterinarian, especially in the relationship of heredity to disease and the extent of the transmission of acquired characteristics. Briefly summarizing it may be said that inherit- ance may be manifested in four ways, \"iz., "Blended inherit- ance," "Exclusive inheritance," 'Tarticulate inheritance," and "Regressive inheritance."' Blended inheritance is a condition in which the character- istics of both parents are equally transmitted and fused. Exclusive inheritance results in the production of offspring which resembles one parent absolutely at the exclusion of the other. Particulate inheritance is represented by the transmission of specific peculiarities from both parents as one eye of the off- spring may be like the male and the other eye like the female progenitor. Regressive inheritance is of prime importance particular to breeders, for it is a condition of a constant tendency to return to the mean or average of the type. INHERITED DISEASES are those transmitted from the parent in spermatozoa or ova and are present at the time of fertilization. Certain characteristics are transmitted from parent to offspring such as genus, breed and individual peculiarities. Thus horses have peculiarities so fixed and constant that they are transmitted to their offspring and differentiate them from other species of the genus Equus. Breeds are differentiated by certain peculiar- ities ; thus Jersey cattle,are brown to light fa\\n in color with a brown or black muzzle, horns turned in and up, they arc small, lean, dish faced; all of which are peculiarities that distinguish 36 VETERINARY PATHOLOGY. them from other breeds of cattle. There are individual peculiar- ities, some of which are the result of the fusion of parental characteristics ; thus the offspring may be of solid color, the result of the fusion of different parental colors, (color blending), or they may be piebald, indicating failure of color blending (mosaic coloring). The extent of intensification of inherited generic, breed or individual peculiarities depends upon the pre- potency of the parental stock. This prepotency depends upon the length of time that the type has existed under similar cir- cumstances. The foregoing illustrates what is meant by the term "heredity," and demonstrates that the breeding of stock is a science. Diseases are rarely inherited, first, because diseased sperma- tozoa and ova are probably incapable of fertilization, and second, there is always a tendency to abortion when an embryo or foetus is diseased. A predisposition may be inherited, i. e., the progeny of diseased parents may be more susceptible to disease than the progeny of a healthy parentage. Infectious diseases are very rarely inherited. It has been demonstrated that spermatozoa are not phagocytic in action and probably ova have no phagocytic tendencies ; the latter, however, has not been proven. The quan- tity of semen and the number of spermatozoa per given volume varies in different animals and in the same animal under differ- ent conditions. Loeb estimated that the average human seminal ejaculation contained about 226,000,000 spermatozoa. The aver- age seminal ejaculation of a dog probably contains about the same number of spermatozoa as that of the human. Lewis found that one stallion ejaculated 65 cc. of semen during one service, each cmm. of which contained approximately 131,750 spermatozoa (total 8,563,750,000) ; another stallion ejaculated 90 cc. of semen during one service, each cmm. of which contained approximately 225,000 spermatozoa (total 20,250,000,000). The quantity and the number of spermatozoa per given volume of semen ejaculated during one service of the bull has not been determined, at least the information has not been found in the available literature. However, it is reasonable to suspect that the number of spermatozoa ejaculated during a single service by the bull is equal to the number ejaculated by a stallion during a single service. It is difficult to collect the entire discharge of semen of a boar, but Lewis obtained 100 cc. from a single service of a boar and by repeated examinations he has determined that the semen from boars contains more spermatozoa per given volume than that from stallions. There would, therefore, be less chance for fertilization with an infected spermatozoon in the GL:NEli.\L CONSIDERATION OF DISEASE. 37 liorsc, OX and liog" than in man. Suppose there were 1,000 tubercle bacilli infecting 1,000 spermatozoa that were ejaculated by a bull in one service, then there would be one chance in from .s,000,000 to about 20,000,0(10 of an infected spermatozoon fertil- izing an ovum, assuming that one seminal ejaculation of the bull contains approximately the same number of spermatozoa as one seminal ejaculation of a stallion. The chance is so slight that it need not be considered. The offspring of animals affected with some infectious diseases are probably more susceptible to those diseases because of inherited weakness. For example, calves of tuberculous parentage are probably mere susceptible to tuberculosis than calves of non-tubercular animals. Neoplasms or tumors are occasionally inherited or at least there is an inherited predisposition to them. Dr. A. F. Meredith of Lincoln. Kansas, submitted a tumorous growth for examina- tion that was obtained from the left eye of a mule. The dam of the mule, as well as four of her brothers and sisters had a similar defect of the same eye. Cadiot refers to a family of dogs in which there were carcinomata of the mammae for two succes- sive generations. ATalformations. though usually of congenital origin, are prob- ably more frequently inherited than is any other type of disease. Thus a cryptorchid stallion was used for breeding purposes in a certain locality in Illinois and about 20'^, of his male colts were cryptorchids. About 5^ of the male progeny of one of ^Missouri's most famout boars, Chief Tecumseh IT. were cryp- torchids. Liberty Chief and Chief I Know, two boars sired by Chief Tecumseh II, were noted boars and from 3 to 5% of their male get were cryptorchids. Chief Perfection IT, also sired by Chief Tecumseh II, was the sire of Cherokee Perfection, which in turn sired about 3% of cryptorchids. Thus this structural defect appeared in at least three generations. A female Belgian hare having one ear, produced a large number of young of which more than ~)0^'', had only one ear. Epileptic domestic animals and those affected with other nervous disorders are usually destroyed or at least are not bred, hence the number of cases of inherited nervous diseases in domestic animals are relatively few in number, but there is little doubt that such diseases, or at least a predisposition to them, may be inherited. La Notte recorded hereditary epilepsy in the progeny of two epileptic bulls, the disease becoming evident in the females after they had given birth to their first calves, and in bulls soon after they were put into scr\ice. 38 VETERINARY PATHOLOGY. Some other diseases are inherited, thus; periodic ophthalmia has occurred in, and affected practically all of entire families of horses. There is a predisposition to spavins, splints and ring- bones in certain strains of horses. This is due to inheritance of structural or conformation defects. ACQUIRED DISEASES. The life of mammals is conventionally divided into two periods, the ante-natal or intrauterine, and the post-natal or extrauterine. Acquired diseases are those contracted after fertil- ization and hence may be ante-natal (congenital), or post-natal. Ante-natal or Congenital diseases are those contracted be- tween the time of fertilization and birth. Some infectious diseases are congenital, for instance, marked lesions of tuber- culosis were found by the writer in 1900 in a three day old calf, and two authentic reports of similar cases have been received since that date. (These cases were not considered as inherited for the reason heretofore given, and in all three cases lesions of tuberculosis were found in the uterus and adjacent tissues of the cows.) Infectious abortion is a congenital disease. The infective agent (B. abortus) is usually readily demonstrable in the diges- tive tube of the aborted foetuses. However, infectious diseases are seldom transmitted from the mother to the foetus because of the relation and anatomical structure of the placental mem- branes. The female is usually either sterile or aborts if the uterus or the accessory parts are diseased, while the male is not likely to be productive if the genital organs are diseased. Exanthematous diseases are frequently congenital. Terato- mas and other malformations are diseased conditions and may be of congenital origin. Post-natal diseases are those contracted r t any time during the life of the animal after birth, as laminitis, actinomycosis, and spavin. In classifying diseases according to extent, two groups are usually described, viz : — local and general. 1. A LOCAL DISEASE IS onc that affects a part or organ ; as urethral calculi, and pulmonary anthracosis. Local diseases proper remain localized although the term is used in a broader sense to designate a circumscribed, local, morbid process that may later become generalized. Thus, tubercular infection of a group of lymphatic glands is frequently spoken of as localized tubercu- losis. GENERAL CONSIDERATION OF DISEASE. 39 2. A GENERAL DISEASE, strictly Speaking, is one invoking the entire animal body, as anemia, but in a more restricted sense it is used to designate the involvement of several parts or organs. Diseases may be classified as to cause as infectious and non- infectious. Infectious diseases are those produced by some microbian agent, as : glanders, tuberculosis and blackleg. Non- infectious diseases are those in which the cause is not of an infectious character, as spavin, laminitis and stringhalt. Etiology. — Disease has been defined as an inharmonious relation between an individual and its environments. This definition is indicative of the various factors concerned in the production of morbid processes. The causes of disease may be conveniently subdivided into two groups, viz. : predisposing causes and exciting causes. PREDISPOSING CAUSES. — Predisposing causes are those condi- tions or environments which render animals more susceptible to disease. It has long been recognized that many diseases of domestic animals are due to induced variations of species that result from selection by breeders. New breeds of the various animals are produced so rapidly, without proper regard of conformation, that the individuals of the new breeds are frequently more sus- ceptible to disease. Rctrogresswc clmnges in anatomical structures predispose to disease. The tarsal joint of the horse is gradually changing from an active to a passive structure ; this change results in a ten- dency to ossification and ankylosis or spavin formation. Pro- gressive changes in various structures are responsible for some diseased conditions, as navicular disease in the horse, and mam- mary diseases of dairy cattle. .Several breeds of horses are char- acterized by small heads and especially diminished facial bones, a conformation that predisposes to dental diseases. Inbreeding has been a cause of decreasing the resistance of animals to disease. Age. The age of animals is an important predisposing factor in the causation of disease. The very young animal is structur- ally more delicate than the matured animal. Tissues are more or less permeable to the various bacteria, and until young animals acquire an immunity, i. e., establish a resistance, they are more or less influenced by bacterial activity. There are some diseases, however, that aflfcct only young animals, as. canine and colt distemper, while other diseases occur primarily or only in adults as carcinomas and bursattae. 40 VETERINARY PATHOLOGY. Sex is of consequence in the occurrence of disease. Parturi- tion predisposes females to peritonitis. Males are especially sus- ceptible to urethral calculi. Genus may be a factor in the predisposition to disease. Glanders is a disease of the genus equus, caseous-lymphadenitis of the genus ovis, canine distemper of the genus canis, rinder- pest of the genus bovis. Breed. — There are certain peculiarities of some breeds of animals that predispose to disease, thus the original Clydesdale horse, which was characterized by a large, round, flat foot, is more susceptible to laminitis than other breeds of horses that have a well formed foot. The thoroughbred, because of its highly developed nervous temperament is more susceptible to heart disturbances than horses of a less highly developed ner- vous temperament, as the draft horses. The Jersey cow has been developed into a high grade butter fat producer at the expense of conformation, in which the thoracic cavity has been dimin- ished and these cows are more subject to pulmonary tubercu- losis than the breeds of cattle that have a large thoracic cavity. White or light colored animals are more susceptible to derma- titis and are more affected by flies than those of darker color. In certain locations there are no white hogs because the hogs in those locations feed upon the roots of Lacuanthis tinctoria. which causes a pink discoloration, (hyperemia), of their bones and causes sloughing of the feet in all except black hogs. Individuals of a resistant strain are sometimes especially sus- ceptible to certain diseases. Locaiion. — The soil of a locality may be deficient in some necessary ingredient or contain some noxious constituent. Some localities may be continually damp and muddy, others dry and dusty, and still others abound in objectionable gases and odors. Any of the above conditions naturally diminish the resistance of animals ; thus pica exists in localities in which the soil is prob- ably deficient in some ingredient, scratches and thrush are com- mon where mud abounds ; broken and cracked feet in dry, dusty regions, and nasal catarrh where irritating odors are common. Climate definitely influences the hairy covering of animals. In Angora, not only goats but also collie dogs and cats have fine fleecy hair. Mules kept in mines constantly for a long time become covered with velvety hair like that of a mole. Season. — Some diseases are more common in certain seasons. Thus pneumonia is more prevalent during the seasons of sudden change as early spring and late fall. liKNKRAl. CUNSlDKKAtlOX OF DISKASi:. 41 Occupation. — The city express horse is particularly liable to diseases of the feet, the thoroughbred to rupture of the heart or blood-vessels, the dairy cow to udder diseases, and the house dog to indigestion. Food and Water. — Excessive, insufificient or unwholesome food and water, also irregularity of feeding or watering are fre- quent causes of depressed condition of animals. In Holstein an enzootic anemia destroys hundreds of suckling pigs annually. The pigs are apparently normal until about two weeks of age. The cause is probably improper food and a predisposition result- ing from excessive stimulation of the reproductive function of the sow. \'ariegated color of parrots is produced by feeding green parrots fat from siluroid fishes. Colic is essentially a dietary disease. The effects of prezioits disease frecjuently leaves an animal in a depleted condition, thus petechial fever is frequently a sequel of pneumonia or "stable fever" (catarrhal fever). Ovcrivork. lack of exercise, variable temperatures, and other minor causes all have their influence in depressing the animal I)ody. Imitation. — Some animals, colts especially, have a tendency to imitate what other horses do, thus colts allowed to run with cribbing horses occasionally become cribbers. EXCITING CAUSES of disease are those acts or agencies which directly and specifically produce disease, as falling, sunlight, chemic substances and infection. Mechanic, physic, chemic and parasitic agencies are the prin- cipal exciting causes of disease. MecJianic. — Diseases are produced mechanically by breaking the continuity of involved tissues, by compression, or by chang- ing the relations of anatomical elements. The condition result- ing from a break in the continuity of a surface soft tissue is termed a wound, of sub-surface soft tissue, a rupture, and of osseous tissue, a fracture. Compression may cause bruising or crushing depending upon the mechanical object inducing the injury, and the amount of pressure exerted. Luxations or dis- locations arc the result of changed relations of bones, tendons and ligaments. Volvuli and intussusceptions are the result of changed relations of the intestine. Hernia is a condition in which there is a changed relation, caused by a break in the continuity of one tissue which permits an adjacent tissue or structure to protrude or sacculate through it. Dogs are more frequently injured by biting than other animals although they may inflict lacerated wounds in other 42 VETERINARY PATHOLOGY. animals, especially hogs. Horses more frequently than other animals become injured by pawing, rearing, kicking, falling and colliding with foreign objects. The majority of barbwire wounds are the result of pawing over or through a wire fence. Rearing •frequently results in straining the plantar ligament, thus producing a curb. Slipping may cause the straining oi tendons, thus producing curbs and spavins as well as tendonitis. Falling may produce strained tendons and is the usual cause of dislocations, rupture, hernia, volvulus and fractures. Runaway horses and mules frequently collide with fences, trees, buildings, and various vehicles, as buggies, wagons, street cars, etc., and thus produce a variety of injuries. Ill-fitting shoes are responsible for contracted feet, strained tendons and ligaments, speedy cuts and bruises by interfering. Ill-fitting collars produce galled shoulders, sore neck, cerebral venous congestion and sweeney. Ill-fitting harness produces Sweeney, sore neck, sore back, galled sides, rump and tail, an ill-fitting bridle causes irritation of the mouth, injuries to the eyes, the ears and the throat-latch region, and poll evil. Except- ing the sore mouth, ill-fitting halters produce the same results as ill-fitting bridles. Ill-fitting saddles produce sore backs, sitfasts, injury in the region of girth and bruises resulting in fistulous withers. Attendants may inflict injuries of various types. Several cows in a dairy were observed to be lame in the right hind leg. Upon closer inspection the right tarsal joint was found enlarged and sensitive. One man had been milking all the af- fected cows and finally admitted that he had either kicked c-r struck each lame cow upon the tarsal joint. Bandages are frequently so tightly wound upon a part that they obstruct circulation thus producing venous congestion, which predisposes to infection. Some cases have been observed in which splints improperly applied to support a part have resulted in venous congestion, oedema and necrosis. Careless individuals will place rubber bands upon dogs' tails, ears, and feet to see the animals remove them. The dog will sometimes fail to remove the rubber band, which, by pressiire, may divide the skin and soft tissues, and finally cause the portion distal to the band to become necrotic and slough. Shooting occasionally causes mechanical injury to animals. Such accidents frequently occur in animals in pastures, especial- ly during the hunting season. Such injuries are more frequent during a war, and a knowledge of the various types of bullets GENERAL CONSIDERATION OF DISEASE. 43 and wounds inflicted by same is of considerable importance to arniv veterinarians. Powdered glass, which is sometimes maliciously incorporated in food for the purpose of destruction of life, may excite gastric and intestinal inflammation. Sand is sometimes consumed in sufficient quantities, by animals grazing upon sandy soil, to mechanically interfere with digestive functions, and mechan- ically injure the gastric and intestinal membrane. Nails, wire, staples, etc., are frequently ingested with food by animals, especially cattle, which objects may cause injury by producing abrasions of the mucous membrane or even by inmcturing the wall of the digestive tract, thus establishing such inflammatory disturb- ances as peritonitis, pleurisy, and pericarditis. Various mechanical contrivances such as operating tables, throwing harness and hobbles, used in subduing fractious ani- mals or confining animals for operative procedure may produce injury. 1. riiysic. — Temperature variations, not only predispose to disease, but may also become an exciting cause. Excessively high temperature is likely to produce overheat, (insolation, heat prostration). Overheat or heat prostration is frequently ob- served in fat hogs having little or no shelter in the summer time, or in hogs being hauled in wagons or cars, or being driven in herds to market. It is also frequently observed in horses worked on pavements in cities during the summer months. Local application of excessive heat produces burns. The lesions produced in local burns vary according to the degree of temperature, the length of time applied and the tissue resis- tance. Three grades of lesions, of local burns, determined by the degree of temperature, may be described. First, short ex- posure to a temperature of from -^0° to C^i)° C. produces an hyperemia or a burn of the first degree; second, exposure to a temperature of (50° to S0° C. for a short time produces inflamma- tion, characterized by a serous exudate that accumulates in the malpighian layers of the epidermis forming vesicles or blisters; third, an exposure to a temperature above ^!^° C. for a brief period, produces necrosis, the dead tissue becoming dry and hard. Burns involving one-fourth to one-third of the cutaneous surface frequently terminate fatally as a result of hemolysis of the red corpuscles, increased heat dissipation and other disturbed cutaneous functions. Excessively low temperature ma\- diminish the body tem- perature, of warm blooded animals, to the extent that the func- tionine is modified or inhibited suflficientiv to result in death. 44 Veterinary pathology. Animal? are naturally protected from the effects of low tem- peratures, in dry weather, by their coat of hair, fur, wool or feathers. When their protective coat becomes wet it no longer pi event? heat dissipation; consequently animals having no shel- ter, as lanch horses, cattle, and sheep, frequently die in great number? during the early cold spring rains. The local lesions caused by low temperature are practically the same as those resulting from exposure to high temperature. Ihus exposure to a mild, low temperature produces hyperemia; exposure to freezing temperature produces inflammation accom- panied by a serous exudation, but the exudate rarely accumu- lates and forms a vesicle as in burning. Exposure to extreme low temperature produces necrosis, the frozen tissue becoming dry and hard. A.nimal£ are most frequently exposed to temperatures suffi- ciently high to produce insolation in the daytime, in the tropi- cal or temperate zones, although overheat is sometimes observed during the night. Exposure to temperatures that produce local burning usually occurs in conflagrations of buildings. Scores of animals die, in the spring, on ranges or large pastures, in the temperate zone, as a result of diminished body tempera- ture induced by exposure to cold rains. These animals are usually depleted because of insufficient or non-nutritious food. Theii coat of hair or wool becomes saturated with water and thus the body temperature regulation is disturbed. Lesions produced by low temperatures are evident only in regions and seasons, where there is a low atmospheric temperature. Local freezing usually occurs in extremities, as the ears, tail and feet. 2. Photic. — Exposure to sunlight frequently produces der- matitis, especially in those animals having a thin, light colored skin. White hogs are quite seriously affected by sunburning, in some localities. This peculiarity prohibits the raising of white hogs, in certain districts in Africa and Central America. R. Paine, F. R. C V. S.. of the Department of Agriculture of Cape Colony, in the Journal of Comparative Pathology and Therapeu- tics, Part 1, Vol. XXI, reported some cases of dermatitis in cattle, that were undoubtedly the result of exposure to sunlight. D, M. Campbell observed about 40 Duroc Jersey pigs affected with dermatitis induced by sunlight. Direct or reflected sunlight is also injurious to the eyes of domestic animals. The injurious effects are noticed more espe- cially in animals driven upon macadam thoroughfares, over light colored soil, or when the ground is covered with snow. Electric and gas lights have also been found to be injurious to the eyes Common Nsme. Erpot Stink Horn Bunch Flower White Kellcbore Calif. HeWebor* Pokeroot Corn cockle Monkshood Wild Monkshood Wild Monkshooa Larkspur (dwarf) Larkspur (purple) Larkspur (Wyoming) Larkspur (tall) Mayapple Wild blackberry Wooly loco StemtcsB loco Rattiebox Wild ur blue pea Wild or blue pea Alslke clover Red Buckeye Horse chestnut Ohio Buckeye Calif. Buckeye Water Hemlock Oreeon Water Hemlock Poison Hemlock Broad leafed laurel Narrow leafed iaurel Great laurel Black nl^•l^'»bade Spreading night- shade Horse NetUe Jlrason weed Tobacco Potato Cockiedur Snec7.ewe*d Doath Camas Sorghum KafJlr com Ciitor *»an ORDEn Hypocra Phallac MelanU Malanth Malantt Phytola. Caryoph Ran unci Ranunci Ranunci Ranunci Ranunc Ranunci K a n u n a Berbcrl^ Prunaca Leguml LegumI; Legumlt Legumli Leguml: Leguml Aescula Aescula Aescula Aescula' Umblllli LOCATION OR DISTRIBCTION I'nlversal Southern States Eastern U. S. Eastern and Northern U S California Eastern 2 /3 of U S Eastern 2/3 of U. S. Universal garden plant N. W. America. North Central U. S., Ga., Pa. Ohio, Ind., Pa., Ky.. N. C, Ga., Ark N. W. U. S. and S. W. Can. Wyoming and N. Colo N. W. U. S. Que.. Pla., Tex. Middle Atlantic States, Dak., Kuns . Tex. Plains U. S.. Mex. and Can. Plains U. S. Mox. and Can N. Car, Fla., S. Dak., Ark.. Mex. western U. S. especially Mo river valley. Uplands and foothills. Central U. S. uplands and foothills. Central U. S. uplands and foothills. Gulf and middle states. Va. to Flo. N. Eng., N. T., N. J. Ohio, Pa.. Ala., Mich., Okla.. Neb. California. Eastern and Gulf States, N. Mex. Umblint >*' ^- U. S. UmbllU Ericace' Erlcace; Ericace Solanaci ^^. E. U. S. and California Allegheny district, Fla., La N. E. U. S. Ga.. Mich., Hud Bay. >;cw Found. Allegheny Mts., Nova Scotia, Ont. Universal Solanaci Ont. N. W. Ter. Kans , Ariz. Solanac Central U. S. also Eastern U. S. Solanaci Universal Solanac. Universal Solanac* Universal ComposI) Georgia, N. Eng, Fla., Neb, Mex. CoTnposI Universal Melanth Western U. S. Gramln« Plains especially. Oramln* plains especially Kuphort Universal BOTANICAT. NAAIB8. INSERT L Common N>me. Erg-ot Stink Horn Bunch Flower White Hellebore Calif. Hellebor* Pokeroot Corn cockle Monkshood Wild Monkshood Wild MonkshooQ Larkspur (dwarf) Larkspur (purple) Larkspur (Wyoming) Larkspur (tall) Mayapple Wild blackberry Wooly loco StemlcBs loco Rattlebox Wild or blue pta Wild or blue pea Alslke clover Red Buckeye Horse chestnut Ohio Buckeye Calif. Buckeye Water Hemlock Orpgon Water Hemlock Poison Hemlock Broad leafed laurel Narrow leafed laurel Great :aurel Black ni(.'li^ahade Spreading night- shade Horse Nettle JImson weed Tobacco Potato (.'ocklet)ur Sncczewe«a Doath Camas Sorghum Kaffir com editor bean ORDJGR OR FAMILY Hypocracaea Phallaceae Velanthacae Malanthacea Malantbacca Phytolaccaceae Caryophyllacea Ranunculaceae Ranunculaceae Ranunculaceae Ranunculaceae Ranunculaceae Ranunculaceae tianunculacpaft Bcrbcridaceae Prunaccae Leguminosae Lcguminosae Leguminosae Leguminosae Leguminosae Leguminosae Aesculaceae Aesculaceae Aesculaceae Aesculaceae Umblllllerae UmbllUferae UmbllUferae Ericaceae Ericaceae Ericaceae Solanaceae Solanaceae Solanaceae Solanaceae Solanaceae Solanaceae Composltae Composltae Melanthaceae Gramtneae Qramlncao Suphorbtacea* GENUS ClavlcepB UathruB Chrosperma Vevatrum Vevatrum Phytolacca Agrostemma Aconltum Aconltum Aconltum Delphlnum Delphlnum Delphlnum Delphlnum Podophyllum Prunua SPECIE purpura columnatus muscaetoxlcum vivide callfornlcum amcrlcana glthago napellus ^olumbianum unclnatum tricorne menzlcBll geyerl glaucum peltatum serotlna Astragalus molllsimus Aragallas (OxytroplB) lambertl Crotalarlc Luplnus LuplnuB Aesculus Aesculua AeacuIuB Aesculus Clcuta Cicuta Conlura Kalmla Kalmla Rhododendron Solanum Solanum Solanum Datura NIcotlana Solanum Xanthlum Helenlum J^y^adenus Andropogon (Hack) Andropogon RIclnui Bagittalls leucophyllue. argentus pavla hlppocastanum glabra California maculata vagans maculata latlfoHa angustofolla maximum nigrum nigrum trlflorum carollnense stramonlurr tobacum canadonse glabratum venenosuB Sorghum Sorghum communis PART OF PLANT POISONOUS entire entire bulbs leaves leaves and seed root entire seeds especially roots and leaves roots and leaves roots and loaves seeds and leaves seeds and leaves seeds and leaves seeds and leaves leaves leaves leaves and stem leaves and stem leaves and seeds pods and seeds pods and seeds leaves and fruit leaves and fruit leaves and fruit leaves and fruit roots roots roots leaves leaves leaves leaves, roots and fruit leaves and fruit leaves and fruit leaves and fruit leaves and fruit tuber jsotyledons entire plant bulbs and leaves leaves leaves seed POISONOUS PRINCIPLE Ergotine Veratrlne Veratrlne Phytolaccine Aconltlne Aconltine Aconltlne Podophyllln (Berberine) Hydrocyanic acid Barium Chloride Barium Chloride Unnamed alkaloid Lupinin Luplnin Aesculln Aesculln Aesculin Aesculln Conine Conine Conine Andromedotoxln Andromedotoxln Andromedi)to.icw Found. Allegheny Mts., Nova Scotia. Ont Universal Ont. N. W. Ter.. Kan«.. Ariz. Central U. S. also Eastern U. S. Universal Universal horses and Universal pigs, cattle & sheep Georgia. N. Eng.. Fla., Neb., Mex horses, cattle and Universal sheep .«hoep and cattl* cattle cattle all Western U. S. Plains especially. Plains especially. Universal GENERAL CONSIDERATION OF DISEASE. 45 of various animals, especially when the lights are allowed to shine directly into their eyes. Epilepsy has been produced in horses by sudden exposure to intense light. The immediate cause of the effects of exposure to sunlight upon the skin is not known but is thought to be the result of the action of the actinic or chemic rays. The eft"ects of exposure to light upon the eyes is excessive stimulation which produces exhaustion, thus predisposing to, if not directly exciting disease. 3. Electric. — Animals are susceptible to the action of elec- tricity. Horses are especially susceptible to its influences. Some authorities have claimed that a direct current of 500 volts, 100 amperes, is sufficient to kill a horse, and an alternating current of 160 volts is destructive to medium sized dogs. A 1,200 pound horse was electrocuted when he stepped upon a wire carrying 220 volts of 230 amperes. Contact with electricity may be the result of lightning, and charged electric wires, or rails. Horses and cattle frequently are struck by lightning while in pastures, and animals used in cities are occasionally accidentally brought in contact with elec- tric currents. Depending upon the amount of electrical current, the results may be a slight singeing of hair, burning, or lacera- tion of tissues in general. Carcasses of animals destroyed by electrical currents have also been observed in which no lesions could be found. On examination of carcasses of animals dead of lightning stroke, there is usually more or less singeing of the hair, hyperemia and hemorrhages along the course of the current and a persistent fluidity of the blood. 4. Chemic. — Chemic substances capable of producing disease are very common and may have their origin from the mineral, veg- etable or animal kingdom, and are inorganic or organic. It is probable that practically all chemic substances may, under cer- tian conditions, be injurious to the tissues of the various animals. Some chemicals are always injurious, others may become injur- ious by chemic change induced by the tissue juices. Those chemicals capable of producing deleterious effects in the animal tissues are poisons. (Poisons are substances which when taken internally or applied externally alter health or destroy life with- out acting mechanically or reproducing themselves). According to their modes of action, poisons have been classi- fied as follows : 1. Corrosive poisons, (caustics and irritants). The action of this group varies from the production of a simple hyperemia to necrosis. The most common agents are mercury, arsenic, sodium and potassium hydroxide and the mineral acids. 46 VETERINARY PATHOLOGY. 2. Parenchymatous poisons. This group produces tissue degeneration, especially parenchymatous and fatty degenera- tions. The most common parenchymatous poisons are the tox- ins, endo-toxins, ptomains, leucomains, phosphorous and silver. 3. Hemic poisons. These act principally upon the red blood corpuscles and may inhibit combination of hemoglobin and oxygen, and cause disintegration of the cells and even produce thrombosis. The principal agents that combine with hemoglobin are carbon monoxide, sulphuretted hydrogen, hydrocyanic acid, the chlorates, and mercury. 4. Nerve and Cardiac poisons. These may produce paraly- sis by over-stimulation of nerve centers, or they may produce variation in the rate and force of the heart beat. Narcotics, such as atropine and solanin are types of neurotoxic poisons. Potas- sium salts depress the rate and increase the force of the heart action. A poisonous drug acts in various ways, depending upon the form of the drug, size of dose and method of administration. The following are the more common inorganic poisons: — arsenic, mercury, sodium, potassium, lead, copper, chlorine, and the various oxides, salts, acids and bases formed from them. Many organic compounds are responsible for poisoning in animals, as phenol, iodoform, picric acid, hydrocyanic acid. In fact most of the medicinal organic compounds are poisonous in large doses. There are many plants that are responsible for extensive losses of live stock in all parts of the United States, Canada and Mexico, and are most common in range districts. Colorado and Montana have had losses aggregating $200,000.00 annually, in live stock, from plant poisoning. The following table gives the common and botanical names of plants that most frequently produce poisoning in animals. (See insert No. 1.) These plants are not all poisonous during their entire devel- opment. The cocklebur is most poisonous in the earlier stage of development, that is, at the time the cotyledons come through the soil and for two or three days after the plant is up. Lupines are harmful principally while the seeds are maturing. Larkspurs are harmful only until the flowers appear. Dry seasons are usu- ally most favorable to the formation of poisonous principles in plants. Ergot develops most extensively during the wet sea- sons. Second growth or stunted kaffir corn and sorghum plants are more likely to be injurious than first growth or well devel- oped plants. GENERAL CONSIUERATION OF DISEASE. 47 Poisonous plants usually have some noxious properties as odor, taste, or appearance that protects them from consumption by animals. Poisoning usually occurs in animals that are hungry or are not accustomed to the location, or at least are not familiar with the plants that abound there. Animals in districts where poisonous plants are found are usually familiar with the dis- agreeable properties of them and let them alone or the animals may become accustomed to the injurious principles of the plant, Fis. Hi. — Ked Bu<-keye i Aesculus Paviai. that is, dc\elo}) a tolerance similar to immunity to infectixe diseases. In their vital activities microphytes (bacteria, yeast and moulds) and microzoa (protozoa) produce chemic substances that are extremely poisonous to animals. Thus saphroj)hytic bacteria produce ptomains in jiutrefying flesh. Fermented, musty or mouldy hay contains injurious substances that produce indigestion in the honee and ox. The specific products of micro- ])arasites will be discussed under the topic of vital or infcctix'C causes of disease. 48 VETERINARY PATHOLOGY. Bees, wasps, scorpions, ants and other animal organisms liberate poisonous chemic substances (zootoxins) which, when introduced into the animal body cause marked disturbances. Poisonous snakes secrete and liberate injurious chemic sub- stances. The poisonous principle, zootoxin or venom is pro- duced by glandular tissue, and is liberated through canals or V '^ tig. 17. — Loco (Astragalus MoUissimus). grooves in their fangs. The exact chemic composition of venom has not been determined but it is not the same in the different venomous snakes. Noguchi has classified the principle action of venom as follows : — 1. Instantaneous production of thrombi. Crotalus (rattle- snake). 2, Neurotoxic action. (Cobra.) GENERAL CONSIDERATION OF DISEASE. 49 3. Produce capillary ruptures and hemorrhage. Crotalus (rattlesnake). 4. Produce hemolysis. Crotalus (rattlesnake). 5. Produce general cytolysis. Crotalus (rattlesnake), and viper berus (adder). The following is the toxicity estimate of venom per kilogram body weight : — Cobra venom .00009 gram lethal dose for horse intravenously. Cobra venom .0005 gram lethal dose for dog subcutanously. Rattlesnake .005 gram lethal dose for rabbit subcutanously. Viper .0001 gram lethal dose for rabbit intravenously. Retrograde metamorphosis in the tissues of the animal body frequently results in the production of leucomains which, when absorbed, are extremely poisonous and cause marked disturb- ances. Over action of muscular tissue may cause the produc- tion of leucomains, thus horses that are overworked, although their food and water are first-class and their digestion is good, are occasionally affected with a severe diarrhoea caused by the action of leucomains. Parasitic or Infections. — During the last quarter of a century pathology has received an impulse by the knowledge of micro- parasites acquired during this time. Although parasitism has been known since the dawn of the 19th century, the importance of microparasites has been recognized only since bacteriology became a science. Parasitism is an evolutionary condition. It is the result of a long continued struggle, and the survival of the fittest, during which there is a necessary adaptation to constantly changing en- vironmental conditions. Parasitic causes of disease include rep- resentatives of both the plant and animal kingdom. Parasitic plants (Phytoparasites) are practically all microscopic in size and are termed microphytes. Pathogenic plants are all fungi and the following scheme gives their position in the plant kingdom : VEGETABLE PARASITES. KINGDOM BRANCH CLASS ORDER FAMILY GENUS SPECIES i. Plant Thallophyta Hyphomycetes Mucidineae Oospo-a Porrigines I (Achorion I schoenleini J2. Plant Thallophyta Hyphomycetes Plecascineae Aspergillaceae Aspergillus Fumigatus iS. Plant Thallophyta Hyphomycetes Plecascineae Aspergillaceae Aspergillus Niger 4. Plant Thallophyta Ascomycetes Protoascineae Saccharomy- Saccharomyces Farciminosu^- cetaceae 5. Plant Thallophvta Schizomycetes Actinomyces Bovis 6. Plajit Thallophyta Schizomycetes , . . , Bacterium Tuberculosis, e^c 50 VETERINARY PATHOLOGY, Hyphomycetes (Moulds). Hyphomycetes or moulds are non-chlorophyllic plants. Structurally they are composed of mycelial threads from which upright reproductive organs may be formed. They are usually multicellular and reproduce by spores. They require preformed foods and thrive best in the absence of light. Oospora porrigines (Achorion Schoenleini) is the organ- ism that causes favus. These organisms have mycelia with Fig. 18. — TrichoiJhjton Tonsurans, showing mycLlium and spore like bodies. hyphae, the latter may be branched and terminate in bulbous ends. The mycelium is later converted into oval spore-like bodies. Favus is occasionally observed in dogs and cats, more rarely in horses and fowls. The disease is characterized by dry scales which are brown, yellow or even white upon the surface and vary from white to sulphur yellow in their deeper layers. The areas involved are usually not more than y2 to ^ inch in diameter, and are usually devoid of hair. The lesion may occur on the head, especially on the forehead, cheeks or ears, and on the abdomen, or outer surface of the hind legs. c;kni:ual co.nsidicration ok diskask. 51 Sporotrichiiim ^ludoiiiiii (Trichophyton Tonsurans; is the fungus that causes ring-worm (tinea tonsurans). This fungus is found in the lesion and is probably strictly parasitic. Structur- ally it is composed of a simple or branched mycelium which may become broken up as a thread of ovoid spores. The spores may also appear in groups in the hair follicles. The disease becomes e\idcnt because of the presence of small circular hairless patches which are covered by grayish crusts or scales. As the disease ])rogresses the central portion of the lesion becomes normal and the peripheral tissue becomes involved. This condition has been observed in the horse and ox ; other domestic animals rarely become affected. Fig. ly. — Aspergillus r'uniig:atU8. Aspergillus Fimiif/atus is responsible for an occasional out- break of pulmonary mycosis ( Pneumo-mycosis, Aspergillosis) in birds. This fungus is of common occurence in nature. Struc- turally the fungus consists of a segmented mycelium which may branch dichotomously and from which upright stems termed hyphae may originate. These hyphae may be segmented and terminate in club-like ^heads. A tuft of hair-like projections (sterigmata) develops from the hypha head and on the distal end of each hair there is a sj)ore l)earing organ (conidium). The 52 VETERINARY PATHOLOGY. entire hyphae head with its spore bearing organs is included in a capsule the rupture of which is necessary for the distribution of the spores. The spores of Aspergillus are present in large numbers in hay, straw, barn-yard manure, etc., and they main- tain their virility in the dormant state for a considerable length of time. The source of infection is contaminated food, water or air. The principal lesions are located in the trachae, bronchi, lung and air cells of bones. The disease is characterized by a fibri- nopurulent inflammation of the mucous membranes of the trachea and bronchi and abscess formation in the lung. Aspergillus Niger is probably responsible for some cases of ear canker in dogs. Saccharomyces. (Yeast). Saccharomyces are the budding fungi. The classification of this group, the yeast plants, is as yet incomplete, their general biologic characteristics not being well known. A few varieties, however, have been studied, one of which, Saccharomyces Cere- visiae, is of considerable economic importance to the brewers. Yeasts are ovoid or spherical single celled non-chlorophyllic plants that reproduce by budding. Structurally the yeast cell has a cell body composed of protoplasm and a double cell mem- brane the latter composed of condensed protoplasm. The cell body may contain vacuoles, granules or foreign substances. Reproduction, which is by budding or gemmation, occurs at one or both ends of the yeast cell and even in some cases from the side of the cell. Budding begins by the appearance of small tubercles or buds which develop until a considerable size is attained. The daughter cell may remain associated with the mother cell or it may become detached and then pass through a similar cycle. Under certain conditions the yeast plant may develop into filamentous threads and in other instances may produce spores. Saccharomyces was, for a considerable time, associated as an etiologic factor in the production of carcinoma. It is prob- able that the "carcinoma bodies" (dense refractile oval bodies) are yeast cells but it is quite evident that they have no etiologic significance in carcinomas. Dermatitis in the human is, in some instances, of a saccharo- mycetic origin and no doubt some of the resistant cases of der- matitis in domestic animals have a similar cause, GENER.\L COXSIUKRATIOX OF DISEASE. 53 The principal pathogenic saccharomyces that concerns the veterinarian is tlie Saccharomyces farciminosus, which has been described by Rivolta as the Cryptococcus farciminosus. This yeast is the cause of epizootic lymphangitis, a disease which affects equines and primarily involves the cutaneous lymphoid tissue. The disease is prevalent or has prevailed in many localities in the United States, and in the Philippines, as well as, in India, Japan, China, South Africa, England and Ireland. The principal lesions are located in the lymphoid tissue which becomes tumefied and inflamed and in which the lymph sinuses are found to be engorged with coagulated lymph Fig. 20. — Yeast (Saccharomyces farciminosus). and pus. The lymphoid tissue later undergoes central liquefying necrosis and this is followed by the formation of pustules or ulcers. After the discharge of the pus the ulcer gradually heals and the related tissue becomes indurated. In a few cases lesions have been observed in tlic li\cr and spleen. Two other pathogenic fungi that have not been satisfactorily classified are the Actinomyces bovis and the Rotryomyces ascoformans. These .are the causative agent of Actinomycosis and Botryomycosis respectively. These micro-organisms as well as the diseases they produce will be discussed Ifiter. 54 VETERINARY PATHOLOGY. Schizomycetes (Bacteria). As will be noted by the foregoing scheme, bacteria are classed among the lowest groups of plants. Each bacterium is a single cell and contains no chlorophyll. The science of bacteriology is of recent development, because early investigators were compelled to use comparatively crude microscopes and because they were hot familiar with the condi- tions required for bacterial growth. The development of bacter- iolog}^ was coincident with the discussion pro and con of the theory of "spontaneous generation." This theory was disproved w s *•-.*.•• «« 1 :i 3 4 5 Fig. 21. — Showing different forms of Cocci. 1. Micrococcus. 4. Tetrads. 2. Streptocois. 5. Sarcina. 3. Diplococcus. by Pasteur about 1865, whose classical experiments also aided in establishing bacteriology as a science. (It is possible that bio- chemists may produce life, (animate objects), by synthesis of inanimate substances which will only represent the achieve- ments of ultratechnical scientists and will not signify that spon- taneous generation occurs in nature). Thirty or forty years 4^^? fx, Fig. 22. — Various forms of Bacilli. ago the study of bacteria was looked upon as a fad by the majority of the people. However, the practical application of bacteriologic knowledge in medicine, sanitation, the various arts and agriculture, has caused bacteriology to assume its present important position as one of the principal biologic sciences. Bacteria are found everywhere that animals or higher plants have grown. They are practically omnipresent. Bacteria are single celled plants, each individual possessing a cell body and a cell membrane. The cell body is principally GENliRAL C0XSII)i:UAT10N OF DISEASE. 55 composed of protoplasm, which may be homojj^eneous or granu- lar. In some instances non-protoplasmic particles may be {pres- ent. Chromatin, the essential nuclear material, is regularly dis- tributed throughout the entire cell body and no doubt functions the same as a nucleus. Granules that are intensely stained with methylene blue occur in the body of some bacteria, but their significance is not known. The cell bodies of some bacteria contain starch granules while those of others contain sulphur ^V H, \\V ',>,<\ H \aiious forms of Spirilla. granules. The cell membrane is of a protoplasmic nature and is probably formed by condensation of the protoplasmic cell body, whereas cellulose constitutes the cell membrane of the cells of higher jjlants. Some species possess organs of locomo- tion called flagella, which are delicate protoplasmic projec- tions of the cell body or cell membrane. Some bacteria, per- haps all. possess a capsule which appears as a gelatinous sub- stance and is probably derived from the cell membrane. The -4^ ^ Fig. 24. — Flagellate bacteria of various forms cell body is the essential structure and presides over metabol- ism. re])roduction and practically all other functions. Circu- latory, nervous and excretory organs are obviously not required in such simple forms of life. The cell membrane protects the cell body. Bacteria are very small, one eight millionth part of a cubic inch has been estimated as the least mass capable of being de- tected with the naked human eye. This space will contain about 2.000.000 ordinary bacteria. The dimensions of bacteria are ex- pressed in the term micron which is the unit of microscopical measurement. (A micron is 1/25,000 of an inch and is desig- nated by the Greek letter "Mu".) The Bacterium tuberculosis averages about 2.5 microns in length and about .5 microns in 56 VETERINARY PATHOLOGY. width, i. e., 1,000 tuberculosis organisms placed end to end would make one inch in length or it would take 50,000 of these bacteria placed side by side to make a linear inch. Some spher- ical bacteria are less than one micron in diameter, e. g., the pyogenic micrococci average .8 of a micron in diameter. Different individuals of the same species may vary considerably in size, thus the Bacterium anthracis may vary from four to ten microns in length. Some diseases are probably the result of infection with micro-organisms that are so small they can- not be detected by the use of present day microscopes and they also pass through the best known germ-proof filters. These in- fectious agents are designated as invisible or ultra-microscopic and may be present in a "filterable virus." Fig. 25. — Bacteria, showing capsule. Morphologically bacteria are very simple. Three principal types of bacteria are recognized according to their form, viz : the rod shaped (Bacilli), spherical (Cocci), and the spirals, (Spirilla). Another type, characterized by branching forms, (Chlamydo-bacteria). has a few representatives but their classi- fication as bacteria has been questioned. The representatives of each of the three principal groups. Bacilli, Cocci and Spirilla, are constant in their morphology so long as the environ- ments remain the same, i. e., the progeny of bacilli are bacilli, etc. Again, each individual is constant in its form, increase in size being the only change that occurs. Frequently, however, unfavorable conditions may cause pleomorphism among indi- vidual organisms. Perhaps the best accepted morphologic classification of bac- teria is as follows : — 1. Coccaceae, spherical shaped bacteria. 2. Bacteriaceae, rod or cylindrical shaped bacteria. 3. Spirillaceae, spiral shaped bacteria. GENERAL CONSIDERATION OF DISEASE. !)7 i Chlamydo-bactcriaccae, branching or irregular torms of bacteria. According to their biologic characteristics, bacteria may be classified as follows : — Aerobic or anaerobic. Chromogenic or non-chromogenic. Zymogenic or non-zymogenic. Saprogenic or non-saprogenic. Photogenic or non-photogenic. Thermogenic or non-thermogenic. Saphrophytic or non-saphrophytic. Parasitic or non-parasitic. Pathogenic or non-pathogenic. Pyogenic or non-pyogenic. etc. Bacteria, like other living things, grow and reproduce under favorable conditions. They grow until they attain a certain size then thev divide, i. e., a cell divides into two equal halves, each half representing an individual bacterium which in turn grows and ultimately divides into two equal halves, etc., thus bacteria grow and multiply. The rate of growth and division is com- paratively rapid. The Bacillus subtilis, under favorable con- ditions may pass through the life cycles incident to attaining its growth and dividing, thus doubling in number, every 30 min- utes. Barber has found that Bacillus coli communis, under optimum conditions may divide by fission, in seventeen min- utes. Beginning with one bacterium, it has been estimated that if division occurred once per hour and continued for three days, the progeny would weigh 7,417 tons. Some other cells, notably the undifferentiated cell in the animal embryo, may divide as rapidly as bacteria, but they do not become developed, and so far as known, there are no other cells that complete the entire cycle of growth and reproduction in so short a time. This method of reproduction is called fission. Fission occurs in the three principal forms of bacteria. Among the Bacteriaceae and Spirallaceae. the division takes place in the transverse diameter, while the Coccaceae may divide in one, two or three planes. Bacteria grow and divide by fission as long as favorable conditions are supplied. When the environments are unfavor- able the organisms cease growing and do not increase m num- ber. Some species produce spores when conditions become unfavorable for further growth and fission. Bacterial spores, generallv characterized by being small, highly refractive oval shaped bodies, are more condensed than the original cell body protoplasm. Spore formation is first indicated by the appearance 58 VETERINARY PATHOLOGY. of small granules in the protoplasm of the parent cell. These granules collect and ultimately coalesce thus forming the spore. The spore may form in the center of the bacterium or near one end. After the spore is formed the remainder of the bacterial body becomes disintegrated. Spores are much more resistant to external injurious influences than are bacteria. The resist- ance of spores is due to the fact that they contain less water than bacteria, moreover they enjoy the protection of a thick covering or cell wall. Spores are inactive, i. e., they remain dor- mant until placed in favorable media and under favorable con- ditions when they germinate and develop as the vegetative form. One bacterium produces only one spore which in turn produces 26. — Bacteria, showing fission. only one bacterium and hence spore formation is not a means of multiplication, but is rather a natural means of preservation or continuation of the species. Those species of bacteria in which no spores are formed usually have a greater resistance to injurious influences than do the vegetative forms of the species which are capable of producing spores. Bacterial food requirements are quite variable. Some types of bacteria require preformed organic compounds and others appear to have the power of synthesizing the simplest com- pounds and available elements into new compounds upon which they subsist. Until recently it was supposed that synthesis was confined to chlorophyllaceous plants but some species of bac- teria are now known to possess the power of building complex compounds from simple materials, e. g., the nitrifying bacteria Parasitic bacteria and most saprophytic bacteria as a rule '■e- quire preformed organic compounds for their food. Some soil GL:NEit.\L considi:ration of disease. 59 bacteria aiH many water bacteria appear to live and thrive on simple inorg:anic substances. In fact most bacteria are capable of adapting themselves to an inorganic food medium. Food sub- stances must be in a dilute form in order that bacteria may subsist upon them. This is probably because of the osmotic differences of bacteria and their surroundings. Some chemic substances, usually considered as destructixe to bacteria, when sufficiently diluted are food for certain bacteria, thus the Bacillus pantotropus produces formalin and then uses it for food. It is said that luicillus pantotropus may live and thrive in a 1 to l."'),oOO solution of formalin. I'.acteria as a rule require food media of neutral or slightly alkaline reaction, (as shown by Fig. 27. — Showinjj si>orc formation. litmus paper) though some grow readily in acid media. While foods are recjuircd in small quantities only for each bacterium, yet because of their rapid multiplication and the resulting enorm- ous numbers, the quantity of food substances consumed by them becomes of considerable importance. Most foods of bacteria like those of animals or higher plants, must undergo modification prejiaratory to assimilation. As I)reviously stated, bacteria do not jiossess a digestive tube, neither do they have the power of enveloping particles of foo bo ■50 = = X5 C rt u O a. 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U t> l> l> h 0000 SE6E 4) a> 4> 4> ' SEE CJ a> o o o o EEEE a 4) O 4) d d d cd 4) o 5 c •a o 2 a S^^E « >. 2 W ft 41 n >■ - -^ d -o C o SEES 3 3 3 3 EEEEEEEEEEEE 333333333333 d£ « =? a <^ ._ k. a 4> ■r 3 EE 0) i| « 5 d d o o « OOtSS 000 5 S c c" O O o o *i -^ *J ^ I d d ej d <- t- u u 3 3 3 3 ft a ft ft ft ft ft ft 3 3 3 3 CC W rn CO r o E A 3^ d 0) 3 3 S t d O 5 S « o ® o > 4> 4) 4) C -l-l <- I. d a Sr^Ert B a Ova C C 4» ccmSD = - 3 e) d o o u 4> o Z; 3 4J u ' i: S d o . .^ o -r >i '-E ft- 00^ >. >. o ft ft >. if d B gSE dz; 3 S5 > U 3 _ ■ 3> §?* bo ai! d 3 "O ft^5 c ^i Ot£5t-SE2 3 d ; ■ 11 -1 I i, S g (U c o g ^ *■= ft ft ft s d ds— ftzS-i: ^•" B ^EE B 3 3 tl o o ^ ^ *" d es «! naa " B B e == = fc O Cj U O 41 000 I to c3ia a B 5 333 3 " " o 8o§o 2 ftftC iRAXCH PKOTOZOA, L'nlcollular animal organ- Isms, asexual. reproduce ay fission, sporulatlon. or suddlngr. PART INFESTED I ORD SPOfl man Liver and Intestine. Repr Lleberkuhn's glands and Intestine. no f Liver and Intestine Muscles, id pig- Muscles. Connective tissue. Intestine. Liver. IXFl Posa repH budd Blood. Blood. Blood. Blood. ANXULATA, Specialized worms com- posed of ring like Beg:c- nienls. simple head and eyes. uFUilly evcrslble dentated pharynx, straight alimentary canal, well de- veloped nervous systera HIR Pllgli sal suck, Skin. Skin. Skin. Anterior respiratory tract and intes- tine. BRANCH PROTOZOA, Unicellular animal organ- Isms, asexual, reproduce by fission, sporulatlon. or budding:. ORDER SPOROZOA, Reproduce by sporulatlon, no flaffella, no cillia. INFUSORIA, Possess cilia or flagella, reproduce by fission and budding. CLASS COCCIDIA. SARCOSPORIDIA. FLAGELLATA. HYPOTRICHA. INSERT III. FAMTLY GENUS SPECIES PSOROSPERMIDAE. SARCOSPORIDAE. CERCOMONIDAE. Coccldlum ovlforme Coccidlum cunlcull Coccidium avium Sarcocystls Miescherl Sarcocystis tenella Balblania glgantea HOST PART INFESTED Rabbits, G. pigs ani man Liver and Intestine. §^^V'*' Lieberkuhn's glands and Intestine. *o^'s. Liver and intestine Pig. Muscles Horse, ox, sheep, and pig. Muscles. Ox, sheep and dog. Connective tissue. Laroblia intestinalls Sheep and dog Monocercomonas hepatica Pigeons. Trypanosoma equiperdura. Horse. Trypanosoma Evansi. Horse. Trypanosoma equinum. Horse. TRTPANOSOMATIDAE. Trypanosoma Brucel. Horse. Intestine. Liver. Blood. Blood. Blood. Blood. ANNULATA, Specialized worms com- posed of ring like segc- nienls, simple head and eyes, usually everslble denlated pharj'nx, straight alimentary canal, well de- veloped nervous system. HIRUNDINEA, .^lightly flattened on dor- sal and vonlral surface, sucker at each end. GNATHOBDELLA. GNATHOBDEIyLIDEA, Hlrudo medicinalis Hirudo troctina. Hirudo decora Hlrudo Tagala Haemopis sangulsuga. Man and horse. Man and horse. Man and horse. Man and animals. Horse Skin. Skin. Skin. Anterior respiratory tract and intes- tine. GENERAL CONSIDIIRATIOX OF DlSEASli. 63 pounds. i)ei)ton, skatol and indol represent aromatic compounds; ptomains probably represent one of the most important putre- factive products. Ptomains are basic chemic substances ])ro- duccd by decomposition of nitrogenous compounds. They are usuall)^ formed outside the body, although they may be formed by putrefaction of the contents of the intestine. Ptomain pois- oning is usually the result of consumption of foods contaminated with ])tomains, although it may result from the absorption of ptomains formed within the intestine. Sufficient ptomains may also be absorbed from necrotic tissue to produce injurious effects. The chemic substances produced by pathogenic bacteria are probably of more importance than any other bacterial com- pounds. Although they have been extensively studied the com- position of most of these compounds is still unknown. Three groups of pathogenic bacterial products deserve mention, they are (1) bacterial toxins, (2) endotoxins and (3) bacterial pro- teids. 1. Bacterial toxins are soluble, synthetical, poisonous, chemic substances elaborated by the bacterial protoplasm and liberated into the surrounding media. The chemic composi- tion of bacterial toxins is unknowm. They are very similar in many respects to enzyms. They are specific, i. e., a given organism always produces a definite toxin. According to Ehrlich bacterial toxins are composed of two combining groups, one the haptophore which combines with the receptors of the animal cells and forms a medium through which the other group, toxophorc. acts. They are the principal product in some infec- tion, e. g., tetanus. (Infection is the invasion into a living body of pathogenic micro-parasites, and the sum total of the disturb- ance produced bv their presence in the body.) During infection the body attempts to neutralize bacterial toxins by the produc- tion of a substance termed an antitoxin. 2. Endotoxins are poisonous chemic products formed and retained within the bacterial body. They become liberated only when the bacteria are destroyed and distintegrated. Although the chemistry of endotoxins is not known, they arc probably constant in composition and produce specific symptoms in in- fected animals. The animal body does not produce antibodies that neutralize endotoxins, but opsonins are produced in the tissues of animals immunized to endotoxins. Endotoxins are the principal injurious substances produced by pyogenic cocci. P>acterium tuberculosis, the organisms causing glanders, pneu- monia, and other specific infections. 64 VETERINARY PATHOLOGY. 3. Bacterial proteids are insoluble nitrogenous constituents of the bacteria cell protoplasm. They are not well understood. (See insert No. 2.) ANIMAL PARASITES. The animal parasites, capable of producing disease in an- imals, are quite numerous and represent the following branches of the animal kingdom : — protozoa, helminthes, and arthropoda. /' V - Fig. 30. — Piroplasma Bigeminum in the red bl^od corpuscles. Protozoa. Protozoa are microscopic single celled animals. They are very simple in structure, being composed of a mass of proto- plasm with or without a cell membrane. The cell membrane, when present, consists of concentrated protoplasm The pro- tozoa having a cell membrane are constant in shape, as the Try- panosoma Evansi, and those not possessing a cell membrane vary in shape from a sphere to an irregular flat mass and are capable of changing their shape whenever occasion demands. Protozoa are larger than bacteria. Protozoa require food similar to the foods of higher animals. Particles of food may be inclosed or incorporated by them pre- paratory to digestion. Digestion is accomplished by means of ferments elaborated and secreted by the protozoa. The digested foods pass by osmosis into the protozoa, the undigested portion being extruded by rearrangement of the cell protoplasm. Res- piration takes place by exchange of gases through the surface protoplasm of the protozoa. They reproduce by fission, budding, conjugation or sporulation. Protozoa are universally distributed. They all require con- siderable moisture. In fact most of them live either in fresh or gait water. A few only are parasitic. GENERAL CONSIDERATION Of DISEASE. 65 The specific action of pathogenic protozoa in the produc- tion of disease is not understood. Some may have a mechanical effect only but the evidence concerning others indicates that most of them produce an injurious chemic substance. Helminthes. This branch of the animal kingdom contains many species that are parasitic. Structurally, animal parasites are much simpler than the closely related nonparasitic animals. The sim- plicity of parasites is a result of adaptation to environments in which essential structures of the nonparasitic type, useless to the Fig. 31. — Trypanosoma Evansi iu a bloodsmear from a horse affected with surra. parasitic type, atrophy because of disuse. The parasitic hel- minthes are of the simi)lest structure, their nervous, digestive and respiratory systems being very rudimentary. Their food is obtained from their host. Some animal para- sites, as the tapeworm (Taenia) absorb digested food stuff from the intestine of their host, others subsist upon the host's blood, (Uncinaria), and till others consume tissue juices and lymph, (Trichina spiralis). The reproduction of helminthes is accom- plished by means of ova, or by the production of living larvae. The life history or cycle of helminthes is very interesting. In some cases the organism is parasitic in different animals during the different stages of its life cycle ; for instance the Taenia cras- sicolilis inhabits the liver of the rat during its cystic stage and the intestine of the cat during the adult stage. Helminthes produce injurv to their host by consuming food, by sucking blood and by liberating injurious chemic substances, 66 VETERINARY PATHOLOGY. Arthropoda. This branch includes many parasitic representatives, as flies and mosquitoes (diptera), fleas (siphonaptera) lice (hemip- Fig. 32. — Sareocystis Miescheri. Drawing made with Camera lucida. 1. Cross section sarcocyst, muscle' cell enclosing carcocyst ruptured. 2. Cross section of heart muscle cell. 3. Fibrous connective tissue. tera), itch mites and ticks (acarina). The entire order, siphon- aptera and hemiptera. most of the order acarina, and many rep- resentatives of the order diptera are parasitic. Of the parasitic arthropoda some are temporary and some are permanent para- KAKCH CLASS «ep PARX rSFBSTKD Intestine Intestine Intestine Intestine Intestine Intestine Duodenum and gall du«4 and fox fain of sheep.) h'f land omnivora > ■PLATTHBILMINTHEJ, , j^g , Flat worma, nearlj* „ _„ ^ hermaphodltea. jTraticepa. ; Small Intestine Small Intestine Small intestln* Small Inlestin» Intestine and omnivora Gall ducts goat, pig, ass. Gall ducts ?'~ « ox I.iver Kumen pig and cat Lungs It. camel, deer lat and deer Small Intestine Small Intestine Intestine Intestine Intestine Intestine Intestine Posterior bowel Posterior bowel Bronchi and lungs Bronchi and lungs Bronchi Bronchi and lungs Bronchi Bronchi Abomasum , , „ Abomasum and duodonuni Small Intestine and abomasum NEMATHELMTNTHBat Round worms, mj goat ^iT'?" '''"■on'i"^rrn'ar\' organs mented, sexes separd dog and man Kidneys and crinarj organs I Heart dog and man d goat I chickens fox d goat p and goat deer p*and goat and cat IntL-stlne Large Intestine Large intestine Tr3.chG£L Region of kidney and liver Small Intestine Small intestine Small Intestine Caecum Large Intestine Caecum Muscles Peritoneal and plural cavltWs R^ght"heart and pulmonary arter- ies Right stomach Stomach , , , ,,_, Flexor tendons asd cervical liga- ments ©•esophageal vail . Tumors of stomach, gullet ana aorta Jastric mucosa pU2f CH CLASS OKDEB s« 8 a a f e e it ''it 5 eo = ^ijtx * at >»•» a a h 41 - 3 « TLATTHEXMINTHES. Flat worma, nearly all hermaphodltes. CESTODA, Ribbon Bhaped, segment- have no fixation apparatus have no digestion apparatus on head. Adult lives In In- testines. TKEMATODA, Fiat worms, nonsegment- ed, have digestive canal, no anus, have one or two suckers on ventral surface. FAMELY TAENIIDAE, Head always has four suckers between which Is found a depression or a proboscis. Segments usu- ally have their gentlal op- enings on margin. GENUS SPECEES HOST BOTHRIOCEPHALIDAE, Found mostly In fishes. DISTOMIDAE, All have two suckers, an anterior and ventral. NEMATHELMINTHES. Round worms, nonseg- mented, sexes separate. ECHINORTNCHIDAE, ACANTHOCEPH A LA. Slender worms, coinplete po^'ef'^in'digeVtTv'^" canal digestive canal, are found ^f vertebrates in all tissues of domestic °^ vertebrates. animals except bone. ASCARIDAE Large firm body, resemble earth worms, nriouth Is surrounded by three lips. Usually found in small In- testine. NEMATODA, Slender worms, complete digestive canal, are found in all tissues of domestic animals except bone. OXTURIDAE, Cylindrold body, pointed, mouth stomach lai'ge. tall nude. STRONGYLIDAE, Body cylindroid, mouth either nude, armed or papillated, oseophagus large. Taenia aaginatta Man (Cyst; Cysticercus cellulosae, of pig.) Taenia solium Jj^q (Cyst; Cysticercus bovis, of ox.) Taenia perfoliata Taenia mamlliana Taenia pUcata Taenia denticulata Taenia expansa Taenia fimbriata Horse Horse Horse Ox Ox and sheep Shewp PART rNTESTBD Intestine Intestine Tntestine Intestine Intestine Intestine Duodenum and gnll du«4 Small intestine Taenia marglnata D^g (Cyst: Cysticercus tenuicolUs of ruminants) Taenia coeaurus nno- nrnic o«/i »-_ r, , . (Cyst: Coenurus cerebralls In spinal c?.d 'and' b.am of'"'sheop ) ^'"^" '"^^"""^ Taenia echlnococcus Dos and wolf small intestine (Cyst; Echmocoocus polymorphous, of herblvora and omnivora ) Taenia cucumerina Dog (Cyst; (1) Cryptocystis irichodectls of Trlchodectes latus.) ^ (Cyst; (2) Cryptocystis pulecldes of Pulex s«Tratlceps. ) Taenia ovis Dog o.„^n t.,i»^h„o, (Cyst, cysticercua ovis sheep.) ^'"'^" Intestine. Bothrbcephalus latus Man. dog, cat Intestine TRICHOTRACHELIDAE, Body slender in anterior portion, enlarged poster- iorly for containing intes- tine, mouth nude, anus terminal, all live In Intes- tine. FILARIDAE, Long thread like body, mouth or triangular .oeso- phagus small- GNATHOSTOMIDAE. Head distinct, oviparous. Distonia hepaticum Dlston'.a lanceolatum Dlstonr.a Amerlcanum Amphistoma cervi Paragonimus Westermanil Echinorhynclius gi.?.TS Ascarls mesralocephalus Ascaris bovis Ascaris ovis ^.•'lus fliaria Strongylus rufescens Strongylus paradoxus Strongylus Osteragl Strongj'lus contortus Strongylus filicollis Strongj'lus gigas Strongylus vasorum Sclorastoma equinum Sclerastoma tetracanthum Sclerastoma hypostomum Syngamus trachealis •Stephanurus dentatui TTncinaria trigonooephala Unclnaria cerniia "Unclnarla radiatus Trlchocephalus affinis Trlchocephalus crenatus Trlchocephalus deprcssiusculus Trichina spiralis Filaria papillosa Fllarla cervina Fliaria immltls Sniroptcra megastoma Sjjiroptera microstoma Spiroptera reticulata Splroptera scutata Spiroptera sanguinolenta Gnathostoraum chelracanthus Herblvora and omnivora Gall ducts Sheep, ox, goat, pig, ass, Gall ducts dog Sheep and ox f.iver Ruminants Kumen Man. dog, pig and cat I.iings PiB Sollpeds Ox Sheep Pig Dog Cat Horse Horse SoUpeds Bovlnes Sheep, go.it. camel, deer SheeT<, goat and deer Pig Ox Sheep, goat .Sheep and goat Horse, ox, dog and man Dog Horse, oy, dog and man Sollpeds Shrep and goat Birds and chickens Pig Dog and fox Sheep and goat Bovlnes Ox. sheep and goat Pig Dog Pig Horse Ox and deer Dng Horse Horse Horse Ox. sheep and goat Dog Pig, dog and cat Small Intestine Small Intestine Intestine Intestine Intestine Intestine Intestine Posterior bowel Posterior bowel Bronchi and lungs Bronchi and lungs Bronchi Bronchi and lungs Bronchi Bronchi Abomasum Abomasum and duodenum Small Intestine and abomasum Kidneys and orlnary organs Heart Int'-stlne Large Intestine Large Intestine Tr3.chc& Rt'glon of kidney and liver Small Intestine i'mall Intestine Small Intestine Caecum Large Intestine Caecum Muscles Peritoneal and plural cavltlfS Rlght°"he"a'?t and pulmonary arter- RiKht stomach Fle^To^r^ undon. asd cervical llga- monts ^ZlTlf sTomach, gullet and aorta Sastrlc mucosa GliNliKAL CONSIDKKATION OF UlSKASi:. 67 sites, and with one or two exceptions they are all external para- sites. The structural peculiarities that differentiate arthropoda from the other branches of the animal kingdom are their jointed ap- pendages, segmented body, and bilateral symmetry. The parasitic arthropoda obtain their food from their hosts. Some of them consume epidermal scales and hair, e. g., the horse louse (Trichodectes pilosus) and feathers, e. g., the M^ ^ 1^^ .j(^::;■^ Fig:. 33. — Taenia Echinorocoiis. Nilps & Neunian. a. Adult tapeworm. After Ncuman. b. Part of hog's liver showing cystic form. chicken louse (Menopon pallidum) others abstract blood, e. g.. the hog louse (Hematopinus suis), itch mite (Sarcoptes scabei variety canis), and still others may consume tissue cells other than blood cells as epithelium. Reproduction of arthropoda is about the same as it is in helminthes. Disease resulting from infestation of arthropoda is due primarily to irritation induced mechanically or by chemic pro- ducts of the parasites, secondarily to loss of blood. Extension of Disease. — Bv extension of disease is meant the invasion and affection of adjacent structures and even remote 68 VETERINARY PATHOLOGY. tissues of the body. Some diseases are necessarily local, i. e., the cause is not capable of being transferred to adjacent or re- mote structures, e. g., ocular filariosis. Other diseases are in their earlier stages local, but later the cause may be transferred to some other part and produce secondary diseased foci or Fig. 34. — Oxyuris Curvula, after Niles. a. Adult worm. b. Cephalic extremity. c. Caudal area. metastases, e. g., tuberculosis. The extension of disease may be produced as follows : First, by the cause of the disease passing along the natural channels and establishing secondary diseased foci, thus, Bray reports that calves become affected with necrotic gastritis and enteritis when allowed to swallow the necrotic tissue during an attack of necrotic stomatitis. Second, by the spread of the cause into adjacent tissues, e. g. : Extension in like tissue, as in muscular tissue, is termed contin- GENERAL CONSIDERATION OF DISEASE. 69 uity and is exemplified in psorospermosis, while extension from one tissue to another of a diiYerent type, as from muscular to connective tissues, is called contiguity and is evidenced in acti- nomycosis. Third, by the lymph and lym])hatic nodes, e. g. tuberculosis. Fourth, by the blood stream in which case the mestastases will be in the lungs, liver, or kidney, — e. g., anthrax. The incorporation of microbian agencies by leucocytes is frequently the means by which infection is extended, in fact it is probable that the leucocytes are the principal factor in lymph and blood extension of infective processes in the l)ody. Fifth, by passing along the nerve fibres as in rabies. Termination of Disease. — Termination is the ending or outcome of the condition or existing disease. Disease terminates as follows : Recovery. — Disease terminates in re- covery when the body tissues are efifectually repaired and all structures have assumed their normal function. Diseases resulting from irritating or non-nutritious foods are corrected by expulsion or neutraliza- tion of the causative agent either by vomition, purgation or chemical union and by repair of the injured tissues, after which normal functioning continues. Tissue attlicted with mechanical injuries as wounds, recover when the destroyed portions have been replaced and the normal function has been resumed. Dis- locations terminate in recovery when the dislocations have been reduced and the parts assume their normal function. A horse recovers from pneumonia when the inflammatory exudate has been removed from the alveolar spaces and all injured tissues have been repaired and the normal functioning has been re-established. In general, recovery is the result of the comple- tion of the protective and reparative processes of the various tissues of the animal body. Partial recovery. — If the normal functioning is not assumed after a disease has run its course, recovery is said to be incom- plete or partial. Partial recovery is observed in old animals or in those that have been depleted because of complications or previous disease. Some diseases are essentially destructive and their influence in the tissue results in incomplete repair, as in Fis. .'55. — Trirlioceplialus Depress! iiM-ii Ills of a Dog, alti-r Kailliot. 70 VETERINARY PATHOLOGY, tuberculosis, glanders, dourine, bovine contagious pleuro-pneu- monia, etc. Injuries and acute inflammation of the parieties of Fig. 36. — Melopbagus Ovinus, after Niles. a. Dorsal view of adult. d. Terminal segmant of leg. b. Ventral view of adult. e. Shell of pupa. c. Mouth parts enlarged. f. Pupa. hollow^ organs frequently terminate in the formation of cicatrical tissue thus contracting the lumen of these organs. This is com- mon in injuries of the oesophagus, intestine, trachea, and ure- thra. Adhesions succeeding pericarditis, pleuritis, and periton- itis are examples of partial recovery. BRANCH CLASS lljr parasitic U en z PART INFESTED Wounds Wounds Skin Skin Wounds INSECT A (HEXA] Air breathers, wh< have three pairs and distinct head, and abdomen. Dgs sheep and dog intmals ARACIINIDA Air breathers with 1 othorax and al have when adult pairs of legs. Tha included are ovlpar^ Skin Skin Skin Skin Skin around perinaeum M M of stomach m' M. of stomach and lntestln» Dorsal cutis and sulicutls Sinuses of head Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin SktM Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin SklQ Nasal cavities BRANCH CLASS ORDER INSECTA (HEXAPODA) , Air breathers, when adult have three pairs of legs, and distinct head, thorax and abdomen. ARACHNIDA All- breathers with caphai- Mvo" ^and abdomen. included I'rf'ovlJa^roua.'^''" DIPTERA Have two wings, two hal- teres, sucking mouth parts, and complete metamor- phosis, includes flies and mosquitoes. HEMIPTERA Wings often absent, when present one pair thick and one pair thin. , Suc;king mouth parts, incomplete metamorphosis, and include the blood sucking lice. MALLOPHAGA Winglea llco with sucking mouth parts, and incom- plete metamorphosis. SIPHONAPTERA Wingless fleas with suck- ing mouth parts, and com- plete metamorphosis. ACARINA Usually short thick, non- articulated bodies, possess oamerostoma. larva usual- ly hexapodal, sexes (sepa- rate. FAMILY MUSCIDAE Have soft probosls adapt- ed for suction, styJ.et of an- tennae plumose to the end. TABANIDAE Broad and slightly flat- tened body, large head, muscular wings, larva car nivarous, are oviparous. I STOMOXIDAE Closely resembles the mus- cidae, SIMULIIDAE Thick body, bulging tho- rax, legs strong. HIPPOBOSCIDAE Flat body, head notched into thorax, legs strong, pupiparous. OESTRIADAE Body usually hairy, large wingb, proboscis very small, oviparous. CULICIDAE Have /ong slendor abdo- men, wings fringed with hairs, antennae plumose in males, oviparous. PEDICULIDAE Blood suckers, proboscis formed of upper and lower lips and armed with small spines, contains protrusile tube or sucker, oviparous RISCINIDAE Not blood suckers, have long masticatory apparatus with o«r Fowls Ox Ox Ox Sporting dogs Horse, ox, aheep and dog Sporting dogs Fowls Fowls Animals Man and animals Horse Sheep Pig Dog Fowls Horse Ox Sheep Horse Ox Sheep Dog Cat Horse Ox Dog Swine Dog PART INFESTED Wounds Wounds Skin Skin Wounds Skin Skin Skin Skin Skin Skin around perlnaeum M M. of stomach M. M. of stomach and intcstlnft Dorsal cutis and subcutis Sinuses of head Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skbi Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Skin Nasal cavities GKNKRAL CONSmKRATIOX OF DISEASE. Fisr. 37.— GastropliiliiH K(|ui, after NiUs. Adult fumale. Adult female. Youn»? larvae. Full grown larvae. Eggs cimcntod to hair. Egg shell showing lifting of operculum. Adult male. Terminal s>gments of male. Terminal se>;mints of female. Fig. ."is. — Oestnit* Ovin. a. Adult female. c. Dorsal view of larva. b. Adult male, after Uily. d. Ventral view of larva, after Rlly and Mlea. VETERINARY PATHOLOGY. Fig 39. — Culex Pungens, after Howard. a. Female. b. Male. c. Larva. GENERAL CONSIDERATION OF DISEASE 73 Death. — Disease mav terminate in the cessation of all func- tions, i. e. death. The more important specific modes of death are as follows: FiK. 4 0. — Distonia llepaticuni. a. Intestines, b. Oral sucker. c. Ventral sucker. d. Uterus. 1. Syncope, or heart failure, a result of paralysis of cardiac nerves or muscles, rupture of heart walls or complete obstruc- ^m Pig. 41. — EcliinorhynohiiH OiRaH, after Nlles. a. Cephalic extremity showing hooks. b. Worm with portion of mucous membrane of inti-stinc attached. tion to emerging vessels of the heart. Nerve paralysis may be the result of poisonous products derived from infectious agen- cies, or chemic poisons derived from katabolism, or hemorrhagic extravasates. 74 VETERINARY PATHOLOGY. 2. Apnoea, or respiratory failure. This may be the result of paralysis of respiratory nerves or muscles, spasms of respiratory muscles, rupture of diaphragm, or occlusion of the respiratory tubes. 3. Apoplexy, or hemorrhage into the brain tissue. This is probably the specific cause of death in apoplectiform anthrax. 4. Hemorrhage, especially rapid loss of large quantities of blood. Any of the above may act independently in producing death, but are probably more frequently complicated one with another. CHAPTER III. IMMUNITY. DEFINITION. IMPORTANCE. lARIETlES. Inherited, (Natural). Definition. Examples. Cause. Ceil Action, {Metchnikoff & Sternberg). Cheniic Substance, (lihrlich & Buclincr). ACQUIRED, (Artificial). Definition. Examples. Varieties. Active. Definition. J'arieties, (Toxic), (Opsonic), (Bacterial) Etiology. Recovery from attack of disease. Inoculation xcitli virus. Inoculation zcitli Z'accine. Inoculation Tcith bacterin. Inoculation with toxin. Inoculation simultaneously Zi'ith 7'irus and antibody. Passive. Definition. Etiology. Inoculation zcith antibody. THEORIES. Exhaustion. Retention. Phagocytosis. Humoral. Ehrlich's Lateral Chain Theory. Immiinitv literally means proof against disease, i. e., it is the name of the condition that enables an animal to resist the action of pathogenic micro-organisms, or to be unaffected by their products. Immunity is only a relative term, the condition is not absolute and permanent neither is it constant and con- tinuous. Whenever an animal is unable to adjust itself to its environments it becomes susceptible to the efYects of the causa- tive agents of diseases, i. c., its immunity, at least acquired immunity, is suspended. The term immu'iitv is ordinarily used in reference to infec- tive diseases, i. e. those diseases resulting from the invasion of microparasites ; although it may be used in designating the resistance to the action of zootoxin, such as snake venom, and possibly also of the poisonous ';ul)stances ejected by centipedes 76 VETERINARY PATHOLOGY. and scorpions, as well as the phylotoxins, such as ricin, abrin, crotin, and robin. Immunity, more than any other problem, directly concerns the medical profession and indirectly the international commer- Fig. 42. — Heniatopinus phalanges ovis, after Niles. a. Adult. b. Egg cemented to hair. cial welfare. It was a laboratory fad of the pathologists until they demonstrated to the practitioners that it was feasible to produce immimity in man and animals. Veterinarians have now Fig. 43. — Pulex Serraticeps, after Tusjijor. iMMi;Nrr\ 17 almost universally accepted :hc proposition and liave at their command the means by which they can immunize animals against the ravages of some of the fatal infective diseases to which thev are susceptible. The increased confidencv-^ of the people is in turn enabling scientists to investigate new phases of the subject. Altlunigh immunization has been known and made use of mure or less for centuries as vaccination against Fig. 44. — Marsarapus .Xnimlatiis, fiinale. Fig. 45. — MargarapuH Annulatus, male. Fig. 46. — >larRarapu8 AnnulatuK, female laying ck(,'3. Fie. 47.— Margarapus Annulatiis, Larva. smallpox by the Chinese before the Christian era. yet the essen- tial ph3'siologic, chemic or pathologic basis for immunity is still nnknown. Immunitv may be natural (inherited) or artificial (acquired). Natural immunity is an inheiited property possessed by or- ganisms (animals). The horse has a natural immunity to hog cholera, the ox to glanders and the hog to tick fever. The concise and exact cause of natural immunity is unknown. It is probably the result of cellular activity in the immune animal, an activity the nature of wliich is not understood. Some inves- tigators, Mctchnikoff in particular, attribute natural immunity to phagocytosis (cellular hypothesis), others maintain that insus- /8 VETERINARY PATHOLOGY. ceptibility to disease is a result of the antagonistic action of the body fluids (humoral hypothesis). Ehrlich's lateral chain the- ory assumes that the cells of immune animals are not capable of combining with the toxins of bacteria, i. e., they have no receptor molecules and hence those animals are not receptive, they are immune. Whether we accept the cellular hypothesis, the humoral hypothesis, or Ehrlich's lateral chain theory, the fact remains that natural mimunity is a characteristic or prop- erty of parental origin that is transmitted to the offspring and is present at the time of birth. Natural immunity may be the result of an acquired toler- ance due to natural selection and heredity. There is a marked variation in susceptibility and resistance in individuals of a given species. A continuous or repeated exposure of susceptible ani- mals to a given pathogenic microparasite will result either in destruction of those animals or the production of an immunity, i. e., those individuals most resistant will survive and their resistance will become more and more fixed and will finally be transmitted to the ofifsprmg and hence be a natural immunity. Thus all native Cubans are practically immune to yellow fever because at the time yellow fever was first introduced into Cuba ihe least resistant individuals died of the malady, the most resistant individuals survived and lived in the presence of the diseases almost continually after yellow fever was introduced into Cuba (It was not eliminated until after the Spanish-Amer- ican war). Consequently the Cubans for several generations developed in the midst of yellow fever and only the resistant individuals survived. This resistance finally became so firm that it was transmitted to their offspring and was then a nat- ural immunity. The resistance possessed by dogs to most diseases is ex- plained in a similar way to the Cubans' resistance to yellow fever. Thus the dog has descended from the jackal and the wolf, two types of animals that have lived largely upon the carcasses of animals dead of various diseases. As the animals fed on carcasses they fought, thus inoculating each other, so in the beginning the least resistant individuals died, the more resis- tant animals survived. Thus the constant fighting and inocu- lating has established in them a firm resistance that is trans- mitted to their progeny as a natural immunity. This immunity lias become so fixed that it does not vary even in the domestic dog. The above is a plausible explanation of race or species immunity. The exact origin of individual immunity is considered immi;nitv. 79 by some to be an aociuircd tolerance, i. e., an ac(|uire(l immunity, and ])y others, as simply an individual resistance not developed by liavinc^ the disease to which the q;iven individual is immune. Acquired immunity is an artficially produced condition bv virtue of which the animal is capable of resistinrj disease, and Fig. 48. — The scab mite of sheep. INoro|ite>. <'iiniimiiiis Ovis, magnified 150 diameter^*. is produced in an animal either in utero or after birth, and may be active (toxic, opsonic or bacterial), or passive (antitoxic). Active acquired immunity is. no doubt, the result of cellular action and may be produced as follows: — 1. By an animal becoming infected and recovering from an attack of the disease, e. g. blackleg. 2. By inoculation of a susceiHible animal with a small quantity of the virulent causati\e microparasites. thus ])ro(luc- ing the disease in a mild form. This is ])ractice(l in immunizing cattle against tick fever. 3. By inoculating a susce])til)le animal with an attenuated virus, (vaccine.) Horses, mules, cattle, and sheep are immun- ized to anthrax by a vaccine. 4. By inoculation of susceptible animals with a bacterin 80 VETERINARY PATHOLOGY. (dead bacteria) colts are immunized to strangles by the use of a strepto bacterin. 5. By repeated inoculations of a susceptible animal with small quantities of a toxin of a specific pathogenic microparasite, tetanus toxin or other active poison as snake venom. This method is used only in the production of antitoxins or in immun- izing animals against zootoxins and phytotoxins. Fig. 49. — Demodex Folliculoruni, variety Canis. Field showing various stages of development. a. Ova. b. Pupa. c. Adult. d. A piece of Scab. Fig. 50. — Demodex Folliculoruni, variety Canis. Adult Male, magnified 400 time.--: showing wide head, with res trum. short legs (3 articles each) 2 claws and elongated body. G. By simultaneous inoculation with a virus and an antitoxin (antibodies, bactericidal substances, etc.). In the Philippine Islands this method is employed in immunizing cattle against rinderpest, and it is also being successfully used in the immun- ization of hogs, against cholera. Toxic immunity is the resistance to poisonous substances as toxins of bacterial origin, zootoxins and phytotoxins. It is common to hear sheep herders speak of dogs that are immune to the venom of rattlesnakes. The dogs are bitten frequently while doing duty on the range and although the reaction from the first inoculation is intense and may even kill, each succeed- ing inoculation produces less reaction until finally the dogs may IMMUiMTV. 81 be bitten or the venom inoculated with impunity. Immunity to intoxication diseases such as tetanus are of this type. The ab- sence of action of various therapeutic agents that have been given repeatedly may be explained on the principles similar to those involved in the production of immunity in dogs to snake venom. Toxic immunity is the result of the presence in the body fluids of an antibody (Antitoxin.) Opsonic immunity is the resistance of an infected animal due to a substance, opsonin that facilitates the destruction of bacteria by leucocytes. This is the type of immunity manifested in the human that is immune to typhoid, and the various animals that are immune to sui)purative processes caused by the pyogenic micrococci. Bacterial immunity is the resistance an infected animal mani- fests to the bacterial invader. It is the result of bacteriolytic substances in the body fluids. PfeilTer demonstrated that bacteria are destroyed when introduced into an immune animal. He introduced the spirilla of Asiatic cholera into the peritonea! cavity of guinea pigs and noted that the bacteria were soon rendered immobile, became swollen and granular and were finally disintegrated. This phenomena has been designated Pfeififer's leaction. Passive acquired immunity consists essentially of the presence in the tissues or body fluids of substances inimical to micro- parasitic activity, or substances capable of union with micro- parasitic products, (toxins) thus rendering them inert. This type of immunity is of short duration. It is usually produced by the inoculation of susceptible animals with antitoxin. In- jured animals inoculated with tetanus antitoxin at the time of injury are thus immunized to tetanus for a brief period. Acquired immunity, like natural immunity, is variable and inconstant. The production of active acquired immunity entails more risk than the production of passive acquired immunity. The causative agents or their toxic products are used in obtain- ing an active immunity and thus disease may be produced and the animal life sacrificed wdiile the anti-toxin is used in the production of a passive immunity, without danger of the pro- duction of disease although transient disturbances may result from hemolysins, contained in the blood in which there is anti- toxin. Theories of acquired immunity. — ^lany theories have been advanced in explanation of acquired immunity. The chief of which are as follow-s: — 8i VETERINARY PATHOLOGY. 1. The Exhaustion Theory. — This theory was championed by Pasteur, who proposed it about 1880. It is based upon the supposition that there are certain substances in the animal body that are food for micro-parasites and that these svibstances are not regenerated. Hence when they have been consumed the micro-parasites cease to develop and the animal becomes im- mune. This theory is not tenable because immunity can be ])roduced by bacterial products and by dead bacteria neither of which consume substances from the tissues of an animal immun- ized. 2. The Retention Theory. — In the study of bacteriology it has been found that bacteria, like most other organisms, can not develop in the presence of a large quantity of their own excrements. This theory presupposes that bacterial products remain in a body after it has been infected and that these products prevent the future development of like bacteria. This theory does not explain the production of an immunity with toxines and is not supported by any scientists at the present time. The theory was proposed by Chauveau. 3. The Phagocytosis Theory. — This theory was proposed independently by Sternberg and Metchnikoff about 1881. The theory w^as the outgrowth of the experimental study of the action of leucocytes upon bacteria and yeast, in which it was found that certain leucocytes are active in the destruction of various bacteria, yeast and tissue debris. These investigators designated those leucocytes active in the destruction of bacteria, phagocytes. Phagocytosis is a state or condition characterized by the development of phagocytes and the display of their special function. The supporters of this theory hold that the cells, which are active in the production of leucocytes transmit the property of phagocytosis to their progeny and thus immunity is perpetuated after it has been acquired. That phagocytes do incorporate bacteria and other foreign substances is not denied but it has not been demonstrated whether phaogocytosis is the cause or the result of immunity. This theory does not explain immunity from such diseases as tick fever. The microzoon of tick fever inhabits and usually destroys the red corpuscles. The leucocytes are probably not affected by them. In fact, the presence of the Piroplasma bigem- inum in leucocytes has not been noted. More recently Wright and Douglas have demonstrated that certain substances in the blood serum are necessary to prepare bacteria for phagocytic action. These substances have been designated opsonins. Opsonins are chemic substances in blood serum that render IMMUNITY. yj bacteria subject to the action of phagocytes. Opsonins resem- ble the amboceptors of EhrUch in action, but they are not iden- tical with them. The action of opsonins is evidenced in pneu- monia, pyogenic infections, tuberculosis and probably in other diseased conditions. The opsonic index indicates the relative power of resistance due to phagocytic action in an animal body. 1. Humoral Theory. — After the phagocytic theory had been found insufficient, immunity was explained from a chemic view point. The supporters of this theory, among v. honi Buchner was acti\'e. demonstrated the bactericidal action of blood serum and lymph obtained from immune animals. Their demonstra- tions established the fact that immunity is due to a chemic substance, possibly an enzyme. But the origin and specific ac- tion of the chemicals in the production of immunity was not determined. The bacteriolytic substance of the body fluid called complement, was found to be destroyed by a temperature of ;).-> C 5. FJirlich's Lateral Chain Theory. — Ehrlich maintains that every living cell contains an active central body which produces unknown chemical substances that combine with and extend nutriment to the cell. These chemical substances, marginal chemic groups or lateral chains as they are variously called, for convenience of description are designated — receptors. These re- ceptors are specific in their nature ; i. e.. there are certain groups of receptors that combine with certain kinds of nutritive sub- stances. TJkcwise there are present normally in the body cells certain groups of receptors which combine with disease produc- ing substances, e. g., toxins, which in turn destroy the body cells. Tt is thought that receptors for certain diseases are absent in certain species of animals and that because of this, there exists a natural immunity : e. g., the dog is immune to hog cholera be- cause his body cells do not have the specific receptors for that disease. If. on the other hand, the receptors that are normally present be increased in amount, an acquired immunity develops. Whenever there is an increase of the receptors in the body they become freed from the cells and are found in solution in the body fluids as antibodies. Experimentation has shown that antibodies are produced by the tissues as a result of the injection of a great variety of substances. These substances are known as antigens. Therefore, an antigen is any substance that when introduced into the bodv will stimulate the tissues to the production of antibodies. An antibody may he defined as anv substance present in the body that has the property of antagonizing, neutralizing, precipi- tating, agglutinating or dissolving the substance (antigen"^ which 84 VETERINARY PATHOLOGY. has induced the production of such antibody. For example, the toxin of the tetanus bacillus when injected in minute, non-lethal doses, stimulates the production of antitoxin by the tissues ; the toxin is the antigen, the antitoxin is the antibody. Likewise, blood serum when injected into a different species of animal would be an antigen and the precipitating substance produced by the tissues as a result, is the antibody. The following are some of the known antigens with their antibodies. This list is by no means complete but serves our purpose for the student of general pathology. Antigens. Antibodies, Toxins Antitoxins Agglutinogens Agglutinins Precipitogens Precipitins Lysogens Lysins or Cytolysins. For convenience of study and because of difference in consti- tution Ehrlich has divided receptors into three separate varieties known as receptors of the First, Second, and Third orders. Ehrlich's receptors of the first order, — (antitoxins). Toxins. — Toxins are antigens that when introduced into the body will stimulate the cells to the production of antitoxins. Excepting the fact that they give some of the protein reactions the chemical nature of toxins is not understood, but they can be demonstrated by certain biological tests. A number of plants and animals are known to produce toxins among which the following bacteria are important : Bacillus diphtheriae, the cause of diphtheria. Bacillus tetani, the cause of tetanus or lockjaw. Bacillus botulinus, the cause of certain cases of botulism or meat-poisoning. Bacillus pyocyaneus, the cause of blue pus. Ricin is a toxin found in the castor-oil bean, abrin comes from the jequirity bean and robin from the bark of the locust. Toxins have also been demonstrated in the venom of snakes, scorpions and spiders. A toxin is composed of two parts — a thermostabile (heat re- sistant) part, known as the haptophore or combining group, and a thermolabile (destroyed by heat at 56°C. for half an hour) group, designated as the toxophore. By careful heating at a lower temperature the toxophore only can be destroyed ; in such a case the remaining haptophore group is known as a toxoid. A toxoid has the property of stimulating the body cells to the pro- duction of antitoxin but cannot exercise a toxic effect. IMMUNITY. yO .Intitoxins. — If a large quantity of toxin, e. g. tetanus toxin, be injected into the bod}' of a horse it will combine through the medium of its haptophorous group with all the available recep- tors (these being limited in amount in normal susceptible ani- mals) and cause death of the organism by destruction of its cells. If on the other hand only a small quantity of toxin be introduced, there will be injury instead of destruction of cells which together with their neighbors will be stimulated to the production of new receptors. Subsequent injections of increasing amounts of toxin further stimulate the production of receptors, which become freed from the cells as antitoxin in the tissues. These free re- ceptors or antitoxin, as they are now known, combine with the toxin which they neutralize and immunity is the result. Anti- toxins as a rule are more stable than toxins but they can be de- stroyed by heat at 60°C. if sufliciently prolonged. Unlike toxins they are composed of only one group known as the haptophore or combining group. I{hrlich's receptors of the second order. (Agglutinins and Precipitins.) It has been found that the blood of an animal immunized to certain diseases, e. g. glanders, when added to a culture of the specific organism causes the bacteria to clump together. This phenomenon is known as agglutination and the substance respon- sible for the process is called agglutinin. Likewise it has been discovered that protein substances used as antigens cause the production in the body of substances, known as precipitins which, when mixed with the protein in solution, will form a pre- cipitate. Unlike antitoxins, agglutinins and precipitins are di- vided into two portions — a combining or haptophore group, and an active agglutinating or precipitating — zymophore group. The zymophore group is unstable, and may be destroyed by heating to a temperature of 60° to 75° C. When an agglutinin has thus lost its zymophore group the remaining haptophore is known as an agglutinoid. Likewise, a precipitoid is the combining group of a precipitin after its zymophore has been destroyed. Antigens which cause the production of agglutinins are known as agglutinogens. l\Tost foreign cells, as red blood cor- puscles, other body cells, protozoa and bacteria act as agglutino- gens when injected into the body. The following pathogenic bacteria cause agglutinin production: Bacillus typhosis. Bacil- lus mallei. Bacillus pestis. Spirillum Cholera, Bacillus tubercu- losis, and others. Advantage is taken of this fact and the ag- glutination test is used as a method of diagnosis in diseases pro- duced by some of these organisms. 86 VETERINARY PATHOLOGY. Antigens which stimulate the production of precipitins are known as precipitogens. Precipitogens are colloid substances in solution and are represented by such materials as, blood serum, milk, meat juices, egg white, etc. Agglutinogens are composed of a haptophore group only. Ehrlich's receptors of the third order. (Lysins or Cytoly- sins.) Lysins are antibodies which have the power of dissolving or disintegrating their respective antigens. Lysins may be sub- divided with reference to their antigens, into bacteriolysins, hemolysins, etc. Antigens which cause the production of lysins are known as lysogens and are represented by a variety of bac- teria, foreign cells as red blood corpuscels, etc. Lysogens are composed of a haptophore group only. Receptors of the third order or lysins are composed of two elements. A thermostabile substance which has two combining or haptophore groups and hence known as an ambocepter, and a thermolabile substance known as the complement or alexin. The amboceptor is specific ; i. e., it will combine only with that variety of lysogen which has caused its production. It is a com- bining element only and its presence is necessary for the lytic action of the complement. The two haptophore groups of the ambocepter are of different action ; one is known as the cytophile and combines only with the lysogen ; the other is called the com- plementophile and unites with the complement. Complement is found in varying quantities in all normal blood. It is non- specific — i. e., it is capable of combining with any variety of ambocepter and through this combination cause lysis. The complement has been found to consist of two groups — the hapto- phore, which combines with the amboceptor, and the zymophore or lytic group. Careful heating destroys the zymophore and the remaining haptophore is known as complementoid. Plate 1 represents graphically the production of the various orders of receptors and a careful study of the figures will enable the reader to grasp the subject more readily. Toxic immunity is explained by Khrlich as follows: Toxins are composed of two essential chemic groups which are desig- nated haptophores and toxophores. The haptophore of the toxin has an affinity for the cell receptors. The union of the toxin haptophore and the cell receptor forms a medium through which the toxin toxophore passes to the central part of the cell where it exerts its action. The toxin haptophores are not injurious except as they enable the destructive toxin toxophore to reach the central cell mass. Grapliif Representation of the Various Forms of Ininiiinit.v According to Ehrlich'8 Lateral Chain Theorj-. 'Fig. 1. — A — The bacterial cell or other substance which produces antigen, a, in the form of soluble toxin, al. B — The body cell which produces side chains or receptors cf the lirst order, t, in the form of antitoxin, zl. a2 — toxin uniting with receptor, z, injuring the body cell and stimulating it to the production of more receptors. zl — free antitoxin which at z2 is seen to be combining with and neutralizing the toxin a3. b — toxophore group and c haptophore group of toxin inolecule. c2 — toxoid after careful heating of toxin and destruction of toxophore bl. c3 — toxoid combining with receptor; such a combination does not produce a toxic effect. Fig. 2. — A — Bacterial cell, foreign serum or whatnot which contains the antigen a, in the form of agglutinogen or precipitogen al. B — Body cell which produces receptors z, in the form of agglutinin or pre- cipitin zl. a2 — agglutinogen or precipitogen combining with the receptor z, and stimu- lating the body cell to the production of more receptors. zl — freed receptor in the form of agglutinin or precipitin which is seen to combine at z2 with the antigen. This union results in agglutination or precipita- tion. X — haptophore group and .v zymophore group of the antibody; careful heating will destroy the zymophore group and the remaining haptophore group, xl, is known as the agglutinoid or precipitoid. x2 — agglutinoid or precipitoid combining with the antigen. Agglutination or precipitation does not result from such union. Fig. 3. — A — Bacterial cell, red blood corpuscle or other body cell which con- tains antiger» a, in the form of lysogen al. B — Body cell which produces receptors z in the form of amboceptors zl and complement y, which together are known as lysin. a2 — lysogen combining with the ambocepter and stimulating the body cell to the production of more ambocepters. y — complement, which is found in all normal serum. zl — freed amboceptor which is composed of two haptophore groups known as the cytoiphile xl, and the complementophile x2. C — shows a combination of lysogen, amboceptor and complement; this union results in lysis of the cell A. D — shows a combination of the lysogen and amboceptor only; the cell A is not destroyed by such union. The complement is composed of a zymophore group vl and a haptophore v2. Careful heating destroys the zymophore and the remaining haptophore is known as a complementoid v4. I.M MlMT'i'. 87 Fig.3 Brawlnff ^, HC.Lure. 88 VETERINARY PATHOLOGY. Toxin toxophores in the absence of toxin haptophores are inac- tive. The result of the union with, or action of, the toxin toxo- phore upon a cell may produce immediate destruction of the cell or it may stimulate the cell to produce more receptors. The presence of toxin in the body fluids stimulates the body cells to produce receptors in excess. The increased receptors may remain in connection with the central body or they may become detached and float in the body fluids. Free receptors in blood serum is the essential active principle of antitoxin. Toxic im- munity may be better understood by giving an example. Examples. — Tetanus is an intoxication disease due to the pro- duction of toxins by localized bacterial activity of the tetanus bacillus. Immunity to tetanus is dependent upon the neutraliza- tion of the tetanus toxin. The tetanus toxin is composed of hap- tophores and toxophores. The body cells possess receptors capa- ble of union with the tetanus toxin haptophores. The union of cell receptors and tetanus toxin haptophores enables the tetanus toxin toxophore to act upon the central mass of the body cell, thus stimulating them to form more receptors. The excess recep- tors become detached and float free in the body fluids and com- bine with the tetanus toxin haptophore. thus preventing the lat- ter from combining with the attached cell receptors. The te- tanus toxophores are not capable of combining with the central mass of the body cells except through the medium of tetanus toxin haptophores and if the tetanus toxin haptophores are locked up with the detached cell receptors, the tetanus toxo- phores remain inactive and the animal is not inconvenienced by their presence and is immune. Toxic immunity is therefore dependent upon first, sufificient free receptors to lock up the haptophores thus inhibiting the action of the toxophore or second, upon the absence of hapto- phores. Bacterial immunity. — From the phenomena observed in Pfeif- fer's reaction Ehrlich has proposed an hypothesis in explanation of bacterial immunity. As previously stated, normal blood serum contains bacteriolytic substances (see humoral theory). Comple- ments are destroyed by a temperature of 55°C. The blood serum of immune animals possess another substance, in addition to complement, not destroyed, by heating to 55°C. These are called amiboceptors. According to Ehrlich, amboceptors, like toxins, are composed of two dififerent combining groups, also designated haptophores and toxophores. The complemental substance of normal serum is not capable of action upon bacteria. The ambo- ceptor haptophore has an affinity for the complement of normal IMMUNITY. 89 serum. The amboceptor toxophore has an affinity only for bac- teria, but is not injurious to them. The amboceptor toxophore combined with or acting upon bacteria produces a condition favorable for the action of the combined amboceptor haptophore and complement, i. e., this enables the complement to cause dis- integration of bacteria. The amboceptor thus renders condi- tions favorable, i. e., makes it possible for the bacteriolytic sub- stance, the complement, to exert destructive action upon bacteria, the amboceptor acting as middle man. Opsonic immunity. — Opsonins are produced by some animal tissue, probably muscle. Opsonic production is the result of stimulation with endotoxins. Endotoxins are products or are an integral ])art of bacteria. Opsonins increase the destroying power of leucocytes or diminish the resistance of bacteria. CHAPTER IV. MALFORMATIONS. DEFINITION. ETIOLOGY. Intruisic (heredity). Extrinsic. Pressure. Atnniottc Adhesion. Excessive Motion. Malnutrition. CLASSES. Single. Result of Arrested Development. Result of Excessive Develofvient. Result of Transposed Visceral Organs. Result of Persistent Foetal Structures. Result of Mixed Sexual Organs. Double or Multiple. Synnnetrical Duplicities. Coviplete. Incomplete. Asymmetrical Duplicities. Multiple. During the embryonic stage of intra-uterine life the special- ized tissues and organs are formed. The foetal period is the time during which the structures formed in the embryonic stage grow and develop. At birth the young of a given species are of a definite shape, contour and type ; the form or type which is most common is accepted as normal ; and deviations from the normal are designated malformations, anomalies or develop- mental errors. Many new strains and breeds of stock have been the result of developmental errors becoming a fixed peculiarity. Thus the polled cattle, the Boston bull-dog, the Mexican (hair- less) dog, and the five toed chicken had their origin. Etiology. — Malformations may be brought about by pre- existing influences in the maternal cells, (internal or intrinsic causes), or from external influences (external or extrinsic causes). Internal or Intrinsic Causes. — Internal causes are inherited peculiarities, i. e., heredity and atavismal influences. These are probably not the usual causes of malformation in domestic ani- mals for malformed individuals excepting cryptorchidism and animals affected with prognathism and some other of lesser de- fects are rarely used for breeding purposes. 90 MALFORMATIONS. 91 External or Extrinsic Causes of malformations are pressure, amniotic adhesions, excessive motion, insufficient or abnormal nutrition, infectious diseases, etc. External causes exert their influence during the embryonic or formative period and they must act in a mild degree or death of the eml)ryo and abortion follows. Typical malformations are approximately of the same form and are usually i)roduced by similar causes. Atypical mal- formations are variable in form and may be produced by a variety of causes. A complete description of all malformations is beyond the scope of general pathology. A general classification with a de- scription and origin of the most striking malformations is all that will be attempted in this chapter. Malformations may be divided into two classes: 1st, Single malformations, and ^nd. Double or multiple malformations. Single malformations are those affecting a single individual. Single malformations may be grouped into five classes as fol- lows : Malformations resulting from; (a) arrested growth or development; (b) excessive growth or development; (c) trans- position of visceral organs; (d) persistent foetal structures; (e) mixture of sexual organs. ARRESTED DEVELOPMENT. — IMalformations caused by arrested development may involve an entire individual or any part of an individual. Arrested development of the entire individual results in the formation of an irregular, fleshy mass, called a mole, in place of the normal foetus. IMoles may be carried in the uterus for the entire period of gestation. In some instances a mole and a normal foetus may be delivered at the same time. Moles have been observed in mares, more rarely in cows. Malformations resulting from arrested development of a part may be manifested by the entire absence of the part (aplasia), bv underdevelopment of the part, (hypoplasia), or by a lack of union or fusion of tissue (schistosis and atresia). The fol- lowing malformations are the result of local aplasia. Acephalus. A name applied to a headless monstrosity. Acephalus is probably the result of amniotic adhesions. Atrichia. A defect in which there is no hair. This results from some disturbance of cutaneous development. Amyelus. A malformation in which the spinal cord is absent. Defects of the primitive streak or failure of production of the neural canal interferes with or prohibits the formation of the spinal cord and is the cause of amyelus. 92 VETERINARY PATHOLOGY. Acardia. A heartless monstrosity. Agastria. A malformation in which the affected dividual has no stomach. This may be due to lack of sacculation of the embryonic gut. Acaiidia. A malformed individual in which the defect con- sists in the absence of the tail. An acaudia fox terrier bitch was recently observed, her mother whelped one or two tailless puppies at each whelping. This bitch recently whelped an acaudiac puppy. Aprosopns. An individual having no face. Dithoracisamelus. Fig-. 51. — Thi.s picture taken when calf wa.s five months old. The animal was abU> to get about by walking in an upright position and could gain its feet unassisted. Case observed by Dr. Smith V. Ewers. Agnatlius. A term used to designate an individual in whih the inferior maxilla is absent. This is common in lambs. Amchis. The name of a limbless or legless individual. Ame- lus is the result of arrested development of leg buds and is usual- ly caused by unequal intrauterine pressure or amniotic adhesions. M onopygusamehis. A monstrosity in which one posterior leg is wanting. This is due to arrested development of leg buds, probably due to amniotic adhesions. Dipygnsaiuclus. The name of a malformed animal in which both posterior legs are absent. Result of arrested development of leg buds. MALFOR.\[.\TI()NS. 93 Mo)i •tlioracisaiiiiiiis ami dithoracisaniclus arc monstrosities in whic t)nc and hoth front k\t,fs arc al)scnt rcs[)ccti\ cl}-. Apus. A name applied to a malformation in which the feet arc absent. This may be the result of intrauterine amputation or amniotic adhesions. Moiwpygiisal^iis is an individual in which one hind foot is wanting and a dii)ygusa])us, an indixidual in which both hind feet are absent. Monothoracisapus. and dithoracisapus, are names im])lying the absence of one or both front feet. The following tualformaticMis are the result of under develop- ment or undergrowth. ( 1 iypoi)lasia). Microccphalus, a term used to designate an in(li\idual hav- ing a diminished sized head, also used to designate the small head itself. This is probably the result of diminished nutrition to the head and anterior part of the bodv during embryonic and foetal development. Micro-card ia. A name applied to an individual ha\ing a small heart. This may be due to excessive pressure. MicroopJitliahiiia. A term used to indicate a malformation in which the eye or eyes are smaller in size than the normal. Tliis is probably the result of insufficient nutrition. Micrognathy. The name of an individual having a diminutive inferior maxilla. These are caused by undue pressure or insufficient nutrition. Microiiichts. A malformation so named because of the dimin- ished size of all legs. This is caused either by diminished nutrition or undue pressure. The following are illustrations of arrested dexelopment mani- fested bv absence of imperfect tissue union, thus producing fissures (schistoses), or resulting in fusion of parts that are normally separate (synactoses). Fissures of the body cavities are due to increased accumulation of fluids in internal organs, increased size of internal organs, prolapse of viscera before body walls have united, the presence of amniotic folds between cleft edges or lack of sufficient tissues to close the margins. CraiiioscJiisis. The name of a condition produced by fail- ure of development and union of the cranial bones and resulting in a cleft. 1 he meninges and in some instances the brain tissue may be ex])osed or there may be protusion of the meninges and also of the nerve tissue, thus producing meningocele or men- ingo-encephalocele. 94 VETERINARY PATHOLOGY. CraniorrhachiscJiisis. A malformed individual so called because of a fissure of the spine and cranium accompanied by exposure or protrusion of the spinal cord or brain. RacJiischisis. A condition in which there is a cleft of the spinal column. This malformation is usually the result of some defect in the margins of the neural groove. If the fissure ex- tends the entire length of the spinal column the resulting con- dition is called holoschisis. If the fissure does not extend the entire length of the spinal column, the condition is termed meroschisis (Gr. Meros^part, and schisis=splitting.) The spinal meninges may protrude through the spinal column fissure Fig. 5 2. — Cranioschisis — Calf. producing spina-bifida. A hernia of the spinal meninx that con- tains cerebrospinal fluid is termed spinal meningocele, and if the cord and meninges protrude, it is called a myelomeningocele. CJieiloschisis, is the condition resulting from arrested develop- ment of the soft tissues covering the maxilla. This is the condition popularly termed hair lip. It is an inconvenience because it inter- feres with sucking the teat, the source of nutrient of the new born mammal. The defect may also involve the maxilla producing cheiliognathoschisis. Palatoschisis. A defect in which the palatine processes have imperfectly developed, thus leaving a fissure through ^vhich there is free communication between the nasal and buccal MALFORMATIONS. 95 cavities. This condition is commonly spoken of as cleft palate. Tlioracoscliisis. A condition resulting from failure of union of the thoracic walls. Tiie thoracic viscera, the lung, heart and large vessels may protrude through the fissure thus producing cctopiacordis or ectopiacordispulmonaris. -ClieilosrliiNii^ ^ibdominoschisis, is the condition caused by failure of union of the abdominal ])arieties. The condition is fre(|uently accom- panied by ]-)rotusion of the abdominal viscera through the fissure. The abdominal fissure may involve only a portion of the cavity or it may be complete. Ectopia gastrium is the condition result- ing from protusion of the stomach through an abdominal fis- sure ; ectopia vesicae, protrusion of bladder, etc. Hypospadias is a condition resulting from arrested develop- ment of the penis and scrotum. The principle defect in hypos- padias consists of a variable cleft in the posterior and inferior 96 VETERINARY PATHOLOGY, Fig. 54. — Palatoschisis. surface of the penis and scrotum. This cleft which represents the urethra is lined \Yith mucous membrane and into it urine is discharged. This is the most common malformation of the male p"enital ortrans. Raymond Pearl reported his observation Fig. 55, — Abdotninoschisis. MALI-ORMATIOXS. 97 (in a case of hypospadias in a lanil) in the American X'ctcrinary Review. Syiiol^litltahnia. or cyclof^ia ( Gr. Kiil<1ops:=mythical single eve monster), is a condition resnhing from the fnsion of the ojitical vesicles. Arrested development of the anteriar cerehral vesicles allows the optical vesicles to contact and in some instances there is one large double eye central! >■ located or there may he two eyes occurring in a centrally located orbit. Cyclopia is usually associated with defects of the nose. Syuactosis is a general term denoting a coiulilion caused by the fusion of parts or organs that are normally se])arate. SmiiiicIus. a malformation caused by the fusion of two legs into one irregular member. Fisr. Sfi. — Synoplit hiilinia or Cyclopia. Syudactyliis. An individual having the digits fused or grown together. An illu-traticn of syndactylism is the soliped hog. The soliped hog usually has two separate digits of three pha- langes each and the ossa pedes are encased in a single hoof. Synmdusdif^iis. A malformation having fused legs and two feet. Syuiiicliis)}wnof'iis. .\n individual having fused legs and only one foot. Syufiicliisaf'iis. .\ monster having fused legs and no feet. Synoirhism. A malformed animal in which the testicles are fused. Arrested developmer.t may be evidenced by the nonappear- ance of the lumen in any of the natural hollow organs, (atresia). The mouth is formed by an ingrowth of the ectoderm and the buccal cavity extends inward until it meets the anterior elonga- tion of the embryonic gut. Later the jiartition separating the buccal cavity and the cavity of the embryonic gut is absorbed and thus the cavities become continuous. Failure of the exten- 98 VETERINARY PATHOLOGY, sion of the mouth cavicy and its fusion with the embryonic gut constitutes the condition atresia oris. Atresia iridis. A defect in the eye cUie to the absence of an opening (pupil). Atresia ociili, a malformation in which there is no opening i)etween the eyelids. Atresia anus is a condition in which there is an imperforate anus, that is, there has been failure of union and fusion of the anal ingrowth and the rectal outgrowth. Atresia anus is of rather frequent occurrence and usually the defect is easily re- lieved. Fig. 57. — A condition of Siceplialic tali. Middle union in double monsters occurs on the venter sur- face from the umbilicus and extends anteriorly. There is usu- ally a single umbilicus ; the abdominal viscera is usually double ; thoracic viscera single or double, depending upon the area of union ; middle union may occur at the xiphoid cartilage, (xipho- pagus), involve the entire sternum, (sternopagus), or the entire thoracic venter surface, (thoracopagus), x'phopagi may survive, the "Siamese Twins.'' were of this type. I^horacopagi are fre- quently unequal in size, the smaller one being designated as a parasite. Anterior union may be dorsal or ventral or the union may be on the anterior surface of the head. Dorsal, anterior union rare- ly occurs, the attachment being on the frontal region. These malformations are designated Craniopagi. Ventral anterior MALFORMATIONS. lo; union occurs occasionally. The union in this type is along the venter cervical region and extends onto the venter thoracic re- gion. The sternum and oesophagus are single ; larynx, trachea and stomach may be single or double; intestine double; there may be two faces or the faces may be fused. Fused-face mon- sters resulting from union of the venter anterior cervical or cephalic regions are called syncephali. hu'oiiiplctc duplicity is the name applied to those malformations in which the greater part of the body is single, duplication oc- curring in only a part. The duplicity may involve any part. These malformations arc not easily differentiated from malfor- mations resulting from multiplicity of parts as polydactylism. ASYMMETRICAL DUPLICITY are those malformations resullmg from the development of two separate, dissimilar. uiie(|ual anlagen of a single ovum, the development of a fertilized polar body or the development of an isolated group of segmentation cells. In asymmetrical dujdicity one body is rudimentary or under-developed, (the parasite), and the other body develops normally or nearly so, (the autosite). The parasite always re- ir.ains attached to the autosite or is included bv it. Parasitic 108 Veterinary pathology. duplicity may occur in any region. Thus the parasite may pro- ject from the orbit, mO'Uth, shoulder or it may be included in the thoracic or abdominal cavities. MULTIPLICITY is the name applied to designate the development of more than two separate individuals in a single chorion. Mul- tiplicity is of rare occurrence. One single case has been authen- tically reported in the human in the form of a tricephalus. CHAPTKR V. CIRCULATORY DISTURBANCES. X'ormal blood circulation is dependent upon normal rate, rhythm and force of the heart, normal caliber of the blood ves- sels and the normal resistance offered by them and the quantity and the (|uality of the blood. Variation of Heart Action. — A marked variation in the heart activity results in imperfect circulation. Depressed or diminished heart action is more common than increased heart action. Di- minished functional activity is most frequently caused by in- flammation of the endocardium, myocardium, epicardium or per- icardium. Valvular stenosis and valvular insufliciency are the result of endocarditis. Myocarditis diminishes the activity of the heart and if the inflammation is long continued the muscle cells are destroyed and then replaced by fibrous tissue thus per- manently impairing the force of the heart. Inflammation of the epicardium and pericardium may be accompanied by volumin- ous exudation which distends the pericardial sac and produces sufficient pressure to hinder diastole, or the exudate may be- come coagulated and later organized attaching the sac to the surface of the heart and thus hindering cardiac systole. Cardiac activity may be diminished by the collection of fluid in the pleural cavity, malformed thoracic cavity, tumors, occlusion of coronary arteries, fatigue and thrombic formation upon the car- diac valves. Diminished cardiac activity results in a diminished quantity of blood being sent out from the heart and an accumu- lation of waste products in the tissues. Increased functional actiznty of the heart is usually only tem- porary excepting in those animals aft'ected with cardiac com- pensatory hypertrophy. The most common cause of increased cardiac activity is reflex stimulation. Increased activity due to reflex stimulation may terminate in exhaustion and syncope in a relatively short time. Increased functional activity, due to a cardiac compensatory hypertrophy resulting from increased resistance as in emphysema, chronic nephritis, etc.. may result in permanent over action of the heart. Anatomical changes in the cardiac-structure, as hypertrophy, fatty degeneration, fragmentation, fibrous formation, or necrosis 109 110 VETERINARY PATHOLOGY. may be evident when the functional activity of the heart is varied. Vascular Variations. — The amount of blood passing into or out of a given organ is determined by the caliber of the blood vessels, provided the heart action and general blood pressure remain normal. \'ariations in the caliber of normal blood ves- sels depend primarily upon the response of the vessel muscu- lature to vaso-motor stimulation. Blood pressure is dependent upon the elasticity of the arteries and the force of the heart. In general, pathologic vascular variations are the result of, first, disturbed arterial elasticity ; second, variation of the normal cal- iber of the vessels and ; third, abnormal permeability of the vas- cular walls. Arteriosclerosis is a condition in which the elasticity of the vessel walls is lessened or destroyed. In the production of arteriosclerosis there is vascular dilatation succeeded by supen- dothelial fibrous formation which continues until the lumen of the dilated vessel is reduced to its normal size. The hyper- plastic fibrous tissue may later become calcified. Sclerotic ar- teries are thick, stifle and nonelastic. Sclerosis is most common in arteries although it occurs in veins. The vascular caliber may be diminished by muscular con- traction or by liypertrophied vessel walls. In animals afifected with chronic nephritis there is contraction of the systemic ar- teries resulting in compensatory cardiac hypertrophy. Arterial constriction is also common in the peripheral vessels of animals afifected with carbon dioxide poisoning. Local diminution of vascular caliber may be produced by parietal thrombi. The vascular caliber may be increased by paralysis of the vaso-motor nerves, a condition which is sometimes observed in animals that have received injuries in the cervical region. Increased permeability of vessel walls usually results from insufficient nutriment to the vascular structures and occurs most frequently in small vessels, i. e., capillaries and venules. In- creased permeability usually accompanies venous hyperemia, although it may exist independent of variations in the quantity of blood. Thus oedema is common in hydremic individuals. Variations in Quantity and Quality of Blood. — The quantity of blood in a part is determined by the caliber of the supplying vessel and by the blood pressure. Acute general anemia re- sults in a diminished blood pressure which, if not corrected in a short time, terminates fatally. Chronic general anemia is ac- companied by a slightly diminished blood pressure and a re- tarded blood current. CIKClLATOKV DISTLRDAXCES. Ill The most important variations in the quality of blood that concerns the student of general pathology are due to the varia- tions of the i)ercentage of water contained. Hydremia is ac- companied by disturbances of the renal function and by oedema. Anhydremia is productive of a slow weak pulse and the sec- ondary changes resulting therefrom. Excess of carbon dioxide or urea in the blood stimulates the vaso-constrictor nerves thus causing arterial contraction. HEMORRHAGE. DEFINITION. ETIOLOGY. PrcdispositKni { hcitiophUia). Ruptured vessel. Rhe.vis or duibrosis. Increased penneability. Diapedcsis. VARIETIES. Location. Tissue. Petechia (flea bite) pin point. Ecchyiiiosis (ovcr-flozv) from pin point to sice of dime. Suggillatwn (sivelling) bruise. Effusion. Hematoma (blood tumor). Infarction. Surface — Skin, mucous, membrane, serous membrane. E pis taxis. Hematemesis. Hemoptysis. Hematuria. Hematidrosis. Hematomctra. Hematocele. Metrorrhagia. Heniathora.Y. Hemococlia, etc. Vessels. Cardium. Arteries. Veins. Capillaries. APPEARANCE. Macroscopic. Microscopic. Tissue hemorrhage. Clot. EFFECTS. Rate of outflow. Location. Secondary change of cxtrazasate. Hemorrhage is the escape of blood from a vessel, (capillary, vein, artery or heart.) Etiology. — .'^ome animals are predisposed to hemorrhage (hemoj)hilia). Hemorrhagic diathesis or hemophilia is an in- herited condition in which there is little or no tentlency for co- 112 VETERINARY PATHOLOGY. aguiation of blood. The cause of this condition is the absence of some blood constituent essential to coagulation. This type of hemorrhage sometimes occurs in colts, usually appearing at the time or within a few days after foaling. In those cases that occur at the time of foaling the hemorrhage is usually from the umbilical vessels although there may be some cutaneous capillary hemorrhage, (hematidrosis). In some cases there may be no evidence of hemorrhage at the time of foaling, but within from 24 hours to three or four days, oozing of blood on to the skin surface may be noticed, the extent of which varies and may or may not be fatal. Gough, of Benton, Ky., reported a case of hemophilia in a mule colt in the American Journal of Veterinary Medicine, July, 1911. A case of hemophilia in a medium sized IT months old Ger- man sheep dog was reported by L. & E. Lepmay. This dog first showed tendency to hemophilia at 15 months of age, by per- sisted hemorrhage from the mucous membrane of the gums. A little later a subcutaneous hemorrhagic extravasate was observed in the thoraco-axillary region and the dog died of acute intesti- nal hemorrhage when about IT months of age. Hemorrhage may be caused by degeneration or ulceration of the vessel wall — thus hemorrhage by diabrosis is produced ; it may be caused by rupture of the vessel wall due to increased intravascular or diminished extravascular pressure and trauma of the vessel wall — 'thus hemorrhage by rhexi's is produced ; or it may be increased permeability of the vessel walls due to increased intravascular press- ure or disease of the vessel wall — thus hemorrhage by diapedcsis is produced. Diabrotic hemorrhage is observed in tumors as a result of the destruction of the vessel wall by the neoplasm ; gastric ulcers particidarly in dogs ; glanders, especially the acute type in which the mucous membrane of the respiratory tract becomes necrotic ; in septic wounds, etc. Hemorrhage bv rhexis is the type most common, it is the type observed in traumatisms, and is sometimes observed in apoplexy resulting from vascular occlusion (apoplectiform anthrax), this type has also been observed in some cases of canine vascular strongylosis due to infestation of the strongylus vasorum. Diapedetic hemorrhage is rather uncommon, being observed occasionally in such disease as purpura hemorrhagica and in some septicaemias. The escaped blood, i. e., the extravasate, may flow upon the surface of the skin, serous or mucous membranes, or into the tissues. CIRCULATORY DISTURBANCES. 113 TISSUE HEMORRHAGES may vary greatly in amount and are designated by the following terms, petechia, ecchymosis, sug- gilation, effusion, infarction and hematoma. Petech'iae are small sharply defined hemorrhagic points and are probably caused by bacterial products in the blood. Ecchymoses are hemorrhagic spots larger than petechiae and less sharply defined caused by rupture of capillaries or precapil- laries. Ecchmymotic hemorrhages are of common occurrence in the nasal and ocular mucous membrane of horses affected with purpura hemorrhagia and equine infectious anemia. ..-O Fis. 64. — Petechial lieniorrliage. Kidney hog cholera lesion. a. Hemorrhagic area. c. Glomerulus engorged with blood, b. Normal kidney tubule. Suggillations and effusions are large indefinable hemorrhagic areas, caused by bruising which ruptures the small vessels. Hemorrhagic infarction is a hemorrhage into an anemic area. This is not a hemorrhage as ordinarily understood, for the blood is within the vessels and escapes into the anemic area because of the diminished pressure. A hematoma is a circumscribed collection of e.xtravasated blood in the tissues and is usually the result of hemorrhage from an artery. 114 VETERINARY PATHOLOGY. SURFACE HEMORRHAGE is designated according to its origin, thus : Epistaxis is hemorrhage from the nasal mucous membrane and is quite common in acute nasal glanders. Hematemesis is hemorrhage from the stomach and is observed in animals poisoned with arsenic and those atTlicted with gastric ulcer or gastric carcinoma. The hemorrhagic extravasate is act- ed upon by the acid gastric content and converted into coffee bean Hke masses. These masses, which are dark in color, char- acterize srastric hemorrhage. r\oe n\ q1 o 1^1 a Fig. 65. — Heinaton':a, caused b.v rupture of spur vein. Hemoptysis is hemorrhage from the lungs. It may be the result of excessive exertion, abscess formation, tuberculosis,. Pulmonary hemorrhage is characterized clinically by the dis- charge from the nose or mouth of a frothy sanguinous extra- vasate. Hematuria is hemorrhage into the urinary tract or bloody urine. The blood may escape from the kidney, and if so there wdll be tubular casts discernible on microscopic examination of the urine ; it may come from the ureter or bladder, and would then CIRCULATUKN DISTLKIJA XCKS. 115 be thoroughly mixed with the urine; or it may have its origin from the urethra and would not be mixed with the urine but would usually precede it. Hciiiatidrosis is hemorrhage from the surface of the skin and is the so-called sweating of the blood and is caused by increased jiermeability of cutaneous capillaries. Entcrorrhagia is hemorrhage from the intestinal mucosa and may be differentiated from hematemesis by the appearance of the extravasate in the feces. The extravasate in hematemesis has the appearance of coffee bean grains in the feces while the entcrorrhagia extravasate retains the hemoglobin color and is not broken up into granules. (The coffee bean appearance of blood extravasated into the stomach is due to the action of the hydrochloric acid of the gastric juice.) Entcrorrhagia is caused by infection as in anthrax and by caustics. Heiiiatomctra is hemorrhage from the uterine mucosa, the extra- \asate being almost entirely retained in the uterus. This is usually caused by improper removal of retained placenta. Metorrlwgia is hemorrhage from the uterine mucosa and the extravasate passes out of the uterus. ISIenstruation in the hu- man is an illustration of metrorrhagia. Hemocoelia is hemorrhage into the peritoneal cavity and is caused by rupture of the peritoneaum or some abdominal organ. Hemothorax is hemorrhage in the pleural cavity, and is caused by ruptured pleura as a result of fracture of a rib, etc. Hematocele is hemorrhage into the tunica vaginalis cavity. This may be the result of laceration or rupture of the tunica vaginalis testis. Effects. — The effects of a hemorrhage depend upon the quan- tity of blood lost and the location and secondary changes of the extravasate. In health the vascular system practically maintains a constant blood pressure by accomodating the capacity of the blood channels to the volume of the blood. The quantity of blood that an animal may loose without be- ing seriously affected varies according to its age and health. The blood tissue of the horse has been estimated at from 1-16 to 1-12 of the total body weight. One-tenth of the esti- mated total amount of blood in the body has been withdrawn from horses used in the production of anti-toxin once every two weeks for from six to eight months without injurious results. From one-third to one-half of the volume of the blood in the body may be withdrawaat once and the animal recover. Hem- orrhage from a small vessel has little effect upon the welfare of the body for the quantity lost is immediately restored from the 116 VETERINARY PATHOLOGY. lymph and other fluids of the body. Thus there may be a con- stant hemorrhage from the digital artery of the horse for twen- ty-four hours without injurious consequences. A sudden large loss of blood diminishes blood pressure and this results in imperfect action of the heart valves. The blood is churned back and forth, becomes mixed with air and this frothy mass accumulates beneath the valves and prevents their closure. Hemorrhage is serious when it occurs in the more delicate or the more highly organized tissues. Thus the amount of ex- travasate into the cerebrum may be very small and yet produce sufficient disturbance to destroy life, while the same amount of extravasate into the muscles of the thigh, forearm, etc., would probably not be observed. The extravasation of blood into one of the body cavities, as the pleural or peritoneal cavity, will be partially absorbed as entire blood before it becomes coagulated, the remaining un- absorbed portion will be in part disintegrated and carried out by the leucocytes and the remaining portion will finally become organized and remain as a mass of fibrous tissue. If the loss of blood is not sufficiently large to materially diminish the blood pressure and the extravasate remains free from infection there will be very little inconvenience from the hemorrhage ; but if the extravasate becomes infected the outcome will be more serious. If the extravasate is into some important tissue the secondary changes will be of more consequence than when in the body cavities. There is a natural tendency for self-arrest of hemorrhage, because, 1st, blood pressure is diminished during hemorrhage and thus coagulation is favored ; 2nd, the endothelium of the injured vessels becomes roughened and thus thrombic formation is favored ; and 3rd, fibrinogen is liberated from vascular endo- thelium and thus the coagulation of the blood is favored. CIRCULATORY DISTURBANCES. 117 LYMPIIORRIIAGIA. DEFINITION. (Extent of lyinpliatic system). (Lymph transttdatc quaiilit\ determined h\' blood pressure). ETIOLOGY. Ruptured vessel or space. LOCATION. Surface, because of lymph spaces and lozv pressure. Thoracic duct. APPEARANCE. Macroscopic. Microscopic. EFFECTS. Lymphorrhagia is the escape of lymph from injured lymph- atic vessels. The lymphatic system in general is the connecting system between the blood capillaries and the jugular vein. Lymph, the fluid in the lymplialic vessels, is that portion of the blood which passes through (or is secreted by), the capilhiry walls into the perivascular spaces and consists of plasma diluted, leucocytes, and usually contains considerable waste material. Lymph varies in its composition, depending upon the source, location and condition of the surrounding tissue. The lymph of the lacteal system depends upon the kind of food-material digested and the length of time since its ingestion. Etiology. — Lymphorrhagia is as a rule the result of laceration or rupture of the lymphatic channels. In rare instances it may be caused by an increased jiermealjility of the lymphatic vessels or spaces. I'ecause of the low pressure within the lymphatic vessels, lymphorrhagia takes place only U])on surfaces or into the body cavities. Lymphorrhagia onto a surface, if long con- tinued, results in the so-called lymphatic fistula. Rupture of the abdominal portion of the thoracic duct accompanied by the escape of its contents into the peritoneal cavity produces the condition known as chylous ascites. Chylous ascites is differentiated from abdominal dropsy or ascites proper by examination of the accumulated fluid. The fluid of chylous ascites and lacteal fluid are practically identical in composition. .Ascitic fluid proper is diluted l}'mph and con- tains no evidence of chyle or lacteal fluid. Lymphorrhagia may also occur into the pleural cavity as a result of the rupture of the thoracic portion of the thoracic duct. The effects of lymphorrhagia depend upon the extent, loca- tion and length of duration of the process. Extensive lymph- orrhagia from a large lymphatic vessel depletes the body be- cause of the loss of food substances, albumin, etc., in the lymph. 118 VETERINARY PATHOLOGY. Lymphorrhagia from the thoracic duct, especially into the peri- toneal cavity, is serious because of the loss of food. OEDEMA, DROPSY OR HYDROPS. DEFINITION. ETIOLOGY. Increased production. Increased permeability (Cohnheim). Increased pressure. OBSTRUCTED OUTFLOW. Valvular insuihciency or stenosis (cardiac). Gravid uterus. Tunior, Abscess, Ligature, etc. LOCATION. Peritoneal cavity (ascites). Thoracic cavity (hydrotlwrax). Pericardial cavity (hydropericardinm). Arachnoid space (hydrocephalus e.vternal). Lateral ventricles (hydrocephalus internal). Tunica 7'aginalis cavity (hydrocele). Subcutaneous l\nipJi spaces (aimsarca), (in legs only, stocking). APPEARANCE. Macroscopic. Microscopic. EFFECTS. Oedema, dropsy or hydrops is the accumulation and reten- tion of an excessive quantity of lymph in the lymph vessels and spaces. Lymph is the conveyor of metabolic substances to and from all tissues of the body except those directly supplied by the blood capillaries. The cjuantity of lymph in the lymphatic channels is determined by the permeability of the capillary walls and the rapidity of lymphatic absorption. In health there is a balance between the transudation of lymph from the blood ves- sels and its absorption into the lymph vessels. In oedema there is either a larger amount of lymph transuded or a smaller amount absorbed. Etiology. — The causes of oedema may be : 1. Increased transudation which may be caused by (A) In- creased permeability (or secretory function) of the capillary walls, thus allowing an increased amount of fluid to escape from the blood (Cohnheim theory). (B) Hyperemia: which pro- duces an increased intracapillary pressure resulting in sufficient injury to the endothelial lining to allow an increased outflow of plasma. Passive hyperemia is more frequently associated with oedema than active hyperemia. Thus, tricvispid stenosis or tri- cuspid insufficiency is usually associated with general dropsy. "Stocking" is an oedema usually resulting from venous hyper- emia. CIRCULATORY I)ISTrRl!AXCI-:S. 119 2. Obstructed utitjlow of lyjiiph. Swollen lymphatic glands, tiic result of inflammatory disturbances or neoplasms, and external pressure hinder the passage of lymph and hence favor its accumulation. As the anastomoses of lymph channels is (|uite complete the obstruction of the outflow of lymph is a minor cause. Varieties of oedema according to location are as follows: — Ascites,: an abnormal accumulation of an oedematous fluid in the peritoneal cavity usually resulting from obstructed ])()rtal cir- Fig. 66. — Dog with Ascites, a n.:^uIt of an licpatlc tumor. culation. Chylous ascites is a condition resulting from obstruc- tion of some of the lacteal lymphatic vessels or the abdominal portion of the thoracic duct, or it may be the result of leakage of the abdominal thoracic duct. Hydrothorax: an abnormal accumulation of oedematous fluid in the pleural cavity or cavities. It is usually bilateral in the horse and is caused by obstruction of the internal thoracic vein. Hydropericardiuiu : an abnormal accumulation of oedematous fluid in the pericardial sac. This variety is very rare as a pri- mary condition. It is caused from venous obstruction of cardiac vessels or vessels of the cardiac sac. Hydrocele: an abnormal accumulation of an oedematous fluid within the vaginal tunic, c. g.. the so-called "water seed," caused by adhesion of the vaginal tunic in the inguinal canal, which is usually the result of improper castration. 120 VETERINARY PATHOLOGY. Hydrocephalus : an abnormal accumulation of oedematous fluid in the serous cavities of the brain or its meninges, caused by venous hyperemia. Thus external hydrocephalus is an affection of the subarachnoidean spaces, and internal hydrocephalus an affection of the ventricles of the brain. Fig:. 6". — Subcutaneous Oedema, caused by valvular insufficiency. Anasarca: an abnormal accumulation of oedematous fluid in the subcutaneous areolar tissue. Appearance. Macroscopic. — Oedema of the body cavities re- sults in their distention and in the displacement of the normal cavity contents as a result of the accumulated fluid. The serous membrane becomes discolored. Oedematous fluid is thin, water- like, pale yellow, or colorless, contains less albumin and is less CIRCULATORY DISTURliANClilS. 121 coagulable than cither blood scrum or inflammatory cxiuhitc. An ocdcmatous tissue is swollen, tlabby, soft and pits \\\n)n pressure, and if incised, a watery, pale straw colored fluid escapes. Microscopic. — The intercellular spaces are increased in extent, hence the cells are farther apart than normal and may be under- going degeneration or atrophy, or be swollen and contain vacuoles. Effects. — The effects of oedema vary according to the causa- tive agent, the tissue involved, and the length of duration of the process. If the etiologic factor is capable of reproducing or increasing in ([uantity, as infectious agents (Bacillus of IMalig- nant Oedema), there is more extensive tissue destruction than when the oedema is produced by other agents. Oedema of the meninges of the brain or spinal cord may result in degeneration and destruction of the nerve cells and death of the diseased animal. On the other hand oedema of the subcutaneous tissues of the metacarpal or metatarsal region is of little consequence. Oedema of brief duration does not, as a rule, produce permanent injury to the involved tissue, but an oedema of long standing is of serious consequence because of the extensive hydropic infil- trations of the cells of the afifected tissue and because of the constant depletion of the system. Hydropic degeneration, thrombosis and necrosis are frequent sequellae of oedema. 122 VETERINARY PATHOLOGY. THROMBOSIS. DEFINITION. ETIOLOGY. Injured endothelium. Mechanical — Artery forceps. Atheromatous degeneration. Insufficient nutrition. Foreign bodies — Parasites, etc. Retarded rate of blood -floiv. Increased coagulability of blood. PROCESS OF FORMATION. LOCATION. Occurs in all vessels, more prevalent in veins and heart. VARIETIES OF THROMBI. Color. Red. White. Mixed. Extent. Partial. Lateral. Parietal (annular). Complete (obstructive). EXTENSION OF THROMBI. APPEARANCE. SECONDARY CHANGES OF THROMBI. Decolorization. Softening. Simple. Infective. Organization. Calcification. EFFECTS DEPEND UPON. Vessels obstructed. Secondary changes of thrombi. Thrombosis is the condition resulting from a coagulation of blood within the vessels or heart during life. A thrombus is the coagulated blood within a living vessel. The accumulation and adhesion of leucocytes on the interior of vascular channels is also spoken of as a thrombus. The term thrombus should not be confused with a coagulum or a clot. A coagulum is coagul- ated blood within a vessel formed after death of the vessel wall, and a clot is coagulated blood formed outside of the vessel. Thrombosis is of quite common occurrence. It is occasion- ally a sequel of parturition. Thrombic formation of one or both of the iliac arteries of the horse is a demonstrated cause of lame- ness. Thrombo-embolic colic of the horse is a sequel of throm- bosis of the anterior mesenteric artery. Ante-mortem clots are of common occurrence and all post-mortem observers are familiar with them. Intravenous or intra-arterial injections are probably always succeeded by thrombic formation at the point of the CIRCULATORY DISTURBAN'CES. 123 injection, but the thrombi resulting therefrom are usually of little consequence. Etiology. — The coagulation of blood involves complex chem- ical changes. From the various investigations it may be con- cluded that three factors are essential in the coagulation of blood. 1st. There must be soluble albumins from which fibrin is derived. 2nd. Fibrin ferment (fibrinogen) which is probably derived from leucocytes and blood plates. (It is probable that vascular endothelium may also liberate fibrinogen.) 3rd. Soluble lime salts. The following are the most frequent immediate causes of thrombic formation. 1. Injury of the vascular endothelium which may be caused by: (A) Mechanical interference, as torsion by artery forceps, or ligation; (B) Extension of disease from other portions of vessel walls, as atheromatous degeneration; (C) Insufficient nutrition the result of passive hyperemia; (D) Foreign bodies. Thrombic formation succeeding injury of the vascular endothelium is apparently a reaction on the part of the injured cells for protec- tion and to prevent hemorrhage until the wound is repaired. Many thrombi are thus formed and later removed by phago- cytes, without causing sufficient inconvenience to be clinically recognized. 2. Retarded flow of blood, which may be caused by a weak heart or the relaxation of the blood vessels especially the veins. Frequently the so-called "ante-mortem clot," which is a throm- bus, is observed in post-mortem examination of horses that have died, of pneumonia, pleurisy, peritonitis and other exhaustive diseases that terminate after a period of a weak heart action. 3. Variations in the composition of blood, as increased number of platelets, (probably because of the production of fibrinogen), contamination with bacteria, and any other factors which has a tendency to increase coagulability. Process of Formation. — Tlie process of formation varies according to the kind of thrombus formed. A red thrombus is formed when there is vascular obstruction and it is formed be- cause of the coagulation of the blood contained in the obstructed vessel. Coagulation in thrombic formation does not diiTer from extravascular coagulation. \\'hite thrombi are formed as a result of leucocytic adhesion, and the deposition of the fibrin from the blood plasma on an injured internal vascular surface. The leucocytes and fibrin may contmue to accumulate until the vessel is obstructed. 124 VETERINARY PATHOLOGY. Location. — Thrombi form in the heart, veins, arteries, and capillaries. They occur more frequently in the heart and veins because of the presence of valves. Varieties of Thrombi. — Thrombi may be classified on the basis of color and extent. 1. Color. Thrombi are variable in color according to their structure and may be red, white or mixed. A thrombus formed in a vessel in which there is complete stasis of blood will occupy practically the entire vessel-lumen and be red. On the other hand a thrombus formed gradually by the deposition of fibrin upon a roughened endothelial surface of a blood vessel will be white. A mixed thrombus may be formed as a result of blood- stasis in a vessel in which there was a white thrombus, or by a red thrombus becoming partially detached from the vessel wall and contracting, thus allowing the blood to pass through the partially obstructed vessel and depositing fibrin (a white throm- bus) upon the red thrombus. 2. Extent. A thrombus may be complete (obstructive), thus occupying the entire lumen of a vessel, or it may l^e partial and thus incompletely obstruct the vessel. A partial thrombus may be lateral and be found along one side of a vessel, or it may also be parietal, i. e.. extend around the entire lumen of a vessel. Extension of Thrombi. — A thrombus may form as a plug in a vessel or may extend a considerable distance in the vessel, the extension usually being in the direction of the blood stream. Thus a bicuspid valve thrombus may extend, by continued deposit, out into the posterior aorta until it has reached the iliac arteries, or a thrombus arising in the metatarsal region may extend up through the metatarsal and continuing veins until it reaches the posterior vena cava. The extension may be the result of direct growth or deposit upon the original thrombus or it may be the result of fragments becoming detached (emboli) and floating in the blood stream until they arrive at the junction of blood ves- sels too small to allow them to pass and so form secondary thrombi or produce embolism. Appearance of Thrombi. — Macroscopic. A red thrombus appears similar to a blood clot but is usually a little more dense. It is red, jelly-like and quite easily broken and may be partial or complete. A mixed thrombus is practically the same as the red except in color. A white thrombus is usually a little more brittle than the red, is yellowish white in color and if formed at diflferent periods, strata may be observed. Microscopic. A red thrombus is practically identical with a blood clot, i. e., it is composed of fibrin in which white and red CIRCULATORY DISTlRr.AXCES. 1. blood cells are entangled. A white thrombus consists essentially of a mass of fibrin in which an occasional leucocyte or platelet may be found. Secondary Changes of Thrombi. — 1. Dccolorization. A red thrombus may become decolorized as a result of degenerative changes in the red blood cells. The contained hemoglobin be- ing liberated may in ])art be converted into other pigments and in part may be carried away by invading leucocytes. Fig. 68.— A Thr.jiiilni.s ii . ]iosteiinous em- boli as a rule pass to the right side of the heart and into the pul- monary arteries and lodge in these arteries or their radicles. Flff. 70. — Embolism. The embolug lodgod at the point of division of an artery. Fragments of thrombi from intestinal veins pass into the portal system and are lodged in the hepatic capillaries thus producing embolism in the liver. Thrombic fragments from the pulmon- ary veins, bicuspid valve and semi-lunar valves pass into the arota and through its various branches and terminals as emboli and finally they occlude the containing vessel and thus produce embolism. Paradoxical" embolism is the name applied to the condition resulting from obstruction of an artery with an em- bolus derived from the venous system and which has passed 130 VETERINARY PATHOLOGY, from the right side of the heart to the left through the foramen ovale. In some rare instances it appears that an embolus travels in the direction opposite to the flow of blood and produces obstruc- tion ; this is called retrograde embolism. Fig. 71. — Anemic infarcts in the spleen, a. Infarcted areas due to emboli in capillaries supplying them. Effect. — The results of embolism depend upon the composi- tion of the embolus, and the vessel obstructed. Composition of the embolus. — Emboli composed of cells having the power to multiply, at the point of impaction (embolism) be- come secondary foci or metastases of the primary pathological condition, as metastatic sarcomata, leukemic infarctions, etc. Pathogenic bacterial emboli not only obstruct circulation, but also produce metastases of that disease as in necrobacillosis, anthrax, etc. Filarial emboli and emboli composed of fatty cells CIRCULATORY DISTURBANCES. 131 produce a mechanical effect only. Air emboli in small vessels mechanically obstruct the vessels but are absorbed after a time. Obstructed circulation. — Obstructed circulation when produced by non-infective emboli will have tire same effects and termina- tions as the non-infective obstructive thrombi. Infarction. — Infarction is the process of obstructing a vessel with an embolus. The area supplied by the obstructed vessel is called an infarcted area. The area of infarction is determined by the region supplied by the occluded vessel and is usually wedge-shaped. An area supplied by an artery that has been in- farcted does not become bloodless at once because some of the blood remains in the vessels of the infarcted area and some may enter the periphery of the infarct through anastamosing capil- laries and venules of adjacent regions. Infarcts may be anemic or hemorrhagic. An anemic infarct is one in which there is limited anasta- moses of venules and capillaries of contiguous areas. The blood remaining in the vessels of an anemic infarct soon becomes de- colorized and the area appears pale in color. Anemic infarcts usually undergo necrosis early because of the lack of nutrition. The type of necrosis is largely dependent upon the nature of the embolus. Infarcts produced by infectious emboli usually suppurate or putrefy and infarcts produced by non-infective em- boli may become liquified, absorbed and replaced with fibrous tissue or it may become caseated or calcified and surrounded by a fibrous capsule and persist for a long time. A hemorrhagic infarcted area is one in which there are anas- tamoscs of the vessels of the infarcted area and the venules and capillaries of contiguous areas through which blood passes and becomes stagnated in the affected area. Hemorrhagic infarcts may become decolorized, there may be inflammation established around their periphery, or the blood and the involved tissue may be disintegrated and absorbed. Infarcted areas may become cystic, caseous, calcareous, ab- sorbed and substituted with fibrous tissue, or they may become infected and there may be abscess formation or gangrene. Infarction occurs most frequently in the kidney, spleen, brain, lung and less frequently in the heart, liver, retina, etc. Typical terminal arteries are common in the kidney and spleen and hence infarction most frequently occurs in these organs. In the kidney anemic infarcts are most common, hemorrhagic and ane- mic infarcts occur in the spleen. Cardiac infarction is not com- mon and is usually caused by thrombosis of the coronary vessels. Cerebral anemic infarction occurs occasionallv and the infarct 132 VETERINARY PATHOLOGY. usually undergoes simple softening, hemorrhagic cerebral in- farction is rare. ISCHEMIA. DEFINITION. ETIOLOGY. Diminished calibre of supplying arteries. Stimulation of vaso constrictor nerves. Inhibition of vaso dilator nerves. Tonic spasms of vessel musculature. Occulsion of supplying arteries. Mechanical. Tu}nors. Thrombi, etc. Collateral hyperemia. APPEARANCE. Macroscopic, pale, flabby, lozver temperature. Microscopic, cell degeneration, atrophy or necrosis. EFFECTS. Depend upon extent and duration and may be atrophy or necrosis. Anemia, as usually considered, is a condition in which there is either a deficiency in the quality or in the quantity of blood. The discussion of this theme will be found in special pathology. Ischemia is a condition in which there is insufficient or total absence of blood in a part of the body. Etiology. — Ischemia may be caused by influences that dimin- ish the calibre or occlude the vessels supplying blood to a part or by collateral hyperemia. The calibre of arteries may be diminished by contraction of the vessel musculature induced by low temperature, high temperature, drugs, etc., which stimulate the vaso-constrictor nerves, or inhibit the vaso-dilator nerves or cause tonic spasms of the vascular musculature. The supply- ing arteries may be occluded b)^ mechanical pressure produced by bandages, ligatures, harness, collar, thrombi, emboli, neoplasms, tissue proliferations and tissue infiltrations. Ischemia in one part may be caused by hyperemia in a related part, because the blood of the entire body is easily contained in the vessels main- tained at the normal calibre, blood pressure causing an equal distribution of it ; and if the vessels of one area are increased in calibre, followed by an increased inflow of blood, the quantity of blood will be diminished in some part, thus a marked hyperemia of the spleen is usually accompanied by ischemia of the stomach. It is possible for sufficient blood to collect in the vessels of the liver to drain the system to a sufficient extent that the animal would die of ischemia of the brain. Appearance. — Macroscopic. — An ischemic tissue appears bloodless and is pale, flabby and of a lower temperature than the CIRCULATORY DISTURBANCES. 133 same tissue with a normal blood supply. If incised the tissue ap- pears dry and there will be limited or no hemorrhage. Microscopic, the blood vessels are practically empty and the tissue cells are more or less shriveled as a result of insufficient moisture. Effects. — The outcome of ischemia is determined by the length of time it exists and the degree of completeness of the condition. Temporary, partial ischemia usually terminates in complete recovery. Continued partial ischemia is a frequent cause of atrophy. Complete absence of blood for a considerable time results in necrosis. HYPEREMIA. Hyperemia is a condition in which there is an increased quantity of blood in a part. The condition is practically local for an increased total amount of blood could not be retained in the general circulation without increasing the general blood pressure which would result in an increased production of lymph and hence diminish the volume of blood. Psysiologic hyperemia is evident whenever an organ or part is active. Local patho- logic hyperemia may be passive (venous) or active (arterial). Passive or Venous Hyperemia. DEFINITION. ETIOLOGY. Enfeebled circulation. Mechanical interference. APPEARANCE. Macroscopic, bluish, cold clannuy. Microscopic, eiigorr/cd z'cins, dc(icucratwn. EFFECTS. Depend upon cause, duration, degree and location, and tnay be varicose veins, fibrosis, oedema, thrombosis, necrosis and recovery. Passive or venous hyperemia is a condition in which there is a normal quantity of blood constantly flowing into an organ or part, but a diminished quantity flowing out. An excess of venous blood consequently accumulates in the part. Etiology. — Passive hyperemia is caused by enfeebled circu- lation due to weak heart, biscuspid and tricuspid insufficiency or stenosis, or diseased vessels and by pressure upon the outgoing vessels by ligatures, bandages, neoplasms, dislocations, fractures, etc. Appearance. — Macroscopic. — The affected tissues are bluish in color and usually feel spongy, cold and moist when palpated. 134 VETERINARY PATHOLOGY. Microscopic. — A tissue affected with venous hyperemia has dis- tended capillaries and venules, the lymph spaces are engorged with lymph and the cells are swollen and their protoplasm cloudy. Effects. — The outcome of venous hyperemia depends upon the cause, degree, duration and organs aft'ected. Thus venous hyperemia resulting from infective phlebitis is more serious than if caused by noninfective agencies. A venous hyperemia caused by complete obstruction of a vein is more likely to be fatal than one resulting from partial obstruction. Venous hyperemia of short duration is usually of little consequence but, if long con- tinued, it results in necrosis or fibrosis depending upon the de- gree of obstruction. Venous hyperemia of vital organs, as the brain or lungs, is more likely to have a fatal termination than if some less important structure as a muscle were involved. Therapeutic Venoiis Hyperemia properly produced results in (a), diminution of pain, probably because of the dilution of the irritating substances (b), destruction of bacteria, the accumu- lated blood serum, possessing strong bactericidal properties (c), increased nutrition because of the increased amount of blood. Bier's hyperemic treatment of open joints by producing venous hyperemia illustrates this type. Pathologic Venous Hyperemia may result in fibrosis, oedema, thrombosis, necrosis, or recovery. A long continued slight ven- ous hyperemia usually results in fibrosis and is noted in the liver of animals aft'ected with a slight tricuspid insufficiency or steno- sis. A marked venous hyperemia, but not caused by complete venous obstruction usually results in oedema, and is noted in the peritoneal cavity (ascites), in animals in which the portal circu- lation is partially obstructed. Venous hyperemia caused by com- plete obstruction results in thrombosis and is observed in intus- susception of the intestines. If other venous channels are unable to convey the blood from a part in which there is a complete venous thrombus, necrosis occurs as in strangulated herniae. Venous hyperemia of short duration, even though it is quite extensive, results in complete recovery if the cause is removed and the tissues are repaired. CIRCULATORV DISTURl'.AXCKS. 135 ACTIVE OR ARTERIAL HYPEREMIA. ETIOLOCV. Increased calibre of arteries. Stimulation of zvso-ditator iicrz-cs. Inhibition of vaso-constrictor nerves. Paralysis of vessel inuscitlatttre. Collateral isclieniia. Piiniiiislied external pressure. APFli.lR.lNCE. .Macroscopic, red, hot, szvollen. Microscopic, engorged arteries and capillaries. EFFECTS. Hypertrophy, hyperplasia, inflainination, recovery. Active or arterial hyperemia is a condition in whicli there is an increased inflow of blood to a part or organ witliout an equally increased outflow. d— . -^ Fig. 72. — H.vperemia, hemorrhagu and oedema of intestine of a horse. a. Surface exudate. c. Area of oedema. b. Engorged ves.sels. d. Suli.surface hi-morrliage. Etiology. — Arterial hyperemia is caused by an increase in the calibre of the supplying arteries, by collateral ischemia and by diminished external pressure. The calibre of the supplying artery may be increased by stimulation of the vaso-dilator nerves, by heat, chemicals, etc., by inhibition of the vaso-constrictor nerves, and by paralysi* of the muscular tunic of the artery. The calibre of the surface vessels is in part of the result of ex- ternal pressure. If the external pressure is materially dimin- 136 VETERINARY PATHOLOGY, ished, there will be arterial hyperemia of the cutaneous arteries as is evidenced in hyperemia produced by cupping. Collateral ischemia may cause hyperemia of the related parts for the same reason that collateral hyperemia may cause ischemia. Appearance. — Macroscopic. — An arterial hyperemic part is scarlet red in color, usually feels dense, dry and has an increased temperature. If the tissues are incised, blood escapes freely. v*^^^^^?^M' ' -"i^; ltk> ''-f^^'iii* -^..- ' * Fig 73. — Hyperemia of Kidney, showing eiigorjjecl capillaries. Microscopic. — Tissues affected with arterial hyperemia contain dilated arteries and capillaries, the lymph spaces are engorged with lymph, the tissue cells may be considerably swollen and diapedesis may be noted. Effects. — The effects of arterial hyperemia depend upon the cause, degree, and duration and organs affected. Arterial hyper- emia caused by infective agencies is more serious than if caused by other means. Arterial hyperemia of a sthenic type is usually succeeded by inflammation and asthenic hyperemia may terminate in recovery. CIRCULATORV DISTURBANCES. 137 Arterial hyperemia of sliort duration is less serious than it would be if long continued, thus, active pulmonary hyperemia is occasionally aborted in the horse and such animals are usually ready for service in 21 to 48 hours, but if active pulmonary hyperemia continues for 24 hours it is succeeded by inflamma- tion (pneumonia). Arterial hyperemia varies in different organs. Affections of the more highly organized structures are usually more serious. Physiologic arterial hyperemia is a condition in which there is an increased amount of blood flowing into a tissue because of increased physiologic demand, thus during gastric digestion an excess of blood passes to the stomach through the gastric arteries. Therapeutic arterial hyperemia, when properly produced in a diseased part, results in (a), diminished pain, (b), resorption of inflammatory exudate, hemorrhagic extravasate, and oedematous transudate, (c) increased nutrition, thus by the alternate use of cold and hot applications an arterial hyperemia is produced and is of value in strained tendons, bruises, etc. Pathologic arterial hyperemia may produce hypertrophy, hyper- plasia and permanent arterial dilatation. Excessive development of a part (hypertrophy or hyperplasia) may result from a long continued active hyperemia as in thickening of the skin as a result of continued application of blistering agents, but arterial hyperemia is as a rule of short duration for it usually terminates in recovery or is succeeded by inflammation. CHAPTER VI. INFLAMMATION. DEFINITION. GENERAL CONSIDERATION OF STIMULI AND REACTIONS. ETIOLOGY. Non-infective. Mechanic. Physic. Chemic. Infective. Nonsuppurative. Suppurative. FACTORS CONCERNED IN INFLAMMATION, (Phenomena). Vascular. Constriction of vessels. Dilatation of vessels. Acceleration of rate of blood How. Retardation of rate of blood Aoiv and leucocytic margination. Oscillation of blood in the vessels and diapedesis. Stasis. Exudation. Exudate. Composition. Physic. Chem ic. Histologic. Varieties. Serous. Fibrinous. Hemorrhagic. Factors determining quality and quantity. Cause of inflammation. Condition of animal. Location of process and of tissue affected. SigniHcance of the exudate. Increased amount of nutrition to the affected part. Dilutes, counteracts, neutralizes or destroys the irritant. Circumscribes the inflammatory process, protects m. m. Spread infection, occludes air cells, produces adhesions. Chemotaxis. Phagocytosis. THE SIGNS OF INFLAMMATION. Redness. Szvelling. Increased temperature. Pain. Impaired function. EFFECTS UPON THE TISSUE INVOLVED. Degeneration. Parenchymatous. Fatty. Mucoid. Serous. Amyloid. Hyaline. Necrosis. Regeneration or proliferation. 138 INFLAMMATION. 139 THE KINDS OF INFLAMMATION. Etiology. Simple. Infective. Nonsuppurative. Suppuratize. Surfiiic. Sub-surface. Exudate. Serous. Fibriftous. Hemorrhagic. Tissue. Parenchymatous. Interstitial. Time, activity and results. Acute. Chronic. Miscellaneous. Catarrhal. Purulent. Ulcerative. I'esicular. Pustular. Proliferative. Specific. TERMINATION. Resolution. Tissue proliferation. Dissolution. CONCLUSIONS. Inflammation is a name applied to a group of pathologic processes including circulatory disturbances, retrogressive and progressive tissue changes. The term inflammation is difficult to define because of tlie several factors entering- into the process and of the variation of each factor. It may be defined as the reaction of a living animal tissue to an irritant. A stimulus is anything that produces action in a living tis- sue. An irritant is anything that produces excessive stimulation in a responsive tissue. Stimuli and irritants differ only in degree. Mild friction of the skin is a stimulus to that structure. When the friction is intensified and the cutaneous function is overstimulated the friction becomes an irritant. All living tis- sues respond to stimuli and likewise to irritants. The response or reaction of a living tissue to an irritant, i. c. excessive tissue stimulation, accompanied by destructive or proliferative tissue changes, and by circulatory disturbances constitutes the pro- cess known as inflammation. The general phenomena of in- flammation will be better understood if some preliminarv con- siderations of the reaction to stimuli are first discussed. General Consideration of Stimuli and Reactions. — It is a 140 VETERINARY PATHOLOGY. well known fact that all living things (organisms) respond to stimuli. A stimulus is that which excites or produces a tem- porary increased vital action, or it is any substance or agent capable of producing activity in a living tissue or producing an impression upon a sensory organ. The extent or degree of response to a stimulus is directly proportional to the organi- zation and complexity of the tissue and especially those tissues which are: (a) capable of being stimulated; (b) capable of trans- mitting an impulse ; and (c) capable of interpreting the impres- sions produced by the impulse. The following discussion of response to stimuli is confined to animal tissues because inflam- mation afTects animals only. Protozoa, although of the simpliest structure, consisting of a single cell, respond to the various stimuli. They respond to light. Thus, if a portion of a cover glass preparation of living amoebae be exposed to intense light, the amoebae in the lighted area will, in a short time, become restless and begin to move about and will finally move away from the area of light. By a specially arranged hot stage, so that there are areas of dififerent temperature, amoebae will be observed to ac- cumulate in the areas of favorable temperature and emigrate from those of unfavorable temperature. That is, they respond to or are responsive to thermic stimuli. In a similar way amoebae respond to various chemical stimuli. If a drop of acid be so placed that it will slowly diffuse into the water or fluid in which the amoebae are being studied, they will move away from the acid. If an amoeba be divided by mechanical means so that one segment contains the entire nucleus and the other segment has no nucleus, it will be observed that the nucleated segment responds to the stimulus by regenerating tissus to re- place the nonnucleated segment which was removed. On the other hand, the nonnucleated segment of the amoeba may survive the shock of separation, but soon begins to degenerate and finally dies. Thus is shown the response of living struc- ture to photic, thermic, chemic and mechanic stimuli. If more complex animals be considered there will be ob- served a similar response to stimuli. Thus, the hydra responds to the various kinds of stimuli and has a remarkable power of regeneration of tissues. Vermes are very responsive to stimuli and all observers have noticed that when an angle-worm is cut in two both ends will crawl away. Vermes are among the lowest forms of animals that possess cells corresponding to white corpuscles or leucocytes of higher animals. These cells are observed to emigrate to the point of injury or to surround INFLAMMATION, 141 the foreign bodies or substances that are experimentally in- troduced into the bodies of vermes. This reaction is analogous lo the reaction of the mammalian leucocytes. The discussion so far, has been with reference to animals that possess no blood or vascular systems, or at least only in a rudimentary form. \'ertebrates are more highly organized and are consequently more responsive to stimuli than invertebrates. Mammalia arc llie most complex in structure of all animals and they are like- wise most responsive to stimuli. The mammalian cornea is a nonvascular structure being composed uf fused layers of fibres arranged parallel to the sur- face. Between the layers of fibres connective tissue cells and lymph spaces are found but no nerves. The cornea is covered externally by the conjunctiva. If the cornea be irritated there will be a reaction, the extent of which depends upon the in- tensity of the irritant. A puncture of the cornea with a sterile needle produces the following reaction or tissue changes ; (a) within a few hours after the injury the afYected area appears swollen and the cells that were punctured begin to degenerate while the uninjured cells immediately surrounding the needle puncture become tumefied and vacuolated ; (b) from twenty to thirty hours after the puncture, wandering cells appear in and around the injured area, and as the cornea is nonvascular they must be migratory connective tissue cells ; (c) by the third or fourth day the punctured cells will have been removed, by solution or otherwise, from the affected areas. Those cells sur- rounding the injury will have divided by mitosis, the newly formed cells replacing those that were destroyed and the wandering cells will have migrated from the injured focus. (The destroyed epithelial cells of the conjunctiva are replaced by those next to the injury). If sterile iron dust, or other insoluble granular material is aseptically introduced into the cornea, a reaction, as described above, will take place, and, in addition, the migratory connec- tive tissue cells will ingest or incorporate the introduced par- ticles and carry them out of the injured focus. When the cornea is injured more severely, as by the ap- plication of a caustic solution (irritant), in addition to the above reaction, a migration of leucocytes from the marginal corneal vessels usually occurs within thirtv hours. Some of the invading leucocytes become destroyed and some of them may multiply, but they usually all disappear from the point of 'njury within from forty to fifty hours. The length of time 142 Veterinary pathology. necessary for repair of such an injury is variable according to the extent of the injury and the readiness of response of the tissue. In vascular tissue the following reaction occurs. An asep- tic cutaneous incision unites almost immediately if the wound margins are placed and maintained in exact apposition. The tumefaction is slight because of the limited extravasate from the severed vessels. There is a slight exudate which coagu- lates and cements the margins or lips of the wound. In a microscopic section through such a wound some cells are found destroyed and others injured. The cells bordering such an in- jury sometimes increase in size to such an extent that they project into the cement between the two incised surfaces. Wan- dering cells and leucocytes in varying numbers appear through- out the entire injured area. The cement (exudate) and the de- generated and necrotic marginal cells are later absorbed. The cells bordering the incision multiply by direct cell division, the newly formed cells replacing those destroyed. New capillaries extend through the newly formed tissue. Finally the leucocytes emigrate and disappear from the injured area. In a more extensive injury, such as a gaping wound that later becomes infected, a more complex reaction is observed. The following changes take place during the first twenty-four hours after an injury of this nature is inflicted. There is hem- orrhage, the extent of which depends upon the size of the ves- sels severed and the gaping of the wound. The extravasated blood accumulates in the wound and also infiltrates the ad- jacent tissues. The injury (irritati(in) causes hyperemia, es- pecially of the arterioles, resulting in engorgement of the capil- laries. From the engorged and dilated capillaries there is marked exudation. The exudate escapes upon the wound sur- face and infiltrates the tissues of the injured area. The ac- cumulation of the hemorrhagic extravasate and the inflam- matory exudate plus the increased size of the vessels (hyper- emia) tumefies or swells the injured area. There is an ac- cumulation of mononuclear leucocytes or wandering connec- tive tissue cells in the injured tissue and an immigration of polymorphonuclear leucocytes. Many cells are destroyed out- right by the injury or by the action of infectious bacteria. Those cells bordering the destroyed cells are injured and be- come tumefied and may later undergo necrosis. The cells, es- pecially the connective tissue cells located peripherally to the injured cells, become enlarged and multiply by indirect cell di- vision. The injured cells are repaired and the newly formed INFLAMMATION. 143 cells are massed together and project outward thus replacing the destroyed cells. The discharge from such a wound after twenty hours con- sists of serum, shreds and fragments of necrotic tissue, dead cells (especially leucocytes) and a variety of microorganisms. The reaction in the above case consists of circulatory dis- turbances, degeneration, necrosis, and regeneration of tissues. Etiology. — The exciting causes of inflammation may act from within the body, hematogenous or lymphogenous, or from without, i. e., extraneous as burning, etc. They may produce their action by direct contact upon surfaces of the body as from a blistering agent externall}^ applied, or, by contact internally, as from arsenic. They may produce their ettect while being ex- creted, as in the production of nephritis by cantharides or tur- pentine. Some harmless agents mav become irritants as the result of chemic change produced by some of the body juices or fluids (lysins). The causes of inflammation may be divided into two gen- eral classes, non-infectious and infectious. NoN-iNFECTious. — The non-infectious causative factors are not as active in producing inflammatory disturbances as the in- fectious agencies, but they are of some importance and should not be overlooked. Some have positively stated that "There is no inflammation without infection." Reasonable interpreta- tions of clinical and experimental observations supply suffi- cient evidence that there is inflammation without infection. The following are the principal non-infectious causes of in- flammation. Mechanic or traumatic. — Surgical wounds which heal by primary union are undisputed examples of mechanically pro- duced inflammation. The reaction taking place in an aseptic incision consists in cell-destruction, slight circulatory disturb- ances, leucocytic immigration and regeneration of tissue. Such a reaction is typical of inflammation and the affected area is devoid of any infection. A sterile needle introduced into a tissue, the surface of which is aseptic, produces a reaction identical to the reaction observed in primary union of tissue. Mechanic or traumatic causes of inflammation may produce, or cause to be produced in the injured cells, chemic substances that are responsible for the reaction. Thermic. — A temporary exposure to a high or low tein- perature is sufficiently irritating to produce a marked inflam- mation. Let those doubting this statement take the chimney from a lighted lamp and hold it in the hand for one minute and 144 VETERINARY rATIIOLOGY. they win acknowledge that heat produces all the symptomatic evidences of inflammation and there is no infection. The prin- ciple object in the use of the thermo-cautery is to produce or establish inflammation. A thermo-cautery, or any severe burn, produces tissue necrosis, as well as the destruction of bacteria in that area (sterilization), and an inflammatory zone is im- mediately established around the necrotic tissue which is sterile and may remain free from infection. A short exposure to an extremely low temperature produces an inflammation. If the exposure is of long duration necrosis is likely to occur. "Chilblains" is an inflammation resulting from temporary exposure to a low temperature. Sloughing following freezing of calves' ears, pigs' tails and cocks' combs are familiar examples of necrosis resulting from long exposure to extremely low temperature. An inflammatory zone is es- tablished around necrotic areas produced by freezing similar to the inflammatory zone observed around necrotic areas pro- duced by burning. Thermic variations may produce chemic substances in injured tissues which are sufficiently irritating to establish inflammation. Electric. — It is cominon knowledge that electricity causes inflammation. Animals injured by lightning usually show evi- dences of cutaneous inflammation. In cities animals as well as men frequently contact wires charged with powerful electric currents and receive local injuries that are usually inflammatory in their nature. Chemic. — There are ma^ny chemicals tliat are irritants. A number of them are used as therapeutic agents when irritants are indicated. Mineral acids, caustic alkalies, mercury salts and arsenic are some examples of chemic agents that produce inflammation when applied in dilute solutions, and necrosis when applied in more concentrated form. A 10 per cent solu- tion of nitric acid applied to the skin for a very short time pro- duces inflammation. Inflammatory symptoms following the nitric acid application appear immediately ; and, as the acid is a disinfectant, the inflammation cannot be the result of infec- tion. In animals poisoned by any of the mineral poisons there may always be observed an inflammation in the mucosa of the alimentary tract more extensive than could have been produced by infection in the limited time of action. Many reptiles, bees, wasps, and ants introduce chemic sub- stances into animal tissues that are extremely injurious and es- tablish inflammation of very rapid evolution. Infectious or vital agencies are the most important etiologic INFLAMMATION. 145 factors in the production of inflammation because they are the most frequent offenders. Infection usuaHy produce inllam- matory disturbances through the action of chemic substances elaborated by the infecting micro-organisms, as metabolic pro- ducts. The infection may be local and produce localized in- flammation as in a superficial abscess and in coccidiosis. The elaborated chemic substances may be absorbed from the local- ized infection and produce inflammation elsewhere in the body. Infection may be general and produce conditions similar to in- flammation in practically all the tissues of the body as in gen- eralized anthrax. Plowever, the term inflammation is usually confined to local disturbances. The extent of irritation pro- duced by any infecting organism is dependent upon the virul- cncy of the given organism and the resistance of the infected ammal. Thus, infection with Streptococcus pyogenes equi may produce pyemia in one animal and only a local abscess in an- other. Again, some bacteria, as the anthrax bacilli, may pro- duce septicaemia in one animal and localized inflammaiion in another. A concise etiological classification of inflammation produced b}- living organisms is impossible because of variations both in the virulency of the organisms and in the resistance of the tissues. Animal parasites are of consideral^le consecpience in tlie production of inflammation. Thev may produce inflam- mation by mechanical interference, as the Echinorychus gigas which inserts its barbed proboscis into the intestinal mucosa thus injuring the tissue as well as opening an avenue for the entrance of various bacteria. 'J'he Trichina spiralis by perfor- ating the intestinal wall and bv burrowing in the muscular tissue produces sufficient irritation to establish inflammation, the results of which are evidenced on microscopic examina- tion of a lesion. It has been suggested that the etiological factor of rabies is an animal parasite; the round-celled infil- tration of the ganglionic nerve cells and perivascular spaces having marked cliaractcristics of the lesions of inflammation. Psorospermosis, a condition resulting from psorospermic in- festation, is inflammatorv in its character. In a general way infective inflammations mav be discussed as non-suppurative and suppurative. The non-suppurative infective inflammations are those in- flammatory disturbances in which there is no purulent fluid or pus produced. As examples the following mav be cited — septic infection succeeding nail pricks in horses feet; blackleg in calves caused by the Bacillus anthracis s^mptomaticus, (Sar- 146 VETERINARY PATHOLOGY. cophysematous bovis) ; malignant oedema caused by the Bacil- lus of malignant oedema. Suppurative infective inflammation is characterized by the formation of pus. The causative bacterial agents of suppura- tion are designated as pyogenic bacteria or pyobacteria. The following are the most important bacteria of this class: Micrococcus pyogenes aureus. Micrococcus pyogenes albus. Micrococcus pyogenes citreus. Strepto-coccus pyogenes. Bacillus pyocyaneus. Factors Concerned in Inflammation. — The animal body is an intricate mechanism composed of different tissues in various combinations. The phenomena of inflammation are the changes that take place in the tissues plus the conditions resulting from those tissue changes, thus including all the changes taking place in the inflammatory focus. The following are the most impor- tant. Vascular disturbances. — These are universally present in animals possessing a vascular system, but inflammation, or a condition analagous to it, occurs in the tissues of animals that have no vascular system, and in nonvascular tissues of animals that have a vascular system. Hence vascular changes are not essential in the process. The vascular changes are dependent upon nervous influence, because the calibre of blood vessels, especially arteries, is controlled by vasomotor nerves. Inflam- matory areas become necrotic when dilatation of the supplying arteries and arterioles is inhibited. In experiments in which dilatation of the arterioles takes place mild inflammatory pro- cesses are limited and usually terminate in recovery in a short time. Necrosis usually succeeds inflammation in tissues in which continuity of the vasomotor nerves have been de- stroyed. For example, the cubital nerve in the horse probably contains the vasomotor fibres that innervate the vessels of the foot and the median nerve the sensitive fibres that innervate the pedal structures. ]\Tedian neurectomy is not succeeded by vascular disturbances, but cubital neurectomy is frequently succeeded by vascular disturbances and excessive exudation that terminates in necrosis followed by sloughing of the hoof. The following vascular changes occur in an inflammatory focus and in the order designated: Decreased calibre of the supplying arteries and arterioles. INFLAMMATION'. 14; Temporary contraction of arteries is the first result of the applica- tion of an irritant. The cause of the constriction of the arteries is a spasmodic contraction, which is of vaso-motor origin, of the muscu- lature of the vessels. This is succeeded by a marked arterial dilatation. Dilatation of the arteries and arterioles. The response to stimuli on the arteries is rapid and always active, in veins slow and usually passive, in capillaries either rapid or slow but always passive. Dila- tation of vessels in an inflamed area is also of vaso-motor origin and is said to be caused bv stimulation of the vaso-dilators or inhibition Fig. "■). — Blood ve.sscl. fhowinK Corpuwles occupying ciiitral portion of .I'.ream, iypical of i)nr;iial ( irculation. of the vaso-constrictor nerves. An increase in the calibre of the arteries results in an increased amount of blood flowing thrtnigh them and into the capillaries. The increased amount of blood in the capillaries mechanically increases their calibre and also in- creases the amount of bloc id which enters the related veins and results in a dilatation of them. l*>y increasing the lumen ot a \essel the resistance to the flowing contents is correspondingly diminislicd and this results in a temporary acceleration of the rate of blood flow. Acceleration of the rate of flow of the blood. The cor- puscles occupy the axial, or central part of the stream as in the normal circulating blood. The arterial dilatation plus the acceleration of the blood flow constitute the essential factors in active hyperemia. 148 \ETERINARY PATHOLOGY Retardation of the rate of flonj. — A long continued dilata-" tion of a vessel results in injury especially to the endothelial lining. The injured endothelial cells become swollen, rough- ened and sticky. The leucocytes begin to appear in the peri- pheral portion of the stream, probably because of the libera- tion of some chemic substance by the endothelium that exerts a limited chemotactic action upon the leucocytes. They roll, O O o o c S^^' '•» ® «- ^o ^ ^. o "^ o „ o o^ "OO^'O or,Or o <-> o^'^ Fig. 75. — Dilated blood vessel showing corpusoles spread throughout the entire lumen typical of first stages of hyperemia. tumble, and creep along over the swollen endothelial cells and finally adhere to their roughened surfaces. The continued at- tachment of leucocytes to the endothelium diminishes the cali- bre of the vessel and increases the resistance thus retarding the rate of blood flow. Oscillation. — The resistance of the flowing blood, due to the roughened endothelium of the vessels and accumulation of leucocytes becomes so increased that the propelling force is momentarily overcome. The blood in the engorged capillaries and arteries may temporarily cease flowing or it may flow toward the heart, i. e. in the reverse direction during the dias- tolic periods. This to and fro movement is termed oscillation. IXFLAMMATIOX. 149 Stasis. — The resistance may become greater than the pro- pelling- force and the circnlatiim cease for a varyin*^ period of time. 'This condition is denominated stasis. Ji.viidatioii. — \ arying qnantities of the iluid and of the cell- ular constituents of the blood pass through the vessels nor- mally and an increased quantity escapes through during in- flammation. The i)ortion of the blood that escapes through the Idood vessels is called exudate. The passing of the exudate -^"■ ^S^^c?-^^-'^^ Fig. 76. — Blood vessel showins marginatlon of leucocytes typical of th,- liist staije.s of inllammation. through the vessel wall is termed exudation. It is a muted •juestion whether the normal tissue lymph is a secretory pro- duct of the capillary endothelium or is jn-oduced bv such physi- cal processes as diffusion or filtration. Tlie source of the in- flammatory exudate is no doubt, the same as the source of nor- mal tissue lym])h. Exudation is a result of th.e vascular dis- tur1)anccs. It has been ])reviousl\- stated that in normal circulatorv blood the corpuscles occupy the axial stream and the plasma the 150 VETERINARY PATHOLOGY. peripheral stream. The corpuscles occupy the axial stream because they have a greater specific gravity than the plasma. The leucocytes enter the peripheral or plasmatic stream in inflam- mation, that is margination is a result of chemotactic influences. After the leucocytes become marginated they pass through the vessel wall as follows : Small protoplasmic processes extend and project through the vessel wall. These processes gradually increase in size until the entire leucocyte has, by protoplasmic extension, passed through. The leucocytes usually pass be- tween the endothelial cells but they may pass directly through O ^ . ^, ^. «..u ^ •^' i'ie 77. — Blood vessel showing diapede^s of leucocytes typical of the exudative stage of inflammation. them. The exudation of erythrocytes is passive, the cells being forced through the vessel wall by pressure. To recapitulate: fluid exudation is either a physical process, such as filtration, or a physiologic process, a secretion ; leucocytic exudation is a physiologic process depending largely upon the chemic influ- ences of the adjacent tissues, i. e., chemotaxis; exudation of erythrocytes is a physical process resulting from intravascular pressure plus diminished resistance of the vessel wall. Exudate. 1. Composition. — Inflammatory exudate contains varying quantities of cells suspended in a fluid (plasma, tissue juice, etc). The fluid part of the exudate contains proteids (serum albumin and serum globulin) in excess of normal plasma. It has a specific gravity of 1018 or more. The quantity of pro- teid is directly proportional to the severity of the process and INFLAAlMATtOX. 151 is never less than 4 per cent and frequently as much as per cent. It usually coagulates readily if witlulrawn from the in- flammatory tissues. The coagulability of intlammatory exudate is so constant that it may be used in differentiating inflamma- tion from oedema. The' exudate is usually acid in reaction. The fluid portion of the exudate is similar to the blood plasma with the exception of the varying percentage of proteids, and the presence of some other soluble substances. Leucocytes are the principal cellular elements found in the exudate, erythrocytes occurring only in certain inllammatory conditions, such as croupus pneumonia. The following types of leucocytes are especially concerned in inflammation : polymorphonuclear leucocytes, lymphocytes small and large. Polymorphonuclear leucocytes with neutrophile gran- ules arc the type most frequently found in an area aft'ccted with acute inflammation, providing the causative irritant was not too severe. About 70 per cent of the leucocytes present are of this type. These cells appear in the affected area in the be- gining of the process. They have the- power of amoeboid movement and may emigrate from the blood and lymph vessels indcpendentlv of the fluid exudate. These cells possess phago- cytic properties and m»-.y produce and lil)erate antitoxic and bactericidal substances. They are the pus cells and constitute the bulk of the exudate in suppuration. These cells may be destroyed and disintegrated in the field of action or when the inflammatory process ceases they may migrate from the in- jured area and reenter the lymph or blood vessels.^ They do not become formative cells and never produce new tissue. Eosinophylic leucocytes, (polymorphonuclear leucocytes hav- pig. 7s . — Types of rolls in inflammatory exudates. Lvmnhocvte " •)— n l'olymorphonu< Uar leucocytes. Mononuclear leucocyte. 6. Endothelial cells from lining ol an arterj . Transitional leucocyte. 152 Veterinary pathology. ing acidophile granules), appear early in an inflamed area. They are usually quite limited in number except in localized inflammation induced by animal parasites. Foci, composed of a mass of eosinophiles, are frequently observed in the liver, kidney, and other tissues, and appear as inflammatory centers. These eosinophilic inflammatory foci are probably the result of invasion of animal parasites. Eosinophiles are abundant in the lesions of bursattae and in epizootic lymphangitis. Their origin is, so far as has been determined, from the blood, the lymph and tissue spaces indirectly, and the bone marrow di- rectly. The specific action of these cells in inflammation is not known. They do not aid in the formation of new tissues. Mast cells or polymorphonuclear leucocytes with basophile granules are observed in subacute inflammation (Adami). Their origin is from bone marrow. Their nuclei apparently become disintegrated in inflamed tissue. The significance of these cells has not been determined. Lymphocytic invasion of the affected areas and an excess of them in the l^lood characterize some of the slow .cooing or chronic inflammatory processes such as tuberculosis and ac- tinomycosis. These cells also appear in afi'ected tissues in the later stage of acute inflammation but are never very abundant. They may have their origin from the blood, the lymph and from adjacent lymphoid tissue. The large lymphocytes may have their origin from the small lymphocytes. Lymphocytes have a very limited power of amoeboid movement. They have never been observed to ingest bacteria although they may in- corporate fragments of destroyed tissue cells or other inert sub- stances. These cells may partake in the formation of new tis- sue but this has not yet been positively determined. Cells other than leucocytes are sometimes observed in in- flammatory foci. Endothelial cells, wandering connective tis- sue cells, giant cells, and red blood corpuscles may be present in inflamed areas. Endothelial or mesothelial cells are especially evident in the exudate of a serous membrane affected with inflammation. They appear later in the process than either polymorphonuclear leucocytes or lymphocytes. Their origin is probably from pre-existing, like cells of the serous membrane. They usually have a sluggish move- ment, are slightly phagocytic and also ingest fragments or particles of inert substances. These cells may be destroyed or they may emigrate from the affected area. Wandering connective tissue cells are usually present in inflamed tissues. These cells do not appear until some time IXFLAM.\[ATroX. 153 after the injury is inflicted because of their slow movement. 'I'heir source is from tissue spaces, and they are the preexist- insjf wandering- connective tissue cells that occur in practically all tissues of the immature animal. They mav l)e phagocytic l)ut this property is not usuallv well developed. They are es- pecially active in the process of repair. Giant cells, so-called, are of common occurrence in some in- tlammatory processes especially tuberculosis and actinomycosis. It is probable that endothelial cells are the progenitors of ..■?-';2^^-''' ''."' ,'^;f '.^^^■■- ■ '•»^V -',,..»i^;f PIgr. 79. — Gastritis, hog, induoed by a caustic, showing- ilestruction of gastric mucosa. giant cells. Wandering connective tissue cells may produce giant cells. The giant cells may be formed either by a multiplication of nuclei without division of the cell body or by a fusion of several independent cells (Syncytium). The latter view is the one most accepted at the present time. The function of the giant cell has not been specifically determined, but those in tubercular lesions frequently contain many tubercle bacilli indicating that they are phagocytic. Red blood corpuscles or erythrocytes occur in the inflam- matory exudate as a result of intense engorgement of the ves- sels. They begin passing through tlie vessel wall after the leucocytic migration. Increased intravascular pressure is the principal cause of their escape from the vessel, their passage through the vessel wall being entirelv passive. 154 VETERINARY PATHOLOGY. 2. Varieties. — Inflammatory exudates mfiy be serous, fibrin- ous, or hemorrhagic. a. A serous exudate continues in the fluid state as long as it remains in the tissues or tissue spaces. It is composed almost entirely of fluid, having very few cells. This variety of ex- udate is characteristic of mild inflammatory conditions. The constancy of the fluidity of the serous exudate is the result of the action of enzyms that continually convert the albuminous substances into soluble compounds as proteoses and peptones. b. Inflammatory fibrinous exudate contains two enzyms, one of which (leucoprotase) is active in an alkaline medium and the other in an acid medium. "These enzyms probably exert their greatest activity in a neutral medium, slight changes in reaction increasing digestion by the one, and suspending di- Fig. 80. — .\cute Pleurisy. Engorged vessels. gestion by the other." In suppuration the acid digesting enzym probably disappears (Barker). A fibrinous exudate is one that coagulates within the tissues or tissue spaces. The coagu- lation of the exudate is identical with the coagulation of blood and is probably due to the liberation of fibrin forming enzyms from disintegrated leucocytes. Fibrinous exudate is the variety observed in inflammation resulting from severe irritation. The exudate usually contains many cells and a large amount c>f proteids. c. Hemorrhagic exudates are those in which the red blood cells as well as leucocytes and plasma have passed through the ves- sel wall. This exudate coagulates the same as the fibrinous IXFLAMMATlrj.V. 155 exudate. Intense irritants arc usually the causative agents of hcnuirrhajric inflammation. Croupous pneumonia is charactcr- i/.eil by a hemorrhagic exudate. A so-called purulent exudate has been described l)ut pus is not purely exudative for some of its constituents are not derived from the blood. Pus is composed of altered leucocytes, tissue shreds, and usually pyo-microorganisms, suspended in a fluid-liquor- puris. Liquor puris is blood plasma and dissolved tissue. Pus contains no fibrin, the proteid constituents being converted into soluble compounds by cellular enzymes and bacterial f( rments. 3. The following are probably the determining factors of the quality and quantity of inflammatory exudate. a. Cause of inflammation: — Generally speaking a mild irritant or injury produces a serous inflammation, and an intense ir- ritant produces fibrinous inflammation. Mechanical injuries, when there are no surface abrasions, produce an inflammation of a mild degree and the exudate is limited m (piantity and is tisuallv of a serous nature. Such injuries, however, usually produce abrasions which fa\or the invasion of micro organisms. Thermal disturbances of mild degree, produce a serous ex- udate, if more severe the exudate is extensive and of a fibrin- ous or hemorrhagic character. The use of a thermo-cautcry is an excellent example of thermal production of inflammation and the severitv of its use demonstrates the intensity of inflamma- tion and the variations of the exudate. An irritating chemical substance injected into a tissue produces intlammation char- acterized by excessive exudation especially of a serous fluid. The more irritating the chemical, the greater the quantity of exudate and the greater the percentage of proteids. External application of chemical irritants produces inflammation char- acterized by a serous or by a fibrinous exudate. This latter may be observed in the application of blistering agents. In- fective inflammation is usuallv accomj)anied by a marked exu- date from the beginning of the infection. The quantity and quality of the exudate varies with the virulency of the organ- ism. There are some exceptitMis however, e. g., tetanus infec- tion causes a verv limited exudate regardless of the virulency of the tetanus bacillus. In some infections, as malignant oedema, the exudate is largely fluid. In suppuration the ex- udate is almost entirely leucocytic. b. Condition of the^ animal effected. The exudate is usually limited in animals having normal vessels, heart action, and blood. In those animals in which the vessels are diseased and especially if the endothelium has been injured there is a ten- 156 Veterinary pathology. j dency to excessive exudation. A weak heart is conducive to excessive exudation, e. g., inflammatorv oedema. Animals pos- sessing- dilute blood (hydremia) are predisposed to excessive fluid exudation. The leucocytic amoeboid movement may be tem- porarily suspended, or it may be increased during inflamma- tion, resulting in an absence or in an excessive number of leucocytes in the exudate. In animals having a clean close build the exudate is not so extensive as it is in those animals of a loose flabby make-up. c. The location and tissue affected. Exudation is in direct pro- portion to the vascularity and density of the tissue. Inflam- mation in compact bony tissue or beneath dense fascia, liga- Fig. 81 — Acute ^leningitis. a. Exudate. b. Engorged vessels. ments or tendons is accompanied by a limited exudate. In- flammation of the cutaneous structure is usually associated with excessive exudation, which accumulates in the subcutane- ous areolar tissue. Inflammation of serous and mucous mem- branes is accompanied with exudation which may in part be discharged upon the surface but is usually accumulated in the substructures. 4. Significance of the exudate. — The significance of the exu- date has had various interpretations. Virchow considered that the irritation producing the inflammation resulted in increased cellular activity in the injured area and that the exudate sup- plied increased nourishment to the area in which there was an excessive metabolism. Others have attributed to the exudate the "flushing out" of the injured area thus mechanically carrying INFLA^[^r.\TIo^^ 157 r-a away the irritant. The exudate dilutes the irritant, especially chemical irritants, thus reducing the activity of the causative agent and mitigating tlie inflammatory process. It has been delermined tliat serum possesses some sub- stances, as opsonins, antitoxins. b.aoteriolysins and bactericides, that are detrimental to infectious agents either Ijy their bacter- icidal action or by chemical union with bacterial i)roducts. Thus the exudate has a ten- dency to reduce the ir- ritation of infection by rendering bacteria in- active or less active, or by n e u t r a 1 i z i n g their products. Phago- cytes are very import- ant factors in the exu- date as they ingest and destroy infectious mi- cro-organisms. In aseptic incised wounds the exudate is of value in cementing the incised surfaces to- gether, although new tissue formation is re- tarded by an exudate. The exudate mechanically protects the in- jured surfaces in ga{)ing wounds and possesses bactericidal proper- ties for a short time after the injury has been inflicted. After the exudate becomes inactive in its protecting ]iro]ierties it is a favorable medium for infection and is then probably detrimental. Injurious chemic substances may result from the aseptic dissolution of an inflammatory exudate. Thus the exudate that fills the air cells in croupous pneumonia may become putrefied by the infection and activity of putrefying bacteria and the absorp- tion of the putrid material would be detrimental to the animal economy. The extent of which would depend upon the condition of the animal body and the quantity of putrid material absorbed. Fibrinous exudates may be injurious or beneficial depending upon the location and the changes taking place in the exu- date. The fibrinous exudate in croupous pneumonia is injuri- ous because it coagulates in the alveoli of the lung thus pre- venting the respiratory function of that area. The fibrinous Fi3. 82. — Inilainmatioii. i;ra> Ileputization. a. Air ctlls ens'rsui "iUi Uucocytes. b. Hyperemia of capillaries. 158 VETEklNARY PATHOLOGY. exudate in serous cavities is beneficial, especially in localized intlammation, because it limits or circumscribes the inflamma- tory irritant or process by coagulating thus producing adhe- sions of the two serous membranes. Many horses upon which paracentesis abdominis or paracentesis thoracis is performed might succumb to generalized peritonitis or pleurisy if the inflammatory process established at the point of the puncture was not circumscribed bv adhesions the result of organization Fig. 83. — Fibrinous Pleurisy, showing an extensive exudate upon surface, of fibrinous exudate. The immediate efifect of a fibrinous exu- date in a serous cavity is beneficial but the adhesions are fre- quently permanent thus interfering with the normal function- ing of the part afifected. The fibrinous exudate is also benefi- cial in croupous enteritis because of the protection of the dis- eased mucosa from mechanical injuries by food stuffs. It is on the other hand injurious in croupous enteritis for the exu- date is a favorable nidus for bacteria and they may produce substances that are irritating to the injured mucosa. The coagulated exudate may also hinder intestinal secretion. The INFLAMMATION. 159 fibrinous exudate of dipluhcritic intlammation is very injurious because of its coagulation and pressure upon the tissues. Inflammatory exudate is usually beneficial in inflamed areas until opsonins, antibodies, and bacteriacidal substances become neutral- ized or inert and the phagocytic cells impaired or destroyed, after which the exudate is usually injurious as it is a mass of foreign dead nitrogenous substances that serves as an excellent food for various bacteria. CiiiiMOTAxis. — It has been iletcrmincMJ by ex]ierinient that chemic substances exert a definite influence upon motile cells. There is always a leucocytic migration into capillary glass tubes previously charged with turpentine or croton oil and tlien in'-ert- ed into living animal tissues. The same migration is obsci-ved when the capillary tubes are charged with bacteria or their products. Negative results are obtained when the tubes are charged with cjuinine or chloroform. This attraction of leuco- cytes toward chemic substances is positive chemotaxis. The repulsion of leucocytes from chemic substances is negative chem- otaxis. The term "Chemotaxis" unmodified includes positive and negative. Leucocytic migration into an inflammatory area is a result of chemic influence or chemotaxis. Phagocytosis. — This is the incorporation and destruction of pathogenic bacteria and other foreign substances by phagocytes. Phagocytes are cells having the power of ingesting and destroy- ing microorganisms and other foreign particles. Polymorpho- nuclear leucocytes ha\ ing ncutrophile granules are the most ac- tive cells concerned in phagocytosis. Endothelial cells and wan- dering connective tissue cells may under some conditions be phagocytic. The phagocytic property of cells is variable depending upon the virulencv of the micro-organisms or strength of the chemic substance and upon the resistance of the phagocyte. Bac- teria are enveloped by protoplasmic extensions from the cell bodv until they are entirely included in the aggressive phago- cyte. After the envclr)j:)ing ])rocess there mav be observed diges- tion vacuoles surrounding the bacteria. The included bacteria are destroyetl bv ferments produced by the phagocyte. It is an intracellular digestion. The length of time necessary for the phagocyte to destroy the bacteria is variable. The bacterial destruction mav be instantaneous or the bacteria may possess sufficient vitalitv to destrnv the phagocyte. There is consider- able evidence that infection is frequently generalized in the ani- mal body by leucocytes that have enveloped bacteria and wan- dered to another portion (tf the body. The included bacteria destroy the leucocyte and, thus liberated, establish a new cen- ter of infection. 160 VETKRIXARY PATHOLOGY. Phag-ocytosis is a very important factor in inflammation. No donbt many localized inflammatory conditions are aborted and the intensity of the attack of other infective inflamma- tory conditions reduced liy tlie process of phag'ocytosis. There is a peculiar variation of phagocytosis occasionally observed, e. g., leucocytes becoming phagocytic toward other leucocytes. Fixed tissue cells may under some conditions become phago- cytic towards leucocytes ; this perhaps is for the purpose of obtaining nutrition for the fixed tissue cells. The Signs of Inflam- mation. — Inflamma- mation may be recog- nized in exposed tis- sues by the so-called "Cardinal signs :" red- ness, swelling, increas- ed temperature, pain and impaired function. These signs are usual- ly perceptible in the early stages of acute inflammation, but they may not be evident throughout the entire process. Mild, chronic inflammation may not be accompanied by any of the above signs. These s.ignj- are very variable in their acute or chronic inflammation of internal or- gans. Redness (Rubor) is a constant sign in the early stages of acute inflammation. It is the result of an excessive amount of blood in the vessels of the afTected area. SiveHiiig (Tumor) is characteristic of acute inflammation. It is the result of the accumulation and retention of the inflam- matory exudate plus the increased amount of blood in the part. The extent of the swelling is in a direct ratio to the density of the tissue. Thus the swelling resulting from subperiosteal in- flammation mav not be detected because of its limited extent. On the other hand, the swelling succeeding inflammation of loose areolar tissue may be very extensive, as in cellulitis. The swelling resulting from inflammation is usuallv firm, dense and quite resistant in contradistinction to swelling resulting from Fig. S4. — .4cute M.vositis. Leiwoojlis exudate. Muscle fibres disinte- grated and vessels engorged. IXI-LAM.MATIOX. 161 oedema, e. gf., the tumefaction accompanyinpr tendonitis is dense, while tlic swelling accompanying^ "slocking"' is soft and doughy. 'J'!u' t'.-iiil'craturc ( Calor ) of tissue affected with active in- flammation is invariably increased. This is the result of the excessive cellular action in the inflamed area and the increased amount of blood flowing into the part. Pain (Dolor) is a common symptom cf inflammation. This may be the result of pressure upon nerve endings bv the accu- mulated exudate. However, oedema is accompanied bv an ex- cessive accumulation of fluid in the tissues, and oedcmatous tissues are not hypersensitive. It seems more probable that in- flammatory pain is the result of the injurious action of the chcmic irritants or soluble protlucts of the exudate upon the sensory nerve endings. The inflammatory pain is often referred to some other part of the body, e. g., in pleurisv the pain frequently appears abdominal. Impaired f\inct'wn (Functio laeso ) is a constant feature ob- served in inflammation. In the beginning of the process the function of the affected tissues (especially secrctc^ry) is in ex- cess of the normal, but this is succeeded in the later stages by depression of the function. The increased function is a result of increased nouri^^hment. increased stimulation, and probably increased pressure is also a factor; the depressed or diminished function is the result of the injurious action of katabolic prod- ucts, produced by excessive cellular action, and of llie irritant producing the inflammatory process. Thus, in the beginning of acute nephritis there is an excessive amount of fluid (urine) excreted, this is succeeded by diminution or complete suppres- sion of the excietion (urine). Effects upon the Tissue Involved. — .\s a result of the inflammatory process the tissues involved may un- dergo various changes. These changes may be dcqcncrativc. necrotic, rcqcucratn'C or prolifcratii'c in character. Degenera- tion usually jirecedes regeneration, but the two conditions may be inde])endent of each other; thus in ulceration, degeneration and necrosris may alone be evident, and in the formation of a tubercle of tuberculosis proliferation is the principal process. Both conditions may exist at the same time in different parts of an afi^ected area, degeneration taking place in the center of the diseased area and regeneration or proliferation in the peri- phery. Inflammation not accompanied by either degeneration or regeneration is rare. The injuries or irritants establishing inflammation may and frequently do produce death of some of the tissue cells; necrotic tissue is sufficiently irritating to pro- 162 VETERINARY PATHOLOGY. duce inflammation, and necrotic areas are usually surrounded by an inflammatory zone. Inflammation is confined to the reactive process of the injured cells and should not be confused with the death of the cells or necrosis. Degeneration and regeneration are distinctly opposite pro- cesses. The former is destructive, resulting in impairment and death, while the latter is constructive, resulting in overgrowth and proliferation. Degeneration is caused by insufiicient food, by the chemic action of certain poisons, or excessive and frequently perverted functional activity. Regeneration occurs when there is an adequate supply of nutrition, and depends upon the rever- Fig. 85. — Chronio Pneumonia. a. Alveolus. c. Wandering leucocytes b. Fibrous proliferation. sion of the cells to the embryonic type or stimulation of the reproductive properties of the cells, the latter usually at the expense of the normal functional activity. Both processes afifect the cellular elements of the tissues, primarily and actively, and the intercellular substances secondarily and passively. Some exceptions will be mentioned later. The leucocytes and wander- ing cells may also undergo changes similar to those which the fixed tissue cells are subject. In general, degeneration character- izes acute inflammation and regeneration characterizes chronic inflammation. The importance of either of the above processes depends upon their extent The general consideration of the two processes has been combined for the sake of comparison; but they will now^ be considered separately. Degeneration. — Practically all degenerations, to which tis- INFLAMMATION. 163 si'cs in general are subject, arc common in inflamed tissues. The following- are the principal ones that have Ijcen dcscriljed. 1. Parenchynialous (k\i;encralion (cloudy swellinm), is the most common type in acute inflammatory tissues. It is indeed rare to examine sections of tissue affected with acute inflammation and not find this degeneratit)n. The presence of parcnch\niatous degeneration is an additional factor frequently resorted to in diff- erential diagnosis of inflammation. This type of degeneration occurs in all tissues, but more especially in glandular structures. 2. Fatty degeneration does not occur as frequently as paren- chymatous degeneration. Like parenchymatous degeneration, it occurs in tissues aff'ected Avith acute inflanuuation. It in- variably occurs in combination with parenchymatous degenera- tion and is usually a seciuel of the latter. The presence of fatty degeneration in inflanuuatory tissue may cause confusion in microscopic diagnosis, esi)ecially if the degeneration is exten- sive. The degeneration is common in epithelium (glandular), muscular tissue and connective tissue. 3. Mucoid degeneration is quite conuuon in inflamed tissues. It is characteristic of catarrhal inflammation. This degenera- tion affects the intercellular substance as well as the cells. Mucus is bactericidal, therefore it is protectant and beneficial, unless produced in sufficient quantity to induce mechanical in- jury. Epithelium and connective tissue are most frequently afifected by this degeneration. 4. Serous degeneration, or more properly infiltration, is char- acteristic of tissues affected with inflammatory oedema or other inflammations in which there is excessive serous exudation. This condition results from the passage into the cells of extra- cellular serous fluid. The infiltrated fluid mechanically inter- feres with the activity of the cell. It occurs most frequently in muscular and connective tissue and occasionally in epi- thelium. 5. Hyaline degeneration is of common occurrence in tissues affected with chronic inflammation. It is the conversion of the tissue into a clear, waxy substance. It is common in the mus- cular tissue of blood vessels in chronic inflammatory foci as well as in fibrous tissue resulting from proliferative inflamma- tion. 6. Am\lMid degeneration lias been observed in chronic inflam- matory tissues (Adanii), although this is not a common se.juel of inflammation. An intercellular degeneration specifically afifecting the ce- ment substances between the myocardial cells has frequently 164 VETERINARY PATHOLOGY. been observed in myocarditis. This causes a separation of the heart muscle cells, i. e., fragmentation, which seriously inter- feres with their function. The striations of muscle cells fre- quently disappear as a result of inflammation. Necrosis (local death). — All degenerations produce impair- ment of function and frequently end in necrosis of the affected cells. Destruction of tissue is a common result of inflammation because of the various degenerations that accompany the in- flammatory process. Suppuration is a type of inflammation and is a liquifying necrosis. Necrosis of inflammatory tissue often occurs independently of suppuration, though both conditions result from the same cause. Destroyed tissue constitutes a fac- tor in the future changes that occur in the affected tissue. Superficial necrotic tissue is usually cast off. Ulceration is the condition resulting from a continuous and sometimes a pro- gressive cellular necrosis. An ulcer is a denuded surface result- ing from continuous and sometimes a progressive cellular necrosis. Subsurface necrotic tissue may be disintegrated or dissolved, and pass out of the affected area in the exudate or be carried out by phagocytes; necrotic tissue may become surrounded and permeated by large numbers of leucocytes which liberate dis- solving ferments, thus forming an abscess ; this liquefied necro- tic mass may become inspissated, a condition termed caseation; the necrotic tissue may become impregnated with calcium salts, denominated calcification ; finally, the necrotic tissue may be- come dissolved and encapsulated, thus forming a cyst. Rcc/cncratioit. — This process usually begins when degenera- tion ceases, although it may be evident from the first. Cells concerned in regeneration undergo a reversionary change, be- coming similar to embryonic cells. Reproduction is an active, vital property of embryonic cells, and this is also the principal function of regenerating cells. The appearance of a tissue con- taining an exudate with the succeeding degeneration has been previously discussed. A concise comprehension of such tissue is essential to a clear conception of the appearance of regenera- tion in an inflammatory zone. Whether degenerated cells are capable of regeneration depends upon the kind of cells and the extent of the injury to them. Regeneration of tissues impaired or destroyed bv acute inflammation consists in the enlargement and proliferation of the contiguous uninjured cells. The exu- date is usually diminished in quantity at this stage. Prolifera- tion in tissues affected with chronic inflammation is, in reality, a fibrous hyperplasia. Cirrhosis of any structure is usually the IMLAMMATIOX, 165 result of chronic inrianimation. The lowest types of tissues, i. e., those passive in function, are most easily and most frequently regenerated, e. g., connective tissue. Surface epithelium is fre- quently regenerated — muscular and nervous tissues are rarely :'«?*'* «■ Hi Fig. SG. — Chronic Hepatitis, showing intralobular fibrous formation, which results in li.\ piitrophic- cirrhosis. regenerated. The age of the individual is an important factor in the regeneration of injured tissues. Tissues in young animals regenerate more readily than like tissues in old animals. The origin or source of the cells that regenerate connective tissue is still a disputed point. It is certain that fi.xed and wander- ing connective tissue cells are capable of this function. Endothelial cells are a type of fixed connective tissue cells which are active in regeneration of connective tissue. ^Fononuclear leucocytes as well as lymphocytes may be capalile of producing connective tissue. The regenerating connective tissue cells (fibroblasts) are either oval or 166 VETERINARY PATHOLOGY. spindle shaped, the latter predominating, especially during the active regeneration period. Endothelial cells are active in the production of new vessels. Inflammatory tissue is usually more vascular than normal tissue. In the vascularization of an inflammatory area the endothelial cells produce long protoplasmic projections. Several of these projec- tions of different adjacent cells may fuse, thus forming an anasto- motic channel, or a single projection may separate in a longitudinal direction, thus producing an extension of the old channel. As the protoplasmic projections become larger and longer there is an activity in the cell nucleus indicative of mitosis, and cell division soon follows. This process of protoplasmic projections and mitosis continues as long as the inflammatory process is active. The irreg- ular blood channels (capillaries) so formed become surrounded by a layer of involuntary muscle tissues and yellow elastic tissue as a result of extension of muscle fibres and connective tissue cells from the adjacent vessel, the whole structure being surrounded by a loosely arranged layer of white fibrous connective tissue. Thus the capillary becomes an arteriole. These cells that are active in vas- cularization are designated angioblasts. They are the progeny of endothelium. Inflammatory injuries to surface epithelium, as epidermis or mucous membrane, are usually repaired by multiplication of the cells bordering the injury. Irregular masses of nucleated protoplasm have been observed in myositis and may represent regenerating muscle cells. Lesions. — The principal lesions of acute inflammation usually consist of arterial hyperaemia, cloudy swelling of parenchymatous cells and the presence of varying quantities of exudate. These lesions are evidenced by redness due to an increased amount of blood, by swelling or tumefaction of the part, and the loss of luster, sheen or gloss of the tissue, the latter change occurs especiall)'^ in inflamed serous membranes. Chronic inflammation is characterized by a relatively mild hyper- aemia and by an increased amount of fibrous tissue. The newly formed fibrous tissue may or may not displace normal tissue. Kinds or Types of Inflammation. — It is difficult to classify inflammation because of the numerous variable factors that com- pose it. The following classification is based upon etiology, exudate, tissue involved, and time or severity of attack. Etiology. — Etiology, inflammation may be classified as simple and infective. 1. Simple inflammation is non-infective and results from me- chanic, physic or chemic interference. INFLAMMATION. !67 Fractures, sprains, bruises and surgical-procedure wounds arc types of mechanic inflammation. As types of thermic inflammation, burns and frozen tissues may be mentioned. Local inflammatory disturbances resulting from lightninj:^ or contact with electric currents are ty])es of electrically established inflammation. The following may be mentioned as chemic inflammations: formalin dermatitis, arsenical enteritis, chlorine pneumonitis, turpentine nephritis, and those induced by the bites of poisonous reptiles, scorpions, bees, wasps and ants ; also those caused by the products of bacteria and animal parasites. The inflammatory processes established by mechanical interference may and usually do become infected cither by external contamination or by the deposition of infectious agents from the blood or lymph. 2. Infective inflammation is of more frequent occurrence than non-infective. It is the kind of inflammation that concerns the practitioner, veterinary inspector and sanitarian because of its tendency to become generalized in the infected animal, and is fre- quently transmissible to other animals. All tissues are susceptible to infective inflammation e.xcept hair. wool, feathers, and the insensitive, nonvascular portions of the teeth, hoofs, claws and horns. Infective inflammation may be either non-suppurative or suppurative. fa) Xon-suppurative infective inflammation is tyjnfied in mal- ignant oedema, blackleg, localized anthrax and the earlier stages of tuberculosis and actinomycosis, and is characterized by the general phenomena of inflammation previously discussed. Infective inflam- mation may be nonsuppurative in the earlier stages and in the later stages be complicated by ty])ical supjiuration. as in tuberculosis. Miore rarely non-suppurative inflammation continues throughout the entire process, as in blackleg. (b) Suppurative infective inflammation or sup])uration. — Sup- puration is inflammation characterized by liquefying necrosis, and may be surface or subsurface, circumscribed or diffuse. The liquefied necrotic tissue produced by suppuration is pus. Pus is a fluid, varying from a thin watery substance to a thick, sticky tena- cious mass, and is usually alkaline in reaction. The color of pus is determined by the infective agent, and it may be white, lemon yellow, golden yellow, greenish yellow, green or black, and is fre- quently tinted red with blood. Pus obtained from solipeds is usually white or grayish white ; from cattle, creamy yellow ; from sheep, greenish yellow, and from hogs, green or greenish yellow. Pus is usually odorless, although it may undergo putrefaction with the evolution of ill-smelling gases. Actinomycotic pus has a nutty odor (Mayo). Pus may have a greasy, smooth, sticky or granular feel 168 VETERINARY PATHOLOGY. when rubbed between the fingers, depending upon its composition. Histologically, pus is composed of pus cells, i. e., leucocytes (the most of which are necrotic, though some of them may possess vital- ity), shreds of necrotic tissue and tissue cells (the type of which depends upon the tissue affected), usually pyo-microorganism in varying numbers (many of them being included in the pus cells) and liquor puris (the plasma or fluid portion of the exudate and the fluid resulting from the solvent action of the various ferments). Animal microparasites are found in the pus resulting from their activity. Practically all of the pus cells are derived from polymor- phonuclear leucocytes, and are usually the neutrophile variety, there being only an occasional nononuclear leucocyte. Extensive nuclear fragmentation and parenchymatous and fatty degeneration of the cell protoplasm are evident in most pus cells, indicating that they have undergone necrosis. Degeneration or necrosis are also present in the fixed tissues of the suppurative areas. The pus found in acute abscesses or discharging from granulating wounds is usually a creamy fluid, yellowish in color. Sanious pus is a reddish fluid result- ing from an admixture with blood. Ichorous pus is an acrid, corro- sive fluid that excoriates the tissues it contacts. j\Iuco-pus and sero- Fig. 87. — Drawing of a pus smear from a case of strangles, showing the organism arranged in chains — the Streptococcus pyogenes equi. INFLAMMATION. 169 pus afe mixtures of mucous and pus, and of serum and pus, respectively. Putrid pus is a thin, ill-smelling fluid, the result of putrefaction. Infection is the usual cause of suppuration. The following IS a brief description of the process. Pyogenic micro-organisms gain entrance either by deposition upon or into a wound by passing through the tissue or are carried and deposited by the blood or lymph, and, finding conditions favorable, develop and multiply. In their development, pyobacteria produce chemic substances that are sufficiently irritating to establish an active hyperemia and also to exert a positive chemotactic influence, the latter attracting at first mononuclear leucocytes and later causing the migration of neutrophilic polymorphonuclear leuco- cytes to the focus of infection. ]\Iultiplication of the pyobac- teria and leucocytic immigration continue. Phagocytosis be- comes evident in leucocytes and some other cells, e. g., endo- thelial cells. Ldberated ferments, produced bv the pyobacteria, leucocytes and other cells, cause degeneration, necrosis and, finally, solution of the tissue involved. Continued pyobacterial multiplication stimulates an increased leucocytic immigration. and the tissues are thus densely packed with cells. There is a marked accumulation of leucocytes around the suppurative focus apparentl}^ attempting to circumscribe the affected area. Thus the process continues, there being a progressive liquefying cen- tral necrosis within and a marginal leucocytic accumulation without. The condition is repeated until the resistant influences of the animal bodv destroy the pyobacteria, or until the pyo- bacteria have destroyed the involved tissue, or the entire ani- mal. (Suppurative osteitis may occur subperiosteal or in the osseous tissue proper. Leucocytes invade the lacunae and pro- duce solution of the mineral matter, and thus the bone becomes porous. If this process continues the bone ultimately liquefies ; this is termed caries.) Surface suppuration (purulent inflammation) is suppuration of a surface tissue. Pas produced in surface suppuration con- stitutes a purulent discharge, and a persistent purulent discharge is termed pyorrhoea. Inflammation of a mucous membrane ac- companied by a purulent discharge is purulent catarrh. In puru- lent catarrh the surface epithelium is infiltrated with leucocytes frequently to such an extent that the epithelial cells are disin- tegrated, become loosened and exfoliate. The surface cells of serous membranes and the skin are similarlv afifected in purulent inflammation. In any purulent inflammation there is always 170 VETERINARY PATHOLOGY. an engorgement of the subsurface Ycssels and the related areo- lar tissue is infiltrated with inflammatory exudate. Subsurface suppuration may be circumscribed or diffuse. Suppurative centers become circumscribed first by a dense wall of leucocytes and later by a fibrous capsule. The capsule is in nearly all cases denser on the side next to the more important tissue. Fibroblasts that form the circumscribing fibrous capsule are probably the wandering connective tissue cells or their progeny. The collection of pus in tissues, or lymph spaces, and as considered by some in body cavities, constitutes an abscess. The circumscribed pus may, by solvent action of its ferments, Fig- a.. Normal kidney tubule. — Suppurative Nephritis. Suppurative focus surrounded by kidney tissue. dissolve or erode the limiting structure (cells or capsule), and be liberated; the erosive action being in the direction of the least resistance. In this way a surface discharge is effected. The channel of exit of the pus may persist and become circumscribed by a fibrous wall, thus forming a fistulous tract. If the pus cavity is completely evacuated by surgical interference or other- wise, and the cause removed, the surrounding tissue will, by proliferation, fill the space previously occupied by the pus. The pus in an abscess may be absorbed and the destroyed tissue be replaced by regeneration. If the capsule is exceedingly dense the contained pus may become caseated and calcified. Abscesses may be classified as superficial and deep ; primary or metastatic (metastatic al)scesses may or may not be embolic), simple or multiple, subfascial and intermuscular. A hot abscess INFLAMMATION. 1/1 results from rajiid. active suppuration, as submaxillary abscesses in strans;les, wliile the so-called cold abscess results from a slow suppurative process, as in tuberculosis. Accumulations of pus in body cavities as the peritoneal, pleural, pericardial, synovial and the facial sinuses constitute empyema. Vesicles may be- come infiltratetl with leucocytes, which become pus cells, and thus the vesicle becomes a pustule. Diffuse suppuration is not limited by any definite border line. Tt is the result of as;encies possessing sufficient strenpjth or virulency to continuously and progressively destroy and licpiefy tissue or it occurs at a time when the resistance of the animal or its tissues is so greatly diminished that there is inability to successfully antagonize the causative agent, rurulcnt infiltra- tion is the permeation of tissues with pus. rhlegmonous in- flammation is the rapid and usually extensive infiltration of tissues with leucocytes (pus cells), and occurs most frecpiently in the subcutem and submucosa. Exudate. — According to the nature of the exudate inllammation tion niav be classified as serous, fibrinous, and hemorrhagic. The physical ])roperties, chemic and histologic composition of inflammatory exudate has been previously discussed. (a) Serous inflammation is characterized by a serous exudate. Inflammation of serous membranes and inflammatory disturb- ances of other tissues than serous membranes, caused l)y mild irritation, may be of this type. Occasionally serous inflamma- tion is the result of intense irritation as in malignant oedema. The terms serous inflammation and inllammation of serous membranes should not be used interchangeably, because in- flammation of serous membranes may be characterized by fibrinous or hemorrhagic exudate. A circumscribed accumula- tion of inflammatorv serous fluid (exudate) in the deeper lay- ers of the epidermis or mucosa constitute a vesicle. Inflam- matorv oedema, a serous inflammation, is the condition result- ing from the difi"usion of an excessive amount of inflammatory serous exudate into tissues as in cellulitis (inflammation of sub-cutem). (b) h'ibrinous inflammation designates that type of inflammatory disturbances in which there is produced a coagulable exudate. The exudate mav coagulate within the tissues or upon the tis- sue surface. Croupous inflanunation is the term applied to the condition resulting froni the c<^agulation of the exudate upon a tissue surface. Diphtheritic inflammation is the condition pro- duced bv coagulation of the exudate within the tissue and upon its surface. Croupous inflammation and diphtheritic in 172 Veterinary MtholoGV. flammation are not distinctly separable although the former is usually milder than the latter. Typical croupous exudate may be detached without serious injury to the surface tissue but the diphtheritic exudate cannot be removed without detaching or extensively lacerating the surface tissue. Croupous pneu- monia and croupous enteritis are examples of croupous inflam- mation, the former being the most frequent type of pneumonia in horses and the latter occurring occasionally in cattle. Roup or avian diphtheria, and diphtheritic stomatitis and enteritis are examples of diphtheritic inflammation, the former being com- mon in fowls the latter in pigs. Fibrinous exudate may be present in inflammation of serous membranes, constituting fibrinous pleurisy, peritonitis, etc. (c) Hemorrhagic inflammation is significant of the action of an extreme irritant. Hemorrhagic exudate coagulates, especially upon surfaces, though it may coagulate within a tissue. Inflam- mation of tissues in which the blood vessels are of meager struc- trure (capillaries), and hence easily permeated or ruptured, is fre- quently of this type. Croupous pneumonia is a hemorrhagic in- flammation. Nephritis and hepatitis are frequently accom- panied by a hemorrhagic exudate. (Mucus and pus have been described as inflammatory exu- dates by some and as inflammatory products by others.) They .1,1 11, CO'^O, Fig. 89.— Hemorrhagic Exudate (Red Hepatization.) lXFLA^r^I.\Tlo^^ 173' are not inflammatory exudates. Inllammation of mucous mem- branes in which there is an excessive production of mucus is catarrh or catarrhal intlanimation. (Suppuration is inflammation accompanied by the formation of pus and may be surface or sub- surface. Purulent inflammation is surface suppuration.) Tissue. — Histologically a gland or organ is composed of parenchymatous and interstitial tissue, rarcnchymatous tissue is the essential or functioning portion of a structure, as hepatic cells. Interstitial tissue or stroma is the supporting framework of an organ or part as the stroma of a lymph node. The pro- cess of inllammation may occur in either the parenchyma or stroma. Classifying upon tlie basis of tissue alTected then, there are the two forms, namely, parenchymatous and interstitial in- flammation. (a) Parenchymatous intlanimatiiMi is usually the result of severe, active irritatinn, the interstitial type results from the long, continued action of mild arritants. "Jlie two types may be present simultaneouslv in the same structure or they may occur independently. (b) Interstitial inflammation is often the sequence of paren- chymatous, although it may be the initial process. Inflammation of the hepatic cells is parenchymatous hepatitis, of the hepatic interlobular tissue, interstitial hejiatitis, etc. Time, .Icti7'ity and Results of the Process. — It is questionable if the length of time an inflammatory process continues should constitute a factor in its classification. r>y common usage, inllam- mation would be classified according to the time basis, as acute and chronic. Formerly this classification was based upon the time element alone, but the duration of inflammation is so \ari- able that it is now recognized as an insignificant factor. The activity and results of the process are the basic essentials relied upon in differentiating acute and chronic inflammation. (a) Acute inflammation is characterized by a sudden onset, by a vigorous action and by production of retrogressive changes in or destruction to the tissue affected. (b) Chronic inflammation is characterized usually by an insiduous onset, bv a mild action, and l)v resutling in prolifera- tion of tissue. The proliferated tissue may induce retrogressive changes, as atrophy, but this is only an indirect result of the pro- cess. F.ither acute or chronic inflammation may occur throughout the entire reaction or they may both prevail at the same time in different parts of the same structure. The causative agents may become less active as the process continues, thus acute inflam- 174 VETERINARY PATHOLOGY. mation is often succeeded by chronic inflammation. Injuries of tendons are usually accompanied by acute inflammation, but this usually subsides early and is succeeded by chronic inflam- mation. Chronic inflammation may be succeeded by acute in- flammation provided that the irritating factor be sufficiently in- creased or the resistance of the animal diminished. Miscellaneous. — a. Catarrhal inflammation is inflammation of a mucous membrane, accompanied by an excessive production and discharge of mucus. b. Purulent inflammation is characterized by the production of pus. This term is confined, by some, to surface suppuration. c. Ulcerative inflammation is one in which there is erosion of surfaces, i. e., the production of ulcers. d. Vesicular inflammation is one characterized by the pres- ence of vesicles. e. Pustular inflammation is one characterized by the pres- ence of pustules. f. Proliferative inflammation is practically the same as chronic inflammation. It signifies the production of new tissue. g. Specific inflammation is one resulting from a specific in- fection, as glanders. Termination. — The tendency of the reaction produced by an injury is always favorable, but the reaction may be so sud- den and extensive or continued so long that its results may be harmful. The termination of inflammation depends upon the extent, intensity, and duration of the irritant and the resistance of the tissues. Inflammation may terminate in resolution, tissue proliferation or dissolution. Resolution embraces the processes of repair and these may be summarized as follows : a. Removal of the cause. b. Re-establishment of circulation. This may be accom- plished in a few hours or perhaps not for several days depend- ing upon the extent of the injury and the kind of tissue injured. c. Restoration of vessels to their normal condition. The length of time required for restoration and the completeness of the process depends upon the severity of the injury and the re- establishment of the circulation. d. Removal of the inflammatory exudate. The time re- quired to remove the exudate depends upon its nature. Serous exudates are usually removed by resorption, i. e., by the lymph channels. Fibrinous and hemorrhagic exudates are usually dis- solved and absorbed, or they may be carried away by phagocy- IN FLA M M ATION. 175 tes. Exudates may in jiart l)c consnnied as nutritiim l)v lucal cells. e. Disposal of necrotic tissue. Necrotic tissue is disposed of by sloughing, absorption, pliagocytosis, or seciuestration. Small areas of necrotic tissue are usually promptly absorbed or dis- posed of by phagocytic action. Considerable time is usually re- quired in disposing of large areas or masses of necrotic tissue, unless it is superficially located and separates from the surroimd- ing tissue and sloughs. .Siil)surface necrotic tissue may be gradu- ally li(|ucficd and absor])ed, discharged through a fistulous tract (submaxillary abscess of Strangles), collected and carried out by phagocytes, encapsulated, or sefjuestrated, and remain per- manently in the tissue. Encapsulated necrotic tissue may be- come infiltrated \vith calcium salts. f. Regeneration of degenerated tissue and replacement of necrotic tissue. The regeneration of degenerated tissue consists in replacing the injured or destroyed cell protoplasm by normal proto])lasm. If only a fe\y cells are destroyed the adjacent cells reproduce and thus rcne\yal is usually rapid. Connectiye tissue cells and surface epithelium are easily and efificiently regenerated, but cardiac muscle, ganglionic nerye and cartilage cells are rarely perfectly regenerated. Large areas of necrotic tissue are usually substituted by fibrous tissue. This proliferated tissue is termed granulation tissue in the beginning and cicatricial tissue after it has become dense and more or less contracted. Granu- lation tissue consists of capillary loops surrounded by masses of cells. These cells are largely fibroblasts and produce fibro- connectiye tissue. After the fibro-connectiye tissue has been formed it contracts, thus becoming cicatricial tissue. Cicatriza- tion is of yalue in closing gaping \younds. but is injurious when it occurs in internal organs as the liyer, because the pressure ])roduces atrophy and obstructs circulation. The capsule sur- rounding pus cayities, after the purulent fluid has been eyacuatcd, becomes a granulating membrane which soon fills the gap with fil)rous connectiye tissue. Exuberant granulation results from excessiye multiplication of cells, undue extension of capillary loops, and failure of contraction of the fibrous tissue. Tissue Proliferation. — The tissue jiroliferated in iiillammatory resolution takes the place of tissues that pre-existed and had be- come necrotic, while that occurring in inflaiumation resulting from long continued mild irritation is not a substitution but an addition to the tissue already existing. In this latter phase tissue proliferation may begin in a yery short time after the in- flammation is established or it may not appear for two. three, 176 N'ETERINARV PATHOLOGY. or several daA's. Fibro-connective tissue is invariably the pro- duct of tissue proliferation. Fibro-connective tissue prolifera- tion is closely associated with chronic inflammation, in fact it is almost inseparable from it. The proliferated tissue appears first in the frame-work of the tissue involved and may later extend into the parenchymatous tissue. If the proliferated tissue is excessive it may, by pressure, produce atrophy of the parenchy- matous tissue. Cicatrization of the proliferated tissue causes an irret^ular lobulation and constriction of the involved organ, as in cirrhosis of the kidney. Strictures of hollow organs are pro- duced in the same way. Adhesions of serous membranes are produced by fibrous tissue formed during inflammation. Dissolution or destruction is a result of intense irritation. Necrosis of tissue is frequently a sequence of inflammation. A single cell or only a few cells may be destroyed or large areas of tissue may undergo necrosis. Ulceration results from con- stant cellular necrosis. Circulation may be obstructed by an inflammatory exudate and cause necrosis in large masses of tissue. It may terminate fatally, in partial recovery, or in reso- lution, depending upon the importance of the tissue involved in the affected animal. Conclusion. — Inflammation is the reaction of a living tissue to an irritant. Inflammation is a complex process, the result of many fac- tors. It is not always a result of infection. It is an adaptive, reparative and protective process. It may produce suf^cient reaction to cause destruction of the portion involved and occasionally of the entire organism. CHAPTER VII. PROGRESSIVE TISSUE CHANGES, RECri:Xl-:RAT10N. PEFIXITION. HXTEXT — Pcf^ctids upon age iind tissue iiit'olved. Blood. Councctize tissue. Fibrous. White. Yelloze. Cartiliu/c — fin rely regenerated perfectly. Bone. Epithelium. Surface — Coviplctc and perfect. Glandular — Irregular and incomplete. Muscle — Perfect regeneration rare. Nerve — Cells do not regenerate, fibres do. Regeneration is the process by means of which destroyed tissues are replaced. Tissue destruction is the result of necro- sis, primarily, and inflammation and dec^eneration, secondarily. Reji^eneration is accomplished by muhi]ilication of pre-existing adjacent cells or l)y invasion and multiplication of wandering connective tissue cells. The proliferating cells assume the charac- teristics of embryonal cells, that is, their reproductive property is over-developed and their other vital functions depressed. The power of regeneration of a tissue is inversely proportional to its specialization. Regeneration of the tissues of the less complex animals is more nearly perfect than that of the tissues of highly organized animals; thus invertebrates regenerate entire organs or parts. Spallanzani cut off the legs and tail of a salamander and observed in the course of three months six crops of these members. In the entire three months GST perfect bones were re- produced and the regeneration was perfect regardless of the point of amputation. The tissues of young growing animals are more easily regenerated than those of mature animals. Single cells or small areas of tissue are more i)erfectlv regenerated than large areas. In some cases destroyed tissues are not regenerated but are replaced by fibrous tissue. The functions of some de- stroyed tissues and organs may be performed bv other struc- tures. Thus, if the tibia of a dog is destroyed, the fibula in- creases in size and assumes its function. Destruction of one kidney is succeeded by a compensatory hypertrophy of the other 177 178 VETERINARY PATHOLOGY. kidney. The law of specificity, i. e., cells beget like cells, is the same in regeneration and in physiologic processes. Regen- eration is the outcome of the unhindered multiplication of cells. Blood is continually regenerated during the natural life of an animal. The normal maintenance of blood is a physiologic pro- cess, but regeneration of blood or some of its constituents may, under certain conditions, be abnormal, as in leukemia. Leuco- cytes are produced in lymphoid tissue of the lymph nodes, spleen and bone marrow, and it is possible that they may multiply in the tissue spaces. Erythrocytes probably have their origin in the red marrow of bones in adult animals. The red blood corpuscles are nucleated in the beginning but the nucleus vanishes by so- lution or extrusion before the cells reach the general circulation except in case of severe hemorrhage or other conditions in which there has been rapid, extensive loss or destruction of blood. Blood vessels are usually the first tissue regenerated in the repair of wounds. Blood vessels are formed in the embryo by canalization of large mesodermal cells, many of which fuse, thus forming continuous canals that later become blood vessels. This -^ Fig. 90. — Vascular Regeneration, showing vascular buds. type of vascular formation is not common in repair of injured .vessels or regeneration of destroyed vessels. The usual manner of vascular regeneration is by the growth and development of endothelial buds from adjacent vessels. These buds are solid, conical processes which extend outward from the capillary en- dothelium. The buds or processes increase in size and become hollow at their base, the cavity being thus continuous with the Himen of the pre-existing vessel. As the buds increase in size PROGRESSIVE TISSUE CHANCES. 179 there is an increase in the number of cells composin*^ Uicni. Union or fusion of buds or processes from different vessels re- sults in anastomosis or inc^isculation. These processes are thus the forerunners of capillaries and l)y a dilatation and an increase in the thickness of their walls due to formation of fibrous and muscular tissue, arteries and veins are formed. The new vessels produced in the repair <>f an injury are invariably in excess of the normal vascular requirements of the part. The excess ves- sels in an injured area are obliterated by cicatrization. Connective tissue is usually completely regenerated. Con- nective tissue is regenerated from pre-existing- connective tissue cells, wandering cells and endothelial cells. Mucoid coniiccth'c tissue is not normally found in the adult animal except in a modified form in the vitreous chamber of the eye. Mucoid tissue is not regenerated, althou.gh it is possible that other types of regenerated connective tissue are mucoid in the beginning. Fibrous connective tissue is rapidly and completely regen- erated. \\'hite fibrous connective tissue is frequently substi- tuted for other tissues. The fibres in regenerated fibrous con- Fig. 91. —Fibrous Regeneration. nective tissue have the same origin as those in normal fil)rous tissue. Regeneration of white fibrous tissue may be studied in the union of the ends of a. tend(Mi after tenotomy. The space between the ends of the tendon is filled with bU)od and 1\ ni])h which escaped from the severed vessels. The pre-existing con- nective tissue cells bordering the wound in the tendon, together with wandering cells, begin proliferating within forty-eight hours, their progeny being fibroblasts. The fibroblasts produce a tangled mass of fibrous connective tissue, and at the same time there is vascularization of the extravasate which occupies the space between the severed ends of the tendon. After the ends 180 VETERINARY PATHOLOGY. of the tendon are firmly united by the mass of newly formed fibrous tissue the extravasate and the fibres, excepting those ex- tending in a longitudinal direction, are absorbed. Finally the repair is so complete that the defect is not visible to the unaided eye and is difficult to detect microscopically. Scars are bands, sheets or masses of white fibrous tissue and indicate imperfect regeneration, the fibrous tissue in scars being largely a substitu- tion tissue. Yellow clastic tissue is not as perfectly regenerated as white fibrous tissue. White fibrous tissue usually is substituted for yellow elastic tissue when the latter has been destroyed. Regeneration of cartilage is very imperfect probably because of its irregular supply of nourishment. Destroyed cartilage is usually replaced by fibrous tissue. In some instances injuries to cartilage are succeeded by excessive cartilaginous prolifera- tion. A case was observed in which the arytenoid cartilage was severed in an operation to relieve roaring; six months later there had developed at the point of operation a cartilaginous mass as large as a goose egg. Perfect regeneration of cartilage does occur, although it is rare. Regenerating cartilage cells are de- rived from the inner portion of the perichondrium. Fibrous tissue formation usually precedes the regeneration of cartilage, alth'^"\gh it may be formed from the beginning. Osseous tissue is usually perfectly regenerated . The cells that produce osseous tissue are called osteoblasts. Osteoblasts are usually derived from the osteogenetic layer of the perios- teum, although they may have their origin from undififerentiated connective tissue cells. The formation of osseous tissue is usu- ally preceded by mucoid, fibrous or cartilaginous tissue. The various stages of osseous regeneration are very similar to those of normal bone formation. Osseous regeneration may be illus- trated by the union of a fracture as follows : Blood and lymph vessels are ruptured when the fracture is produced. Blood and lymph escapes into the surrounding tissues and the interstice between the two ends of the fractured bone. The injury pro- duces necrosis and establishes inflammation. Vascularization of the injured area initiates the process, after which there is solu- tion of the extravasate, exudate and necrotic tissue. Osteo- blasts accompany the newly formed vessels and produce irregu- lar masses of fibrous tissue which later calcify. The calcareous tissue is infiltrated with osteoclasts derived from the blood which dissolve out regular canals in the regeneration of long bones, and irregular cavities in the regeneration of flat or irregular bones. Osteoblasts appear in the canals and cavities, formed PROGRESSIVE TISSUE CHANGES. 181 by the osteoclasts, and produce til)ri)us lamellae which arc later calcified. This process continues until the canals or cavities arc filled with lamellae excepting- a small central cavity which ctjn- tains blood vessels, thus Haversian systems are frecjuently com- pletely regenerated. Excess of osseous tissue formed over and around bones at the line of fracture (provisional calli)us), is usually later reabsorbed. .Idiposc tissue is not a t\])ical j)riniary lis.-uc. It is derivccl from the undifTerentiated connective tissue cells by the C(jnver- sion of their protoplasm into fat. Adipose tissue is consumed when the food supply is deficient, and the cells become typical connective tissue cells or are destroyed. Adipose tissue is also formed when the food supply exceeds the demand as a result of production and accumulation of fat in the connective tissue cells. Pi'iitiiic is not replaced except in some of the lower animals. Epithelium of surfaces is constantly destrox'cd and regen- erated. The outgrowth and shedding of the su])erficial ei)i- dermal cells is a physiologic process. Mpithelization of small abrasions of the epidermis and mucous membranes is rapid and comjilcte. the regenerating cells having their origin from the epithelium bordering the injury. If tlie denuded surface is large regeneration may proceed from the cells of the sweat glands of the skin, or mucous glands of mucous membranes as well as the epithelium bordering the injur}-. S(jitaiiioiis cpithcUuui is more com])letely regenerated than columnar. Constant destruction of columnar cells may cause the production of short columnar cells and finally squamous cells. This, however, is rare, as the law of specificity is practi- cally without exception. Glandular epithelium of large glands as the kidney liver pancreas and salivary glands is not regenerated as perfectly as surface epithelium. The cDithelium of sweat glands, oil glands, mucous glands, gastric glands, Brunner's glands, crypts of Lieberkuhn and uterine glands, is generally quite perfectly regenerated even after destruction of practically all of the glandular epithelium. .\ny of the latter will regener- ate from small islands of cells either in the duct or body of the gland. The epithelium of the mammary gland in creases in amount during lactation and diminishes when lacta- tion ceases. Wx ol^scrvation it has been determined tliat mam- mary epithelium regenerates after it has been destroyed by ab- scess formation or other destrucli\-e processes, prox-ided newly formed fibrous tissue is not substituted. P.y analogy it might be supposed that the destroyed epithelium of salivary glands 18f Veterinary pathology. and of the pancreas may be regenerated, but this has not been clinically or experimentally demonstrated. The liver is a tubu- lar gland and regeneration of a single cell or a few cells is not uncommon, but large areas of liver tissue are probably never regenerated, although some pathologists claim that they have observed the regeneration of the major portion of a liver lobe in the dog, cat and rabbit. Kidney cells, especially of the tubules, are constantly regenerated, although the regeneration of an entire tubule has never been observed. The testicular and ovar- ian tissues are probably never regenerated except m the physio- logic maintainance of spermatogenesis and oogenesis. Muscular tissue is imperfectly regenerated. Injuries of invol- untary muscular tissue are usually repaired by the substitution of fibrous tissue which may later be replaced by involuntary mus- cular tissue, the latter being derived from the adjacent muscle cells. Two or three days after an injury to a voluntary muscle fibre, the nuclei near the injury divide and a multinucleated protoplasmic mass is formed on the damaged fibre. These pro toplasmic masses extend into the substituted fibrous tissue and may split longtitudinally into regular fibres but more frequently they die and disintegrate. Destroyed heart muscle cells are invariabl}- replaced by fibrous tissue. Nerve cells are not regenerated, at least in adult animals, although their processes, axones and dendrites, are regenerated in peripheral nerves. After a nerve fibre is injured the axone degenerates to the distal end and to the first or second node of Ranvier proximally. A few days after the injury the axone, if its continuity has not been destroyed, begins to elongate, ex- tending peripherally, in the direction of least resistance, which is in the old sheath. If the axone extends in the original sheath the tissue deprived of its nerve supply may become perfectly innervated. The rate of growth of an axone has been variously estimated at from .1 mm. to 1mm. in twenty-four hours. Foot lameness in horses that has been completely relieved by meta- carpal and metatarsal neurectomies, sometimes reappear, in from eighteen months to three years after the operation, thus indicating that there has been reinnervation. If the proliferating axone does not continue in the original nerve sheath it may become entangled and coiled up in the scar tissue, of the wound, thus producing sensitive scars and amputation neuromata. TRANSPLANTATION AND GRAFTING. Transplantation is the process of partial severing a piece of tissue from its connection and moving it so that it occupies a new position. Such transplantation usually grows and this PROGRESSIVE TISSUE CHANGES. 183 method is resorted to in the surgical rehef of wounds and in plas- tic operations. Grafting is the process in which a piece of tissue is removed and transferred to some other part of the body or a piece of tissue may be obtained from one individual and grafted into another. Grafts are not as likely to grow as are transplantations, how- ever, it has been found that grafts of the same kind of tissue in the same individual, if properly placed, usually take and grow and become a part of the individual. In some instances the graft is rapidly absorbed, while in still other instances the graft persists for a while, ultimately dies but has served the purpose for some little time. Grafting is much more successful in the lower animals, although it has reached rather a high state of efificicncy in the higher animals, even the body of man. The success of a graft depends somewhat upon its size and upon the length of time that the graft has been kept out of the tissue. Alexis Carrell perfected a method of patching an abdom- inal vessel with a flap of peritoneum, subperitoneal tissue and vol- untary muscle, and by a series of experiments has demonstrated that an artery can regenerate itself by using heterogeneous anatomical elements. The regeneration was so perfect that in less than two years after the operation on the aorta it was nor- mal, although the wall was composed of tissue different than the normal but the shape and lumen had not been changed. 184 VETERINARY PATHOLOGY. (Ccplhilic, ccri'ical, thoracic, etc.) WOUND HEALING. DEFINITION. CLASSIFICATION. Etiology. Traumatic. Therm ic. Chciiuc. Location. Surface. Subsurface Character. Incised. Punctured. Lacerated. Contused. Stab. Gun shot. Bites. Condition. Aseptic. .Septic. HEALING. Primary union, (First Intention.) Hemorrhage arrested. Approximation of zvound margins. Adhesion of zvound lips zvith e.vudate. Multiplication of related cell-:. I'^ascularization. Epitheli::ation. Cicatrization. Substitution. Secondary union, (Second Intention.) Hemorrhage arrested. Immigration of leucocytes to zi'oitnd margins. Infection. Suppuration. Granulation. Cicatrization. Epithelization. Substitution. The regeneration of the individual tissues has been discussed. The simultaneous regeneration of the tissue-complex of an area in which there has been previous tissue destruction constitutes wound healing. A wound is the result of sudden interruption of the continuity of tissue or tissues. Some have restricted the term 'wound' to those conditions resulting from traumatisms; others confine it to injuries of soft tissue, and again some main- tain that wounds occur only upon a surface. There is no good reason for restricting the term, because both thermic and chemic influences produce tissue destruction not distinguish- able from wounds meclianically inflicted. A fracture is a break in the continuity of osseous tissue and is repaired in the same way as wounds of soft tissue. Rupture of the liver or spleen is PROGRESSIVE TISSUE CHANGES. 185 characterized by tissue destruction and regeneration, the entire process being identical with that in surface wounds. Wounds resuh from sudden and violent action. Thus ulcers or necrotic tvibercular centers are not wounds. A bruise may or may not be a wound, depending upon the nature of the lesion, i. e., whether or not the interruption of tissue has been affected. Wounds may be classified as to cause, location, cliaracter, and condition. 1. Etiologically wounds may be traumatic, thermic or chemic. 2. According to location wounds may be, surface or subsur- face, abdominal, cervical, thoracic, etc. 3. As to their character, wounds may be incised, punctured, lacerated, contused, stab, shot, or bullet and from bites. 4. Wounds may be noninfectious and infectious. Traumatic wounds usually heal more readily than wounds re- sulting from thermic or chemic causes because traumatisms arc caused by mechanical force only and the destructive influence ceases immediately upon removal of the cause ; whereas the in- fluence of thermic and especially chemic causes are more lasting as their action continues after the wound has been produced. Cell reproduction is probably the result of physiologic auxetics as kreatin, globulin, and xanthin, which stimulates cell multiplication. In persistent ulcers cell proliferation succeeds the local application of a solution of 5 parts globulin and 2 parts kreatin. The more rapid healing of an ulcer succeeding scarification is probably because of auxetics liberated from cells destroyed by the curette. Wound healing hlay be of one of two types, healing by pri- mary union (first intention), and healing by granulation (sec- ond intention or secondary union). These two modes of heal- ing differ only in the extent of tissue reaction. Other meihods of healing have been described as immediate union, healing by third intention, and healing under a scab. Immediate union, signifies union of parts of a cell or the cut ends of fibres, etc., and is now thought to be impossible ; healing under a scab and healing by third intention are properly discussed under the caption of prim- ary union or granuation. Healing by Prinmry Union. — This is the most desirable method of wound healing and is usually obtained in veterinary practice only in surgical wounds and recently inflicted, clean cut wounds. This mode of healing is of short duration and is ac- 186 VETERINARY PATHOLOGY. companied by little if any infection and limited inflammation. Healing by primary union takes place only in clean cut wounds, i. e., when the tissues are smoothly and evenly divided and in which hemorrhage is limited and easily controlled. After hem- orrhage ceases or has been arrested the extravasate coagulates thus agglutinating and drawing the wound margins together. If the incised surfaces or severed tissues be approximated by surgical procedure the coagulated extravasate and exudate as- sists in maintaining them in that position. In surface wounds varying quantities of serum and lymph discharge and coagulate upon the surface thus forming a scab. An injury producing a wound and the extravasate are sufficiently irritating to es-" tablish hyperemia and in some cases slight inflammation ac- companied by a serous exudation and a leucocytic immigration. The hemorrhagic extravasate is gradually disintegrated and re- moved by phagocytes and at the same time, there is enlarge- ment and extension by multiplication of the marginal tissue cells of the wound into the coagulum which serves as a support for the regenerating tissue. Vascularization accompanied by fibrous formation initiates the process of regeneration in the healing of a wound by primary union. Vascularization is usually limited because of the small size of the wounds. The newly formed vessels are capillaries and supply the regenerating tissvie. Fibrous tissue is produced in sufficient quantities to replace all tissues destroyed. Disintegration of the coagulum and regeneration of new tis- sue thus proceed until the newly formed tissue has entirely re- placed the extravasate. The scab which is hemorrhagic extravas- ate and inflammatory exudate is firmly held upon the wound surface by fibrils continuous with the subsurface coagulated ex- travasate and exudate and as the latter is absorbed the scab grad- ually becomes loosened and finally drops ofif leaving a shining surface. The regenerated tissue formed in the extravasate is embryonic fibrous tissue the amount of which depends upon the quantity of coagulum. Upon the embryonic tissue thus formed, in surface wounds, epithelization is usually rapid and complete. The scar appears pale pink and is tender until cicatrization takes place and then appears white, dense, firm and hard. Whether the fibrous tissue produced in wound healing is substituted later by the normal tissues of the part involved depends upon the gen- erative power of the tissues destroyed. PROGRESSIVI-: TISSUI-: CHANGKS. 187 To recapitulate, healing by primar}- union embraces, coagula' tion of the hemorrhagic extravasate, agglutination of the wound margins, hyperemia, inflammation, vascularization, fibrous form- ation, disintegratit)n of the hemorrhagic extravasate and in- flammatory exudate, cicatrization, cpithelization and substitu- tion. sti- tution. In some individuals the formation of fibrous connective tis- sue is continuous and there is formed large masses of cicatrical tissue known as keloids. Keloids are classified with neoplasms by some authors. HYPERTROPHY. ETIOLOGY. Inhciifed. Antenatal. Uneqiuit pressure. Amniotic adhesions. Post-natal. Increased nulrition. Increased function. ■Internal secretion. Diminished pressure. APPEARANCE. Macroscopic. Microscopic. TISSUE AEEECTED. EFEECTS. Hypertrophy literally means excessive nulrition. P.v usage the term has come to mean, an abnormal increase in the size of an organ or part. In a more restricted and definite sense, hy- pertrophy is a term ai)plied to that condition resulting from ati abnormal increase in the size of the essential cells of the part. Thus an increase in the size of the liver as a result of an in- creased amount of the interstitial tissue or an increase in the size of a kidney due to an accumulation of an intlammatory ex- 190 VETERINARY PATHOLOGY, udate or oedematous transudate is not an hypertrophy, al- though such conditions have been called false or pseudo-hyper- trophy. Tumors produce an increase in the size of the struc- ture affected, but this should not be confused with hypertrophy. Hyperplasia is a condition resulting from abnormal increase in the number of the cells though it is difficult to diff'erentiate from hypertrophy. Compensatory TTvrKRiROPiiv is the name applied to that type of hypertrophy caused by increased functional activity. Thus an increased blood pressure maintained for some time induces compensatory hypertrophy of the heart. Concentric hypertrophy is a term denoting an hypertrophy of the tissues of a hollow organ, accompanied by a diminution in the lumen of the hollow organ, e. g., hypertrophy of the heart, oesophagus, intestine, or any other hollow organ in which the hypertrophied tissues occupy a portion and thus diminish the lumen of the organ. In some instances hypertrophy represents a normal, physio- logic process. The increased size of the pregnant uterus, and the enlargement of the mammae during the gestation period are examples of physiologic hypertrophy. Increased size of the heart and voluntary muscles in horses trained for racing rep- resents a physiologic hypertrophy. After the destruction of one kidney by disease or the removal of one by operation, the re- maining kidney increases in size and ultimately performs the function of both, this is functional or physiologic hypertrophy and also compensatory hypertrophy. In fact practically all hy- pertrophies are physiologic, however, the hypertrophied struc- tures are abnormal, therefore the condition is pathologic. Excessive development of an entire animal i. e., giantism is designated by some as general hypertrophy. Excessive development of a part as one foot is designated local hypertrophy. Local hypertrophy is much more common than general hypertrophy. \ Hypertrophy may be inherited, (natural) or acquired. Ac- quired hypertrophy may be antenatal or postnatal. Etiology. LvHERfTEn HYPERTROPHY. — Thc cause of inherited hypertrophy is unknown except that there is an inherited impulse to grow large. This type of hypertrophy is noted in giants. Antenatal hypertrophy is usually the result of unequal pres- sure and amniotic adhesions. PROGRESSIVI-: TISSUE CHANGES. 191 The CAi^sATiVE factors of postnatal hypertrophy are. 1st, in- creased nutrition, 2ncl, increased function, ;?d, a stimulus, prob- ably an internal secretion, that causes the affected tissue to con- sume excessive quantities of food. Two or more of these etio- logic factors are usually evident in all cases of hypertrophy. lucr^'oscd nntrition. — A long continued, mild arterial hypere- mia in a tissue insures increase of the nutritive supply to the affected part and such parts usually become hypertrophic. Increased function is the prime causative factor of physiologic or functional hypertrophy. Increased function is intimately associated with increased nutrition, in fact long continued in- creased function without increased nutrition is not possible. Tn the production of functional hypertrophy the part must be accustomed to the extra work gradually. An excessive amount of work, assumed at once, by any structure will produce atrophy or degeneration. Cardiac hypertrophy is invariably functional as it usually is the result of valvular defects. Hypertrophy of the involuntary muscle anterior to a stricture is also functional as it results from increased muscular action to force the contents of the intestine past the stricture. \'oluntary muscular hyper- trophy is also functional. Some unknown cause is active in the production of certain hypertrophic conditions. This unknown cause is probably an internal secretion, at least this would appear to be the cause of hypertrophy of the mammae and uterus in pregnant animals. That certain internal secretions are required to sustain the nor- mal balance in the growth of tissues is evident in disease of the pituitary body which frequently results in excessive develop- ment of certain parts (acromegaly). By diminishing the external pressure, experimentally, some parts have been noted to become hypertrophic. This is because of arterial hyperemia produced bv diminished pressure. Appearance. Macroscopically. li\'pcrtroijhied organ? or parts are larger and heavier than normal and may be regular or irregular in shape. The general api)earance of hypcrtropliicd parts other than size is not usually sufficiently distinct to differentiate them from normal. Microscopic. — Renal compensatory hypertrophy is charac- terized by increased length and size of the uriniferous tubules. Hypertrophy of muscular tissue is characterized by increase in the size of muscle cells. In general hypertrophied organs or parts contain an excess of parenchymatous tissue. 192 VETERINARY PATHOLOGY. Effects. — The effect of hypertrophy varies according to the tissue affected. There is usually an increased functional capac- ity in an hypertrophied structure. The heart musculature may become hypertrophied to such an extent that its force ruptures some important blood vessel and causes death. Increased func- tion of hypertrophied suprarenal bodies tends to increase blood pressure by the production and elimination of large quan- tities of adrenaline which causes constriction of arteries and cardiac dilation or rupture. HYPERPLASIA. DEFINITION. VARIETIES. Parenchymatous. Interstitial. ETIOLOGY. APPEARANCE. Macroscopic. Microsco}>ic. TISSUE AFFECTED. EFFECTS. Hyperplasia, according to the derivation of the word, is ex- cessive formation. Hyperplasia and hypertrophy are incorrectly used interchangeably by some. Hyperplasia should be used to FiR 94. —Hyperplasia Interstitial Testieiilar Cells. a. Interstitial hMierplastic tissue. b. Seminiferous tubuUs not fully developed designate the condition resulting from an abnormal increased size of a part due to an increase in the number of cells of the part. Accepting the last definition, hyperplasia may be due to an increased number of parenchymatous cells, or an increased PROnR!-S?T\'I^ TIS!^rF CTIAKGF.S. 193 number of interstitial cells the two types beinj:^ called parenchy- matous hyperplasia and interstitial hyperplasia respectively. Parenchymatous hyperplasia and numerical hypertrophy are sometimes used synonymously. Interstitial hyjjerplasia is prac- tically the same as fibrous hyperplasia. Pitrciichyiiialoits hypcrlylasin is not of common occurrence It is usually either inherited or congenital. Interstitial hyperplasia is quite common as it is usually evident in chronic intlammatory tissues and it is also occasionally observed in structures affected with functional fibrosis as is evi- dent in the liver of animals afiflicted with disturbances of the cardiac valves. The descended or scrotal testicle of single cry])- torchids is usually enlarged because of an increased amount of parenchyma ami hence is an example of interstitial hy])erp]asia. Etiology. The cause of parenchymatous hyperplasia is unknown. Inter- stitial hyperplasia is produced by the long continued action of mild irritants or other substances tliat produce over stimulation. Fig. 95. — Pen drawiiif,' of an ll.vperiilaNth' Iretcr, Appearance. Miii IOSCO pw. ix. n.Ttural size. rarentliymatiiu.^ hyi)cr])lastic structures arc regularlv or irreg-ularly enlarged and arc heavier tlian normal. Interstitial hyperplastic parts vary in appearance according to the amount of hyperplastic fibrous tissue. The part may vary 194 VETERINARY PATHOLOGY. from normal to dense, hard, pale irregularly lobulated masses of fibrous tissue. Microscopic. — Parenchymatous hyperplastic structures have the same appearance microscopically as sections of normal tissue. Sections of tissue afifected with interstitial hyperplasia con- tain an increased quantity of fibrous tissue which may be readily recognized microscopically especially if the section is stained with hematoxylin and picro-fuchsin. Effects. A part affected with parenchymatous hyperplasia will have an increased functional capacity. The effects of an increased functional capacity of a structure depends upon the part in- volved, and may or may not be injurious to the animal in which it occurs. Interstitial hyperplastic structures have an increased quantity of fibrous tissue and usually a diminished amount of parenchy- matous tissue and a diminished function. Interstitial hyper- ^ ' ~ "■ " '' (9 *» «* Fig. 96. — Fibrous Tissue Ossifloation. a. Fibrous tissue. b. Osteoblasts. plasia of the walls of hollow organs may cause irregularity of the lumen (intestine) and hinder passage of the organ's con- tents. pr()(;ki;ssivic tissi'I': chancks. 195 METAPLASIA. Metaplasia 1;=^ the name applied to the conversion of a devel- oped or matured tissue into another closely related. Under normal conditions a inaturcd tissue has specific cells and a char- acteristic structure. The character of a tissue may be chan_<::;ed by certain pathologic conditions. Metaplasia should not be con- fused with degenerative or infective tissue changes which are observed in functional or inflammatorv fibrous formation. Meta- plasia is usually concerned in the conversion of one variety of a primary tissue into another variety of the same tissue as fibrous tissue into bone and occurs in i)hysiologic processes as well as in disease. Metaplasia occurs in scars, the conditions consisting of the replacement of fibrous tissue by osseous tissue. This type of metaplasia is also evident in bone spavin, ringbone, sidebone, as well as in scars resulting from fistulous withers, poll evil, etc, Metaplastic osseous formation was recently noted in the omen- tum of a sheep. The conversion of lymphoid tissue into adi- pose tissue is metaplasia. The replacement or substitution ol sqnamus epithelium for cubic or columnar epithelium repre- sents a type of metaplasia. Metaplasia is of little significance except as a pathologic con- dition. CHAPTER VIII. RETROGRESSIVE TISSUE CHANGES. DEFINITION. ETIOLOGY. Variations in nutrition. Chemic poisons. Clieniic reaction of tissue. Variations of temperature. J'ariations of function. VARIETIES. Atrophy. Degeneration. Infiltration. Pigmentation. Physiologic cell growth and function are dependent upon nor- mal metabolism. Retrogressive processes are those conditions in which normal cell growth and function are diminished or sus- pended. Retrogressive tissue changes are caused primarily by abnormal cell metabolism or abnormal functioning, and are accompanied by structural or chemic alteration of the cell proto- plasm or diminution in the size of the cells. Metabolic disturbances may be caused by the following: Diminished nutritive supply caused by (a) occlusion or di- minution of the calibre of nutrient vessels ; (b) insufficient supply of food to the animal ; (c) incomplete or lack of digestion of the ingested food; (d) failure^of absorption of digested food; (e) inability of the cells to utili^ digested food that has been carried to them. Nutrition may W supplied in excess of the normal requirements, thus disturbing the metabolic equilibrium. Excess nutrients may be stored within the cells or they may be converted into energy by oxidation. In the former the stored food is a mechanical hindrance to cell action and in the latter the cell is overworked in converting the food into energy. With- holding of nutrient substances from cells produces destructive metabolism and ultimately cell death. Chemical substances, i. e., poisons exert their action on cells by combining with some of the protoplasmic constituents or by accelerating, inhibiting or suspending the action of the cell enzyms, thus interfering with metabolism. Chemic reaction of a tissue influences the action of celj 196 RKTROGKFSSIVF. TTSSl'E CHANGES. 197 enz}'ms, and hence is a factor in metabolism and in l)rin|nfin.c: about retrogressive tissue changes. / ariations in tcinpcraturs. — The various albumens of protop- lasm are coagulated at different temperatures. An increase of 15. G° V. is sufficient to coagulate one groui) of all)uniins and an increase of U" F. is usually fatal because of the coagulation t)f other impor- tant albumi" constituents of the cell prott)plasm. I'ever is invariably accompanied by coagulation of some alljuminous constituents of protoplasm although it is possible that cheniic substances as well as the high temperature may have some influence in this coagulation. Diminished temperature retards metabolic process- es and if tissues are exposed for a sufficient time to a low tem- perature the protoplasm dies and nietal)olism ceases. Diminished or increased cell functioniiuj are factors in the causation of retrogressive changes. Diminished functioning for a considerable length of time results in atropliy and if functitni- ing of a specific part is decreased progressively through several generations there will be failure of development of that part (aplasia). Excessive functioning, to a limited extent, in a part supplied with an excess of food, produces hypertrophy. Functioning beyond the nutritive supply produces degeneration and finallv destruction of the cells. Retrogressive tissue changes include atroi)hy, degeneration, infiltration and pigmentation. ATROPHY. nr.FixiTfox. DIFFERENTIATION. KINDS. Physiologic. Pathologic. ETIOLOGY. Physiologic. Senility. Pathologic. Disturbed nutrition. Disturbed function. I'nduc pressure. .IPPEAR.INCE. Macroscopic. Microscopic. TISSUE AFFECTED. EFFECTS. Atrnpliv is that condilion in wliicli there is a decrease in the size of an organ or tissue caused b\- a decreased size or a dimin- ished number of the composing cells. In some instance the interstitial tissue increases and replaces the atrophied cells and the affected organ docs not diminish in size. The term atropliy 198 VETERINARY PATHOLOGY. is usually restricted to a local diminution in size, as, of an organ or part, although it has been applied to the condition resulting from a general wasting away of all the tissues of the body, i. e., emaciation. Atrophy is differentiated from degeneration by the fact that the former is purely a diminution in the size of the part, (a result of decreased size or diminished number of the cells and without any alterations in the cell protoplasm) while the latter consists of chemical changes of the cell protoplasm and may result in in- creased or diminished size of the cells. Atrophy and degenera- tion may occur simultaneously in the same structure, the result- ing condition being known as atrophic-degeneration or degenera- tive-atrophy. Hypoplasia is an underdevelopment in contradis- tinction to atrophy, which is diminution in the size after the part has been developed. Atrophy may be physiologic or pathologic. PHYSIOLOGIC ATROPHY is a term used to designate the normal diminution in the size of an organ or part. This occurs in the thymus gland which is well developed at the time of birth. Soon after this it begins to diminish in size and is practically extinct by the time the animal matures. The mammary gland atrophies after lactation ceases. Testicles and ovaries atrophy after the period of reproduction or sexual activity. Senile atrophy is a term employed to designate all atrophic conditions occurring in the tissues of old or aged animals. Senile atrophy is a physio- logic process. PATHOLOGIC ATROPHY is a term used to designate abnormal diminution in the size of an organ or part. Pathologic atrophic disturbances involve muscular, glandular and nervous tissue although no tissue is exempt. Th^ type of atrophy is of fre- quent occurrence, viz., diminution of mjuscle cells and the size of the muscle in lameness and sweeney, and the diminution in the size of the liver in hepatic atrophy. Etiology. — Pathologic atrophy may be the result of either disturbed nutrition or disturbed function. Disfiirbed Nutntion. — Atrophic disturbances resulting from mal-nutrition are most frequently the result of insufificient food. Cells receiving insufficient food gradually shrink in size, possi- bly because of auto-digestion. Insufficient nutritive supply may be due to a diminished quantity of blood or an impoverished blood. Diminished quantity of blood, i. e., a local anemia, is a result of diminishing the calibre or obstructing the supplying vessels. Thrombic formation, aneurisms, etc., may cause partial or even Retrogressive tissue changes. 199 complete ol)Strnction of nutritive vessels and thus be a causative factor in atrophy. Starvation, or failure, of assimilation of food is a cause of atrophy (general). However, in such cases atro- phic de52:eneration of the cells is usually evident by the time the body \vei.e:ht has diminished Vm of the total weight. Certain chemic sul)stances mav indirectly be of significance in the pro- duction of atrophy, but they influence either the cell nutrition or function. Excess nutrition may induce metabolic disturbances of suffi- cient gravity to cause the cells to become sluggish and more or less inactive to such an extent that they will become atrophied. However, excess food is a much less frequent cause of atrophy than insufficient food. Disturbed function. — Diminished or excessive functioning are causative factors in producing atrophy, the former being the most frequent cause. Tissues deprived of function usually be- come more or less atrophied. When an afferent nerve fibre is disconnected from its end organ, (the mechanism by which it picks up impressions), it begins to atrophy at once, probably because of its failure to function. Muscles not functioning atrophy. Thus there is muscular atrophy during most cases of lameness. Diminished cardiac function resulting from dimin- ished blood pressure, is succeeded by atrophy of the heart muscle. Glandular structures become atrophied because of disuse. Excessive functioning, long continued, causes fatigue and in some instances paralysis, the latter usually being succeeded by atrophy. Atrophy from excess function is sometimes observed in race horses, show animals and is not uncommon in musicians, acrobats, trapeze operators, etc. Pressure. — Aside from the influence of the vaso-motor mech- anism there may be sufficient pressure from tumors, hyperplas- tic formations, mechanical contrivances, as harness, etc., to dim- inish or obstruct vessels and cause atrophy. Pressure may also exert influence other than diminishing the blood supply, for con- stant pressure alone causes atrophy, e. g. pressure atrophy of osseous tissue. Pressure atrophy, accompanying cirrhosis of glandular structures as the liver or kidney, is usually caused by pressure of the newlv formed fibrous tissue which partially ob- structs the nutrient vessels. However, the compression of the parenchymatous cells disturbs their metabolic equilibrium and is also a factor of some importance. Appearance. Macroseopic. Atrophied organs are usually di- minished in size, are irregular or regular in shape, have a dry shrunken anemic appearance and are usually pigmented. The 200 VETERINARY PATHOLOGY. parenchymatous tissue is most frequently involved, interstitial tissue rarely becoming atrophied. The diminution in size may be uniform throughout, the atrophied part thus retaining its nor- mal shape, or the diminution may be unequal in different parts, thus producing a lobulation of the affected portion. Atrophied bone usually maintains its normal external shape, as the process is essentially a rarefication in which the Haversian and medul- lary canals are increased in size . Pulmonary atrophy may con- sist of diminution of the alveolar membranes to such an extent that they rupture, thus produciing large cavities. Atrophic mus- cular tissue is usually more intensely pigmented than normal muscle. The source of the excess pigment in atrophic muscles may be from the atrophied muscle cells or it may have its origin from the blood. Microscopic. — The cell body and nucleus shrink in size in simple atrophy without previous alteration in the cell structure. In numerical atrophy the cells first diminish in size and then dis- integrate and die. Thus atrophy, disintegration and necrosis are evident in numerical atrophy. The appearance of atrophic tis- sues vary according to the structures involved. Atrophic kidney tissue is characterized by the diminution in the size or in the number of the glomerular and tubular cells. The tubules and glomeruli may collapse the supplying capillaries becoming oblit- erated by pressure of the hyperplastic fibrous tissue. In muscu- lar atrophy, the muscle cells diminish in size probably because some of the fibrillae disappear. Effects. — The effect of atrophy depends upon the structure involved the extent of the condition and the age of the animal. If the involved structure is no/ vital and the atrophy is of only slight extent and in a young animal, in which the regenerative power is good, the part will recover if the cause is removed. Extensive atrophy of vital structures in old animals is usually fatal or at least predisposes to other conditions that are fatal. Again, a part may partially recover after atrophic disturbances. RETROGRICSSIVK TISSl'l'. CHANGES. 201 CLOUDY SWELLING. DEFINITION. OCCURRENCE. ETIOLOGY. Chcuiic. Bacterial products. Phosphorous, Arsenic, etc. Thermic. APPE.IR.INCE. Macroscopic, Microscopic. TISSUE AEEECTED. Epithelium. Muscle. Nerve. EFFECTS. Cloudy swelling-, albuniinous, granular or parenchymatous degeneration is a retrograde metamorphosis in which the proto- plasm of the cell becomes granular. The granules in cells affected with cloudy swelling arc albuminous, at any rate they are solu- ble in an excess of a 2% solution of acetic acid or a 1% solution of potassium hydroxide, and give the typical albumin reaction to the xanthoprotein test. Active glandular cells, especially those that produce ferments, are normally granular; but the granules in tiiese cells do not respond to the foregoing tests and hence are not albuminous. Cells in the earlier stage of fatty degeneration are granular but the granules are not dissolved by solution of acetic acid or potassium hydroxide, and they are dissolved by ether or chloroform and are stained red with Sudan ITT. There- fore they are fat granules. Cloudy swelling probably occurs more frequently than any other retrogressive change. It invariably affects parenchymatous cells in areas afflicted ^vith acute inHammation and is usually associated with infective diseases. Etiology. — The causes of cloudy swelling may be divided in- to two groups, Chemic and Thermic. Chcmic substances jiroduce cloudy swelling either by influ- encing the action of cell enzyms. thus causing the separation (coagulation) of the cell albumins, or by combination with the albumins of the cell protoplasm thus forming new compounds (albuminate of mercury, etc.) that are of no value to the cell. Excessive quantities of all)umin()Us substances may be assimi- lated l)y the cells, the unused portion becoming coagulated or rendered insoluble as it accummulatcs, thus producing cloudy swelling. The chemic sijl)stances that produce cloudy swelling are usually soluble and are in solution in the blood or lymph from which they readily dift'use into the cell body where they exert their action. 202 VETERINAR.Y PATHOLOGY. Of the chemic substances capable of producing cloudy swell- ing bacterial products are the most important. The diphtheria toxin is probably the most active of all bacterial products in the production of cloud}- swelling. Other organic substances as leu- comains and phenol are capable of producing this degeneration as well as many inorganic substances as arsenic, mercury, phos- phorous and the mineral acids. Thermic disturbances, especially high temperature, is prob- ably a cause of cloudy swelling. Halliburton has demonstrated that certain high temperatures produce turbidity or granular degeneration of cells. P'rom experimental evidence it is appar- ent that different groups of the albumins of the cell protoplasm are separated (coagulated) at different temperatures. The high- er the temperature the more fixed the coagula and the more difficult they are of solution. From the present known facts, although the chemistrv is not determined, it is evident that high 7 » - \>y^ -~ Fig. 97. — Cloudy Swelling, showing granular degeneration of kidney cells Rl-TROr.RKSSIVF. TISSl'I-: CIIAXGF.S. 203 temperature is at least a predisposing if not an exciting cause of cloudy swelling. Appearance. — Macroscopic. — An organ or part afl^cctcd with cloudy swelling, has a parboiled appearance, it is lusterless and lighter in color, softer in consistency, and is slightly enlarged. Microscopic. — An organ or part affected with cloudy swelling appear cloudy, because of the presence of many small albuminous granules, and the cells are slightly enlarged, hence the name cloudy swelling. The increased size of the cell results from co- agidation, the coagula occupying more space than the non-coag- ulated protoplasm. If the tissues of an organ are examined with the high power microscope the cell may appear slightly sw'ollen and its limiting membrane quite distinct ; it may be considerably swollen and have an indistinct membrane ; or. finally, it may have ruptured and the space it previously occupied may contain a mass of granular deljris. The protoplasm of the cell body may con- tain small, irregular granules, the nucleus mav be almost normal, slightly degenerated, or it may even be entirely disintegrated. Tissues Affected. — Epithelium, muscular, nervous, and con- nective tissue are aft"ected with cloudy swelling, the frequency being in the order mentioned. Cells of excretory organs are especially affected because of their eliminative function. Effects. — The effects of cloudy swelling depend upon the structure involved, the extent of the involvment, and the age of the affected animal. Affected muscular tissue has a diminished contractile power. T\cnal tubules may be occluded because of the swollen tubular cells and the affected cells may also have a diminished functional capacity. The function of any structure is decreased and in extreme cases inhibited by cloudy swelling of its component cells. Cloudy swelling is usually a repairable process, providing the cause is removed before the cells are destroyed. 204 VETERINARY PATHOLOGY. FATTY CHANGES. PHYSIOLOGIC (Fattv luiihraiion'). DEFINITION. ETIOLOGY. Excess ford. Insufficient exercise. Heredity. Influence of disease. Unsexing. Lactation. Venesection. APPEARANCE. Macroscopic — Greasy, pale color. Microscopic — Droplets of fat between cells. TISSUE AFFECTED. Normal depositions. Epithelium, muscle. EFFECTS. PATHOLOGIC (Fattv Degeneration). DEFINITION. ETIOLOGY. Insufficient food. Inability of cells to utilise food. Excessi7'e activity. APPEARANCE. Macroscopic — Greasy, pale, light. Microscopic — Droplets of fat in cells. TISSUE AFFECTED. Epithelium. Aluscle. Nerve. EFFECTS. Adipose tissue is not a specific tissue, but represents a modi- fied connective tissue. The cells that later become fat cells, are originally flat or spindle shaped and usually occur in clusters or groups. There are certain locations, called fat depositories, where fat usually occurs. Normally the principal fat depositories are located in relation to the kidney capsule, subserosa (parietal, visceral and omental peritoneum), subcutem, intermuscular areo- lar tissue, and in the orbital fossa. A well fattened animal has accumulations of fat in all the fat depositories. In an emaciated animal limited quantities of fat occur only around the kidney in the omentum, and orbital fossa. Normal adipose tissue varies in color and consistency in the dififerent animals. In general it is white or yellow and appears lobulated when cut across. The consistency depends upon the melting point of the fat. Olein is the principal kind of fat in the hog, stearin and pal- Kiitin in the ox, and stearin in the sheep. It has been demon- RETROGRESSIVE TISSUE CHANGES. 205 strated, however, by Prof. Hopkins, of the University of Illi- nois, that the body fat is the same as the ingested fat. (Hogs were fed on cotton seed oil and the presence of the same kind of fat was demonstrated in the hog tissue.) It has also been found that butter fat in cow's milk is the same as ingested fat. Opinions are at variance in reference to the digestion and assim- ilation of fat. The fat splitting enzyms convert the fats into fatty acids and glycerine. Tlic alkali present in the intestines unites witli a part of the fatty acid, forming soap, the latter and the glycerine i)ass bv osmosis into the intestinal epithelium or through the mucous membrane where the glycerine is substituted for the alkali, the alkali passing back into the intestinal lumen to form more soap (Hammersten). Some of the fat may be so finely emulsified that it passes directly into and through the in- testinal epithelium, and some of it may be incorporated by leu- cocytes, and thus carried from the lumen of the intestine to the lacteals (Ilowellj. Fat droplets are present in the circulating blood. The exact manner of the prt)duction of fat cells in normal adipose tissue has not been determined. All normal animal tissues contain varying quantities of neu- tral fat. As much as 23 per cent of fat has been extracted from kidnev tissue (.\dami). The proportit)n of neutral fat in the same kind of tissue varies in the same animal under different conditions and in animals of different species under the same conditions. Thus the quantity of fat in the muscular tissue of an emaciated animal is less than in an animal in good flesh. The muscular tissue of the hog contains more fat than the muscular tissue of the ox, sheep, horse or dog. In fact the presence of fat droplets betwen the nuiscle cells is a distinguishing characteris- tic of porcine muscular tissue. There is no definite limit to the quantity of fat normallv contained in the tissues of any animal. Certain abnormal fattv changes occurring in the various tis- sues have been described as fatty infiltration and fatty degen- eration. These changes, although originally thought to be en- tirely distinct, are closely related and may represent different stages of the same process. These fatt\- changes mav be dis- cussed as physiologic fattv changes (fattv infiltration), and path- ologic fattv changes (fatty degeneration), although there is no good reason for the division of the subject other than to recog- nize the previous classification and prevent undue confusion. 206 VETERINARY PATHOLOGY. Physiologic Fatty Changes. (Fatty Infiltration.) Physiologic fatty changes is a condition in which there is an excessive accumulation of fat, but the function of the altected part is not materially changed. Etiology. Excess Food. — House dogs and cats and many family horses are usually fed to excess, resulting in the deposition of exces- sive quantities of fat in practically all tissues, thus producing general obesity. The "Strassburg goose" is force-fed with dough balls in excessive quantities until excessive obesity is produced, the liver especially becoming the seat of marked fatty accumulations. In fact all prime "butcher stuff" is affected with physiologic fatty changes or dietary obesity. Insufficient Exercise. — Animals kept in tie stalls or in close quarters have a tendency to become excessively fat, especially if they are fed a full ration, because there is diminished oxidation on account of lack of exercise and the bulk of the consumed food is stored as fat. Venesection. — Frequent bleeding diminishes the percentage of red l^lood corpuscles and thus indn-ectiy diminished oxidation and favors fat accumulation. Disease. — Some diseases appear to influence the physiologic deposition of fat. The early stages of tuberculosis in cattle and hogs and distomatosis in sheep is accompanied by physiologic fatty deposition. During convalescence from some diseases there is an increased deposition of fat. Lactation. — The early period of lactation is accompanied by fatty accumulation especially in the liver. (Possibly the liver may act as a distributing center of fat.) The fatty accumulation in the liver is evident regardless of any variations in the composi- tion of food stuff. Heredity. — Some animals, especially hogs, except the Tamworths and Yorkshires, appear to have an inherent tendency to become excessively fat. Castration. — Removal of the gonital glands favors fat accumula- tion in the tissues. Castrated dogs and cats, especially if cas- trated when mature, become obese. In general the exciting causes of physiologic fatty changes are excess of food or diminished oxidation, heredity being a pre- disposing factor. RETROGRESSIVE TISSUE CHANGES. 207 Appearance. — Macroscopic. — Tissues affected with fatty infil- tration are greasy or oily, more friable than normal, and paler in color, the color being uniform throughout or mottled. The quan- tity of blood in the fat varies, there being more, in general, in the fat of young animals. Muscular tissue in which there is a fatty accunuilation contains areas or strata of fat and strata of muscular tissue. The dejiosition of fat may be so extensive in muscular tissue of hogs that there is little evidence of muscle. Subserous accumulations of fat may be localized, giving the ap- pearance of masses of fat, or it may be accumulated diffusely as thick layers of fat. In dogs and cats the excess fat is usually deposited around the kidneys. Microscopic. — In the early stages of physiologic fatty changes, small droplets of fat are observed between and within the cells. The intracellular fat gradually increases and assumes the space within the cell, the nucleus being crowded to the margin of the cell and may ultimately disappear. Fig. . — Fatty Infiltration, liver, hog, showing Infiltration of globulis from piriiihery of lobule toward Its center. Tissue Affected. — All tissues are subject to fatty accumula- tions, excepting the normal depositories, the liver being most prone to the afifection. Effects. — The influence of physiologic fatty changes is de- pendent upon the extent of the condition and the duration of 208 VETERINARY PATHOLOGY. the process. If the nuclei of the cells are not injured and the process is discontinued the infiltrated fat is disposed of and the part recovers. If non-regenerative cells, such as heart muscle, are destroyed, they will not be regenerated, even though the fat is reabsorbed. The destroyed heart muscle cells may be replaced w-ith fibrous tissue. Pathologic Fatty Changes. (Fatty Degeneration.) Pathologic fatty change, or fatty degeneration, is a condition in which the protoplasm of the afifected cells diminishes because of an increase of the intracellular fat. Fat or some of its cleav- age constituents is probably constantly present in varying quan- tities in all active cells. Pathologic fatty changes are of frequent occurrence, being associated with diseases of malnutrition, and occurring in acute febrile diseases and many of the infective diseases. It is espe- cially evident in chronic phosphorous poisoning and some other chemically induced diseases. Pathologic fatty change is differentiated from cloudy swelling as follows : The droplets of fat are soluble in ether and chloro- form and are not dissolved with dilute acetic acid or potassium hydroxide; while the granules in cloudy swelling are insoluble in ether and chloroform, but are soluble in dilute acetic acid or po- tassium hydroxide. Again the fat droplets are stained red by Sudan III, while the granules of cloudy swelling are not. Fatty degeneration is difficult to differentiate from fatty infil- tration, and in some instances it is impossible to differentiate them ; in fact, future investigation may confirm the identity of the two processes. In the early stages the fat droplets are usu- ally intracellular in fatty degeneration, and intercellular in fatty infiltration. Etiology. — In general, fatty degeneration is the result of the disturbance of cell metabolism. The production of energy, be- ing intimately associated wnth the metabolism of fat, becomes a factor in the causation of fatty degeneration. Specifically, disturbed nutrition is the principal cause of fatty degeneration. Disturbed nutrition may be the result of, 1st, variation in the composition of the blood, 2nd, diminished quantity of blood, ord, diminished oxygen supply, and 4th, changed environments of the peljs. Insufficient supply ot cell nutriment is the principal inj RKTROCUI'-SSIVIC TISSl'K CIIAXGi:S. 209 fluence resulting from circulatory disturbances or altered com- position of blood. Diminished oxyi:;;en supply results in incom- plete oxidation of the a\ailable intracellular fat which is then accumulated within the cell. Changed environments include the variation of the chemic reaction of a tissue, the tissue tenii)era- ture. amount of Huid, etc. Disturbance of the environments in- fluences the cell metaljolism and may cause the union of cleav- age products of fat tliat exist within the cell, or the infiltration and intracellular accumulation of fat may be favored. Changed environments may also render the cells unable to utilize the food brought to them. The causes of cloudy swelling are also etiological factors in the production of fatty degeneration, in fact, fatty degenera- tion is frequently associated with cloudy swelling. Disturbed metabolism is produced by insufficient or improper food, dimin- ished supply of oxygen, or inability of the cells to utilize the food or oxygen supplied, the inability of utilization being a re- sult of the damaging influence of chemic or thermic variation of the environments of the cells. Appearance.— Macro^cof'ic. — A tissue affected \^•iith fatty de- generation varies in appearance according to the extent of the process. Tn general, affected tissues are paler in color (change in color is frequentlv in patches which appear yellowish), lighter in weight (in extreme case, liver tissue afifected w'ith fatty de- generation, floats in water), greasy or oily in appearance, (a knife blade that had l)cen used in sectioning a fatty tissue is usuallv smeared with drops of oil or fat), and usually sw^ollen or enlarged in the early stages, succeeded by diminution in size as the fat is resorbed. Tissues afifected with fatty degeneration are less elastic, and more friable. Microscopic. — Tn the very early stages the cells contain small granules that are differentiated from the granules of cloudy swelling only by the chemic test referred to above or by special stains, as Sudan III. As the degeneration progresses, the minute fat droplets coalesce, forming drops sufficiently large to be rec- ognized microscopically, as small, clear spots or holes in the cell protoplasm in sections of tissue fixed in fluids that are sol- vents for fats and as fat drops in fresh tissues. The affected cells are swollen to an extent which is proportional to the degree of tlie degeneration. l"^ltimatelv the cell membrane ruptures and the enclosed fat is liberated, thus producing a condition not 210 VETERINARY PATHOLOGY. differentiable from fatty infiltration. The nucleus is usually not involved in the beginning, but as the degeneration progresses in the cytoplasm, the chromatin network disappears and the entire nuclear structure finally becomes disintegrated, producing the so-called granule cell. The degeneration may be continuous throughout a tissue or it may be more or less patchy. The ex- tent of involvement of the cells in an afTected area is usually unecjual, some cells being only slightly affected, others contain- ing considerable fat, and still others being entirely converted into fat. fig-. 99. — Fatty Degreneration of the Liver, showing the early stage of the process around the central vein. Tissue Afifected — Glandular tissue, particularly the liver, is probably most prone to become affected with pathologic fatty changes, or fatty degeneration. Muscular tissue is quite subject to fatty degeneration, especially heart muscle. Epithelium other than glandular, nervous and connective tissues, are not exempt from this process. Tumors are occasionally observed to be affected with pathologic fatty changes. Necrotic tissue fre- quently becomes a fatty mass or an entire cadaver may be con- ri:tr()(;ki:ssivi-: i issri". cii.wci'.s. 211 \crtccl into a fatty mass termed adipocere, whieh is no doubt the result nt" i\Tment> !il)eraled iruni the dead tissue. Effects. — llie e(in\ersiun of tlie cell protoplasm into fat im- pairs tb.e eell funetion. At least diminislied cell action, as well as disturbed cell metahnlism is e\ident in cells affected with patholos^ic fatty change. In cells slii^htly affected, the droplets are either oxidized or are extruded from the cell (absorbed when the cause is removed). L'ells more extensi\el\- alYected may be destroyed, leavings a meshwork of \-essels and fibrous tissue. The area may later be filled w ith the new i)arenchymatous cells arisiui^- from the surrounding less affected zones, and, like those destrt)3-ed. it ma}- persist as a mass of fibrous tissue, i. e., a scar. If regeneration occurs there must be an adecpuite blood supply. The degenerated cells may become caseated as a result of the con\ersion of the fatty material into a cheese like mass. The usual cause of caseation of fatty debris is diminished or obstructed blood supply resulting in gradual absorption of the tluids, saponification of the fats and in some instances the forma- tion of cholesterin. Caseated material derived from the fatty debris may later be liquified or calcified. AMYLOID CHANGES. Df.riXITION. ETIOLOCV. APPEARANCE. Macroscof^ic. Microscopic. TISSUE AEPECTED—Subcndothclium. EEEECTS. Some masses may be found in the acini of the prostate gland, especially in old dogs and aged liumans, that respond to the iodine test and are considered by some authorities as amyloid bodies. I'lnsiologic amvloid formations ha\e not been observed other than in the prostate gland and they proltably have a pathologic iirigin. Tims a physiologic prototype of amyloid formation is unknow n. Annloid sul)stance (am^lin) is an all)uminoid. insoluble in water, alcohol, ether, eldoroform. xylol, dilute acids or alkalies and is not acted upon by pepsin. When tissue containing amy- loid substances is immersed in Lugol's solution the amyloid areas assume a malioganv brown color and the normal tissue is stained a vellowish brown. ("To make this test wash the aflfected tissue thoroughly until all blood has been removed, apply a lib- 212 VETERI^■AR^' PATHOLOGY. eral quantity of Lugol's solution for one or two minutes, wash the excess of tlie reagent off and the above color reaction will be observed). The test is equally applicable to macroscopic and microscopic sections. If the sections, macroscopic or micro- scopic, are immersed in dilute sulphuric acid, after the application of Lugol's solution, the amyloid area will assume a blue color, the normal tissue a brown color. The analine dyes usually stain amyloid substances some shade of red. The source of amylin is not definitely known. It may be derixed from the blood or from tissue cells. The formation of am}lin may de})end upon variations in the percentage of some chemic substance in the blood or tissue juices. Amyloid formation is not common in the domestic animals. Occasionally a dog is observed that is aft'ected with amyloid ac- cumulations in the prostate gland. One case has been observed n a hog in which the liver was affected, and, excepting this, the carcass showed evidence of no other lesions. Etiology. — The cause of amyloid change is not known, al- though it has been assumed by some pathologists to be associ- ated with chronic suppurative conditions, as, tuberculosis, and other chronic debilitating diseases, as carcinomatosis. The tissues from several animals affected with chronic suppurative processes, as fistulous withers, poll evil, quittor, tuberculosis, glanders, casecais-iymphadenitis, as well as tissue from animals affected with tumors have been examined, but amyloid changes have not been found. Increased or diminished quantity of some of the salts of the blood may be found to be an etiologic factor in amyloid changes. Appearance. — Macroscopic. — Aft'ected tissues or organs are larger, paler, and firmer than normal. The amyloid areas are homogeneous and translucent in appearance. The entire organ or tissue appears homogeneous when the amylaceous material is diffuse. Microscopic. — Amyloid substance is deposited in the frame- work beneath the endothelial cells lining the blood vessels. It appears as an annular homogeneous mass encircling the vessel. The amyloid substance may accumulate to such an extent that the vessel is obstructed. After the capillaries have been gorged beyond their resistance they rupture, thus allowing the amyloid substance to permeate the interstitial spaces where it appears microscopically as irregular homogeneous masses. Tissue Affected. — The blood-vascular subendothelial con- nective tissue is the principal location of amyloid formation, although it may occur in lymph vessels and even the perimysium Ri:rK(>(;Ri;.ssi\i-: rissri-: iii.\.\c.i-:s. 21.> and ciuldiinsium may be aft'ccted as well as the struma of the mucdiis membranes. The liver, spleen, and kidney are the most frc(|uent locations of the jirocess, pro])ably because of the lartji'e number of capillaries in those organs. — c\ Fig. 100. .\iii>li)i«l I)»'neiu^erali«>n, I.iver. a. I^ivir ctlls b. Amyloid material. Effects. — The cdnditiun is so rare lliat it is not ])OSsible to generalize upon the effects of the i)rocess. The amylaceous ma- terial is insoluble in the body fluids and it is (|uite probable that if a part becomes atYected, it remains so permanently. IIVALJXi: CHANGES. /)/•:/•/ A7770.V. liTlOLOGV. .irPRARANCE. Macroscohic. Microscof'ic. TISSUE AFFECTED. I'cssds, Muscles. EFFECTS. This is a i)athologic condition characterized by the conversion of the cell substance into a homogeneous material called hyaline. In the phenomena accompanying the physiologic changes of the corpus luteum "f pregnancy, a hyaline substance is produced. The physiologic formation of hyalin, aside from that produced in the corpus luteum of pregnancy, has not been recorded. The formation of hyalin is quite common in the muscular 214 VETERIXARV PATHOLOGY. portion of the blood vessels of tissues affected with chronic in- flammation and in the blood vessels of sarcomata. It has also been observed in voluntary and heart muscle in certain diseased processes. Hyalin, an albuminous substance very similar to amylin, does not respond to the iodine test, and is not acted upon l)v alcohol, ether, chloroform, acids, ammonia, or water. Acid stains, as eosin and acid fuchsin, have an affinity for hyalin and stain it quite intensely. Etiology. — The specific cause of hyaline formation is not definitely known. Certain predisposing factors, however, are of interest. Wells found that lactic acid injected into voluntary muscle was succeeded by hyaline formation, and it may be as- sumed that the cause of hyaline changes in voluntary muscle is in some instances at least is due to an excess of sarcolatic acid. Some diseased processes, as chronic inflammation, tuberculosis, and sarco- matosis appear to produce conditions that favor hyaline formation. Fig. 101. — H.valine Denegration, Vessels. a. Hyaline around arteries in maxilla of colt. Appearance. — Macroscopic. — Rarely does this condition be- come sufficiently marked to be recognized with the unaided eye. The hyaline substance appears as a translucent, homogen- eous, firm mass, intermingled with the normal tissue. Microscopic. — The hyaline substance appears as glassy areas, and the adjacent tissue frequently becomes less distinct. Except for the affinity of hyaline substances for acid stains and its fail- KF.TROCRF.SSTVR TTSSri'. CTTAXr.F.S. 2l5 lire to react to iodine it is difficult to differentiate from amyloid change. Tissues Affected. — IMuscular tissue, involuntary muscle, especially of the blood vessels, voluntary muscle and heart mus- cle are subject to hyaline changes. Connective tissue is less fre- quently involved and epithelium rarely, if ever. Effects. — When hyaline has been formed in small quanti- ties ana che cause is removed the hyaline substance is probably resorbed and the affected cells repaired. If the production of hyaliri has replaced the protoplasm of large cell masses, especially of mus- cular cells, the area will probably not be repaired with muscular tissue, but it may be substituted with fibrous tissue, provided the cause is removed. MUCOID CHANGES. Physiologic. DEFINITION. ETIOLOGY— Phvsiologic, pathologic. APPEARANCE. Macroscopic. Microscopic. TISSUE AFFECTED— Connective, epithelium. EFFECTS. The transformation of cell protoplasm into mucus is evident in the physiologic production of mucus in the surface epithelium of mucous membranes as well as in mucous glands. The physi- ologic conversion of protoplasm into mucus is the result of in- tracellular enzyms, or at least depends upon protoplasmic activ- ity. As the mucus is produced the cell becomes enlarged and ultimately ruptures, discharging the mucus. The mucus may be formed only in the distal end of the cell or it may entirely re- place the protoplasm of the cell. In the former the remaining protoplasm of the cell regenerates the portion destroyed. In the latter the adjacent cell multiplies, thus filling the gap. Mucus is a viscid, glairy stringy nitrogenous fluid. The principal ingredient of mucus is mucin, a giucoproteid, although there mav also be present pseudomucins. Mucin imbibes water, thus becoming swollen, and from this swollen mass there is pre- cipitated a stringy material by addition of alcohol or dilute acetic acid. Pseudomucin forms a gelatinous mass when dissolved in w^ater, but by the addition of alcohol to this gelatinous mass a stringy precipitate is formed which is redissolved in excess of water, differing in this respect from mucm. 216 VETERINARY PATHOLOGY. Pathologic. Pathologic mucoid formation affects cells and intercellular substance. Cellular pathologic mucoid change is identical to normal mucus formation except that it is in abnormal locations or is in excess in those locations in which mucus is normally produced. Intercellular mucoid formation is a condition result- ing from the conversion of fibres, matrix of cartilage and bone, or other intercellular substances, into mucus. Pathologic mucoid changes occur rather frequently. It is evident in catarrhal in- flammation, in cyst formations and as a retrogressive process in many tumors. Etiology. — The cause of pathologic mucoid changes is not known. Excessive cellular mucoid formation accompanies mild inflammatory disturbances of mucous membranes — so calied catarrh. The increased production of mucus in catarrhal inflam- mation may be the expression resulting from the exaggerated function of the mucous membrane induced by the excessive quantity of blood supplied. Intercellular mucus formation may result from improper nutrition or injurious influences induced by chemic substances. It has long been thought, although it has never been proven, that some product is evolved when the thyroid gland is dis- eased that causes a mucus degeneration of all fibrous tissue in the body (myxoedema). Some sarcomata and carcinomata are affected with mucoid changes, probably the result of chemic sub- stances elaborated by the tumor cells. Appearance, — Macroscopic. — ^Mucus of pathologic origin is not differentiable from physiologic mucus. In pathologic conditions accompanied by mucus formation the mucus is frequently mixed with other substances, as blood, pus and food stuff. Thus the mixture assumes various appearances. A discharge composed of mucus and pus (muco-purulent) is common in practically all catarrhal inflammation, being the characteristic discharge of catarrhal pneumonia and is the usual discharge from the respira- tory tract and conjunctiva, in dogs affected with distemper, in horses afflicted with "stock yard fever," etc. The appearance of a tissue affected with pathologic mucus changes, regardless of whether the cells or intercellular sub- stance is involved, depends upon the quantity of mucus pro- duced. If there is a limited quantity of mucus and it is equally distributed throughout, the affected tissue will appear swollen and soft. If more extensive and diffuse the affected tissue will be soft, spongy, and slimy. If the entire structure has practically been converted into a mass of mucus, it will appear as a slimy, Ri:Tk()(;Ri:ssiV[-: tissui-: ciiant.ks. 21; strinj^^y. jnilpy subslance from which varying- ([uantilies of mucus mav be expressed. The mucoid changes may afYect circumscribed local areas that appear moist and soft, spongy, or even cystic in contradistmction to tlie surrounding- luirmal tissue. Microscopic. — Mucu>^ appears as a stringy substance containing varying (|uantitics of detritus. Fixing agents coagulate mucin in which case it apjiears as a more or less homogeneous mass containinu- man\- fibrillae nr threads of coatrulatcd material. C- t I ^ a' '^ / - r~a^'C^ '■^^^~^ ',>^ ^ an. \r d SP ~\ Fig. 102. — .Mucoid Degreneration. Fibrous tissue. c. Mucoid ci.lls. Mucous substance. Microscopic appearance of a tissue atTected with pathologic mucoid changes is variable according to the extent of the pro- cess but in general the picture observed is the same as that of the normal tissue plus the muctis. Tissue Affected. — Epithelium and the cells and iuicrcellular substance of connective tissue as well as some tumors arc sub- ject to mucoid changes. Effects. — The effects depend upon the extent, duration, and regenerative ability of the affected tissue. 218 VETliRIXARV PATHOLOGY. COLLOID CHANGES. DEFINITION. ETIOLOGY— Unknoivn. APPEARANCE. Macroscopic. Microscopic. TISSUE AFFECTED. Tlivroid, prostate, tumors. EFFECTS. The term "Colloid" has rather an indefinite meaning and by present day writers is used to indicate a variety of substances. "The word colloid is merely morphologically and macroscop- ically descriptive of certain products of cell activity or disinte- gration, which have nothing in common except the fact that they form a thick glue like or gelatinous, often brownish or yellow- ish substance" (Wells). One type of colloid substance is a physiologic product of the thyroid gland, it is in part a secre- tion of the thyroid cells and in part a conversion of those cells into colloid material. This product is normally absorbed as it is produced though it may accummulate in small quantities in the gland acini, especiallv in aged animals. Chemicallv the physiologic thyroid colloid is composed of iodo-thyreoglobulin (a compound of globulin and thyroidin). Thyroid colloid is glue like in consistency and varies in color from brown to yellow\ Colloid and mucous are closely related. Colloid does not increase in bulk when it is suspended in water, neither is it precipitated bv alcohol or acetic acid — two tests that are usually sufificient for differentiation of mucus and colloid. Pseudo-mucin is more difficult to differentiate from colloid. The latter, however, contains iodine and tlie former does not. Pathologic colloid changes are conditions resulting from the excessive production and retention of collagenous material. The disturbance induced by excessive colloid accummulation is usu- ally not serious although it may cause fatal termination. This condition occurs more frequently in old dogs than in other ani- mals. Sheep occasionally show lesions of this condition, in some instances the entire flock becoming affected. Pathologic colloid accummulation is a constant lesion in the thyroid gland of animals suffering from exophthalmic goitre. Colloid changes have been observed in cattle, sheep, horses, mules and one case has been recently noted in a calf. Etiology. — The specific exciting cause of pathologic colloid changes is not known but undue exposure to inclement weather is a predisposing cause of considerable moment. Exposure, in some instances, appears to become an exciting cause of thyroid Ki.i ut)(iKi;ssi\i'; Tissri'. i ii.\\(;i:s. 210 colU)id accuninuilation. iV Hock of 12S l>«aUliy, yfarling- sheep >hipped from smith central Xew ?\Iexico to the Kansas City stock \ar(ls, were all found to have enlarj^ed thyroid !;nands at the lime of slaughter, which was about 2[ hours after their arrival at the stock >ards. The iliymid glands were fimnd on niicro- scropic examination to l)e aliected with patholngic colloid accum- ulation. This occurred in .April, the sheep, having been sheared iust previous to shipment, and the weather having been very inclement during the entire time that they were in transit. ( Jtlier entire flocks of sheep that lia\c been unduly exposed have been affected in a like manner. Fig. 103. — Iliniu.yiMi.h ..I ., ili.Muid Klaiul ulliri.a witli Colloid DeKeinriiticin. I-Indemic goitre in the human is indicative of an infectious cause though the individual cases in non-affected areas dispels tlic infection theory. The absence or diminished quantity of iodine in the food, water or air, may be a causative factor in the production of goitre and other colloid accummulations in the thyroid glands. Appearance. — Macroscnpic. — Colloid most frefpiently oc- curs in masses, varying in size from mere microscopic points to bodies as large as a lead pencil rubber or even cyst like bod- 220 VETERINARY PATHOLOGY. ies as large as a black walnut. More rarely the colloid material may have infiltrated the tissue spaces and become ditifuse. Col- loid varies in consistency from a watery to a jelly like mass, is usually of a clear amber color, although it may be translucent or of a deep mahogany tint. An affected tissue contains variable sized areas of hyaline, rather firm, amber or mahogany colored masses deposited ir- regularly throughout the entire structure. iMicroscof>ic. — The cells are noted to contain small droplets of colloid material which is constantly produced and passed out of the cells and accumulated in the acini, tubules, or intercellu- lar spaces. Other entire cells are converted into a colloid Fig. 104. — Colloid Degeneration, Thyroid Gland. a. Colloid material completely filling tlie acini of gland. mass. The conversion of a large number of cells into colloid material in one vicinity produces colloid masses or the so-called colloid cysts. Colloid substance is homogeneous or slightly gran- ular and is stained, by acid stains. It assumes an orange color when stained according to \'an Giesen's method. Tissue Affected. — Epithelium is probably the only tissue in which colloid formation occurs. The thyroid gland is most commonlv affected. There is a degenerative change occurring in carcinomata that is similar to the colloid formation although it may be pseudomucin formation. McFarland states that col- loid casts occur in the uriniferous tubules, in kidneys affected with chronic inflammation. Ziegler regards the prostatic con- cretions, of the human, that do not react to iodine, as colloid. Ri:TRor,Rr.?siVF TTSsri' ciiAxr.F.s. 221 Effects. — The efifects of colloid accumulation depend upon the extent of it. The exact function of the thyroid ^land has not hcen determined hut it is quite eertain that the iodine compound, iodothyrein or thyroiodin is the acti\e principle of the thyroid secretion. It is not known whether the thyroid secretion has some action vroii cell metabolism or neutralizes various poison- ous substances that result from metabolism or poisons intro- duced into the body from without. The colloid accummulations in p^oitre contain less iodine per given volume than the nc~)rmal secretion, but the total quantity of iodine is materially increased resultinor in circulatory disturbances, as rapid weak pulse, in- creased metabolic actixity especially of protcids, increased secre- tions, irritability, etc. Diminished iodine i)roduction, as ob- served in m}\\uedenia, is not common in colloid accummulation. SEROUS IX FILTRATION. DEflMTIOX. ETIOLOGY— (Ocdcvia). APFEARASCli. Macrosco/^ic. Microscopic. TISSUE AEI-ECTED. EFFECTS. Serous infiltration is a condition in which excessive quantities of lymph or serous fluid infiltrates the cells. In the anatomo-physioloi^ic discussion of the cell, tlie nutri- ents were said to be obtained by specific selective action of the cells and by osmosis. Osmosis is j)rol)ablv the most important mode of passai^e of extracellular suljstances into the cell. In hydremia or other conditions in which cells are bathed by excessive c|uantities of fluid, there is a tcndenc\- for them to become hydropic. Serous fluid that enters the cells in serous infiltration is thin, watery and contains small quantities of protcids and salts. Etiology. — Tlie cause of serous infiltration is an excess of serous fluids in tlie tissues. Serous infiltration is, therefore, an accompan\ini;' condition of oedema and the causes of oedema would likewise be tlie ])rimar\- cause of serous inhlt ration. A second cause ma\- be the im])airment of the cells in whicli they are stimulated to iiiil)il)e more lluid. Appearance. — .][aci'oscof^is. — because of the simultaneous occurrence of oedema and cellular serous infiltration and in view of the fact that oedema is so cons])icuous. the serous infil- tration is not recti!.;nizable in c^ross examination. ^9^ \i:tkr! xarv PATiior.ocv Microscopic. — When examined in the fresh state the cells arc enlarged, the extent of which depends upon the quantity of fluid imbibed. The infiltrated fluid accumulated in the cells appears as clear spaces or vacuoles. The vacuoles occur either in the cyto-plasm or the nucleus and in extreme cases, thev occupy the entire cell and mav even cause its rupture. Tissues Affected. — I'racticalK- all tissues are subject to serous infiltration. Those tissues in which oedema occurs are most frequently afl'ected. Epithelium is quite frequentlv in- volved in serous infiltration because this tissue forms the sur- face of those structures afl'ected with oedema. Effects. — The eft'ects depend upon the extent and duration of the condition. Some vegetable cells are capable of imbibing fluid to a sufficient extent that thev increase their size one hun- dred times. Animal cells cannot imbibe fluids to such an extent as vege- table cells without being rent asunder. After the cells have been subjected to serous infiltration for sometime, the nuclear chromatin appears to dissolve and diffuse through the cell bodv. This necessitates an impairment of the cell activities. GLYCOGENIC IXEILTRATIOX. DEFINITION. ETIOLOGY — ( Disturbed carhoh\dvatc victubfllisvt). APPEARANCE. Macroscopic. Microscopic. TISSUE AFFECTED. EFFECTS. This is a condition characterized by the infiltration of exces- sive quantities of glycogen into cells that normallv contain a limited amount of it or the infiltration of glycogen into cells normally glycogen free. The source of glycogen is not definitelv knowai. Accord- ing to some physiologists, glycogen may be formed from either carbohydrates or proteids. The digested carbohydrates are probablv stored up in the form of glycogen, at least glycogen is readily converted into dextrose wdienever carbohydrates are needed. Glycogen can be demonstrated in the normal liver cells, kidncv cells, and in muscle cells, although it occurs in limited quantities. Glycogen is soluble in water and insoluble in alcohol, chloro- form and ether. Its presence in tissue may be demonstrated by smearing the tissue on a slide and allowing it to dry inverted, ri:tr()(;ki:ssi\i-: tissi'i-: (.hancms. 2^3 over crystals of iodine. The c^lycoo-cn appears as hrownisli areas in the cells. Il may also he denionstratecl hv immersing in a mixture of four parts of alcohol and one part of tincture of iodine, sections that have been hardened in absolute alcohol, the glyco- gen assuming a port wine color. Pathologic glycogenic infiltration occurs in pus cells of supi)U- rating processes. The blood cells, esi)ecially leucocytes, contain some glycogen in those animals afifected with septic infection or sapremia. Thus horses afflicted with sapremia induced by punct- ure wounds of the foot show glycogenic infiltration, of the blood cells. In diabetes mellitus the liver and kidney cells are infil- trated with excessi\e (piantities of glycogen. Etiology. — l)isturl)e(l carl)ohydrate metabolism is inseinir- ably associated with glycogenic infiltration although the specific relation of disturbed carbohydrate metabolism and glycogenic infiltration is not known. Glycogenic infiltraiiim has some asso- ciation also with certain infectitnis and intlammatorv disturban- ces as well as tumor formations. Appearance. — Macrosci)pic. — Glycogenic infiltration d(^cs not produce lesions sutficientlv characteristic to l)e recognized with- out the aid of a microscope. iMicroscof'ic. — The affected cells contain transparent colorless areas near the nucleus. Jf the specimen has been hardened in absolute alcohol, the areas of glycogen may be stained port wine color b\- four i)arts of alcohol and one part tincture of iodine. The areas are \ariable in size depending u]:)on the ex- tent of the condition. In extreme cases the glycogen may be observed in the intercellular spaces. Tissues Affected. — Liver, kidney, muscle, and blood cells are most sul)iect to glycogenic infiltration, the frequency in the order named. Effects. — 1'he glycogen is readily reabsorbed jiro\ jded the cause be removed. The condition being associated with cither pathologic conditions, their removal becomes essential before the glycogenic infiltration can be overcome. 224 VliTKRIXARV PATHOLOGY. URATIC INFILTRATION. GENERAL DISCUSSIOX. DEFINITION. ETIOLOGY — Deficient uric acid secretion. APPEARANCE. Macroscopic. Microscopic — Needle like crvsfols. TISSUE AFFECTED— Articulaiions. EFFECTS. Uric acid is formed by the kidneys from urea and passes out normally with the urine. If not promj^tly eliminated, it com- bines with sodium carbonate of the blood to form sodium urate (cjuadriurate and biurate). The ciuadriurates are unstable but the biurates are quite stable. Uric acid and urates do not nor- mally exist as such in the blood of birds or mammals. The urin- ary excrement of birds is composed of urates but no urea. In birds the ureter terminates in the cloacum ; the kidney excretion, which is almost solid in consistency, is thus mi.xed with the feces before it is eliminated from the body. This anatomic arrange- ment probably favors the resorption of uric acid. At any rate uratic infiltration is more common in l)irds than in any other domestic animal. Sodium urate is the usual compound found in uratic infiltra- tions and when examined miscroscopically appears as a feltwork of radiating clusters of needle like crystals. If urate of sodium be treated with a few drops of nitric acid, and then evaporated to dryness, and to the amorphous residue a few drops of ammo- nium hydrate be applied, the entire mass assumes a purple-red color, or if potassium h}-droxide be applied, the mass becomes bluish-purple. Etiology. — L'ratic infiltration is due to deficient excretion of uric acid by the kidneys. It may be caused bv ligation of the ureters or by any obstruction to these ducts. An exclusive meat or other nitrogenous diet, sometimes produces uratic infil- tration in fowls. Old age is a predisposing factor. Appearance. — Macroscopic. — The phalangeal, metatarsal and tarsal joints are most frequently afifected in fowls. In the begin- ning the condition is e\-idenced by a soft, painful, dififuse swell- ing becoming more circumscribed as it Ijecomes larger. The skin over the affected area becomes thickened and scales off as the swelling increases in size. The nodular swellings ultimately rupture, the contents l)eing buff" ccdored and crumbling as it is discharged. Scimetin.ies masses of the urates accumulate as small stones (tophi) under tendons, etc. The articular surfaces are frequently eroded. ri-:tri)(;ri;ssivi-: tissuk changes. 225 Microscopic. — The needle like crystals of sodium urate, in addition to more or less detritus from necrosis of the tissue, is characteristic of sections or smears of tissues aiTected with uratic infiltration. Tissue Affected. — Articulations are the usual location of uratic infiltration, especially those in the metatarsal region. The skin and visceral organs may he aiTected. Effects. — The accumulation of the urate crystals in the artic- ulation, produces erosion of the articular surfaces, and thus interferes with movement. Tophi beneath tendons also produce disturbance of mobility. KERATOSIS. DEFINITION. GENER.AL DISCUSSION. ETIOLOGY. Dcssicatioii of surface epithelium. Excess of iiitercellulay cement. APPEARANCE. Macroscopic — Horny grozvths. Microscopic. TISSUE AFFECTED— Epithelium. EFFECTS. Epithelium becomes cornified thus forming the hard horny hoofs, horns and claws. The conversion of epithelium into horn- like substance (characteristic of the hoof) consists of a dehy- dration of the cells and the production of a glue like material that cements the dessicated cells together. The ergots and chestnuts in the skin of the horse are produced by the accumu- lation of dessicated cells cemented together. The cornified epithelium that characterizes keratosis varies from dried scales to dense horn tissue. Pathologic cornification is of rather common occurrence in the domestic animals. The skin covering the carpus of oxen fre- quently becomes materiallv thickened and cornified, one case having been observed in which the cornified mass accumulated until a projecting horn like structure some ten inches long and six inches in diameter at its base, was present. As a general condition it is observed in the skin of animals affected with ich- thyosis. Etiology. — Irritation appears to be a causative agent in keratosis. The condition may be a sequel of inflammation and sometimes occurs in scars. Whatever increases dessication of 226 VETERINARY PATHOLOGY epithelium and stimulates the formation of excessive quantities of cellular cement favors keratosis. Appearance. — Macroscopic. — Keratotic accumulations appear like so much irregularly formed horn tissue. The resistance of the cornified epithelium varies according to the completeness of cornification. Fig. 105.— Photograph of a Keratotic, horn-like grovvUi removed from region of withers of an ox. Microscopic. — The cornified epithelium usually appears as a mass of debris, although in some instances there may still be evidence of cellular elements. The epithelial pearls of epitheli- omata probablv represent a type of keratosis. — the pearls appear- ing as whirls of scale like elements suggesting the gross appear- ance of a section of an onion. Tissue Affected. — Epithelium is particularly affected. Some tumors are afifected, especially epitheliomata. Effects. — The area involved is incon\enienced. If the en- tire skin is involved there may be secondarv constitutional les- ions. ri:tr()(;ri:ssivk tissi'k rir.\xci:s. 227 OSSTFICATK^v. rilYSIOLOGIC. PATHOLOGIC. ETIOLOGY. Irritation. Ini/^ropcr nutrition. APPEARAXCL. Macroscopic — Osseous tnasscs. .Microscopic — Osseous plates. TISSUE AFPECTED. Muscle. Arteries. Tumors. EFFECTS. Ossification, as in the formation of bone, is a normal process. The process consists in the formation of fil^rous lamellae that are later calcified. Osseous bodies are sometimes formed in such structures as the falx cerebri and tentorium cerebelli. These osseous formations assume the sliape of the oriq-inal structures, and are called osteophytes. Pathologic ossification consists in the formation of a bone like substance in abnormal locations, as n-tuscles, arteries, tum- ors, etc. Etiology. — Ossification probably results from chronic irrita- tion, improper circulation, or impoverished nutrition. Appearance. — Macroscopic. — Ossified muscle appears as a porous osseous mass. In an autopsy of a horse the flexor bra- fhii muscle, was found to be a porous osseus mass, and appeared like cancellated bone. Muscle ossification is usually designated myositis ossificans. An ossified falx cerebral or tcnt(~irium cere- bellar osteophyte appears as an irregular bony mass. Microscopic. — The porous osseous tissue formed in pathologic ossification is found ^ lbs.) was found. Gage reported a case in which a calculus w^eighing .9 kilo- grams produced fatal results. Hodgkins and Son of Hanley, Eng- land, recently obtained three enteroliths, each weighing 1.6 kilo- grams (314 lbs.) from the intestine of a horse. Bikiary Oalctili (Cholfliths) are not rare in the domestic ani- mals. They vary from the size of ia pea to a baseball, are tinted yellow, brown, red, green, or may be chalk white in color. Fre- quently they occur in large numbers, are variable in shape, and structure. They are usually composed of biliary pigme.>its in 238 VETERINARY PATHOLOGY. combination with calcium, although carljonates and phosphates are common ingredients. J miliary calculi may form in the iMiiary collecting tubules of the liver in the bile duct or in the gall blad- der. The results of their presence depend upon their location and size. If they are small and cause no obstruction there will be no inconvenience from them. If they are of a size that they can be forced through the bile ducts they will produce severe colickv pains at the time of passage. They may be sufficiently large to obstruct the bile duct of some principal collecting tubule and produce a stagnation and resorption of bile, resulting in %A^^^^ Pig. 112. — Biliary Caleuli, Ox. 1. Showing Facets. -3. Showing Crevice. 2. Showing Facets and Lamination. various disturbances because of the presence of the bile in the blood. Pancreatic calculi, or calculi in the ducts of the pancreas, have been observed particularly by veterinary inspectors. These calculi produce obstruction of the ducts and there may be reabsorp- tion of some of the pancreatic secretion. Fatty necrosis sometimes succeeds obstruction by pancreatic calculi. Lacteal Calculi (galactoliths) may be formed in the galacto- phorus sinuses, particularly of the ox. They are usually com- posed of calcium phosphate. ki;tk()(;ui;ssi\i-: tissi'i'. ciiaxgks. 23') Phlcholitbs or calculi in veins have l)ccn (>l)^c^vc(l l)v Spoon- cr in abdominal \cins and hy Sininmnds in the jui^ular vein. Idiey are prohably the result nf calcineaticm of thrombi which have later 1)econie detached from the vessel walls and are true calculi. Thcv produce an obstruction in the vessels in which they occur. They may be of slight significance or may cause a fatal termination, depending upon the importance of the vessel and extent of the collateral circulatit)n or anastomoses. These calculi are usually composed of calcium compounds. .IrtcrioliUis are calculi formed in arteries. Their cause, for- mation, composition and termination being practically the same as that of phleboliths. Litlwpcdia are calcified foetuses. In extra-uterine foetation the foetus occasionally lives only for a short time. Dead extrauter- ine foetuses frecpiently become impregnated with lime salts, producing the so-called lithopedia. Lithopedia may also occur within the uterus. This class of calculi is (juite common in swine and some cases have been observed in cattle and sheep. CONCRE^IENTS. DFJ-IXITION. ETIOLOGY. VARIETIES. Hair balls. Fecal matter. Bile. Pus. Milk. Cerumen. Concremeiits are abnormal accumulations of ori^anic material in the cavities of hollow organs. Their effects are practically the same as the efi'ects of calculi. Their formation depends upon the collection and massing together of organic substances derived either from the body in which the concrements occur (M- from some extraneous source. They mav be homogeneous or hetero- geneous in structure; oval, spherical, or angular and faceted in shape, variable in size, color and number. (S^;} oat hair concre- ments were found in the great colon of a horse by C. Roberts. M. R. C. \'. !^.). They may be composed of hair, mucus, fecal matter, casein, inspissated pus or bile, ingesta of various kinds, etc. 240 VETERINARY PATHOLOGY. Hair Balls (Egagaropiles or Trichobezoars) are accumulations of hair into masses. They occur most frequently in animals that lick themselves as the ox and deer. Other animals are affected as the hog, dog and cat, also man, espe- cially barbers, hair-sorters, hair- dressers, etc. Dr. A. Trickett observed a Persian, cat that womited a mass of hair ^}4-inch in diameter and 3 inches long. Egagaropiles vary in size from a pigeon's egg to a basket ball. They are in some cases simply masses of hair in others they are impregnated and incrusted with mineral substances, giving them the appearance of calculi. Hair balls incrusted with min- eral salts taken from the deer by someone's grandfather or great- grandfather is the ordinary "mad-stone" in use at the pre- sent time. Recently a hair ball (bristles) completely filling the stomach was obtained from a hog slaughtered in a packing house. Hair balls are usually found in the abomasum or large intestines of the ox and in the stomach or large intestine of the hog. The presence of a hair ball produces the same effects that would be produced by any other indigestible body of the same size in the same location. Fecal Concrements. — The intestinal contents may accumu- late into compact masses. These '^TEgairopn"!)'"^''' concrements interfere witli the t^l'.TROCKKSSIVl-: TISSUK CIIAXGKS. 241 movement of food-stuff throiiii:^h the canal and may completely obstruct it. Apjiendicitis in the liuman is frequently a result of a fecal concrement in the vermiform appendix. These concrements occur most frequently in the horse, dog and cat. They arc usu- ally composed of cellulose in the horse, of bones and bone frag- ments in the d(\g and cat. The large intestine is the usual loca- tion of them in the liorse and the small intestine in the dug or :at. Maxwell reported a case in which alfalfa accumulated in the large intestine of a horse, the ci increments being irom 1T}4 to 22yj cm. (7 to 9 inches) in diameter. The fine hair of clover or oats (phytobezoars) frequently accumulates and forms concrements. The results of fecal concrements depend upon either mechanical interference in the passage of intestinal contents, erosion of the intestinal mucous membrane or perforation of the intestinal wall, or a combination of two or more of the above. Inspissated Bile. — Tf the outHow of bile is obstructed it will become condensed or ins|)issated to a degree depending upon the length of time of obstruction. Inspissation of bile frequently occurs. The animals most frequently affected are the ox and hog. An ox liver, containing several concrements composed of inspissated bile in the interlobular ducts has been observed. Bile in this condition may form masses which in general ap])earance resemble biliary calculi. It is sometimes impossible to differen- tiate biliary calculi from ins])issated l)ile, and, in fact calculi are )'i- III. 1. InxpiNNaled pim fmtn luiiu absccsp. ;'. IiittpiHHated piiN, guttural piiucli. horsf. 242 VKTKRIXARV TATHOLOGY. frequently of secondary origin, the thickened bile forming the nucleus. The results of inspissated bile depend first upon the resorption of bile into the system and. second, upon the absence of bile in the intestine. Inspissated Pus. — Empyema sometimes terminates, when there is no surgical interference, in resorption of the liquor puris. after which the solid constituents frequently mass together, forming concrements. These concrements may form in any cav- ity in which the suppuration is slow going or chronic, provided the movement of the part is limited. Their formation has been noted in the guttural pouch. After formation they may become calcified. They are of little importance except as pathologic phenomena. Lacteal concrements result from the coagulation of the casein of milk and its accumulation in the galactophorous sinuses. These concrements occur in the cow and can usually be expelled through the lacteal duct by manipulation. Ceruminous concrementf^ occur in animals in which the hair or wool extends far into the external auditory meatus. They are composed of cerumen and are the result of an excessive pro- duction or limited excretion of it. They may form into sufftcient masses to completely occlude the external auditory canal and thus interfere with hearing. Concrements have been found in the bronchial tubes. Their formation depends upon the accu- mulation and condensation of mucus or purulent fluid. They may obstruct bronchioles and produce atalectasis. Prostatic concrements frequently occur in old dogs. They are present in manv of the enlarged prostate glands. They con- sist of masses of accumulated colloid-like material. The results depend upon the pressure that they may exert. Thus there may be an obstruction to the outflow of urine, PIG.AIEXTARY CHANGES. Physiologic pigmentation is variable. The color and extent of pigment varies in dififerent animals and in the same animal under difi:'erent conditions. All physiologic pigmentation is the result of deposition of hemoglol)in or some of its derivatives. The skin of animals is usuallv extensively pigmented, with the exception of albinos and some white skinned animals not albinos. The production of the cutaneous pigment is not well understood but probablv results from metabolic activity of the deeper layers of epidermal cells. Because of the intense cutan- Ri;'i"R()(;Ki:ssi\'i". i issri-: chancks. 243 eons pigmentation of animals, erythema, hcmani;i(»mata and other I)ath(.)logic processes are not as e\i(lent as like conditions in the human. The excessive cutaneous pignuntation protects the skin I'rom the injurious inthiences of sunlight. Hair, wool, fleece, fiu' and feathers are variously colored, the color depending upon the soluble pigment in the cortical portion of the cutaneous appendages. The color of the skin is usually an index to the color of the hair or similar epidermal appendages. The color of hoofs, horns, and claws is prol)ably dependent upon cutaneous pigment. X'oluntary mtiscle tissue is pigmented with varying quanti- ties of hc-moglobin, excepting the so-called white meat of fowls (the sternal muscles and nuiscles of the pectoral arch). The pigmentation of the voluntary muscles varies in the dift'erent animals. The e(|uine muscles are the most intensely red, the intensity of pigmentation in the muscles of other animals being in the following order: bovines, ovines, porcines, canines, felines. The flesh of duck and c|uail and the dark meat of other fowls is darker even than equine muscle. Heart muscle is verv dark in color because of the excessive quantities of pigment, (iizzard muscle is intensely pigmented. Involuntarv muscle of all ani- mals is very ligiit in Color, because of the limited quantity of pigment contained. Ihe significance of the pigmentation of muscle is not known, i)ossibly the hemoglobin of the muscle cell has some important metabolic function. The mucous membrane, particularly of the mouth, is fre- rpiently pigmented, 'ihc buccal mucous meml)rane of the sheep and dog is often black. The uterine mucous membrance of •the bitch is occasionally quite black as a result of ])igmentation. this i)igment being derixed from the uterine glands, and no doubt is indirectly a (lerivati\-c of hemoglobin. r>ones, especially the internal portion of the articular extremi- ties, are frecpiently pigmented from the red marrow that occupies the spaces in the cancellous bone. The liver and spleen are natin-ally deeply pigmented because of the excess of free hemoglobin in those organs. The kidney also appears pigmented, probably because of the excess quantitv of blood contained in it. The choroid tunic of the eye is deeply pigmented with a substance not unlike melanin, the purpose of which is to absorb rays of light. 244 VETERINARY PATHOLOGY, EXCESSIVE PIGMENTATION. (Hyperchromatosis.) DEFINITION. ETIOLOGY OR SOURCE. Hematogenous. Hemoglobin. Hemosiderin. Hematoidin. Hepatogenous. Bilirubin. Biliveridin. Cellular. Suprarenal — Addison s disease. Tumor — Melanin. Pregnancy. Freckles. Extraneous. Pneumonokoniosis. Anthracosis — Carbon. Siderosis — Iron. A rgyriasis — Silver. Plutnbosis. Hydrarqiriasis.. TATTOO.' EFFECTS. Excessive pigmentation, also known as pigmentary infiltra- tion, is a pathologic condition characterized by the presence of an excess of pigment in the tissues. Pathologic pigmentation is quite common. Icterus, melanosis, and anthracosis are types of pathologic pigmentation. This condition may be congenital as melanosis maculosa of calves, or it may be acquired as in icterus. Etiology. — In pathologic pigmentation the coloring matter may be derived from internal sources, as blood, bile and cells, or from external sources as coal dust, silver, lead and various pig- ments. Blood. — Pigmentation as a result of deposition of hemoglobin of the blood is designated hematogenous pigmentation. Hemo- globin is the principal hematogenous pigment, although hemo- siderin and hematoidin, both derivatives of hemoglobin, are of some importance. Hemoglobin is the normal coloring matter of the red blood cells and muscle. It constitutes about 90 per cent of the solids of red blood cells. It is a compound proteid and exists only in combination with lechithin. Hemoglobin splits up readily into RETROGRESSIVE TISSUE CHANGES. 245 globin and lieniochromogen, the latter combines with oxygen lO form hematin. iIemogIol)in is liberated from the red blood cells and in all con- ditions in which there is rapid destruction of these cells, as in tick fever, anthrax, hemorrhagic septicemia, toxic doses of chlorate of potassium, lead i)oisoning, and other hemolytic agents, excessive quantities of hemoglobin is set free. A portion of the liberated pig- ment is eliminated by tlie liver and kidneys, thus excessive quan- tities (if bile and bloody urine (l.emaglubinuria) are a feature of tick fe\er, lead poisoning, etc. The- liberated hemoglobin n((t eliminated from the body is deposited, especially in the vessel walls, but ultimately diffuses into the lymph and infiltrates prac- tically all tissues. Post-mortem staining is the result of hemo- globin deposition into the dependent tissues. Hemoglobin is also liberated from muscle tissue in azoturia and other diseased •'/.•t/A-.v '"rir; -V --..;■•■..- .'*^*» ««^ i-s^.- f ■>- ^ ;.'©' tf>. ^'\'.:- *l••^ '...'.^V-. .\ <*3 ■••":*v • « % Jp ffi c& «s» .^ /i^'^l'/-"*^'" ,ri:'/^i i& Flff. 115. — HemoHidrrin IMjcinentation. a, Tiihulos ((int.aiiiinK rtoposlts of liemosiili riri in the lells. b. Xormal kidney tubules. 246 VETERINARY PATHOLOGY. conditions of muscle. The hemoglobin liberated from muscular tissue is disposed of in the same way as that derived from red blood cells. Hemoglobin pigmentation, the results of bruising, is common in the superficial tissues of animals bruised in transporta- tion and slaughtered immediately after shipping. Hcuiosidcrin is a derivative of hemoglobin. It is yellowish brown in color, is insoluble in water, alcohol, ether, chloroform. dilute acids and alkalies. It contains iron and gives the typical iron reaction with potassium ferrocyanid. Hemosiderin is the common pigment observed in tissues that have been previously stained with hemoglobin. Extravasated blood observed in pete- chiae and hematomata appear as typical hemoglobin pigmenta- tion for a few days, after which the hemoglobin is converted into hemosiderin and the affected parts become a yellowish brown. Hemosiderin pigmentation is observed in tissues of animals vhat have been bruised three or four days prior to slaughter. It is also observed in post-mortem examinations of animals that have been afifected with diseases accompanied by hemorrhages for a period of three to five days, as purpura hemorrhagica, acute tick fever, anthrax, etc. Hemosiderin pigmentation is of common occurrence in tumors. Hcjiiatoidin is an iron free pigment, probably derived from hemosiderin. It is soluble in chloroform, but is insoluble in water, alcohol and ether. It occurs in rhombic crystals and is occasionally observed in old hemorrhagic foci. Blood pigments, hemoglobin, hemosiderin, and hematoidin are deposited in the cells and intercellular substances. The pig- ments are removed by solution and resorption of the dissolved pigment or bv leucocytes which incorporate the insoluble pig- ment granules and carry them out. Blood pigmentation has little efifect upon the tissue in which deposition occurs, but the flesh of food producing animals is usually condemned when pigmented because of its unsightly appearance. The deposition of a brownish or blackish pigment in tendons, ligaments, cartilage and bones (ochronosis) is occasionally observed in the carcasses of cattle which were apparently in good health. The cause of this pigmentation is unknown. It probably does not injure the tissues or the meat for food, but such meats are usually condemned because of their unsightly appearance. Another brown- ish pigmentation of muscular tissue (xanthosis) is associated with muscular atrophy or disease of the suprarenal bodies. This con- kETROGRESSIVE TISSUE CIIAXGES. 247* dition is of no consequence except public sentiment prevents the -ale of such meat. Bile pigmentation results from the resorption of bile and its depositie)n in the tissue. Bile pigmentation is designated hepa- togenous pigmentation and the condition produced is commonly known as icterus or jaundice. Obstruction of the bile duct or any of its ratlicks 1)\- pressure, duodenitis, calculi, etc., will result in retention of the generated bile which is later resorbed into the blood. In some instances it is possible that extensive destruc- tion of red blood cells and the chemic change of the hemoglobin into bilirubin or biliveriden may produce bile in the blood vessel and thus cause the so-called hematogenous icterus, again destruction of considerable numbers of liver cells or diminution of their func- tion may possibly result in the retention in the blood of those products that are normally converted into bile, and thus produce a hematogenous icterus. Excessive production of bile, as in acute tick fever, is frequently accompanied by resorption of some of the bile and its deposition throughout the body, thus producing a generalized icterus. Bile staining is most e\idcnt in the conjunctiva and ocular sclera of the living animal where it produces a lemon or greenish yellow discolorization. If resorption of bile is very extensive simcmm^^' Fig. 116.— Icterus affecting lymphatic tissuf. Normal tissue.- b. Deposit of bll«' pigment. 248 VETERINARY PATHOLOGY. it may appear in the urine. In carcasses, biliary pigmentation is most evident in the adipose tissue, especially the subcutaneous fat, although it is usualU^ well marked in the subserous fat and may be detected in the lymph nodes, spleen, kidney and muscu- lar structures. The bile may be deposited in the cells or between the cells as greenish-yellow amorphous granules. The granules are read- ily soluble in alcohol, hence they are best detected in frozen sec- tions. The effects of resorption of bile are variable. The tissues are discolored ; there may be pruritus, as the bile appears to act as an irritant on nerve endings; putrefactive changes may occur in the intestine, and the heart may be depressed. Other inconstant symptoms may appear, especially if the quantity of resorbed bile is large. Cells. — Aside from hematogenous and hepatogenous pigmenta- tion the products of certain body cells become a factor in hyper- chromatosis. The principal pigment produced by cellular activity is mel- anin. Melanosis maculosa is a congenital, cutaneous, pathologic pigmentation of calves resulting from the excessive production of melanin bv cutaneous cells in certain areas. Melanotic deposits are of common occurrence in the various glandular tissues, especially the liver, kidney, and suprarenal glands. The deposits in the glandular tissue may occur in the cells or intercellular spaces, and may appear as irregular yellow- ish-brown or black masses. Melanin may occur in the form of fine granules or be flocculent. Black kidneys are occasionally observed, in abattoirs, especially in hogs. These usually result from deposition of delicate, flocculent masses of melanin in the kidney cells. Melanosis is of most frequent occurrence in white animals, although it has been observed in Aberdeen angus cattle, red short horns, black and bay horses, and black and red hogs. Melanotic tumors are pigmented with melanin. The melanin may be a product of the tumor cells or of the adjacent tissue cells. The principal melanotic tumors are the melano-sarcomata, although there may be a benign melanotic tumor called a mel- anoma. Melanotic deposits occur in practically all tissues. The author observed the heart muscle of an ox, that was slaughtered in an abattoir, in which there was extensive melanotic deposits. F. G. RETROGRESSIVE TISSUE CHAXGES. 249 Edwards reported an interesting case of melanotic pigmentation in the cerebellar meninges and lymph nodes in a horse. In a disease of the snprarenal capsule in the human (Addi- son's disease) there is a peculiar bronzing of the skin. This con- dition has not been noted in the domestic animal, probably be- cause of the dense pigmentation of the skin. It is thought to be a form of melanosis. A pigmentation has been noted in atrophic tissues, especially atrophied muscles. The pigment of atrophic muscles may be the result of disturbed cell metabolism or it may result from con- centration of the pigment, because of the diminution in the size of the cells. Rrown atr(i])hv of the licart is a condition in which pigmentation is prominent. Freckles are pigmented areas of the skin in the human, the result of cutaneous cellular action. Because of the intense pig- mentation of the skin in domestic animals, freckles are not easily observed, except in white animals. Pregnancy in the human is frc(|ucntly accom])anic(l by local- ized pigmented cutaneous areas. Such areas have not been re- corded in domestic animals. Aside from tlie blood, bile and cellular activities, pigments may be introduced into the body from without. The most common external substance that produces pigmen- tation is carbon. The most extensive pigmentation by carbon is in the lung, producing the condition known as anthracosis. Anthracosis is a common condition in the lungs of animals used in and around coal mines, in cities in which there is large cpuin- tities of coal smoke, in cats and other pet animals confined in coal bins, engine houses, etc. The inhaled carbon is largely ex- creted in the mucus discharged from the respiratory tract, al- tliough some of it is deposited in the epithelium of the air cells, and ultimately may be found in the interstitial tissue of the lung. Anthracosis apparently produces little harm unless it is exces- sive, when it predisposes to inflammatory (listurl)ances. When examined in gross the lungs varv in color frt^m a gray to a deep black. Microscopically small particles of carbon may be observed in the cells and intercellular substances of the lung tissue. .Iryyriasis is a condition in which silver is deposited in a tissue. After the silver is deposited it is combined with sulphur, thus forming silver sulphid, which is brownish black and imparts a similar color to the tissue. Argyriasis is not common in animals except those used in andan und silver smelters or as a result of the application of some silver preparation to the tissues. 250 VETERINARY r.\TIIOI,OGV. Sidcrosis is a condition in wliich iron is deposited in a tissue. Iron, like silver, usually combines with sulphur, forming the sulphid, which is brown or black in color. Siderosis is not common in domestic animals, except in the intestinal epithelium of animals that have been medicated with iron preparations. Hydrargirosis is a condition resulting from the deposition of mercury in a tissue. This condition is present in the intestinal mucosa after medication with calomel or other mercury prepara- tions. The mercurv sulphid, which is brown or black in color, is the usual pigment in hydrargirosis. Phiv.ibosis is a term applied to pigmentation with lead. This form of pigmentation mav be evident in the intestine in chronic lead poisoning. It appears as a bluish black pigment. Tattooing is the introduction of insoluble pigments into tissues. In tattooing, the tissues are first punctured or injured, after which some insoluble pigment is introduced into the wounds. Some of the pigment is carried out by leucocytes and some of it is entangled in the cicatrix of the healing wound, wdiere it re- mains permanently. Tattooing is a very valuable means of marking stock, as it gives a positive means of identification. Registered cattle, horses, sheep, hogs, dogs, etc., are tattooed in the ear, and fowls on the legs. The wound is made with an instru- ment similar to a hog ringer, in which slugs containing needle points arranged in the form of figures or letters are used. This instrument is used to punch holes into the inner surface of the external ear, immediately after which carbon is rubbed into the wound. When the wounds are healed, the tattoo may be easily observed. Effects. — Excessive pigmentation of a tissue or tissues is of little pathologic significance. Pigmented tissues are probably not hindered in their physiologic activities, excepting in so far as the cause of the pigmentation is an etiologic factor in the dis- turbance of the functioning of a part. Icteric pigmentation may be of consequence because of the action of the bile upon nerve cells. Pigmentation, especially when excessive, is a basis for the condemnation of meat and meat products because of public sen- timent. ABSENCE OF, OR DIMINISHED PIGMENTATION. (Hypochromatosis.) Visible pigmentation may be less than normal, and in some instances there is a complete absence of pigfment. Areas con- RF.TROCRFS^TVF. TTSSrK CHAXCFS. 251 taining less pig^inent tlian iKirnial and depigmented areas are permanently white in color, as they are not afifccted with sun- liq;ht or any other conditions that tend to produce pif^mcntation. This condition may be of antenatal or jiostnatal orifjin. Etiology. — Antenatal al^sence of, or diminished pii^mentation may be inherited or it may l)e caused by disturbances of the embryonic cells that produce normal pi.nnientation. Postnatal absence of, or diminished pi,q:mentation is usually the result of disease in which areas of tissue have been destroyed and later substituted by cicatricial tissue. The total absence of pigment (achromatosis) is not of com- mon occurrence, being- most frequent in rabbits, birds and rats (albinos). An albino is an animal devoid of cutaneous and chor- oid pigment, the condition being inherited or congenital. The animals thus have white skin and usually white hair and their eyes are pink or red because of the absence of choroid pigment, the blood being- observed through the transparent ocular struc- ture. 'J'hc so-called "Wall-eyed"' horses ha\e little if any \ng- ment in the choroid tunic, and frequently they have depigmented localized cutaneous areas. Depigmentation is probal^ly never generalized. Permanent localized depigmentation, leucoderma or vitiligo, is a character- istic symptom afifecting the external genitals of horses afflicted with dourine. It is also observed in cicatrices resulting from burns or extensive operative procedure. Surgeons usually make incisions in an obliciue direction in order that th.e hair in the ad- jacent skin may cover the scar. Scars are usually devoid of hair, and when hair is present it may lack pigment. The application of some medicaments on the skin of some animals causes the hair to lose its pigment. Temjwrary depigmentation is evident after an attack of coi- tal exanthema, vaginitis accompanied by an ichorous discharge. and by many otlier conditions characterized bv erosion or necro- sis of cutaneous tissue. Effects. — The absence of i)igment is of no serious conse- (|uence except in some animals. Hogs that are white skinned cannot be raised in some localities because of the effects of tht: sunlight. Depigmentation of the choroid is also of some conse- quence. l,>ecause the eye is exposed to the effects of excessive light. CHAPTER IX. NECROSIS AND DEATH. NECROSIS. DEFINITION. ETIOLOGY. Suspended nutrition. Thermic. Burning. Freezing. C hemic. VARIETIES. According to cause. Inanition. Thermic. C hemic. According to character of necrotic tissue. Coagulation. Colliquation. Caseation. Gangrene. Mummification. Miscellaneous. Senile. Fatty. Focal. Jack-sores. TISSUES AFFECTED. DISPOSITION OF NECROTIC TISSUE. Absorption. Exfoliation. Encapsulation. Sequestration. EFFECTS. Necrosis is local death. It is death of a part of a living body. The term necrosis is applicable to the death of any kind of tissue, glandular, muscular, osseous, etc. Necrosis is usually a rapid process, that is, it is sudden death of a part. Death of a cell or a group of cells that have been previously afTected with degen- eration, i. e., a slow or lingering death, is termed necrobiosis. Caries is a term used to designate necrosis of dentinal or osseus tissue. Cells are constantly worn out and destroyed in physiologic active tissues. The physiologic destruction of cells is not usu- ally thought of as necrosis although the cause and manner of death may be similar, and there may be no difference in the ap- pearance of cells destroyed by physiologic and pathologic pro- cesses. kECROSlS ANb DEATH. 253' The term necrosis is applicable to the pathologic death of a single cell, althougli such a limited necrosis is rarely recognized. Clinically necrosis is usually not noted except when the area is sufficiently large to observe with the unaided eye. All tissues of aH animals are subject to necrosis, and it may occur upon a su'-^ace or in subsurface structures. Bursattae is a disease characterized by necrosis of the skin. Necrotic stoma- titis, a disease in puppies, calves and pigs, is accompanied by necrosis of the buccal mucous membrane. Tuberculosis, glan- ders, actinomycosis, and caseous-lymph-adenitis are diseases in which there is surface or subsurface tissue necrosis. Etiology. — Necrosis may be primary but it is more fre- quently secondary. Secondary necrosis is a sequel or result of some other pathologic process, as hemorrhage, oedema, throm- bosis, anemia, hyperemia, inflammation, degeneration, infiltra- tion and infection. Primary necrosis is the result of; (1) obstructed nutrition; (2) chemic substances; (o) temperature variations. Obstructed nutrition. — A tissue or part, from which nutri- tion is entirely obstructed, will die after all the available nutri- ents have been consumed. Nutrition mav be obstructed from a part by some mechanical means. An occasional result of mechanically obstructed nutri- tion is observed in dogs in which a rubber band has been placed upon a leg, an ear, the tongue, or the tail, the circulation being thus obstructed the part distal to the rubber band soon becomes necrotic. The improper adjustment of bandages, especially when used to support fractures, is frequently a cause of necrosis. Tumors, cysts, abscesses and other pathologic enlargements may exert sufficient pressure to obstruct circulation and produce necrosis. Fractures and herniae mav mechanically occlude blood vessels and result in necrosis. The seriousness of omental hernia or, in fact, any hernia, is due to the fact that the vessels supplying the hernied structures are occluded, resulting in ne- crosis and the absorption of the products of the necrotic tissue. The plugging of a terminal vessel by a thrombus or an em- bolus (infarction) produces necrosis if collateral circulation is not established. Thrombo-embolic colic is a condition usually caused primarily by the larvae of the Strongylus armatus enter- ing and producing a parietal thrombus in the anterior mesen- teric artery, fragments of the thrombus become detached, pass down to and occlude the terminal mesenteric arteries, resulting in ischemia of the walls of the intestine, and if the circulation is not soon established the ischemic area becomes necrotic. 254 VETERINARY PATHOLOGY. A part or organ separated from the remainder of the body undergoes necrosis sooner or later, the time depending upon the condition of the tissue and the temperature in which the sep- arated portion is kept. Maceration and bruising produces ne- crosis to a varying degree, depending upon the extent of the in- jury. Big. 117. — Photograph showing Necrosis above the foot of a horse. Clicmic substances.— Certain chemic substances as phenol, arsenic, mercury bichloride, strong solutions of the caustic alka- lies and mineral acids, as well as the products of a large number of bacteria, are tissue destroyers. Phenol abstracts water from all cells to a sufficient extent to destroy their vitality, and it pro- duces a rapid disintegration of red blood cells. Arsenious tri- oxide is frequently applied on tumors because of its erosive action. Bichloride of mercury combines with the cell albumins, forming albuminate of mercury, thus inhibiting the cell action, and when all of the cell albumin is combined the cell is de- stroyed. The caustic alkalies and mineral acids coagulate the cell albumin or abstract the cell water, thus destroying them, The Bacillus necrophorous produces chemic substances that cause coagulation of the cell protoplasm (coagulation necrosis). NKCROSIS AND DKATII. -:r."' Dc Sclnvcinilz lias described a cheniic substance produced by the Tubercle bacillus, as necrotic acid, which is thought to pro- duce necrosis in tubercular lesions. The toxin of the diphtheria bacillus produces focal necrosis in practically all tissue in an individual aftlicted with diphtheria. The products of pyogenic bacteria produce marked tissue destruction. Cheniic substances produce necrosis by coagulation of the Fig. 118. — IlacilliLs Nej-ropluiriis— PU omoiiihic form. albumin by dehydration or bv the formation of new cell com- pounds, thus inducing metabolic disturbance and cell death. Temperature lariaiions. — All active cells have a maximum and a minimum temperature. Thermic variations beyond these means are injurious and destructive if the variation is extensive. The high temperature causes coagulation of the cell protoplasm (cloudy swelling), which, if extensive, destroys the cells. Necrosis resulting from burning is of common occurrence. Low temperature is not as rapicllv destructixe as liigh temperature. I-'reezing pniduces necrcjsis of the tissues of warm blooded ani- mals, probablv because of cell disintegration induced by the for mation of ice in the cells. Types or Varieties of Necrosis. — Se\eral factors may be used as the basis for the classification of necrosis. pj'whniy. — According to the cause, necrosis may be: a. In- anition necrosis, b. Thermic necrosis, c. Chemic necrosis. !S6 VCTHRINARV PATHOLOGY. Inanition necrosis is that type resulting from obstructed nutrition. As an example of this type may be mentioned the necrosis of the scrotum and its contents in rams induced by placing- a rubber band moderately taut around its upper portion. i:/ Fig. 119. — Photograph oC the Erarnt of R.ve. This is a m.ethod frequently resorted to in the castration of old rams. Bed sores observed in tlie superficial structures in ani- mals afflicted with diseases that cause them to constantly assume the decubital position, are the result of obstructed nutrition in- duced by pressure upon the nutrient vessels or thrombic forma- tion secondary to bruising. Thermic necrosis results from exposure to extreme tempera- tures. Thus necrosis of cutaneous tissues is of common occur- rence in animals as a result of conflagrations or undue exposure NliCROSIS AND DKATII. ^?/ to the solar heat rays or thcniKj-caiiU'ry. Xccrosis induced by freezing is very coninu)n in calves, pigs, and chickens, in tlie temperate and frigid zones. Cheniic necrosis is represented by the extensive destruction of the buccal, oesophageal, gastric, and intestinal tissues induced by the ingestion of lye. Corrosive sublimate and arsenious tri- oxide destroy the mucous menil)rane and frequently the deeper tissues of the alimentary tract in animals poisoned with tliese agents. Location. — Xccrosis ma\- be surface or subsurface. Surface Fig-. 120. — Erg«it roisunini; in Cattle. Photograph by Dr. W. T. Spencer. 1. Sloughing abovu the feet. 2. Sloughing of the ends of the tails. necrosis may be of the skin, mucous or serous membranes. Sub- surface necrosis may be of any tissue, muscle, bone, glandular, etc. Xaturc or condition of the necrotic tissue. 1. Coagulation necrosis. — This type of necrosis is character- ized by the coagulation of the necrotic tissue. It is the result of the presence of some enzxm that produces the formation of fibrin or some allied substance. Coagulation necrosis is evident in tlie coagulation of bloofl and intlammatorv exudates. The exudate in fibrinous inflammation (croupous and dijihtheritic) usually becomes firmly coagulated. r)n the r)ther hand, coagulation is rarely observed in collections of lymph, as in ascites, etc. The necrotic tissue in anemic infarcts, especially in the kidney, is sometimes coagulated. 2. Colliquation necrosis. — The conditi'jn resulting from solu- 258 VETERINARY PATHOLOGY. tion of a substance or surface area of necrotic tissue is colliqua- tion. Solution of the necrotic tissue is the result of enzyms that dissolve or digest the dead tissue. Suppurative processes (as abscess formation, etc.), are examples of this type of necro- sis. Liquefication of anemic infarcts, inflammatory exudates and thrombi, with or without the formation of cysts, is colliqua- tion necrosis. In the brain of horses that have died of the so- called blind staggers areas are found containing liquefied nerve tissue. 3. Caseation necrosis. — When the fluid is absorbed from li- quefied necrotic tissue, the remaining solids may become cheese- like, thus producing the condition known as caseation. Caseation may be primary, but it is more frequently secondary to liquefying necrosis. Caseous material is granular, soft or crumbly in con- sistency. Caseation is characteristic of the typical lesion of cas- eous-lymph-adenitis in sheep and goats. Liquefaction precedes caseation in this disease. Tubercular lesions, especially in the bovine, is characterized by caseation, although they later become calcified. Necrotic centers of a caseous nature are observed in the lesions of bursattae. 4. Mummifying necrosis (mummification, dry gangrene). — Necrotic tissues superficially located may become dessicated, thus producing the condition known as mummifying necrosis. This type of necrosis occurs upon a surface that is freely exposed to air and of tissues in which there is little moisture. The ear, tail and hoof lesions, characteristic of ergotism, are the most typical examples of mummifying necrosis. In ergotism, the lesions are produced by constriction of the arterioles. This in turn in- creases blood pressure, and, consequently, the work of the heart. This ultimately results in the diminution or complete absence of blood from the extremities, and the latter sooner or later become necrotic. The necrotic tissue, as ears, tails, etc., in animals aft'ected with ergotism become mummified because blood is prac- tically shut off from the affected parts and the contained moist- ure soon evaporates, for they are freely exposed to the air on two or more surfaces. Frozen tissues may become mummified. The umbilical cord in new born animals undergoes mummifica- tion. 5. Gangrene. — Bv the laity, the term "gangrene" is used to designate any type of necrosis, and by some medical men it is used to signify death of soft tissue en masse. Gangrene is that type of necrosis characterized by putrefaction of the necrotic tis- sue. Gangrene invariably occurs in tissues in which there is a good supply of moisture, as in a tissue affected w'ith venous con- Nl-A KOSIS AM) DIATII. 250 gestion, and usually occurs upon a surface because infection is more likely to occur there. Parenchymatous mammitis of the bovine is frequently succeeded by necrosis and putrefaction of the necrotic tissue (gangrene). Gangrenous pneumonia is not uncommon and may be the result of embolic metastasis of organ- isms from sc])tic metritis, etc.. or it may be induced by medica- ments introduced into the king. Miscellaneous. 1. Senile X'ecrosis. — 'i'his is a type of necrosis occurring in old age. It is not uncommon in old dogs and aged horses, and is usually the result of inelasticity of the arteries and an insufifi- cient sui)plv of nutrition. 2. Fatty Necrosis. — This is a condition characterized by the Fig. 121. — >Iultii)le I-atty Neorcisis. Fat cills undiTt'oiiiB disiiUcgraliou, bi;caus.- of Saponiluatioii. conversion of fat into fatty acid and glycerine, that is, saponifica- tion of fat. The name fatty necrosis is a misnomer, as the condi- tion is not necrosis. It should he called saponification of fat. In fact, a fullv developed fat cell represents that amount of stored, available food, and there is in reality no vitality in the cell, and necrosis in dead tissue is not conceivable. Again, the real exist- ing condition is sajionification of the fat. not necrosis. The prol)- able cause of fatty necrosis is resorption of steapsin induced by pancreatic disturbances, although steapsin may be absorbed from the intestine. Some ftmr or five cases have been observed in the dog. several cases in the slice]), and one horse was examined that was afifected with fatty necrosis. In each of the a1)ove cases 260 VETERINARY PATHOLOGY. there was evidence of pancreatic lesions, as inflammation, hem- orrhage and atrophy was noted in one case. Recently it has been suggested that this condition is caused by disturbances of the islands of Langerhan. The areas affected are at first soft and spongy, but later be- come more or less calcareous as a result of combination of lime salts with the free fatty acid. Fatty necrosis usually involves the omental fat, and espe- cially that in close proximity to the pancreas, though all fatty tissue is subject to this condition. In gross appearance the involved portions are dull, lusterless, opaque, slightly raised, usually circumscribed areas, of a yellow- ish white color. If the lesions are advanced, calcareous granules may be observed by palpation. In microscopic section the cells of the affected areas may contain needle-like crystals, or the cell substance may appear as a granular mass. 3. Focal necrosis. — In certain infective diseases it has been noted that small foci of the various parenchymatous tissues un- Tis,. 122. — A necrotic tubercle: lung. x250. Showing- necrotic center surroundta by small round cells, cpitheloid cells, and leucocytes, NECROSIS AND DEATH. 261 dergo necrosis. In many instances, this occurs in the absence of any circulatory disturbance, indicating that the exciting cause, chemic substance, is carried by the blood and appears to have a selective action for certain tissue. This type of necrosis is com- mon in diphtheria and typhoid fever in the human and in hog cholera, glanders, generalized tuberculosis and probably some other infective and chemically induced diseases of the lower ani- mals. The areas afifected are frequently not sufficiently large to observe with the unaided eye. Microscopic sections show the cells in various stages of necrosis. The nucleus may be appar- ently normal or entirely disintegrated, the cell body may be granular or hyaline, it may be intact or appear fragmented. Leu- cocytic invasion of the necrotic area is of frequent occurrence, and may at first give the impression of an infected focus. Necro- tic tissue in focal necrosis may be absorbed and the destroyed tissue regenerated; it mav become liquefied, thus forming a cyst; it may become infected and be succeeded by abscess formation, or it may be substituted with scar tissue. 4. Jack-Sores. — This is a name applied to a very prevalent condition in I'acks in which there is necrosis of the skin and sub- cutaneous tissue. Perhaps jack-sores should not be classed as a separate or distinct type of necrosis, but it is so common that it merits a special mention. The skin and subcutaneous struc- tures of the legs, venter surface of the abdomen and thorax, and maxillary region are most frequently afifected. The necrotic areas may be very extensive, in some instances involving the entire metatarsal or metacarpal region. The etiology of "Jack-Sores" is not known, but no doubt it is the result of malnutrition and probably an irregular, indefinite lymphatic circulation is the primary cause. Tissue Affected. — No tissue is exempt from necrosis. The tissue afi'ected depends upon the cause, the animal and geog- raphical location. Disposition of Necrotic Tissue. — Necrotic tissue or products derived from it are more or less irritating and may produce an inflammation in the living tissue around the necrotic mass. The perinecrotic inflammation insures an increased number of leucocytes around and in the necrotic area. The necrotic tissue, leucocytes and other living cells may produce enzyms that will ultimatelv dissolve' the necrotic tissue. There may be a contraction of the necrotic tissue and later it may separate from the surrounding normal tissue. The reaction of the adja- cent living tissue may be limited and cause the production 262 VETERINARY PATHOLOGY. around the necrotic area of a fibrous or osseous capsule, cr ever. cause a fibrous formation throughout the entire necrotic mass. From the foregoing it is apparent that necrotic tissue may be disposed of as follows: 1. Absorption. 2. Exfoliation. 3. En- capsulation. 4. Sequestration. Absorption. — The necrotic mass is more readily absorbed when it is in a liquid state (colliquation), although leucocytes, and various other cells may produce enzyms that are capable of dissolving coagulated necrotic tissue. Absorption of fluid ne- crotic tissue is in part accomplished by means of the lymphatic tissues, and in part by means of leucocytes that incorporate and convey fragments of necrotic cells to the various organs that dispose of waste materials. Necrotic infarcts are occasionally entirely absorbed. Exfoliation. — Necrotic surface tissue is frequently disposed of by separation of the dead from the living tissue as a result oi inflammation or contraction of the necrotic mass. The separated necrotic mass is the sphacelus. The process of separation and sloughing is exfoliation. Exfoliation is the usual disposition of necrotic extremities induced bv freezing and by ergot poisoning. Encapsulation. — The irritation produced by subsurface ne- crotic tissue may be insufficient to cause an acute inflammation, but it may stimulate fibrous hyperplasia. Thus a fil^rous capsule or wall is built around the necrotic mass, i. e., it becomes encap- sulated. In some instances the encapsulated necrotic tissue later becomes calcified, or it may become liquefied, the capsule retain- ing the liquid, thus a cyst is formed. Fibroblasts may extend into the necrotic area and form fibrous tissue throughout the entire mass, thus there would be a mass of cicatrizing fibrous tissue permeating the necrotic mass. Sequestration. — This is a term applied to the separation of subsurface necrotic tissue, more especially necrotic bone, from the surrounding healthy tissue. The separate necrotic portion is termed the sequestrum, and the process of its separation sequestration. An osseous sequestrum may be encapsulated, the capsule later becoming osseous, thus forming an involucre. Effects. — Necrosis is the condition resulting from tissue des- truction. The efifects of tissue destruction depend upon the variety of tiss'.ie, t'le extent and location of the condition, and the age and condition of the animal in which it occurs. If the tissue destroyed is capable of regeneration, or if it is limited in extent, and the animal is otherwise in good 'condition, the efifects will be insignificant. If the tissue destroyed cannot be regener- NFXROSIS AND DEATIt. 263 atea and is extensive, the animal will ])e deprived of that quan- tity of tissue and if the function of the destroyed tissue is of prime importance, the animal will die. Necrosis is invariahlv associated with inflammation, which is especially active around the necrotic area, and the results of this inflammatory reaction must also be considered in estimat- insj the sum total of the effects of necrosis. DEATH. DEFINITION. ETIOLOGY. Suspended heart action. Respiratory arrest. Stispciided hraiii action. SIGNS. Post Mortem Staining. Temperature cinnige. Muscular rigidity. Decomposition. TESTS. Mirror. Blister. Incision. Relaxation of sphincter muscles. Death is the condition resultinj^ from the permanent arrest of all functions. Death should not be confused with necrosis. The former refers to somatic death and the latter to the death of a part. It is difficult and in fact impossible to determine the exact time when life ceases in a body. The various body tis- sues do not all become lifeless when the individual as a whole dies. The length of time that vitality is retained in the tissues of a dead animal depends upon the variety of tissue, the ai^e of the animal and the cause of death. The less highly organized, the tissue, the longer its vitality is retained. The tissue of young animals possess their vitality for a longer time than the same tissues of an aged animal. r>eath results from disturbance of certain vital centers and these tissues, as well as all others speci- ficallv acted upon by the agency that causes death, lose their vitality earlier than tissues not acted upon. Death may be physiologic or pathologic. Physiologic Death. This is that type of death observed in old animals. During em- bryonic life the principal function of all tissue cells is reproduc- tion. As the tissue becomes more matured, the reproductive prop- ertv of its cells graduallv diminishes and has practically disap- 264 VETERINARY PATHOLOGY. peared in old age. Cell repair is complete in early life, but gradu- ally diminishes as the animal becomes aged. The activity of cells and their life cycle is limited as is that of all active structures either animate or inanimate. Therefore, if new cells are not pro- duced and the old cells are not repaired their energy or vital forces are finally exhausted and they degenerate and die. If large numbers of cells of all tissues die the animal involved is incapaci- tated and ultimately sufficient cells die to diminish the function of the vital organs to such an extent that there is collapse and som- atic death. Physiologic death is initiated by a gradual decline which may continue until the individual dies. Or after a long per- iod of slow decline, death may be sudden as a result of a sudden- ly diminished function of a vital organ. Physiologic death is sim- ilar in a way to the collapse of the one horse chaise which, as the story runs, was used until it literally fell to pieces. Very few domestic animals die a physiologic death. Those animals whose flesh is used for food are butchered long before physiologic death would intervene, and those animals used as beasts of burden are usually destroyed when their earning capacity is monetarily less than the food they consume. Pathologic Death. Pathologic death signifies the ending of life prior to the time that the vital forces have been exhausted. Etiology. — Pathologic death is that type caused by accident or disease process. Death is primarily the result of permanent suspension of heart action, respiration or brain functioning. Snspoidcd heart action may be caused by influences acting upon the cardiac nerve centers in the medulla or upon the heart mus- culature direct. The significance of suspended heart action is self evident. There being no blood circulating the tissue would soon consume all available nutriment and then succumb. Tem- porary arrest of heart action is called syncope. Respiratory arrest is usually the result of nervous influences though clonic spams of the respiratory muscles would produce a similar efifect. The absence of respiration implies the absence of oxygen to oxidize the blood and the tissues and the absence of oxygen for a considerable length of time results in carbon- dioxide poisoning and death. Apnoea is a condition in which respiration is arrested. Permanent arrest of all brain functioning even for a brief period results in cessation of all the principal functions and death. NECkOSIS AND DEATH. 2^5 Thus, suspended brain function results in arrest of heart action and respiration either of which results in somatic death. Coma is a term used to designate a condition in which all conscious- ness or recognition of environments is suspended but the con- trol of \ilal functions is still maintained. Signs of death. — The changes that occur in dead tisstie are of considerable importance especially to inspectors of carcasses of ani- mals, the Hesh of which is intended for human consumption. The most important post mortem changes in tissues are as follows ; post mor- tem staining (livores mortis) ; temperature change (algor mortis) ; death stiffening (rigor mortis) ; and decomposition or putrefaction. Post Mortem Staining. — The blood usually undergoes changes immediately after death. The disintegration of red blood cells allows of the liberation of hemoglobin which is deposited more or less extensively upon the inner lining of the blood vessels and heart and also filters through the vessels and stains the peri- vascular tissues. The length of time after death that post mor- tem staining becomes evident depends upon the cause of death. In fact the purplish staining along the cutaneous vessels evident in dead bodies may be evident in the living body of animals. Thus liberation of hemoglobin takes place during life in the blood of animals affected with septicemic diseases. Temperature changes. — The carcasses of all dead animals assume the temperature of the environment sooner or later. The length of time necessary for the body heat to pass out of a dead body depends largely upon the cause of death. In some diseases, those in which tissue change is limited, the temjierature is sub- normal at the time of death and rapidly assumes the environmen- tal temperature after death. In other diseases, those in which tissue changes are extensive, the temperature may vary from normal to considerably above normal at the time of death and may increase for several hours after death. Temperature changes may be extremely variable in a carcass. Also a remarkably low subnormal tem])erature has been observed in many living ani- mals, especially those in a comatose state and vet the animals recover. The thermic variations should never be relied upon in determining whether or not life is extinct, at least not within 48 hours after the animal is supposed to be dead. Rigor Mortis. — That the body of an animal becomes rigid after death is common knowledge to all observers. Rigor mortis re- presents a condition of tlie muscle fibre in which it becomes rigid as if in a tonic contraction. The length of time after death that rigor mortis appears and the length of time that it persists de- pends upon the condition of the animal at the time of death. 266 VETRRINARY PATHOLOGY. Thus muscular rigor appears usually in a few minutes after death and is of brief duration in animals, that have died as a result of a long continued exhaustive disease, as chronic tuber- culosis. On the other hand rigor mortis may not become evi- dent until 24 hours after death in animals that have been killed while in a perfect state of health and it may continue for from two to four days. In catalepsy, muscular rigidity is a charac- teristic symptom. Other conditions, however are sufficient to dififerentiate this from rigor mortis. Decomposition or putrefaction is caused by the action of putre- fying bacteria. The decomposition of a tissue is sufficient evidence of the fact that it is lifeless. Decomposition or putrefaction is not easily detected in the early stages. The evolved odor is usually the accepted sign of decomposition and during some seasons of the year, decomposition may not become evident for several days after death. The carcasses of animals dead of septic infections usually decompose immediately after death, e. g. carcasses dead of anthrax, hog cholera, etc. Tests. — Because of the uncertainty of the above signs espe- cially, during the first 2i or 48 hours after death, certain tests are recommended to determine the presence or absence of life in a certain body. They, like the above signs, are not absolute. TJie mirror test. — .Respired air contains more or less water vapor. Respiration is not always perceptible. Water vapor is condensed upon a cold surface. The procedure of this test con- sists in holding a mirror over the nostril and if any air is ex- pired the watery vapor from the expired air will be condensed and rendered visible upon the surface of a mirror. This test is not infallible for the respiratory functions may be so diminished that the moisture (watery vapor) of the expired air is insufficient for condensation upon the mirror. Blister Test. — Blisters or vesicles can usually be produced by heat or chemic vesicants applied to the skin of a body in which life still exists. The formation of vesicles is not possible in dead tissue because the production of a blister represents the response of a living tissue to an irritant and only living tissues are cap- able of reacting. Vesicle productions varies in living animals and in some cases they are not produced. Incision. — Because of the elasticity of living tissues, all incised wounds gap in the living body. Tissue elasticity disappears when the tissue dies, consequently incised wounds in dead tis- sues do not gap. XFXROSIS AXD OKATII. 2^)7 Certain pi^st morlcni clian^cs arc rather constant in the eye. These changes consist of a cUnuHness of tlie lens and the acjue- ous humor, the condition gradually becoming more intense. The surface of the eye, i. c., the conjunctiva, becomes dry and scaly in appearance. All sphincter muscles arc usually relaxed at the time of death and remain so permanently. Still Birth. — The expulsion of a dead matured foetu?; from the uterus is denominated a still birth. A variety of conditions may cause the death of a foetus, as: ruptured umbilical vessels, stran- gulation of the umbilicus and various diseases of the foetus. \'eter- inarians arc frequently asked to determine whether a foetus has been dead or alive at the time of its expulsion from the uterus. The principal evidence is found in the lung, which in the case of a still birth is solid as it has never been inflated. Chapter x. TUMORS. (Neoplasms "{ DEFINITION. FREQUENCY. STRUCTURE. Cells. Intercellular. J'essels. Nerve tissue. SIZE. SHAPE. COLOR. CONSISTENCY. NUMBER. GROWTH. EXTENSION. NATURAL RESISTANCE. RETROGRESSIVE CHANGES. CLINICAL CONSIDERATION. ETILOLOGY. VARIETIES. Occurrence. Primary. Secondary. Recurrent. Structure. Histoid. Organoid. Teratoid. ■ Clinically. Benign. Malign. Tissue. Adult. E/^itlielial and connective — Pat '=''~>^ o c? s "g^ jr <:iS^% ^- gp ^ & % « 1 ^^ c==> V <^ ,=--. f 0> ^ ^i^ ■ C^ ^ h (~~tr^ CSS I. c ''-^334^ ?^//:oo - ^9t/HN^:.i Fig. 128. — Section of Myxoma from the orbital fossa of a horse, showing stellate cells. TUAfORS. 285 Vv'liich tlic cell procej^ses arc apparciuly coiUimMus with the pro- cesses of adjacent cells. Myxoma cells have an cjval nucleus and the spaces between the cells and cell processes are filled with mucus, which appears as a stringy, ijray substances that stains red with eosin. Myxomatous cells produce both kinds of fibres, i. e., glia and collagen fibres. The collagen fibres are more or less separated from each other by a varying quantity of fluid containing" mucin. JMyxomata are prone to degeneration, result- ing in the formatit)n of a cyst, or the fibrous capstile may become eroded, allowing the degenerated contents to escape into the sur- rounding tissue or upon a surface. In the latter case the degen- erated contents is usually absorbed. Cicatricial tissue is usually produced in the cavity or space occupied by the myxoma. Sub- surface, myxomatous, degenerated areas luay bccoiuc infected, resulting in abscess formation. Clinically, myxomata are benign tumors. They grow slowly by interstitial expansion, do not recur when rciuoved, and ex- tend only bv Continuity or contiguity. These tumors are difi:'erentiated from muc(>id degeneration, as the latter contains no stellate cells, and there are usually some of the cells i)resent in mucoid degeneration that are normally present in that area. Clinically, it may at times be difficult to distinguish between mucus retention cysts and myxoma, but by the exploring needle the contents of the cyst may be evacuated and thus the nature of the mass will be determined. CHONDROMA. A chondroma is a cartilaginous tumor. Thev occur in cattle, sheep, dogs, horses and fowls. They are found most frecptently in the location in which cartilage is normally found. The ster- num seems to be a favorite location for their development, prob- ably because of the frequent injuries of the sternal cartilage due to the fracture of ribs and other injuries. Thev not infref|ucntly occur in other bones, possibly developing from islands of cartil- age that have not ossified, or from marrow or periosteum. They also occur in glandular tissue as the thyroid, parotid, ovary and testicle, and a few cases of rhondromata of the lung have been reported. These tumors appear as hard, nodular, well-defined growths, unless they are undergoing degeneration. In this case they may be of the nature of cysts, or if their capsule is ruptured, they may be soft, spong-y, diffuse masses. They are variable in size. A chondroma weighing l"? kilograms (26 1/5 lbs.) was obtained 286 VETERINARY PATHOLOGY. from the sternum of a sheep killed in a Kansas City abattoii. Another about the size of a pigeon's egg and attached to the sternum of a small hen was found by a city meat inspector. Prof, G. H. Wooldridge reported a case in the "Veterinary Jour- nal'' in which there was a chondroma 4 or 5 times as big as a man's fist between the humerus and scapula and chest wall of a cat. Their shape is very irregular, but they are most frequently oval. As a rule they have a regular surface, though they may be lobulated. They are usually separated from the surrounding tissue by a fibrous capsule, but they may be firmly adherent to the adjacent tissue. In cutting, the tumor gives a resistance sim- ilar to cartilage and th.ey may be gritty because of calcification or ossification. The ablated tumor is bluish-white if it is a pure chondroma. Degenerated areas w'ill vary in color according to the kind and degree of the degeneration. Necrotic centres appear dull gray or yellowish-white and white if calcified. If the tumor is mixed the color will vary according to the contaminating tumor tissue. Chondromatous tissue is composed of cartilage cells and an intercellular substance. The cells are irregular in size and shape and the number found in each lacuna is more variable than that in normal cartilage. The size, shape and arrangement of cells in dififerent areas in the same tumor is variable. The cells are fre- quently degenerated, the nucleus fragmented and the cell mem- brane ruptured, allowing the cells to fuse as a homogeneous -^ - cs ^^ - ■ ;« S> - ' (S ffl -> «. " » ® %** Ji f>(^ ^^^^ ^:.]G o ufftV£^-'i. Via. 129.- Sr< tinii ,,t' ('hoiulninia t'lnm st.Liiuin nf a sheep, sliowing lacunar with indosiil caitilagt- ct-lls. TUMORS. 287 mass. The lacunae are not so distinct as those in normal cartil- age, and their capsule may be absent. The intercellular substance is usually homogeneous, as in normal hyaline cartilage, or it may be fibrous, as in normal fibro-cartilage or elastic cartilage. The in- tercellular substance becomes fibrous towards the margin of the growth and finally forms a perichondrium. The cells mav be arranged in rows near the perichondrium, but the}- are more likely to be irregularly distributed. The microscopic appearance of a degenerating, necrotic or mixed chondroma depends upon the kind and extent of the condition existing. Clinically, chondromata are usually benign, but the\- mav be- come malignant because of their extent. Some surgeons have recorded esses of metastatic chondromata. These tumors are frequently lobulated and may be multiple. They have little ten- dency to recur when removed. LIPOMA. Lipomata are tumors composed of adipose tissue with a con- nective tissue framework supporting the vascular supply. They occur quite commonly in the horse, ox, and dog, but none of the domestic animals are exempt. Thev usually develop where adi- pose tissue normally exists, as the subcutaneous tissue, submu- cosa and subserosa. omentum, etc. They may also occur in tissue that contains no fat, as the liver, kidnev and even the brain. They occur most frequentlv in the subcutaneous tissue in the horse; in the intestinal and omental subserosa of the ox and hog; in the subcutum and conjunctival submucosa in tlie dog, and in the uterine submucosa of the sheep and the cow. Lipomata are usually circumscribed, but they may be diffuse. The accompanying cut is from a photograph of a two-year-old colt in which there is shown a clifTuse subcntancons lipoma of the left hind log. These tumors mav ])cconie enormous in size in the horse and ox, some cases having been reported of lipomata as large as a wash-tub and weighing 30 to 70 kilograms (fiO to l')4 lbs.). In consistency, these tumors mav be firm and dense or soft and flabby. The\- arc usuallv surroimded by a fibrous capsule and in section those from the peritoneum and omentum ere vellowish or white in color. Peritoneal, omental, subnnicc^us and subcutaneous lipomata have a smooth surface; intestinal lipomata are usuallv lobulated. Bands of connective tissue may divide the tumors into lobes or lobides or the connective tissue may be diffuse througkotit the entire structure. In cutting a lipoma the resistance varies acccrding to the (|uantity ()f fibrous connective tissue it contains. If osniic acid is applied to the free 288 VETERINARY PATHOLOGY. surface of the gross specimen it stains the adipose areas black but has no efil'ect upon other tissue. Occasionally groups of adi- pose cells become necrotic and calcify, thus forming gritty areas. Complete necrosis with sloughing or calcification is not rare in the larger lipomata. pig. 130. — From photograph taken 6-20-'7 of a colt affected with a Subcutaneous Liltnma. Photograph presented by J. U .AI\ the spinal cord or in the gray matter of the cerebrum. Tliey do not become large and they are usualK- not encapsulated. Tlie\- are composed 1 of cells that are very similar io normal neuroglia cells. The glioma cells mav be slightly larger than neuroglia cells but they have the fibre-like processes characteristic of them. These tumors do not form metastases but are likely to produce a fatal termination by pressure upon nerve centers. ODOXT( ).M.\. Odontomata are tun^ors composed of dental tissue and usu- all\- occur in connection with teeth. j)articularly the superior molars. ()dontomala are of fre(pient occurrence, the majority of dental diseases in two lo five-\ear-old horses beiniiia. The spaces in cavernous hemangioniata are lined by endotbeliuni ibat is supported by a very limited amount of white fibrous connective tissue, yellow elastic tissue being practically absent. Fif,-. 136. —Photograph of spleen of doff affected with an Henianffioma C'arvernosiiin. Ilcmah>gionia hypcrtrophicum is a blood-vessel tumor composed of masses of relatively small vessels, in which the vessel walls are hypertrophied. One of these tumors occurring in the subcu- taneous tissue of the metacarpal region of a horse has been observed. It appeared as a mass beneath the skin and was about the size of a lien's tgg. Pulsations could be observed and by palpation they were quite distinct. The tumor when removed was a tangled mass of blood-vessels with comparatively small openings. Microscopically, the vessel walls were found to be hypertrophied. The vessels were held together by fibrous con- nective tissue. Cirsoid aneurisms are tumors composed of dilated and enlarged 298 VF.TKRIXARV PATHOLOGY, tortuous arteries. This A'ariety of hemangioniata is not common in the domestic animals. Lymphangiomata are tumors composed of newly-formed hm- phatic vessels. These tumors are not common; in fact, onl\- one ^ i^ ^^0 ^3' ■-,,■ 1' 5' . (f 'ii^-^ ^^' ^^ ./' 29o. Fig. 137. — Section of lieniangioiiia H.viiertrophicuni, showing an increase in the number of the vessels and an h.\perlroiJhy of their walls. or two cases have been reported by veterinarians. The tumors may be conveniently divided into capillary and cavernous. Angiomata are usually benign tumors, although by rupture they may produce fatal hemorrhage or lymphorrhage. MYOMA. Myomata are muscle tumors. They are divided into two classes: 1. Leiomyomata or the smooth muscle tumors. 2. Rhabdomyomata or the striated voluntary muscle tumors. My- omata, found occasionally in the human, are rare in the lower animals. TT'>rous. 200 Leiomyomata arc fiuiiul iiiosl ;';-c'(|ik'iii1\ in lhii>e' locations in which involunlary nuisclo tissue normally exists, as the uterus, bladder, intestine, etc. They are nodular or dift'use, dense, pale pink masses appearing; \crv similar to fibromata. ]\licr()sct)pic- ally they are composed of miscellaneously arrani^cd involuntary nuiscle cells. They ditiler from fibromata in that the muscle cells are thicker and usually not as lonij as the fibres of fibromata. Frc(|ucntlv thev are combined with fil)romata forming a leiomyo- fibroma, makini;- the diai^'nosis more difficult. Leiomyoma cells ma\- be very similar to the cells of a spindle-celled sarcoma, but 13S. — J.eioin.'Kiiiia, small inUsUnc, iiiul< the nuclei of the former are loni;- and rod-shaped while those of the latter are o\ al in shape, a ch;iracteristic usually sufficient for diagnosis. The c\to])la^ni of .tlu' leiomyoma cells stains densely witji acid stain-. Rhabdomyomata ha\e been found in the kidney, ovary and testicle. They are ])robabl\- the result of the de\elopmcnt of misplaced embryonic myoblasts. These tumors arc usually pale in color. In microscopic section the cells are irrencularly striated, 300 VETERINARY PATHOLOGY. and are variable in shape and arrangement. These tumors are benign. Fig. 139. — I>ei<)iii,Mniia. Smooth nucleus cell, showing nucleus. SARCOMA. A sarcoma is a tumor composed of embryonic connective tissue cells. Sarcoma occasionally succeed an injury and are .common where globin is prevalent, as in muscle, bone, etc. The cells have no tendency to become mature but constanly appear as undiffer- entiated mesoblastic embryonic cells. Sarcomata are of frequent occurrence in all domestic animals. They have no predilection for tissue or location, and are variable in size and shape. They may be circumscribed but are more frequently diffuse. Metastases are frequent in the lungs, liver and kidney. Metastatic sarcomata are usually circumscribed. TUMORS. 301 Sub-surface sarcomata may produce necrosis of the surface tis- sue, the tumor projecting as a red. granular mass, which appears very similar to exuberant granulation. The surface tissue may not be destroyed, in which case the tumor appears as a sub-surface nodule or diffuse mass. Some sarcomata are encapsulated and are easily enucleated, but the mali.c^nant varieties have no cap- sule and it is impossible to differentiate the surrounding tissue from that of the tumor. Sarcomatous tissue may be soft and spongy or hard and dense, depending upon the extent of the intercellular substance and the kind of cells composing it. In color they vary from gray or white to pink and they may be mottled, depending upon an excessive amount of blood or hemorrh- agic extravasate, pigmentation, or necrosis. The microscopic appearance varies witii the different varieties, but in general they are found to be composed of embryonic cells Fig. 140, — Photograph of a h<>rs<' afCeoted with Sarrniiia of th-- Mfdia^iliniini result- ing in obstrurtid circiilatinn. (a) Oedema inferior thoracic region. (c) Subcutaneous veins, i'o) Jugular vein engorged with blood. 302 VRTKRIXARV PATIIOLOGV. having a limited amount of intercellular substance. The cells may be round, spindle, or myeloid, and the intercellular substance may be mucoid, fibrous, cartilaginous or osseous. The cells contain a large centrally located ovoid nucleus, which occupies practically the entire cell body. ^Mitotic figures are common in rapidly growing sarcomata. Frequently there are multipolar mitotic figures indi- cating the possible division of a cell into three or more daughter cells. Karyolysis or nuclear fragmentation is well marked in those cells that are centrally located in the tumor, and especially in degenerating centres, and in the cells of sarcomas that are not y 4- Fig. 141. — Section of tumor, showing mottled appearance, a result of Ne"i. ^ <*/» ifl> *ft ff _^ .c * ji . ^ W • '"*• 0.n*.***-**^*^tV* Fig. HL'. — Round cmII Sari'imui. The rapid devcloiunent and the irregular distribution of blood \e>sels ])redisposc sarcomas to destructive ])rocesses. Mucoid degeneration frecpienlK- occurs and ma\- result in the complete destruction of the tuuKjr. Necrosis is also cpiite common, and suppurative conditions are not rare. If the normal tissues are eroded, exposing the Jumor tissue, septic infection is common and sometimes results fatally. This group of tumors may be 'dassified. according to their 304 VETERINARY PATHOLOGY. cellular elements, as (1) round-celled sarcomata, (2) spindle- celled sarcoii;ata, and (3) myeloid-celled sarcomata. Round-cell sarcoma. This tumor is composed primarily of round cells (spherical cells) and is rather common. They de- velop in any tissue and are, as a rule, the most malignant tu- mors of this entire group. They are soft, spongy, and usually quite vascular, and, as a rule, are not encapsulated. Structurally the cells of this varietv approximate the embry- onic epithelial cells more closely than do those of any of the other types. According to the size of the cells two classes may be recognized, viz. : small and large. There is, however, no dis- tinct line between the two classes. The small, round cells are about the size of lymphocytes while the large, round cells are as large and sometimes much larger than mononuclear leuco- cytes. The nuclei of this type of sarcoma cells are, relatively, much larger than the nuclei of lymphocytes or leucocytes. In fact, the nucleus occupies practically the entire cell body. The intercellular substance is very limited and is usually mucoid or reticular. Blood vessels are usually numerous, and their walls are frequently formed by sarcomatous cells. Metastatic growths are frequently of this type. The cut on page 274 is from a pho- tograph of the lung of a horse, showing metastatic round-celled Fig. 14 3. — Photograph of sheep's heart, showing a lympho sarcoma of the pericardium. TUMORS. 305 f0m ^'' '^ % ' f'^'f'^^'W'^i ^ Fig. 144. — Sfction of a L.vinplio San-oma of a dog's omentum, showing Uu' lymph Vessels and sarcomatous tissue. sarcomata. The primary tumor involved the eye-])all and hiiall}' de.^^troyed the soft structures of the entire orbit. In this case two or three metastatic tumors were observed in the liver also. The cut on pag^e "SOI is a photograph of a horse in whicli there was an extensive sarcomatous fcirmation in the thoracic cavity involvinor the mediastinum, pericardium, pleura and some smaller nodules in the lung. (The lung- nodules were, no doubt, metastatic formations.) because of their tendency to form metastases and the rapid peripheral infiltration these tu- mors usually cause a fatal termination. Lympho-sarcomata arc a variety of round-celled sarcoma, and are called lymphomata by some authors. They are quite com- mon in all domestic animals. These tumors have their origin in lym])hoid tissue and are extended by the lympli. Two cases have been studied in the ox in which the primary lesion was in the wall of the abomasum. One case of generalized lymphosar- comatosis has been observed in a chicken. A pericardial lym- 306 VETKRIXAKV rATIIOLOGV. phosarconia was found in a post-mortem examination of a sheep. An omental lymphosarcoma in a dog was reported in the Ameri- can Veterinary Review, December, 1905. The color, consistency and size of lymphosarcomata is quite variable. Microscopically these tumors are found to be composed of lymphoid cells, the tumor cells being- supported by stellate cells. Lymph vessels are usually quite numerous and their structure is similar, if not identical, to that of normal lymph vessels. The stellate supporting cells and the presence of lymph vessels are the distinguishing characteristics of lymphosarcomata. There is no leucocytosis in animals alTected with lymphosarcomata. while in those affected with leukemia leucocytosis is well marked. These tumors are malignant. They form metastases through the lymph and blood channels. They are usually surrounded by a very thin capsule. 1-.. H -—2 Fi^. 145 Photosrnph of a niiiio affected with a spindle cell Sar .>■ ■^^ " ^>- -- K . :^ '«^. ■^z •'*'\^ ^^ A SiPO ^ Fig. HG. — Pi^ftidii from spindU- 'Nil Sarcoma ol' :i mules lyiliil. and are sometimes quite persistent regardless of surgical inter- ference. The cells vary from short, thick fusiform cells to elong- ated fibre-like cells. Spindle cells are more matured than the cells of round-cell sarcoma. Round cells have no tendency to become spindle cells, neither do spindle cells become either round cells or matured connective tissue cells. The cells in spindle- cell sarcomata have no definite arrangement but extend in all directions. In microscopic section some cells are cut trans- versely, others obliquely, and still others longitudinally. The nucleus is centrally located, is usually spherical or oval in shape, and is not as large in proportion to the size of the cell as that of the round cells. Some have suggested a classification of this 308 VETERINARY PATHOLOGY. group into large and small-celled varieties. The cells are usu- ally held together by reticular connective tissue. This may be demonstrated in sections in which the sarcoma cells have been dissolved out by acetic acid. The density of the tumor depends upon the relative quantity of protoplasm the cells contain and the amount of intercellular material. A tumor composed of short, thick spindles is less dense thau one composed of fibre- like cells. Blood vessels usually have normal vessel walls and are not as numerous as they are in round-cell sarcomata. Fig. 147. — M.veloid or Giant cell .Sarcoma of the Humerus. a. Giant cells. b. Sarcoma cells. These tumors are usually encapsulated, rarely form metas- tases and are, in general, not as malignant as the round-cell variety. They may be mistaken for fibromata, but a careful study of a microscopic section is usually sufftcient for differen- tiation. Fibromata contain no elements that appear like trans- verse sections of s|)indle cells. Leiomyooia may be differen- tiated by the shape of the nucleus and the selective action of stain as picrofnclisin. Myeloid-Cell Sarcoma (Giant-Cell Sarcoma). — This is a variety of sarcoma characterized bv the presence of myeloid or large multinucleated giant cells fmyeloplaxes). Giant cells of at least two types occur in tumors, one of which results from multi- ple mitosis and usually indicates rapid growth and may occur in a variety of different tumors. The second type of giant cells is due to TUMORS. 309 r. ^ ^? the fusion of invading endothelial leucocytes and occur most fre- quently in bone tumors. The latter are therefore not true tumor cells, although they usually receive the name. Surgeons and patho- logists frequently find myeloid sarcomata in man, but they are rare in domesticated animals. They are invariably found in relation to, or in connection with, bone-marrow, or more rarely in relation with periosteum. They frequently contain cartilaginous, osseous or calcareous centres. Ball in "Journal de ]\Ied. \'et., et de Zoo- techny de Lyon," reported a case of giant celled sarcoma alTected the right front foot of a 6 year old cat. i\Iicroscopically, they are com]:)Osed of myeloid cells and round or si)indle cells. The myeloid cells are the distinguishing elements of this variety of sarcoma. The size of the myeloid cells is variable, frequent- ly being 80 to 100 microns in diam- eter and with an irregular outline, \arying in shape from a sphere to an elongated mass. Their protoplasm may be quite gran- ular or almost clear. They have many nuclei — 150 being observed in one cell. These nuclei have no de- finite arrangement but occur miscel- laneously through- out the entire cell body. The round and spindle cells are like those occurring in round and spindle-cell sarcoma. There may ba an excess of one or the other or they may be equal in number. The intercellular substance varies from mucoid to calcareous in nature. There is usually an exces- sive blood supply, the blood vessel walls being usually normal Fig. 148. — Photograph of hor.se's head affected with mixed cell Sarcoma. 310 VETERINARY PATHOLOGY. in Structure. Degeneration as well as necrosis and calcification are of frequent occurrence in myeloid sarcomata. These tumors may not be completely encapsulated, though there is always a tendency for them to be circumscribed. They are the least malignant of all sarcomata. They rarely form me- tastases. Mixed-Cell Sarcoma. — This is a variety of sarcoma charac- terized by the presence of variously shaped cells, as round, spin- dle and even stellate cells. This variety is not as common as either the round-cell or spindle-cell varieties. They have been observed in the horse, hog and ox, but they doubtless occur in all domestic animals. They affect bone, glandular tissue, and meninges of the brain, in fact, no tissue is exempt. An inter- esting case of mixed-cell sarcoma of the inferior maxilla of a horse was described in the December Veterinary Review, 1905. The tumors frequently degenerate and become necrotic. Mi- croscopically they are composed of round cells and spindle cells that are identical in structure with those described in the discussion of round-cell and spindle-cell sarcomata. Stellate cells may be present, and are very similar in structure to mucoid connective tissue cells. The cellular elements are supported by reticular tissue or by fibrous connective tissue. The number of blood vessels is variable. There is an excess of vessels in those Fig. 149. —Photograph of 3faxilla of horse shown in Fig. 162, showing 3 bony points; the remainder of the maxilla being completely destroyed by the sarcomatous tissue. tT'%rOR?. 311 made up principally of imuikI cells and in those that have a lim- ited amount of intercellular substance. The vessel walls may be normal or thev may be composed of sarcomatous tissue. De- p^cncrate (^r necrotic chauijes in the tissue necessarily alter the microscopic apjicarance. Fig. 150. — Section of a mixed cull .Sart-oma of th. inferior maxilla of a horso These tumors are usually diffuse ; that is, they are not encap- sulated. They form metastases, and hence are malii^nant. Alveolar Sarcoma. — This is a sarcoma characterized 1)y tlie arranij;ement of the sarcoma cells into t^roups or nests, and is occasionally found in domestic animals, especially in the i)x and hog-. The reproductive ,Q;lands, ovary and testicle, are the struc- tures most frequently invaded by them. They may become quite large. An alveolar sarcoma obtained froni the ovary of a heifer weighed lo kilograms ('^'^ lbs.) and was alxmt t?n cm. (S in.) in diameter. Microscopically the cells arc usually round, although they vnay be spindle-shaped. The stroma of the tumor is made up oi 312 VF.T1:R1 XARV PATHOLOGY. two portions. One portion is usually composed of spindle cells which are connected into dense bands extending- in various direc- tions and forming- alveoli ; hence the name alveolar. The other portion of the stroma is intercellular and corresponds to that of the round-cell sarcoma. The arrangement of the cells into nests is suggestive of a carcinoma, but the differentiation is not diffi- cult and depends upon; first, the presence of intercellular sub- stance between the cells which is present in sarcomata but is absent in carcinomata ; second, sarcomatous cells are embryonic connective tissue cells and hence contain nuclei relatively large in proportion to the size of the cell, while carcinomatous cells are embryonic epitlielial cells and contain nuclei relatively small in proportion to the size of the cell. Fig'. 151.— Section of Alveolar Sarcoma from ovary of lieifer showing alveoli filled with sarcomatous cells. These tumors grow slowly. Thev are usually encapsulated and have no tendency to form metastases. They are very mildly malignant. Endothelioma is a tumor composed of endothelium. This is a tumor that is not specifically a sarcoma, but m?.y be so classed. Endothelium has the same origin as connective ti'^siie, i. e., the TUMORS. 313 mesoderm. Embryonic endothelial cells are structurally iden- tical with embryonic connective tissue cells. These tumors are not very common in domestic animals. An endothelioma was observed in the lung of a dog, another in the testicle of a bull. These tumors may have their origin from, the endothelium lining blood or lymph channels, peritoneum, pleura, pericardium, arach- noid membrane, any organs developed from mesothelium, or deflections from any of them. They are variable in shape, size, color and consistency. Microscopically they are composed of cells that most fre- Off ^ ^«s* fp-f" 9^ ^^?,%'^(f^ ■^ .'^ & e ^ ^.3^ r^^ 7j'oUiiF/E~ Fig. 152. —Section of Endothelioma fr • f Endothelioma from a bull's trsticle. Xote the bands of nective tissue and arrangement of cells. quently resemble sarcoma cells, although they may approximate the structure of carcinoma cells. The cells may be arranged in tubules, transverse or oblique sections appearing as sections of gland tubules or acini. If arranged in columns transverse or oblique sections appear as cell nests. The cells are usually cubical or spherical in shape, although they may be spindle or even squamous. The stroma varies according to the tissue in- vaded and may be dense fibrous or mucoid. Blood vessels are usually quite numerous, and if the endothelium is derived from 314 VETERINARY PATHOLOGY the endothelium of a vessel, the vessel may be very irregular in calibre and structure. If the cells occur in columns or nests it will be necessary to differentiate them from carcinomata. This differ- entiation involves the comparison of cells derived from mesoderm and those derived from entoderm or ectoderm. The only essential diff'erence, and that is not constant, is the size of the nucleus. The differentiation may also be governed to some extent by the distribu- tion of the blood vessels. If the cells occur in tubules, their differ- entiation from the adenoma will be necessary. Adenomata may be « •- '#:*#• ^"*-% --^- > .*« Fig'. 153. — From drawing- of a Nodule of a Mediastinal endothelioma. 1. Column of endothelial cells. 2. Diffuse mass of endothelial cells. differentiated by observing the same factors that are used in differ- entiating endotheliomata from carcinomata. Alveolar sarcomata are very difficult to differentiate from endotheliomata, in fact it is some- times impossible, and they may be considered in one class or group. These tumors are not encapsulated and usually form metastases. They usually occur in internal organs and hence surgical relief is impossible. Fatal termination is the usual outcome. Psammo-Sarcoma. — The existence of this type of tum.or is questioned by some authorities. They are composed of sarcomatous tissue and have calcified masses or cells within. They are rather TUMORS. 315 rare One case was observed by Harvey, an army veterinarian, and another case was reported as a cholesteatoma in the Journal of Comparative Pathology and Therapeutics These tumors occur most frequently in relation to the brain and particularly the lateral ventricles, in whicli they are intimately associated with the choroid plexus. Because of their location they invarial)lv produce symp- toms evidencing brain disturbances. Microscopically modified sarcoma or endothelioma cells vari- ously arranged constitute the minute structure of psammo-sarcoma. There is usually evidence of calcification of small centers and there may be cholestcrin crystals present Fibrosarcoma. — This is a tumor composed of both adult and embryonic connective tissue. They are quite common, espe- cially in the eyelids and in labial commissures of horses and "^ Fig'. 151. — Photograph showing location of tumor in ventricle. 1. Cerebrum. 2 Left lateral ventricle. 3. Cerebellum. 4. Medulla. 5. Psammoma. 316 VETERINARY PATHOLOGY. mules. Several cases of dense tissue growths in the withers of horses have been observed. These animals when presented ap- peared to be affected with chronic inflammation of the subcutan- eous tissue or deeper structures. Alost of the above cases were clinically diagnosed as fistulous withers and an operation recom- mended. The operation usually consisted of dissecting away the dense masses of tissue. The ca^es were usually returned in Fiff 155 — Photomicrograph showing nature of connective tissue, leucocytes, neo- plasm c&lls, lime deposits and one blood vessel surrounded by hyaline like substance. WF mi^H r .. "* i^lHH ..,-^' --*' . H .a HH ,. " ■ ^»^J '^ '^^::S:^:^ ^2^-^i»i ^ ,^^^^ :«_ -^^., j'.jim IBS* ' fs^_-^ . "^^ % -, '"» '"* "^^H ^H r ^ ,W j| RK ''^ H l» % % fl IBl* "• % J Fig. 156. — Higher magrnification of No. 2. from four to six weeks after the operation with growths larger than those present before the operation. The operation was usually repeated two or three times with the same results. On microscopic examination these growths were found to be fibrosarcomata, being composed principally of fibrous connective TUMORS. 3i; tissue in which there were some spindle cells and occasionally a few round cells. The presence of both fibrous and sarcomatous tissue is the principal characteristic of these tumors. The num- ber, size and distribution of blood vessels are very irregular. These tumors are not distinctlv encapsulated, but they do not form metastases. They are prone to recur after ablation. They may destroy life after a considerable time, as their growth is Fiff. 157. — A so calkd srupe burioma from uterus of a cow. 318 VETERINARY PATHOLOr.Y. relatively slow. Operation usually stimulates them to grow more rapidly. Melanosarcoma. — A melanosarcoma is any variety of sarcoma in which melanin is deposited in the tumor cells. These tumors are quite prevalent. Gray horses seem to have a special predis- position to them, but thc)^ are also found in bay and black horses, black or red cattle, black hogs, and, in fact, all varieties of do- Figr. 158. — Melano Sarcoma of hog skin. mestic animals regardless of color. On microscopic examination, melanin is found deposited in the tumor cells. The melanin may be in masses or granular and occasionally it mav be found out- side of che cells. Excepting the deposit of melanin, these tumors have the same microscopical appearance as the round or spiiidle- cell sarcomata described before. TTMOKS. 319 Melanotic sarcomata are frequently malignant. In an autopsy of a gray mare metastases of melanosarcomata were found in the liver, lung, spleen and kidney, the primary growth being located in the subcutaneous tissue on the rigiit superior portion of the anus. Another case was obser\ cd in which there was general- ized mclanosarcomatosis in a short-horn cow. Myxosarcoma. — This is a tumor com]:)osed of m\ xuniatous and sarct)niatous tissue. The existence of this group of tumors ^ @ «i ^ 6 <9 , L^® 159.- .Ltiuu ni .Melaoo .*iiia ui" a liuisi's livi deposit of melanin in the tumor cells. showing,' th. is doubted by some pathologists because sarcomata are prone to undergo mucoid degeneration, and, because if the mucoid degen- eration is of limited extent and generalized throughout the en- tire tumor, dift'erentiation would be practically impossible. If the mucoid degeneration atfects localized areas the differentia- tit)n is not difificult. ( !ne m\xosarcoma has been studied. It in- volved the right lobe of the liver of a cow but was not the cause of death. The tumor, about the size of a goose egg, was encap- sulated, soft and ])ale pink in color. Microscopicallv it was composed of stellate cells, the pro- cesses of which were apparently united, thus forming alveoli. 320 VETIiRI XAR Y PATHOLOGY, There were also round cells, some areas being composed almost entirely of round cells and others of stellate cells. The round cells were like the round cells found in sarcomata. The alveoli formed by the stellate cells were filled with a stringy mucus ma- terial. A few blood vessels were observed but they were not as numerous as in pure sarcomata. These tumors may be malignant. When they occur upon or near available surfaces they usually become necrotic, slough and produce no further trouble. Fig. 160. — Section of a -Myxo-Sareoma, from a cow's livei-, showing: 1. Spaces formed by the union of the processes of the stellate cells. 2. Sarcoma cells. Chondrosarcoma and tumors composed of chondromatous and sarcomatous tissues are not common. They usually occur in the location most favorable for chondromata. A chicken affected with a chondrosarcoma of the sternum was obtained at a butch- er's stall at the city market in Kansas City. Microscopically, these tumors are found to be composed of a mixture of chondromatous and sarcomatous tissues in varying proportions. Sometimes the chondromatous tissue is apparently stroma for the sarcoma tissue proper. In other cases the stroma is apparently formed of sarcomatous tissue and the chondro- matous tissue is the essential portion of the tumor. TL'.MORS. 321 These tumors may grow to an enormous size. They are not as malignant as pure sarcomata and metastatic tumors are rare. 'I'hey should be difl'erentiated from chondrofying sarcomata and from sarcomata involving cartilage. Osteosarcoma. — Tliis \'ariety of tumors is composed of osseous and sarcomatous tissues. They are rather common, occurring in the horse, dog and ox. Microscopically, osteomalous and saicomatous tissues are arranged in \arious proportions and in various relations, but [he combining tissue in any case must be new growth tissue. Ossifying sarcomata are not osteosarct)mata. neither are sarco- mata of osseous tissue osteosarcomata. These tumors are usually malignant, but they do not form metastases. Hemangiosarcoma. — These tumors are composed of heman- giomatous and sarcomatous tissues. They are relatively com- mon, occurring in the location common for haemangiomata and may afTect anv of the domestic animals. These tumors are essen- tially very vascular and are highly colored. In microscopic examination variations are observed in diflfer- ent hemangiosarcomata. The sarcomatous tissue in some cases appear to have had its origin from the tunica adventitia of the vessel wall ; in other cases the sarcomatous tissue appears to have had its origin independent of the vessels. x*\gain. the ves- sels may act as the supporting stroma for the sarcomatous tissue. The vessels mav be cai)illarv or cavernous, sinusoid or plexiform. The vessel wall may be practicallv normal, but more frc(|uently it is either hypertrophied, as a result of increased number o^ the cellulcir elements or increase in the size of the cells, or it may be thin, scale-like and alro]:)hicd. Sometimes the endothe- lial cells lining the vessels are cubic or columnar in shape, thus diminishing the lumen of the vessel. The sarcomatous cells may be either spindle-shaped or round. These tumors are cpiite malignant, and thev usuall\- grow rai)idly. The metastatic tumors are most frequently pure sarco- mata. PAPILLOMA. (Wart.) Papillomata are fibro-c])ithclial tumors. These arc perhaps the most common of all tumors. They occur upon the surface of the skin, and upon mucous, serous, and synovial membrane^. They are very common upon the skin of calves, especially around the eyes, ears and poll. Thc}- occur mroRs. 323 invaiial)ly fuund upon the skin and cnnsliuUcs the growths ordi- narily known as warts. Thev may also be soft, and are then found upon mucous, serous or synovial membranes, in which case the covering- epithelium is not cornified. Hard papillomata or warts may appear as tabulated masses, as fungoid growths or as a mass of villi. Any of the above forms may have a smooth surface or be fissured with a xevy irregular surface. They vary in size from a millet seed to an ap])lc. They may be single but are more frequently multiple. Microscopically, the}- are composed of adult epithelium and of fibrous connective tissue in varying prc>portions. They sug- gest the structure of cutaneous papillae. In fact, they have been % ».'o c t Fig. 162. — Sfclion of I'aiiilloiiia iruiu OeHO|)liaKUH of cow, showing bands of slroina covertd by epithelium. described as h_\pertrophied i)apillae. The fibrous tissue is the supporting structure or framework of the tunn'r and contains the blood vessels and nerves when they are present. The epi- thelium is the covering mantle of the fibrous tissue. In the hard papillomata the epitheliiun is stratified and the surface cells are cornified. In soft papillomata the epithelium may be single or stratified but the surface cells are not cornified. The proportion of fibrous tissue and epithelium in ]-)ai)illomata may be the same 324 VETERINARY PATHOLOGY. as in normal papillae or the fibrous tissue or the epithelial tissue may be in excess. Hence some papillomata are apparently sub- epithelial fibromata and others are masses of epithelial cells upon a very limited fibrous matrix. Papillomata have the same relation to underlying structures that normal papillae have. The stroma of the papillomata has a definite connection with the dermis in cutaneous papillomata and the epithelium apparently originates from the lower layers of the epidermis. Transverse sections appear as areas of stroma surrounded by epithelial cells, while epitheliomata are composed of columns of cells surrounded by a stroma. These tumors are essentially benign. They may result fatally because of luechanical interference, as in the occlusion of the oesophagus or the urethra. They may undergo necrosis, thus providing an entrance for infection and result in fatal septicemia. Papillomata do not form metastases, but they are frequently multiple. Cases have been recorded where the condition papil- lomatosis has been transmitted from one animal to another. By constant irritation some epithelial cells may become enlarged in the subsurface, thus providing a centre from which an epithe- lioma may develop. They respond to medicinal treatment and surgical interference. EMBRYONIC EPITHELIAL TUMORS. This is a group of tumors composed of embryonic epithelial cells, and for description mav be divided into three varieties, — (1) carcinoma, (3) epithelioma, and (o) adenoma. Carcinoma is an epithelial tumor characterized by the group- ing of cells into nests or alveoli. They are of rather common occurrence but not as common as sarcomata. Horses and mules, cattle, sheep, hogs and dogs have been observed affected with carcinomata. These tumors have no selective action for any tissue. They have been found aft'ecting mucous membranes, glandular structures, invading muscles and even in bone. They are usually diffuse, although they may be limited by a membrane resulting from reaction of the surrounding tissue. They are usually soft (encephaloid), but thev may be quite hard (scir- rhous), depending upon the amount of stroma or fibrous tissue contained. The color of a cut section of a carcinoma is usually gray, dirty-white or pale pink. They may be mottled because of degenerating or necrotic centers or hemorrhage. Lobules may be observed, especially in those carcinomata formed by the cel- lular infiltration into dense areolar tissue. Small blood vessels may be present, but the blood supply is usually very limited and the vessels occur only in the stroma. TUMORS. 325 jMicroscopically, these tumors arc found to consist of embry- onic epithelial cells arrang;ed in nests, the cells ha\inc^ no inter- cellular substance between theni. The cells are variable in size and in shape, they may be squamous, spherical or columnar. The nucleus is usually much smaller in proportii)n to the size of the cell than the nucleus of sarcoma cells. The stroma is usually .7: .*■ •#'*♦** ^ Fig. 103. — Enrephaloid (arcitiuina. Eye ball, horse. appropriated from the pre-exi.sting- tissue and therefore is vari- able in quantity and structure. In some cases sarcomatous tissue constitutes the stroma. The stroma forms alveoli in which the carcinoma cells occur. In fact, the alveoli are, in many instances, simply dilated lymj^hatic spaces which have been invaded by carcinoma cells. Lymph is usually quite abundant and bathes the nests of the carcinoma cells in the alveoli. Because of the freedom of anastomosis of lymph spaces and the constant flow of lymph, carcinoma cells are easily and rapidly diffused. Karyo- kinetic fi^^ures are of common occurrence in rapidly p^rowincf carcinomata. There is usually an inllammatory reaction accom- 326 VETERINARY PATHOLOGY. panied by a leucocytic infiltration in the adjacent tissue. In rap- idly growing carcinomata the cells frequently completely ob- struct the flow of lymph through the alveoli, resulting in degen- eration or necrosis. Mucoid degeneration is perhaps the most frequent variety, thus producing a mucous mass. Clinically, these tumors are malign. They are not circum- scribed, hence their extirpation is practically impossible. In fact, surgical interference usually stimulates them to more rapid de- velopment, and, in addition, opens an avenue for infection. They Fib. 164. —Section of an EpitlTelioma of thf liock of a liorse: was the sequel of an Injury. Note the ingrowth of the columns of epithelial cells. form metastases. The metastatic tumors usually occur in the first lymphatic gland that the lymph passes through from the area alYected with the carcinoma. Then by metastasis they will be extended on to the next group of glands and finally reach the blood stream and form carcinomatous emboli in the lungs, liver, etc. These tumors should be differentiated from alveolar sarco- mata, endotheliomata and papillomata. The sarcoma cell has a much larger nucleus in proportion to the size of the cell and the cells are usuallv smaller than carcinoma cells. In a cross-section of a tl'MORS. 32; papilla from a papilloma the cells will be found arrang-ed around the stroma instead of in nests as in carcinoma. Carcinomata arc sometimes associated with other tumors as fibromata and chondromata, but they are more frecjuentlv in combination with sarcomata, in which the sarcomatous tissue forms the stroma of the carcinoma. The sarcoma cells are usually of the spindle-celled variety. Epithelioma. — This type is the result of an inorowth of epi- thelium into the underlying structures and has been classed by some as a sub-variety of carcinomata. In this variety of tumors t'lK' 1C5. — Kiiitlu'lioniii from cyo of an ox. there is considerable evidence that thev are secondary to surface injuries. A horse with a large fungoid growth beneath the left eye was sent to a Kansas City veterinarian for treatment. The history of the case brought out the fact that the tumor was the secjuel of a wire cut. Tw^o similar cases of epitheliomata oc- curred in the eye of two cows after severe attacks of keratitis. Epitheliomata are not' rare and may afYect any of the domestic animals. They always occur primarily in rclati(-)n to epithelial surfaces. The surface is usually denuded and there is usually an acrid, fetid discharge. They may appear as elevated nodular .128 VETERINARY PATHOLOGY. masses or as ulcerated surfaces and are rarely encapsulated. Their consistency varies with the amount of connective tissue stroma present. Their color is usually white or gray, although it may be quite variable as a result of degeneration or necrosis. The quantity of blood depends upon the vascularity of the tissue invaded. Microscopic sections of epitheliomata are usually very similar to carcinomatous sections, indeed, it is sometimes impossible to dififerentiate them from carcinomata. In the beginning of the tumor formation, if sections are made perpendicular to the sur- Pig. 166.— Section of a pearl cell Epitbelloma of the Subcutum of a 14-year-oId dog, showing pearl cells and columns of epithelial cells, face, the ingrowing epithelium will be observed as columns of cells. These cell columns extend into the areolar lymph spaces and are then distributed the same as in carcinomata, the pre- existing tissue stroma becoming the stroma of the tumor. The presence of the epithelial cells or their katabolic products some- times produces a chronic inflammation of the stroma. The pres- sure produced from the thickened stroma upon the columns of epithelial cells may result in the formation of "pearls." Epithe- liomata containing the "pearls" are designated pearl-cell epithe- liomata. TUMOKS. 329 CHiiicall\- these tumors are not as niali.i^naiit as carcinoniata proper, and they have less tendency to form metastases. They are fre(|uentlv completel}- destroyed hv siirtjical interference. Adenoma. — This is a glanduhir tumor. While it is similar tea i;"land it is functionless or has a perverted function. Though occurring- nn)re fre(|uently in glands, as the kidney, mammae, mu- cous or sebaceous glands, testicle, liver, etc., they may occur in any tissue. Swine and dogs are most frequently affected with them. Thev are usually circumscribed, rather firm, nodular, white or grayish-white masses, varying in size from a pea to a A I'ig. 1G7. — I'holograiJli showiiib' Maiuniarj Adeuoniu uf a bilch. man's head. In section the gross specimen usually appears lobu- lated, and. if the tumor is large, there are usually necrotic centres here and there tlirough it. The blood supply is limited, the ves- sels usually being obstructed by the pressure of the new-formed adenomatous tissue. In microscopic sections glandular cells are found in various arrangements as tubules, acini, etc. The mimicry, however, is not complete, and there is usually little diflficulty in differentiat- ing adenomata from normal gland tissue. The cells vary in shape from short cubical to tall columnar. They arc usually 330 VKTKRTX.\R^■ I'ATTTOLOGV. arranged in a single layer, although the tubules or acini may be entirely filled with cells arranged layer upon layer. The type of cells adheres to the description given in discussing carcinoma. The stroma is usually composed of fibrous connective tissue and is variable in amount. Blood vessels are found within the stroma. The cells lining the acini may be active and the secre- tion is frequently retained, thus resulting in a cyst-adenoma. The accumulated secretion may cause degeneration of the stroma, and the acini rupturing one into another produce a large cyst. Fig. 168.— Section of an Adenoma from the frontal sinus of a mule, showing the arrangement of tumor tissue into acini and tubules. Clinically these tumors, as a class, are malignant, but do not produce fatal results as rapidly as carcinomata. Many individual adenomata are benign. A horse's tail was amputated that for three years had been affected with an adenoma of the sebaceous glands. These tumors rarely recur when removed. From experience it has been found that mammary adenomata of the bitch frequently result fatally immediately after operation. (The operation appears to produce sufificient shock to destroy life.) Adenomata are extended Tu^roRS. 331 'by means of the lymph. \'ariou.s combinations of adenomata are common. Adeno-Sarcoma. — This is a tumor composed of adenomatous and sarcomatous tissue, l^hese tumors are sckUnn observed dur- ing life because they occur in the kidney, and it is not an easy matter to palpate the kidney in the domestic animal unless there is extreme emaciation. They usual! v atYect only one kidney. They occur in young animals and are most common in the hog although one has been observed in a horse. These tuuK^rs grow rajiidly and may become very large. Day reported one that \veighed "'7.2 kilograms (GO lbs.) fi.und in tlic kidney of a hog. Renal adenosarcomata usually have their origin near the kid- ney pelvis. The renal tissue is gradually displaced bv the tumor, and in some instances the kidney tissue is entirely destrovcd as a result of piessure atrophy. The tumors arc usualK- confined to the kidney, but they forui metastases, in tlie lung (througli the blood), or in the sublumbar lymph nodes (througli the lymph.) In gross appearance, these tumors are irregular in outline. They are usually surrounded by a thin fibrous capsule from which fibrous bands project into the tumor dividing it into Fig- 169. — Section of an AdeiKi-Sarromn of the kidney of a hop, showlnp the sarcomatous tissue between the acini and tubules. 332 VETERINARY PATHOLOGY. irregular lobes. These tumors are usually mottled, though they may be uniform and of a white or light gray color. Microscopically, adenosarcomata are composed of epithelium and connective tissue. The amount and arrangement of the two types of tissue are variable. Some areas may be entirely epi- thelium (adenomatous) and other areas connective tissue (sar- camatous). The epithelium is arranged as glandular tissue, the tubes and acini of which are irregular in shape and size and may contain disintegrating, epithelial cells or their products. The epithelium is usually arranged in a single layer in the tubes and acini though they may be grouped in some instances and .'^-^. ^^-r\sf:, -^< ^'' '-^-.►N. y_^_- Fig. 170. — Siitiun of a Cystadenoma of the mammary gland of a sheep, showing': 1. Coagulated cystic contents surrounded by an atrophied acinous wall. thus appear similar to carcinomat(ms nests of cells. The epithe- lial cells are small and usually contain finely granular chromatin. The connective tissue cells are usually fusiform although they may be nearly spherical in shape. They contain relatively large nuclei in which granules may be observed. Cystadenoma is also common, especiallv in those adenomata that produce secretion. They are found in the adenomata of the mammary and sebaceous glands. Hypernephroma are tumors wliich mav be classed either with TU^[ORS. 333 sarcomas or carcinomas and is composed of tissue similar to adrenal tissue. They occur most frequently in the kidney, ovary or ad- renal body itself. Mns^le reported case a hyjjcrnephroma in a 23 years old mare, llloody urine was the first evidence of disease in Fingle's case. On autopsy a renal tumor about one foot in diameter was observed. Hypernephromas are rarely diagnosed as such in living- domestic animals. They are variable in size, fre- quently weighing- as much as five kiU)grams (11 lbs.) Usually gray in color and invariably containing hemorrhagic areas they thus appear mottled. There is usually an encapsulating mem- brane present. lUood-vessels are numerous, especially in the stroma. Degeneration and necrosis is of common occurrence. ^ /«> ■ ft - XZfo Fig. 171. — II.v|)erne|)liroiiia nf ihe kidney of nn ox, sliowing large typical hyperne- phrfimalous cells containing fat droplets. Microscopically, these tumors are found to be made up of large cells similar to ei)ithelial cells and usually containing fat droplets. These cells are arranged in rows or columns, the columns being separated from each other by a small amount of stroma. The columns of cells may be quite variable in their diameter, appearing at times as long, slender columns and again as rather long nests of cells. The stroma is composed of fibrous connective tissue and contains many blood-vessels. Clinically, these tumors are very malignant, and, although 334 VETERINARY PATHOLOGY. they are encapsulated, they form metastases through the blood. They frequently result fatally in the human, even after operation, probably because of the liberation of considerable of th« adrena- lin substance which increases blood pressure to oich An extent that heart failure supervenes. PLACENTOAIA. (Syncytioma.) A placentoma is a tumor composed of tissue similar to the chorionic villi. . These tumors have been described under a variety of names as syncytioma malignum, deciduoma malignum, chorio-epithel- ioma, epithelioma seritonale, chorio-carcinoma. Only recently have placentomata been recognized as distinct tumors. A placentoma is essentially a tumor of the uterus. They are not common in domestic animals but this may be because of fail- ure to recognize them. The uterus or fallopian tube is their most frequent location. They occur more frequently after spur- ious or mole-pregnancy and usually appear a short time after parturition. Abortion is a predisposing cause. The primary tumor almost invariably occurs in the uterus though a few cases have been reported in women in which the primary tumor was in the kidney. They are very malignant. These tumors appear as soft, spongy, villous, bleeding masses and are variable in size. They have the general appearance of placenta or foetal membranes in both the primary and the metas- tatic tumors. They begin to develop at the cotyledons or zone of placental attachment and rapidly extend into the uterine mus- cular tissue and invade blood vessels, thus metastases occur in a short time after the tumor appears. Because of their struct- ure (embrvonic cells and rich vascular supplv) thev grow rap- idly. The presence of a placentoma is indicated by uterine hem- orrhage occurring a few days after normal parturition or abor- tion. The uterus is enlarged and the affected individual rapidly becomes anemic and emaciated. The uterine discharge usually contains shreds of the tumor and the cavity of the uterus is occupied with a soft bleeding mass. Microscopically, these tumors are composed of a protoplasmic ground-substance, which is arranged in an irregular network forming alveoli. The protoplasmic mass is usually continuous, there being no evidence of cell partitions, and it contains many nuclei thus forming a syncytium. Within the alveoli of the pro- TUMORS. 335 toplasmic mass occur nian\- small variously shaped cells. lUood cavities and canals are abundant and liemorrhai;ic areas are not uncomnum. 'ri:RA'r( ).ma. These tumors are composed of the different kinds of tissues that approximate the structure and arrangement of normal tissue so closely that it is difficult in some instances to differentiate them macroscopically or microscopically from normal tissues and organs. Teratomas are also so closely related pathologically to malfor- mations, that in some cases it is impossible to determine which condition exists. Structurally they are found to be composed of either embryonic or adult tissues. Cutaneous structures are the most frequent tissues observed in this class of tumors, although tissues of bone, muscle, intestine, rudimentary eyes, brain, etc., have been found in them as well as sarcomatous and carcinomatous tissue. Kig. 172 and Fig. 173. — Dermoid Cysts, natural size. These tumors are (|uite variable in size, shap-e and color. In consistency, they vary from a viscid mass to dentine and enamel. Tliey are usually single, grow slowlv and rarely form metasta- ses, although a few have been observed that grew rapidly, metas- tasized and recurred when removed. They frecjuently undergo degeneration tending to cystic formation. Clinically, teratomata are benign, onlv rarelv terminating fatally. 336 VETERINARY PATHOLOGY. Etiologically, they are as mysterious as the other types of tumors. They may have their origin from tissue inclusions. Some teratomata may succeed imperfect tissue union. The theory of parthenogenesis may be apphcable in the explanation of some of the m, but the specific cause or causes of teratoma- ta has not yet been determined. Teratomata are of frequent occurrence in all domestic ani- mals but are more prevalent in equines. They are found in any tissue and in all parts of the body although they are more frequent in the skin, ovaries, testi- cles, kidneys and parotid glands. Be- cause of the hetero- genous structure of teratomasa they are difficult to classify. Dermoid cyst are teratomata com- posed primarily of skin and its appen- dages (hair, sebace- ous glands, horns, teeth, etc.) These cysts are due to the dislocation of epithelium during development. The most common location is in the connective tissue of the head and neck. They may be solid, but are more frequently cystic. In size they vary from a pea to a basket ball. There is usually sur- rounding them a dense capsule from which a villous mass may be Flgr. 174. — Dermoid C.vst from eye of a steer, showing tuft of hair, growing upon cornea. TUMORS. 337 observed projecting into the cyst cavity. Extending from the vil- lous projection are tufts of hair or teeth. The villous is, in struc- ture, very similar to skin. In some teratomasa hair and teeth are produced directly from the inner portion of the cyst \vall. Cys- tic dermoids usually contain hair and a pultaceous marcial de- rived from the sebaceous glands or they contain teeth and a vi'j- cid fluid. Dermoid cysts without any capsule are occasionally observed. The accompanying cut illustrates hair extending from the anterior surface of the eve. Those found in the ovaries ^i\< V ■.cYiJ. 3^S^ Fig. 175. — DentigeroiiN C.vst on left inferior maxillary of S years old colt containing 4.'?1 tfi'th. Removed Dec. 11, 1905, by H. M. Stevenson. Perry. Iowa. usually contain elements of all three germ layers. Those of the te.sticles may contain vestiges of all the germ layers, but are usually cystadenomatous or cystocarcinomatous in type although they may contain cartilage, teeth, osseous tissue, etc. Solid der- moid cysts are a heterologous mass, of embryonic or adult tissue. Dentigerous cyst is_the name applied to those dermoid cysts containing teeth. These are the most important to the veterin- arian because they are of the most frequent occurrence. They are invariablv encapsulated and mav or niav not Ciitain a villus 338 VETERINARY PATHOLOGY. projection. The teeth vary from an irregular conglomerated mass of dental tissue to those perfect in form and structure. The con- stant production and accumulation of the containing- viscid fluid results in enlargement of the cyst and frequently rupture of the capsule and the production of a fistula. The most frequent lo- cation of dentig-erous cysts is near the base of the ear in the region of the parotid gland although they may occur in any other place especially in the ovary and testicle. They are most common in horses. Cholesteatoma is a teratoma composed of pearl like masses of endothelium in which there is more or less cholesterin. They are not common but have been observed in the brain, (choroid plexus and tuber cinereum) and urinary organs. CYSTS. DEFINITION. ETIOLOGY. Retained secretion. Obstructed outflozv. Excessive production in ductless glands. Retention of hemorrhagic extravasate. Colliquation necrosis. False hursae. Parasites. STRUCTURE. VARIETIES. Retention; Atheroma. Exudation; Hygroma, Shoe boil, Capped Iiock, Meningocele. Extravasation ; Hematocele, Hematoma. Degeneration; Colliquation necrosis, Hydatiform Parasitic; E cJiinoccosis, Measley pork. Dermoid; Cutaneous, Dentigerous SECONDARY CHANGES. EFFECTS. A cyst is a bladder like growth surrounded by a capsule and containing a liquid, semiliquid or gelatinous material. Cysts are not true tumors. However, a tumor ma}/ become cystic, (Cystoma,) and the capsule surrounding a cyst may proliferate and become a true tumor. Collections of inflammatory and oede- matous fluids, are not usually considered as cysts. Cysts may be single or multiple. The latter arc designated multilocular cysts. Cause. — Cysts may be caused by, 1. obstruction of gland ducts, thus favoring accumulation and retention of a normal secretion Tl'NfORS. 339 or excretion, e. g.. renal cysts ; 2. By excessive secretion into duct- less structures, e. g., distension of bursae ; 3. By extravasation into the tunica vaginalis sac, e. g., hematocele ; 4. Liquefying necrosis, e. g., formulation of cysts in the cerebrum of horses atTected with "blind staggers." 5. Parasites, e. g., Cysticercus cellulosae. Structure. — The cystic wall varies according to the age of the cyst. In the beginning it may represent th.e original gland structure or a condensation of the normal tissue of the part. Later the cystic walls may be lined with epithelium or endothel- ium, which actively secretes as long as the cyst grows. The cys- tic capsule mav be composed entirely of filjrous connective tissue. In some instances the primary capsule is fibrous and later an endothelial lining develops. The cyst wall or capsule may be firmly adherent to the adjacent tissue or it may be loosely at- taciied. Tig. 176. — C.VHt on AIkIoiiumi of Miilr. (Courtesy of Amerlcnn \ ct^ rinary Review) 340 VETERINARY PATHOLOGY, The cystic contents varies according to the nature of the cyst. Urine, milk, saliva, mucus, semen, liquor folliculi and other secre- tions and excretions are represented in cystic contents. Blood i. e., hemorrhagic extravasates and various tissues that have undergone colliquation necrosis may represent the contents of cysts. The various secretions, excretions, extravasates, exudates and necrotic tissue usually undergo some modification when re- tained within a cyst. Varieties. — Retention cysts, those resulting from the accumu- Fig. 177. — Uterine C.vst the capsule of which had become osseous. lation and retention of normal secretions, e. g., renal cysts, mam- mary cysts, testicular cysts, ranulae, mucus cysts, sebaceous cysts (Atheromata). Of 3,000 kidneys from swine 108 were found to be cystic. An ovarian cyst in the ovary of a goat was reported by Hebrant & Antonie. The ovary in this case was about the size of a three gallon pail. Exudation cystS[, those resulting from excessive secretion into ductless glands or cavities, e. g., ovarian cysts, hygroma, capped hock, meningocele. Extravasation cysis, those resulting from hemorrhage into tis- sues or closed body cavities, e. g., hematocele, hematoma. Degeneration cysts, those resulting from liquefaction of ne- crotic tissue ,e. g. colliquation cerebral cysts. Parasitic cysts, those resulting from the development of para- sites in the tissue, e. g., cysticercus cellulosae, cysticercus bovis, cysticercus echinocogcus, etc. TUMORS. 341 Dermoid cysts, those resulting from inclusion of cutaneous tis- sue. These have been discussed under the head of teratomasa. hnplantation cysts, those resulting from transplantation of epi- dermal cells into the sub-epithelial connective tissue. When such transplanted cells continue to multiply and form a continuous epi- thelial mass the central part of which sooner or later undergoes necrosis and l;ecome of a semisolid consistency, thus forming a pultaceous mass. Secondary Changes. — The cystic wall may become the seat of inflammatt)ry disturbances, neoplastic formation or necrosis. In some instances cysts are destroyed because of the disintegration of their capsule, by disease. The cystic contents may undergo degeneration, become in- spissated or calcified. Effects. — The effects of cyst formation depend upon the tissue involved and the size and nature of the cyst. The cysts frequently become so large that the entire organ is destroyed, e. g., ovarian and renal cysts. In some cases tiie cysts may destroy life, especially if a vital organ, e. g., the brain is in- volved. Cysts may persist for years and be of no serious con- sequence, on the other hand they may seriouslv inconvenience the functional activity of the part involved and impair the healtii of the animal from the beginning. CHAPTER XI. FEVER ( Pyrexia ) . DEFINITION. ETIOLOGY. — To.vins; ptuimiuis; kataholic tissue products; drugs. PERIODS OR STAGES {Course). Onset (Stadium hicrementi). Acme (Stadium Fastigium) . Decline {Stadium Decrementi). Convalescence. VARIETIES , according to Course. Regular. Irregular. Duration and temperature variation. Ephemeral. Continuous. Remittent. Intermittent. Severity. Sthenic. Asthenic. SYMPTOMS. Chill, diminished secretions, increased h.^art c:iion and respire I ic n^ nervousness and restlessness. LESIONS. Parenchymatous degeneration, hemolysis, hyaline degeneration, loss of fat. Body heat is a product of metabolism. Hie body heat or temperature of warm blooded animals is practically constant, although changed environment, diet and use or occupation pro- duce some variations. Thus a horse confined in a barn has a temperature .5 to 1° F. higher than when not so confined, pro- vided the diet is the same in both conditions. A narrow ration is conducive to increased oxidation and consequently a higher temperature. Animals in action have a higher temperature than when at rest. Thus a dog's temperature is from 1 to 1" F. higher immediately after than it is before a chase. The accurate regulation of body temperature is accomplished by- the action of the thermo-regulating center or centers. Tissue action is always accompanied by increased heat production, and frequently diiTerent parts of the same animal may vary 1 to 6° F. in temperature. The equalization of body heat and the distribu- tion of heat to the different parts of the body is accomplished by means of the circulating blood. Heat is continually produced in the animal body and is constantly eliminated from the body 3 4 2 FEVER. 34.1 in the excretions (air, perspiration, urine and feces), as well as by direct radiation. The relative amount of heat dissipation by the excrementation and by radiation varies in different animals. Normal temperature is the balance of equilibrium maintained between thermo.<:^enesis (generation of heat) and thermolysis (dissipation of heat). The normal temperature of an animal used during the day is about 1° F. higher in the evening than in the morning. Fever is a condition in which the equilibrium between ther- mogenesis and thermolysis has been overthrown, i. e., there is a disturbance of metabolism accompanied by increased tempera- ture. It is not a disease but a symptom complex, common to several different pathologic conditions. Fever should be dif- ferentiated from heat stroke and sunstroke. In heat stroke there is no disturbance of thermogenesis or thermolysis, but the ther- molytic centers are unable to cope with the existing external conditions, and there is accumulation of heat in the body, whereas fever is a result of disturbed equilibrium between thermogene- sis and thermolysis. Sunstroke is a condition produced by the action of actinic or chemic rays of the sun upon the nerve cen- ters, temperature variations being only a predisposing factor. Etiology. — Fever is usually caused by bacterial products as toxins, endotoxins and bacterial proteids. Tissue products as leucomains, peptones and various albumins are also capable of producing fever. Certain therapeutic agents may be causative factors of fever. Course. — The course of a fever may be divided into four per- iods or stages, as follows: Onset (stadium incremcnti) is the period of increase between the time of normal temperature and the time that the tempera- » ? 3 4 r J s 9 10 II n n 't /f n n (* (? If V tx i' u sr u «7 u «? Jo S( zx ^•f=- -^1 ^ .-- ^^ ^ ■p "*■ -X', s ^ ^ r N / >f' \ "^ / \ ll )^ ^ / N u L. _ L ^ L_ L_ Si. Fife'. 178.— Charts wliowinj: two fever curves. On the left is glv.n tho t.mp.raturo and on the top each nunibi r 8i(,'nilk-8 one day or 24 hours. From 1 to 13 Is the onset; from 13 to 17 and 20 respectively the Acmf, from IT to 32 is a gradual decline (lysis); and on -" 's shown a rapid declined (crisis). 344 VETERIXARY PATHOLOGY. ture reaches its average height. The length of the onset and the temperature during this period is variable. Acme (stadium fastigium ) is that period of time that the temperature remains high. It is the time from the termination of the onset to the beginning of the decline. Decline (stadium decrementi) is the time extending from the termination of the acme until the temperature reaches the nor- mal level. A sudden decline, i. e., when the temperature sud- denly changes from acme to normal, is called crisis. In a large percentage of the cases of fatal equine pneumonia the tempera- ture suddenly drops from the acme to normal, or even subnor- mal, the sudden change (crisis) causing death. Excessive varia- tions, as a sudden rise of temperature of a sudden fall of tem- perature (may be to subnormal) are of rather frequent occur- rence a short time before death and is called the moribund or premortal stage, A gradual decline from acme to normal is called lysis. Convalescence is that period extending from the time that the temperature becomes normal until the animal has recovered. This period varies in length, a long continued fever essentially requiring a long period for convalescence. The temperature variation during this period is inconstant, but usually there is only slight fluctuation from the normal. Varieties. — Fevers may be classified according to course, to duration, and to temperature variation as follows : According to the course fevers are regular and irregular, typi- cal or atypical. A regular fever is characterized by the appear- ance of the various stages or periods of fever as described above. An irregular fever is one in which the stages are not distinct or are not regular in their appearance and duration. According to duration and temperature variations, fever may be ephemeral, continuous, remittent or intermittent. Ephemeral fever is of brief duration, usually lasti^ng not longer than 2-t hours. It is the type of fever observed in nervous, ex- citable animals. This variety of fever may be produced at will by some nervous women. Continuous fever is that type in which there is a continuous high temperature. In continuous fever there are usually morn- ing and evenings variations the same as in the normal tempera- ture. Croupous pneumonia without complications is an example of disease in which there is a continuous fever. Remittent fever is characteristic of pyemia and is recognized by the irregularly periodic variations of temperature in which the temperature is always above normal. FEVER. 345 Intcrmittcuf fr:rr i? the name applied to that type in wliich there arc periodic xariations, the temperature becoming- normal between the fever periods. Intermittent fever is observed in equine pernicious anemia. Fever mav also be classified as: 1st. Sthenic. 2nd. As- thenic. Sthenic fever is active, vigorous and destructive. As- thenic fever has an insidious onset and is slow in action. p-1 f s f^ r 6 7 9 9 r^ p-ii-. It rs — '- pii-| '' , » — t' t> »I »» 11 f ;i 17 2i >1 Jt IZ — 1 ^ \. .y \ /^ \ r ^.y \\ -sl ^ y ~-- — A- V- ""- "■M- -^^s fl'l / 7^ ~~'^ / ^> 7^ i_ _ _J _ _ — Fig. 179. — Continuous fe^ er I'hart showing morning and evoninK variations, but a continuoua high temperature. Symptoms. — Fever is usually ushered in by a chill because of the constriction of cutaneous vessels which thus diminishes the temperature of the skin and produces the sensation of chill- ing. There are diminished secretions, as perspiration, saliva and urine. In long continued fever there is constipation because of absorption of fluid from the intestines. The pulse rate is usually • t }, •^ r t 7 > 9 i„ ,j 'J /^ 'f u ,-, „ If to ti 31 Cl st i' t!. f) t« J? .V • 1 >1 ^ r N y r -» y x'* Si lef f < \ / \, ^>' y' > /"' V,. ^.H — ^.- y ^ / ^. * -.' ( /■ t? ^/ / _ Fip. 180. — Keniiltent fe> er «'liart, showing variations in whitli Ihi- temperature is always above normal. increased and its character is changed because of the action of katabolic products on the nerve centers. Respiration is increased probablv because of an efYort to eliminate large quantities of air and waste material, and thus there is a tendency for the tem- perature to be diminished. The affected animal is more or less nervous and restless. 346 VETERINARY PATHOLOGY. 1 pl_ 3_ r-^ s 1, 7 -^ 9 — — li 19 It- IS It p /« /y Jo JLI »». 28 8f 8t If jt _5£_ »( 3Jt t' A r^l ,_ ^ y, / 1 \ 1 N / '" \ i \ I \ / \ / \ f 1 i / >' \- ■N / \ V- •> — "- '*' "" ._ Vl. -- ->" rsf ~^^-r _ Fig. 181.-~Interinittent fever chart in which tluif are periods of normal tempera. ture. Lesions. — All parenchymatous structures are afifected with cloudy swelling-, the extent of which depends upon the degree of temperature and its duration. Hemolysis is more or less ex- tensive. Chronic or long continued fever usually causes hyaline degeneration, especially of the vessel walls. The affected animal rapidly diminishes in weight because of the consumption of fat. CHAPTER XII. INFECTIVE GRANULOMATA. Infective s^ranukimala embraces a group of specific inflam- matory conditions characterized by the proliferation of endothe- lial cells, fibroblasts and other cells. Though the consideration of the following diseases belongs more properly to a discussion of infective diseases, their description will be of value to the stu- dent of general pathology. TUBERCULOSIS. Tuberculosis is a specific, infective disease, caused by the bacterium of tuberculosis afifecting practically all of the higher animals and also some of the lower forms of animal kind. Extent. — McFarland states that 14% of the deaths in the hu- man family are from tuberculosis. It is probable that 25% of all himians have or have had tuberculosis. The prevalence of animal tul)erculosis is variable in different communities, the percentage depending upon methods employed for control and eradication under different sanitary laws, upon transportation rules and regulations and upon the conditions un- der which the animals are maintained. The exact percentage of tubercular animals in any country is not known, but the relative number has been determined by tuberculin testing and by post- mortem examination at abattoirs. In the United States the percentage, generally speaking, is low in comparison with other countries. According to the post-mortem findings of T^G^l.Tn cattle slaughtered in United States establishments having official inspection during the fiscal year beginning July 1st. 1906, and ending June 30th, 1907, 29,835, i. c.. A'/r were tubercular. This percentage is probably below the actual percentage, as dairy cattle are more extensively affected than beef cattle. The Secretarv of Agriculture in his report for 190S holds that 1% of beef cattle anrl lo% of dairy cattle are tuberculous. According to the above report 2% is the estimated prc\alcnce in the United States of tuberculosis among swine. Porcine tuberculosis is apparentlv on the increase in the United States. In Germany it varies from 1-7%. Equine tuber- 347 348 VETERINARY PATHOLOGY. culosis is not common in the L'nited States, or at least only a few cases have been reported. Tuberculosis is usually found in those horses and mules that have been fed on tubercular cows' milk. Tuberculosis of goats is rather rare and the disease is still less common in sheep. Dog and cat tuberculosis is not uncommon and is usually observed in pets of tubercular humans, although barn cats, espe- cially those fed milk from tubercular cows, frequently become tubercular. (A dairy was recently inspected in which 68% of the cows were tubercular and on autopsy three barn cats also were found to be afifected in a like manner.) Tuberculosis of fowls is more prevalent in the United States Fig. 182. — Bacterium Tuberculosis Bovine. Pus showing leucocytes and bacterium tuberculosis. than is ordinarily suspected, although the percentage of afifected birds is difficult of determination because there is at present no official inspection of fowls. Etiology — Tuberculosis is caused by the Bacterium tuberculo- sis. This bacterium has rounded ends and is frequently slightly Ujent. It varies from 2 to 5 microns in length and from .3 to .5 in width. (These bacteria may appear as long, delicate, mycelial threads, branching forms, or even as a ray like fungoid growth, the form depending upon the environment. The pleomorphism of this micro-organism has caused some doubt as to its classifica- tion as a bacterium.) The Bacterium tuberculosis may occur singly or in pairs, and it is not uncommon to find several lying INFKCTIVK r.RANri.OMATA. 349 side by side. They do not form spores, l)ut ihey may contain i^ranules and vacuoles, and they may have a beaded appearance because of fragmentation of their cytoplasm. Tlie IJacterium tuberculosis is extremely resistant to external injurious intluences, probably because of a wax-like substance that constitutes about one-third of the body weight and forms the i)riiicipal jjart of the external covering or capsule. (These bacteria are stained with difficultv but when once stained retain their stain even though subjected to tlie action of alcohol and acids.) The staining peculiarities are prol)abl\- due to a fatty substance they contain. Source of infection. — The bacteriuiu tuberculosis may be transmitted direct from tubercular to healthv animals, but infec- tion is more frecpiently obtained from foodstutifs, or barns, feed racks, watering troughs, posts, soil, etc. Tubercular animals are almost constantly eliminating the ])acterium which contam- inates everything that tiie tubercular discharges contact. The cadavers of tuberculous animals are usually deposited in the soil, and, in many instances, the proper precautions are not taken to destroy the infecting micro-organism. Infected manure is spread upon the soil and thus it becomes infected. The various crops, including hay, grown upon a tubercular infected soil, may be contaminated with the Bacterium tuberculosis and infect sus- ceptible animals that consume such food. Sometimes the car- casses of animals dead of tuberculosis are thrown into rivers or creeks, thus infecting the water. The waste products of many small slaughter houses are fed to hogs and this affords oppor- tunity for them to become infected. Skimmed milk and whey ivom creameries and cheese factories are also sources of tuber- cular infection. Channel or avenue of entrance of the infection. — The Bacter- ium tuberculosis may gain entrance into the tissues of a healthy, susceptible animal through the mucous membranes or through abrasions of the skin, though the latter mode of infection is not of common occurrence in domestic animals. Cutaneous infec- tion is occasionallv observed in the mammae of sows and in the castration wounds of barrows. From clinical and experimental evidence and autops}' lesions observed in al)attoirs, it seems evident that the digestive tract is the principal channel of entrance of the Bacteritun tubercu- losis in hogs, cattle and fowls. It was originally erroneously concluded that the presence of pulmonary tubercular lesions was positive evidence that the infection had gained entrance through the respiratory tract. Tubercular free experimental animals fed 350 VETERINARY PATHOLOGV. foodstuff contaminated with the Bacterium tuberculosis have frequently become affected with primary pulmonary tubercular lesions. (The possibility of inhalation of the infection was care- fully guarded against in these experiments.) It is presumed that the Bacterium tuberculosis is incorporated by leucocytes in the digestive tube and that the leucocytes then pass through the intestinal wall into the lacteals and thence to the thoracic duct to the right heart and on to the lung, the first capillary system encountered, where they may lodge and establish tubercular foci. No doubt the respiratory tract is the channel of entrance in some cases of tuberculosis, but the number of animals infected through this channel is very small. An occasional case of tuberculosis may be the result of infec- tion through the genito-urinary organs. Thus the penis of a bull may become infected by serving a cow afflicted with uterine or vaginal tuberculosis, and this same bull by copulation may infect other cows. Tubercular lesions are occasionally observed in the superficial inguinal glands of steers, and this may be the result of infection in the castration wounds. Conjunctival infection may occur as a result of forcible dis- charge of infection from the respiratory tube of an affected animal. In summarizing, the digestive, respiratory, cutaneous abra- sions, and genito-urinary organs are the principal channels of entrance of the Bacterium tuberculosis, the frequency being in the order mentioned. Lesions. — The characteristic lesion of tuberculosis is the tubercle. A tubercle is a nonvascular nodule, composed of leu- cocytes, endothelial, giant and connective tissue cells, wath a tendency for the central part of the nodule to undergo necrosis. The lesion may vary in animals of different genera and in differ- ent animals of the same genus. Thus tubercular lesions in hogs may differ in some particular from those in cattle because of variations in the resistance of the hog and ox. Variations of the tubercular lesions in different individuals of the same genus occur because of variation of individual resistance of the infected ani- mal and variation of the virulency of the infecting organisms. Tubercular lesions may be modified or obscured by lesions re- sulting from secondary infections. The initial or primary lesion may occur in any tissue or organ. Lymphoid tissue, however, is more frequently affected than anv other. The Bacterium tuberculosis and its products are the etiologic factors in the formation of a tubercle. The bacterium having lodged in a tissue favorable for its growth and development, be- INFF.CTIVE r.RAXrr.ONFATA. 351 gins to nuillip'.y aiul to eliminate those products that stimulate the surroundini;" connective tissue and endothelial cells to in- crease in number, and, at the same time, exerts a positive chemo- tactic action upon leucocytes. If the influence of the bacterial products is exerted upon the connective tissue and endothelium, the resultins:^ tubercle will be composed of connective tissue cells and endothelial cells, and if the intUicnce of the bacterial i)ro- ducts is of a chemotactic nature, the tubercle will contain leu- cocytes. Structurally, a younq- tubercle consists of a cellular focus in- fected with varyino- numbers of the Bacterium tuberculosis. As Fig. 183. — Mmall cellular tubercle; liver, x.'iOO. Showing small round colls with tu- bercle bacilli scatt<-ro(l hi-r<> anil thirc. also a few partially destroyed hepatic cells. 352 VETERINARY PATHOLOGY. rhe bacteria multiply the quantity of their products is increased, and these stimulate cellular multiplication and accumulation, and thus the tubercle grows. The formation of a tubercle constitutes a tissue reaction, but there is no vascularization ; that is, no new blood vessels are formed, and the existing capillaries in the invaded tissues are finally ol^literated. A tubercle is, therefore, strictly non-vascular, although in the very beginning the afifected zone may be hyperemic. Cells constituting a tubercle obtain nutriment from adjacent tissues by absorption. Tubercles grow by multiplication of the peripheral cells, the central cells becom- ing degenerated after they have consumed all available nutrition. The structure and appearance of a tubercle varies according to its age, thus : a tubercle in the very early stages is a cellular mass, a little later the central portion of the cellular mass becomes necrotic, and at about the same time a median zone, consist- ing of bacteria, endothelial, and, in some cases, giant cells, becomes evident ; the outer zone is the active zone and is com- posed of bacteria, connective tissue cells and leucocytes. As the tubercle becomes larger the necrotic zone extends to the median and outer zones toward the periphery. Necrosis is usually evident in tubercles that have attained the size of a pea. The central necrosis is primarily of the coagulation type, but the coagulated necrotic tissue may become liquefied, always be- comes caseous and usually calcified according to the quantity of fluid contained. The calcification may be limited in extent, the necrotic tissue containing small calcareous particles that cause the necrotic tissue to have a "gritty feel," or it may be so ex- tensive that the tubercle cannot be dissociated except by the use of a sledge. Liquefied tubercular necrotic tissue (pus) is yellow- ish in color in the ox, dirty white in hogs and yellowish in fowls. It is not sticky, although it becomes quite thick and is finally caseated.i. Tubercles may vary in size from a microscopic point to large masses. All tubercles are small in the beginning and are usually entirely cellular. Small cellular tubercles in which there is no necrosis are designated miliary tubercles. Miliary tubercles ap- pear as minute, grayish, translucent, pearl-like specks or nodules. If all the lesions in an afifected animal are miliary in character, the disease is termed miliary tuberculosis. Miliary tuberculosis is common in hogs. The appearance of a tubercle changes when central necrosis begins. The color of caseous and calcareous tubercles varies from a dirty white to a yellow color. The tubercles may or may not be encapsulated. The capsule of a tubercular lesion is rela- INFKCTIVli GRANULOMATA. 353 tively thin, though it is tough. Secondary tubercles may develop from a primary tubercle, and daughter tubercles may develop from a secondary tubercle, thus are produced the irregular nt)du- lar tubercular masses. The tissues contiguous to a tubercle are ischemic, prt)bably because of the enfringement of the affected areas with lymphoid cells. ' Little difference is noted in tubercular lesions in the various Fig. 184 A Lesion of Tuberculosis from the rost-pliar.vnKeal L.rinph Gland of an Ox. A — giant-cells; b — caseous center wltliin the tubercle; c — fibrous capsule. tissues e.xcept possibly osseous ti.ssue and serous membranes. Tubercular lesions of osseous tissue are usually associated with extensive suppuration of the osseous structures, while tubercular^ lesions of serous membranes are frequently entirely cellular in structure and do not undergo central necrosis. Bovine tubercular lesions are usually encapsulated and become quite extensively calcified. The age of the lesions is sometimes important in medico-legal cases. Calcification usually begins 354 VF.TF.RIXARV PATHOLOGY, when the tubercle is from six to eight months of age and is ex- tensive by the time the lesion is one year old. Tubercular masses are occasionally observed in the lung, bronchial or mediastinal glands, and in the liver. These masses may contain all stages of tubercular formation or the entire mass may all be in the same stage of development, as liquefying necrosis, caseation or calcifi- cation. Tuberculosis of serous membranes of bovines should receive special mention because of the characteristic appearance of the lesions. Bovine serous membrane lesions vary in size from a millet seed to a walnut, but are usually about the size of a pea. These lesions are frequently thickly studded over large areas of a serous membrane. The nodules are surrounded by a firm cap- sule which causes them to appear as pearl-like bodies, and hence Fig-. 185. — Photograph of a tubercular mamniary Kland, Ox. the name, "pearly disease."' Sometimes serous membrane tuber- cular lesions are very extensive ; this type may be called "mass tuberculosis." Porcine Tubercular lesions are characterized by enlargement of lymphatic glands, the formation of tubercles of variable sizes in or upon serous membranes and within the substance of glandular organs, bones and other connective tissues. The tubercles pro- duce increased density of invaded soft tissues and are, therefore, easily detected except in very recent infection. The tubercular nodules in the early stages present about the same color as the surface of the tissue invaded. In sectioning the tubercle the cen- tral portion is caseous and slightly yellow or fibrous and white. INFECTIVF. GRANULOMATA. 355 Sometimes there is a coml)ination of botli conditions and occa- sionally the tubercles contain calcareous j^ranulcs. The central portion of porcine tubercles rarely contains litiuefied necrotic tissue.) J Microscopically porcine tubercular lesions are always cellular in the beginning. The cellular tubercles are fairly constant in structure regardless of the tissue in which they occur. The center is at fiirst represented by a mass of lymphoid cells, the other cellular elements occurring as the tubercle develops. Necrosis, or fibrosis, succeeds the cellular stage in the por- cine tubercular lesion. Necrosis of tubercles is probably the result of the activity of very virulent bacteria or the low resis- tance, of the infected animal. The necrotic center may be sur- rounded by a cellular zone (lyniphoid and endotiielial cells), or it may be surrounded by fibroblasts. The necrotic material is invariably caseatcd and later becomes calcified. Fibrous lesions vary from the formation of small ([uantities of fibrous tissue to dense fibrous centers. Fibrous lesions are probably produced by bacteria of low virulence, or occur in ani- mals having a marked resistance. The central portion of the fibrous lesion mav become calcified. The so-called arbor vitae gland is a fibrous center in which the fibrous tissue is arranged similar to the trunk and branches of a tree, hence the name. This lesion is observed in the hog in the cervical lymph nodes. The bacterium tuberculosis has been demonstrated in about 30 per cent of arbor vitae glands. The lesions of porcine tuberculosis are in brief either cellu- lar, necrotic and calcified tubercles, or cellular, fibrous and calci- fied tubercles. The lesion is always non-vascular as in other animals. ' Ai'ia}i tubercular lesions arc very similar to mammalian tubercles, and mav occur in practically any tissue. Microscopically, avian tubercules are found to contain giant cells, endothelioid cells, small round cells and connective tissue cells, the arrangement of whTch is the same as described in mammalian tubercles. Avian tubercular lesions have been found in the liver, spleen, intestine, mesentery, kidnev. lung, skin, and bones, the fref|uency being in the order mentioned. Avian tubercles in glandular tissue, i. e.. in tlie liver, kidney, spleen, etc., begin as small, dirty, white cellular foci. They usu- ally occur singlv. though thev may occasionally become conflu- ent, thus producing nodules a quarter of an inch in diameter. As the tubercles in glandular tissue undergo necrosis, they as- sume a yellowish color. Intestinal tubercles are about the same 356 VETERINARY PATHOLOGY. size as those in glandular tissue. The intestinal lesions are usu- ally quite hard and dense and present a glistening appearance. Necrosis frequently destroys the intestinal wall and thus a tuber- cular intestinal ulcer is produced. Mesenteric tubercles are fre- quently pedunculated and they invariably present a pearf like appearance. Extension. — Tuberculosis, except in some cases of the acute form, is essentially a localized disease. However, the disease, even in the chronic form, has a tendency to extend and involve new tissue. The extension may be accomplished by means of, first, the lymphatic system, second, the digestive, respiratory and genito-urinary tubes, third, the blood vascular system and fourth, by continuity and contiguity. Tuberculosis is usually extended by the lymphatic circulation. Thus the first group of lymph nodes through which the lymph passes from a tubercular lesion is almost invariably involved. In fact this is a characteristic of the disease. The large per cent of lymphatic lesions is also evidence of extension by means of the lymph. It has been previously stated that hogs are invariably infected by ingestion of tubercular material and in 93 per cent of tubercular hogs the submaxillary lymph nodes are affected, which is further evidence of lymphatic extension. The fact that infec- tion may extend along the digestive, respiratory or genito-urin- ary tracts, has been demonstrated. Thus the discharges, con- taining the Bacterium tuberculosis from a pharyngeal tubercle may pass through the oesophagus and stomach and find a nidus favorable for its development in the intestine. In a like manner the lung tissue may become affected by extension from laryngeal, tracheal or bronchial tuberculosis and prostatic tuberculosis may result from extension of renal tubercular lesions. In extensive or generalized tuberculosis the tubercles not infrequently in- volve and produce necrosis of the blood vessel walls and the virulently contamin.ated necrotic material being discharged into the blood resulting in tubercular metastasis. Thus tuberculosis is extended by means of the blood. Extension by the blood in- variably results in generalized tuberculosis which is usually acute. In the discussion of tubercular lesions, the formation of sec- ondary and daughter tubercles was mentioned. The production of secondary and daughter tubercles is a means of extension. If the newly formed tubercles are in tlie same kind of tissue as the primary tubercle then the extension is by continuity. If the secondary or daughter tubercles are in tissues dissimilar to that INFRCTIVE r,R.\xrr.OM.\T.\. 357 in which the primary tubercle occurs the extension is by con- tiguity. In the majority of the cases of lymphatic extension and in some of the cases of blood extension the Bacterium tuberculosis is incorporated in and transported by leucocytes. The leucocytes usually have sufficient vitality to destroy the incorporated bac- teria but occasionally the leucocytes may be destroyed after having transported the bacteria a considerable distance. Thus a Bacterium tuberculosis from a pulmonary tubercle may be incor- porated by a leucocyte and carried to the kidney and the leuco- cyte being destroyed the liberated bacterium may establish a tub- ercular focus in the renal tissue. The occurrence of Bacterium tub- erculosis in the milk of cows having no mammar\' tubercular lesions as well as the fact that ingestion of tubercular material frequently causes pulmonary tuberculosis, may be due to leuco- cytic incorporation and transportation of the infecting micro- organism. Elimination. — From the sanitary point of view it is always of considerable importance to know the channels or avenues through which infectious agents are discharged in order that they may be destroyed. Tuberculosis aff'ects all tissues and the Bac- terium tuberculosis may not be eliminated from the affected ani- mal or it may be discharged in one or more of the secretions or excretions. It has been determined by the Department of Agri- culture that about 40 per cent of tubercular cattle eliminate the Bacterium tuberculosis in their feces. The same investigators also found, in a limited number of dairies, that about 25 per cent of tubercular cows, regardless of location of the lesions, eliminated the Bacterium tuberculosis in their milk. These are facts of prime importance in adopting means for checking the progress or for suppression of the disease. The discharges from tlie respiratory tract of tubercular animals fre(|uently contain the Bacterium tuberculosis, especially if they have pulmonarv lesions of the disease. The urine and discharges from the female genital organs may be contaminated with the infection. Renal tuber- culosis, ho\vever, is not of frequent occurrence and it is not probable that the Bacterium tuberculosis is eliminated in the urine of tubercular animals in which there are no renal lesions. In general the ch.annel of elimination of the bacterium tuber- culosis depends largely upon the location of the lesion. Tuberculin and Tuberculin Test. — Tuberculin is a bio-chemic material containing the ])roducts and the disintegrated bodies of the Bacterium tuberculosis. It is prepared by growing the Bacterium tuberculosis in glycerin.e bouillon for a certain length 358 VETERINARY PATHOLOGY. of time. The glycerine bouillon culture is filtered and the fil- trate sterilized by heat and concentrated to the desired strength by evaporation over a water-bath. The active principle of tuber- culin is probably a nucleo-proteid or its chemic derivatives. Tuberculin is a very reliable diagnostic agent. Its chief use in veterinary medicine has been in the diagnosis of tuberculosis in cattle. It is practically as reliable in the detection of human, porcine and probably avian tuberculosis as in the detection of bovine tuberculosis. A tuberculin reaction consists of a local, focal and general or systematic reaction. The local reaction is manifested at the point of injection of the tuberculin and is the reaction evidenced in intradermal and ophthalmic tuberculin testing. The focal reaction consists of a hyperaemia and increased tissue action around the tubercular centers and is probably responsible for the systematic disturbances evidenced in the ordinary thermal or sub- cutaneous tuberculin test. The principal method of application has been by subcutaneous injections and noting the temperature changes in the suspected animal. The normal temperature of the animal is ascertained previous to the injection and the tempera- ture is taken every two hours, beginning eight hours after tuber- culination. On the day svicceeding the injection a rise of from two to three degrees Fahrenheit is considered a reaction and this sig- nifies that the patient is tuberculous. This reaction is probably due to the specific irritating action of the injected tuberculin upon the tubercular foci producing intense hyperemia around and disintegration of the tubercle. Thus there is a sudden dis- charge of tubercular products into the system and the intense re- action, thermic and constitutional follows. A purified tuberculin used directly in the conjunctival sac is now on the market. The ophthalmic reaction consists of the production of a marked hyperemia of the conjunctiva in from six to ten hours after tuberculination. The intradermal tuberculin test is the official test in the state of Missouri. ACTINOMYCOSIS. Actinomycosis is a specific, inflammatory granuloma, caused by the Cladothrix actinomyces and characterized by the formation of tumorous masses of fibrous tissue in which there usually develops suppurating centers and fistulous tracts. Distribution and extent. — Actinomycosis is prevalent in Eu- rope, Australia, Africa, North and South America. The extent of the disease varies in diiTerent countries. According to the 24th Annual Report of the Bureau of Animal Industry there were slaughtered in establishments having federal inspection 7,621,717 cattle, of which 22,742 were found to be affected with actinomy- cosis, or one in about each 340, The actual per cent is even INFECTIVE GRANULOMATA. 359 larger, for many animals afflicted with actinomycosis are slaugh- tered where there is no official inspection maintained. Susceptible Animals. — Cattle are more frequently affected with this disease than other animals, though actinomycosis of sheep, goats and hogs is occasionally reported. A few cases have also been observed in the horse, mule, dog and wild ani- mals. Etiology. — A fungus, the Cladothrix actinomyces or actino- myces bovis, is the specific cause of actinomycosis. The life his- tory of this organism is not known, but it is thought that it passes a part of its life cycle upon some of the grasses. Each matured fungus is composed of a central body 10 to 40 microns in diameter, from which the radiating filaments (mycelia) extend outward for a distance of from 5 to 30 microns, then becoming enlarged, terminate in club-shaped bodies from 10 to 50 microns in length. Thus the matured fungus has the appearance of a rosette and is commonly called the "ray fungus." Detached clubs are capable of reproducing the entire rosettes as described. The fungus can be cultivated in artificial media where it develops a tangled mass of mycelia. Source. — The Cladothrix actinomyces is probably most fre- 1^ , Fig. 1S6. — Drawing iii.vc«>s i l;ay fungus) in sncti,>ii of tongue. 360 VETERINARY PATHOLOGY. quently obtained from vegetation, especially wild rye (Hof- dium murinum) consumed by the animal. Infection occurs most frequently in animals fed on dry feed as fodder, stover, straw or hay. During January and February, 1908 .86% or 376 cattle of 41,405 slaughtered had actinomycosis of the tongue or submax- illary lymph nodes, and of 12,484 cattle slaughtered in July, 1908, 44 or .34% were affected with actinomycosis. Some rather exten- sive outbreaks have been investigated in which it seems highly probable that infection has been direct from one animal to an- other, or indirect by means of the discharge of actinomycotic ani- mals that liad been smeared on rubbing posts, feed racks and feed troughs. (Of 98 head of cattle, three of which were actinomycotic when placed in the feed lot in November, 42 head were affected with actinomycosis when inspected 2^^ months later.) Channel of Entrance. — The causative fungus may gain en- trance into the system by way of the digestive tract, the respira- tory tract or through the skin. Abraded surfaces appear to be essential for infection, though it has not been proven that the fungus cannot penetrate uninjured surfaces. The digestive tract is the most frequent channel of entrance in cattle. The tongue, especially the dorsal surface at the junction of the base and apex, is subject to injury by the rough, harsh food consumed by cattle. Tongue injuries may also be inflicted by licking boards, posts, etc., containing nails and splinters. Awns of wheat, barley and rye, chaff, splinters and hair accumulate in the erosions or wounds of the tongue, producing the so-called "hair sores." More than 12% of 48,000 cattle slaughtered during the winter months in one of the Kansas City packing houses had "hair sores" upon their tongues. The "hair sore" is intimately associated with lingual actinomycosis ; indeed it is rare to find actinomycosis of the tongue or submaxillary lymph glands when there is no "hair sore." Diseased teeth, especially if the gingival mucous mem- brane is involved, also provide an entry for the ray fungus. The possibility of the infection passing through the intestinal or gastric wall explains the cases of peritoneal actinomycosis that are occasionally observed Respiratory infection is not of common occurrence. This type of infection probably occurs by inhalation of chaff or awns con- taminated with the Cladothrix actinomyces. The skin is probably the most frequent channel of entrance in hogs. Actinomycotic scirrhus cords are quite common, the in- fection taking place in the castration wound. Mammary acti- nomycosis is sometimes observed in sows, especially those run- ning in stubble fields, the infection taking place through abra- INFECTIVK GRAN ULOM ATA. 361 sions produced by the stubble. Abrasions resulting from rub- bing on stanchions and feed b(X\es may be a source of infection in dairy cattle. Lesions. — Macroscol^ic. — Actinomycotic lesions may be sur- face or subsurface. The fungus may invade and prc^ducc tlic lesion in any tissue. Surface lesions begin as small inflammatory centers which usually thicken and become elevated above the general surface. The lesion gradually increases in size, and in some cases assumes a fungoid appearance. At this stage the lesions vary in size from a small pea to a walnut. The surface tissue may become eroded as a result of the extension of necrosis from the lesion and tiie typical actinomycotic pus discharged or more frequently the lesion becomes encapsulated bv the formation of a dense fibrous capsule. The capsule usually limits the development of the lesion and it may be diminished in size by the contraction of the filjrous tissue constituting the capsule. Subsurface lesions, though beginning as inflamniatorv centers, are invariably (circumscribed by a dense, fibrous wall. As the disease progresses the center of the lesion undergoes lique- fying necrosis. The necrosis extends, producing Irregular, tor- tuous sinuses that may extend through the capsule and into the surrounding normal tissue. Ultimately tlie lif|uified necrotic tissue (pus) would ordinarily be discharged upon a surface, or the fungus contained in the necrotic tissue (pus) w-ould perfor- ate the primary capsule and cause the production^.of a secondary fibrous capsule. Thus the lesion is frequently composed of sev- eral communicating cavities (multilocular) containing actinomy- cotic pus. If such a lesion is incised and pressure applied the typical beads of actinomycotic pus will appear in various places upon the cut surface. Actinomycotic pus is crcamv, sticky, tenacious, yellowish-white and contains small, yellow, gritty granules. The pus has a greasy feel and may have a slight odor. If tiie pus is permanently maintained within the capsule, its fluid content is absorbed and becomes caseous. Osseous actinomycosis is of common occurrence. The fungus having gained entrance produces inflammation, which is suc- ceeded by disintegration of the osseous tissue and the formation of cavities or pockets. By growth and extension of the infect- ing fungus, inflammation and disintegration is favored, and thus rommunicating cavities a'e formed in the affected bone. As the process of rarefaction continues within there is new osseous tis- sue deposited without. Thus bone affected with actinomycosis 362 VETERINARY PATHOLOGY, becomes enlarged and cancellous and has a honeycombed ap- pearance. Microscopic. — The presence of the Cladothrix actinomyces in a tissue produces an irritation resulting in an accumulation oi INFECTIVE GRANULOMATA. 363 small round cells, the production of endotheloid and giant cells by the invaded tissue, and finally the development of a fibrous cap- sule around the entire mass. The fungus may appear in the be- ginning as mycelial elements, but later it has the typical rayed appearance. In old lesions the central portion or body of the fungus becomes calcified. Surrounding the clubs or mycelium in the early stages are varying numbers of small, round cells (lymphocytes). As the disease progresses, the matured fungus is more or less surrounded by giant cells that actually contact the fungus. The actinomycotic giant cell is very irregular in shape and size and has varying numbers of nuclei scattered indiscriminately throughout the cell body. Endotheloid cells appear marginally to the giant cells. These cells are similar in appearance to the endotheloid cell of tuber- culosis, having a relatively large cell body and a small, single nucleus. The small, round cells are first noticed immediately around the fungus, but later they infiltrate the surrounding tissue also, and are in excess of all other cells in the lesion. Fibroblasts appear in the margin of the early lesion, and through their activity a thick fibrous capsule is produced. Actinomycotic pus is found to be composed of tissue shreds and fragments, lymphoid cells and some polymorphonuclear leucocytes, an occasional endotheloid cell and the Cladothrix actinomyces. Extension. — The extension of actinomycosis has usually been described as taking place only by growth in continuity or contig- uity, or by passing along the respiratory, digestive or genito- urinary tubes. By a careful observation of over 72,000 cattle slaughtered, it has been found that many cases, in which there were "hair sores" but no actinomycotic tongue lesions, showed actinomycosis of the submaxillary lymph nodes. The majority of cases of lingual actinomycosis are accompanied by involve- ment of the submaxillary lymph nodes. That practically all cases of actinomycosis of the submaxillary lymph nodes occurred in animals having "hair sores'' is indicative of lymphatic exten- sion. It is therefore quite probable that actinomycosis may be extended in the animal body by means of the lymph. Differential Diagnosis. — Bovine actinomycosis may be con- founded with tuberculosis, nodular disease, abscess formation and various tumors. Tubercular lesions calcify, actinomycotic lesions rarely be- come cakified. Tubercular pus is usually quite different from 364 VETERINARY PATHOLOGY. actinomycotic pus. The former is not sticky or tenacious, and does not contain the small, yellow, gritty granules found in the latter. The capsule of an actinomycotic growth is thicker and denser than the capsule of a tubercular growth. The two diseases can be differentiated positively by microscopic ex- amination of the pus and the lesion. The Bacterium of tuber- culosis would be found in tubercular pus and the Cladothrix actinomyces in the actinomycotic pus. Tubercular lesions are characterized by the presence of the horse shoe giant cell, the actinomycotic giant cell is irregular in outline and size, is poly- nuclear, the nuclei being scattered indiscriminately through the the cell body. Nodular disease, though not very prevalent in cattle may be mistaken for actinomycosis. The nodules of nodular disease are in the intestinal wall. The pus in the nodule is greenish yel- low in color, and though fluid in the early stages, it later be- comes caseous but never contains the calcareous granules. Microscopically the finding of the Cladothrix actinomyces in actinomycotic lesions or pus and the absence of this fungus in the lesions of nodular disease is sufficient for differentiation. From abscesses the differentiation may be made by the pecul- iarity of the pus, and the capsule, which is usually much more dense in actinomycotic lesions than in abscesses. Osteosarcomata may produce lesions in bone similar to actin- omycotic lesions. A microscopic examination is always suffi- cient for dift'erentiation of these diseases. Ovine actinomycosis may be confounded with ovine caseous lymphadenitis and nodular disease. Ovine caseous lymphaden- itis is essentially a disease of lymphoid tissue characterized by the formation of greenish yellow pus that later caseates in con- centric layers, but never contains gritty granules. The color of the pus and the arrangement of the caseated necrotic tissue is usually sufficient for differentiation of ovine caseous lymphaden- itis from actinomycosis. The remarks on the differentiation of nodular disease in bovines is equally applicable to ovines. GLANDERS. Glanders is a specific, infective disease, especially affecting equines, caused by the bacterium mallei. Glanders is prevalent in all countries with the possible ex- ception of Iceland, Australia, and some isolated islands. The disease is found in practically all parts of the United States. It is i^iFECTIVE GRAXIT.OMATA. 365 more prevalent in those portions of a country in which there is extensive horse traftic. The invasion of a province or a country by an army is usually succeeded by the appearance of glanders. Etiology. — Glanders is caused by the Bacterium mallei. This organism was described by several different investigators in 188'.^. It is similar in appearance to the Bacterium tuberculosis, has rounded ends, is from 2 to 3.5 microns in length and .3 to .5 microns in width. This bacterium occurs singly except that when grown upon potato medium, pairs or even long filaments are not rare. Like, the Bacterium tuberculosis, it produces ple- omorphic forms when cultivated in different media or under varying conditions. In old cultures it frequently becomes short and is sometime coccoid in appearance. Branching forms are not uncommon. It does not form spores. The Bacterium mallei is stained by aqueous solutions of ana- Fig. 188.— Bacterium Mallei. xlOOO. line dyes that are slightly alkaline in reaction, such as Loef- tler's meth}lene blue. It is so-called "Gram negative," i. e., it is decolorized by Gram's solution. Source of Infection. — Infection probably occurs most fre- fluently in an indirect manner, i. e., the infection is obtained from some surrounding object or thing that has been contamin- ated with the infected. discharges of a glandered animal. The Bacterium mallei is strictly parasitic and the source of the micro-organism is either the discharges from an infected animal or the carcasses of animals that have died of glanders. Fortunately this bacterium possesses little re- 366 VETERINARY PATHOLOGY. sistance to light, dessication and other external influ- ences and consequently the infection in discharges is as a rule, promptly destroyed. The length of time that the Bacterium mallei may exist outside of the animal body and retain its viru- lencv has never been absolutely determined. Authentic cases of glanders have appeared in horses that had been placed in stalls that had been vacant for one year, but prior to that time occupied by glanderous horses. A few reports are indicative of the fact that the Bacterium mallei may retain its virulence in infected buildings for two or even three years, but these re- ports need further substantiation. It seems probable from clin- ical and experimental evidence that, except in the animal body, the virulence of Bacterium mallei is rarely retained longer than one year. In cities, public drinking fountains, hitching posts and feeding troughs are probably the greatest sources of infection. The purchase of second hand harness, wagons, and other equipment should be regulated by ordinances or laws to prevent the spread of such infections as glanders. The Channels of Entrance of the Infection. — All exposed surfaces and natural openings of the body may permit the Bac- terium mallei to gain entrance to the tissues. In glanders, as in tuberculosis it has been quite conclusively demonstrated experimentally that the majority of the cases of glanders results from the ingestion of the Bacterium mallei. No doubt infection may occur by inhalation of the infectious agent, the discharges con- taining the Bacterium mallei becoming pulverized and carried by air currents, and an occasional case may be the results of cutaneous inoculation. Farcy may or may not result from cutaneous infec- tion. Such inoculations are easily accomplished by bridles, harness, saddles, currv combs, etc. More rarely the conjunc- tival membrane may be the channel of entrance. For example a horse, afifected with nasal glanders may sneeze or cough and thus infection be forcibly introduced onto the mucous mem- brane of the eye of another horse. "Lesions.— Macroscopic. — The lesions of glanders are found especially in the mucous membrane of the anterior respiratory passages, lymph nodes, lung and skin, the frequency being in the order mentioned. It is probable that the Bacterium mallei primarily affects lymphoid tissue. The gross lesions may be diffuse or circumscribed, depending upon the virulency of the infecting organisms and the resistance of the afifected animal. Dififuse fflander lesions are usually found in animals having* INFECTIVK CiRANULOMATA. 367 little resistance and in which the disease assumes an acute form. In the nasal mucous membrane, diffuse, glanderous les- ions appear as severe inflammation in which the submucosa is extensively infiltrated. The engorgement of the tissue may be sufficient to obstruct circulation and result in necrosis of the mucous membrane thus producing ulcers variable in size and ir- regular in contour. The submaxillary lymph nodes are invari- ably liard and enlarged and may or may not be adherent to the maxilla. Pulmonary, ditluse glander lesions vary in size from a hazel ntit to a basket ball and are irregular in shape. These lesions are grayish or dirty white in color. The lesions may undergo a central necrosis or they may become fibrous in nature. The necrotic material ma\- be of a semi-solid or caseous consis- tency and in the smaller foci there may be calcification. In practically all cases of pulmonarv glanders the bronchial and mediastinal lymph nodes are enlarged and contain cellular necro- tic or fibrous centers. Difi"use cutaneous lesions are not of common occurrence. Tiiey may be present in acute general glanders, the manifesta- tion in the skin being of the nature of a diffuse gangrenous der- matitis. Cutaneous nodular lesions may become diffuse as a result of rapid and extensive necrosis. Diffuse lesions occur in lymphoid tissue. Splenic lesions are usually nodular though a few cases have been reported in which there were dift'use lesions of the spleen. Osseous lesions are usually diffuse and appear as a suppi rativc osteitis. Circumscribed or nodular lesions are common in animals that have a marked resistance or in those cases infected with mildly viru- lent bacteria. In chronic glanders the lesions are usually nodular. The appearance of nodular lesions in the nasal, pharyngeal and tracheal mucous membranes as well as in the nmcous lin- ing of the facial sinus varies according to the age of the lesion. In the beginning the lymphoid tissue of the mucosa or submu- cosa becomes swollen and the tumefaction is surrounded bv a hyperemic zone. As the disease progresses there is necrosis which not only involves the lesion but also the surface tissue, thus producing an ulcer. The size depth and contour of the ulcer necessarily depend upon the extent of the necrosis. In some instances the nasal septum and facial bones max- be per- forated. Tlie ulcers \arx' in size from mere points to areas a> large as a silver dollar. The large ulcers are usuallv the result of two or more necrotic centers becoming confluent. Tb.e de- nuded surface is usualK limited or surrcninded bv a raised 368 VETERINARY PATHOLOGY. border, the latter being the result of cellular infiltration. The tissue adjacent to the denuded surface may finally produce sufificient new tissue or granulation tissue to repair the injury. If the necrosis involves only the superficial epithelium the re- pair will be complete and there will be no scar, but if the necrosis lias involved the mucosa and portions of the submucosa. ^'S- 1S9. — Nasal septa, sliowing ^landiTous ulci-rs. A A nasal st-ptum from glandered horse. 1. A crateriform ulcer having a thick raised border with a depressed granulating center. 2. Shows characteristic outline of an ulcer, also fusion of two or more primary ulcers. 3. Thumb tacks. B. A nasal septum from a second glandered horse. 1. Typical crateriform ulcers and large necrotic area the result of fusion ol se>-w;ral ulcers. 2. Cicatrices shown as irregular white spots ?. Thumb tackg. TNFECTIVF, CRAKI'LOMATA. 360 there will be large quantities of cicatricial tissue produced and cpnsequently a scar. In nodular glanders of the anterior air passages, the submaxillary lymph nodes arc invariably enlarged and contain fibrous, caseous or calcified necrotic foci. Pulmonary nodular lesions are usually dirty white in Ci.iltr and vary in size from pin point centers to masses as large as a man's head. These nodules in the beginning are entirely cellu- lar and are surrounded by an hyperemic zone. As they become larger the central portion usually becomes necrotic and the hyperemic zone becomes infiltrated with fibroblasts that pro- duce a fibrous capsule. The small nodular lesions may be small and thickK' distributed throughout the entire lung. The large Vie. 190. —Cutaneous Glanders — Farcy. 1. A IfiTge erosion or ulicr (I'arcv bud) on tlir int. rii.Tl surface of fetlock, 2 3 and 4. Other ulcvrs appearing along tbo course of the lymphatics. 370 VETERINARY PATHOLOGY. lesions are usually few in number and they may be formed l.-y two or more nodules becoming confluent. The central caseous necrotic tissue in the small foci frequently becomes calcified. Calcification is usually not evident in the large pulmonary les- ions. The bronchial and mediastinal glands are invariably in- volved and they may be caseous, calcified or indurated. Nodular lesions of the skin are found in the superficial por- tion of the dermis or in the subcutaneous tissue. The nodules in the skin rarely become larger than a pea but those of the subcutaneous tissue may become as large as a hen's egg. The central portion of the cutaneous and subcutaneous nodules and Fig. 191. — Microscopic Section through a glanderous ulcer. Margin of ulcer-necrotic tissue. Normal nasal mucous membrane. Showing depth of erosion. Small round cells. Epitheloid cells. Fibrous tissue. the superficial tissue covering them become necrotic and a sticky, tenacious, semi-fluid material is discharged onto the surface. The related lymphatic vessels are all engorged and the lymph nodes are enlarged and later becoiue indurated. The tissue destroyed in the lesions of cutaneous glanders may be partially regenerated, but are more frequently repaired by the substitution of fibrous tissue thus producing a thickened fibrous skin. Small nodular lesions have been noted in the spleen, liver and kidney. The splenic lesions may be caseous or calcified. Hepatic lesions are usually caseous. The portal lymph nodes are usually involved when lesions are present in the liver and INFECTIVE GRAXULOMATA. 371 the Ivmph nodes along the hilus of the spleen are invaded in splenic lesions. Microscopic. — The bacterium Mallei multiply in the invaded tissues and their metabolic products produce a progressive cell necrosis indicated first by karyolysis and later by a complete dis- integration of cells. Smaller lesions are the result of a diffuse proliferation of lymphoid and endotheloid cells and migration of polymorph leucocytes. The proliferated cells may accumulate in groups, thus producing- nodules. In the beginning there is usu- ally a well marked hypcremic zone around the cellular center The cells constituting the central portion of the lesit)n later un- dergo necrosis and about the same time the hyperemic zone becomes less evident. A fibrous capsule may or may not en- close the lesion, depending upon whether it is diffuse or nodular. In the nodular form of the disease there is a proliferation of fibroblasts in the tissue that was previously hyperemic. The fibroblasts produce the capsule that characterizes nodular gland- ers. In the older subsurface centers there is formed caseous material and in the small centers calcareous particles. In sur- face lesions, necrosis or fibrosis is evident. Diagnosis. — Mallcin is a filtrate obtained from a glycerinated bouillon culture of the iSacterium mallei. Alallein is of diagnostic value only. Reaction to mallein consists of a local, focal and systematic disturbance. The cause of the reaction of glandered horses to mallein is due to increased tissue action. The reaction noted in glanders after the subcutaneous injection of mallein con- sists in a thermic disturbance, a swelling at the point of inocu- lation, stififness in gait, general depression and there is usually fref|uent urination. The temperature variations in glanders range from 3° F. to i^° F. The maximum rise of temperature usuall}- occurs in from ten to twelve hours after malleination, though it may not a])i)car until the eighteenth hour after injection of the mallein. The high temperature evidenced in a mallein reaction is maintained for a period of from 24 to 60 hours. The swelling is usually quite large and is very sensitive. The lymphatic ves- sels that are related to the swollen area become engorged and present a knotted appearancee. The swelling characterizing a mallein reaction persists for several days. Stiffness of gait may be due largely to the disturbance induced by the swelling at the point of injection, but at least in some cases it is evident that the stifi'ncss of gait is not proportional to the size of the swell- ing. Aside from stififness the reacting animal has a dejected appearance. The cause of frequent urination is not known. 372 VETERINARY PATHOLOGY. The ophthalmic mallein test is now the recognized test by the United States government. The test is made by applying specially prepared mallein into the conjunctival sac. The reaction consists of an intense hyperaemia within 16-18 hours after the application of the mallein. 'Agglutination. — The bacterium mallei produces an agglutinogen which causes the animal body to produce an agglutinin. A spe- cific agglutinin is found in small quantities in the blood serum of normal horses and in larger quantities in horses with gland- ers. The agglutination test for glanders depends upon the same principle, as that upon which the typhoid agglutination depends. The agglutinin appears to cause the bacterial cell membrane to become sticky and thus the bacteria acted upon adhere to each other when they are brought into contact and clumps or clumping of the bacteria results ; this constitutes the agglutination reaction. Blood serum is obtained from the suspected animal and placed in a normal salt solution in which are suspended dead Bacteria mallei. A series of four tubes is usually used in order that different dilutions may be made. In the 1st tube the dilution is made 1 to 200, i. e. one part of serum is taken to 200 parts of salt solution in which the Bacterium mallei is suspended. In the 2nd tube, the dilution is made 1 to 500, the 3rd tube 1 to 800 and in the 4th tube, 1 to 1200. These tubes are placed in an incubator. The reaction consists in a deposit of clumped or agglutinated Bacteria mallei in the bot- tom of the tube. Normal horse serum usually contains suffi- cient agglutinin to produce a reaction in tube number one, that is in a dilution of 1 to 200. A deposition in tube number two is considered suspicious and deposits in tubes three and four is positive evidence of glanders. The reaction time is from 24 to 60 hours. The agglutination test is an accurate means of diagnosis if the test fluid is properly prepared and has been properly pre- served and if the operator uses care in making the test. The time required is much less than the time necessary in making the mallein test. Another advantage is that the blood serum of an animal dead of suspected glanders can be as readily tested as the serum from a living animal — hence it is useful in medico- legal cases. The complement fixation test has been used in the identification of glandered horses. This test is very reliable if properly con- ducted. It is a technical laboratory test in which many variable factors enter in and amateurs are likely to encounter more or less difficulty should they attempt this test. IKFFCTTVK ("R A NT LONf ATA. Z7?> EPITHELIOMA CONTAGIOSUM. Epithelioma Contagiosum is a specific infective disease of fowls and it may be transmissil)le to pigeons. The disease is widespread in the United States. It is, according to Gary the most serious drawback to the ptiultrv industry of the south. It is quite prevalent in Hawaii, and has been described in many ditfercnt localities in Europe. Etiology. — The cause of contagious epithelioma is unknown. The evidence obtainable at the present time indicates that the ciologic factor is either a protozoon, (coccidium ), or an ultra microscopic or filterable virus. Lesions. — Macroscopic. — The disease is initiated by a catarrlial inflammation of the mucous membrane of the head and neck. The disturbance may be localized in the eye, nose or mouth, or may involve all those parts. The inflammatory disturbance stim- ulates or is accompanied by a proliferation of epithelial cells in the eye, nose, mouth or even on the wattles and comb. These epithelial new growths are at first grayish, have a smooth, glis- tening api)earance and are surrounded by a h3-peraemjc zone. Later the growths, which become nodular, undergo -degenera- tion, especially upon the surface. The necrotic tissue' may re- main and form a scab or it may slough leaving a ragged, brown- Figr. in2. Left side of htad. showing ^o with cxtinsiv.- accumulation of caseous n.crotlo matL-rial. ish or grayish indurated surface. These nodules may become as large as a pigeon's t^^. They frequently entirely obstruct vision and in some cases destrov ilic eye ; those appearing in 3/4 VF.TERINARY PATHOLOGY. the nostril may seriously interfere with respiration or even obstruct the air passages ; and nodules in the buccal cavity may prevent eating or the prehension of food ; while those that occur in or upon the wattles and comb may be so extensive that these structures are practically destroyed. These nodules may entirely undergo necrosis, the necrotic tissue becoming dry and scaly or necrosis may begin in the center of the nodule and be of a liquefying character and when the entire nodule has undergone necrosis the mass is discharged as a thick, --vatery fluid containing flakes of coagulated necrotic tis- sue. Again the discharge may be thick and creamy or if. -n?' -rven be of a caseous nature. Fig. 193. Right side, showing growtlf from eye, nasal cleft, and mouth. TXFrxTivr: cranitlomata. 375 Microscopic. — Tlicse nodules are found to be composed largely of ej)ilhelial cells sujiported l)v irrei^ular bands ()f connective tissue in which there is a limited blooil supply. The majority of cells are very large. Some of these cells contain oval re- fractile bodies that have been considered as protozoa by some. These bodies are also observed between the cells. The epithelial cells, especially those in the center of the nodule, usually show more or less of a nuclear disintegration. The marginal cells in the nodules are usually more or less flattened. The cell nests FiK. 194. -.Mic rosc.ipic S' ctioii nl' K|>itlieliattae (L.Bursa. purse.) Small bur- sae or vessels. A disease of the skin characterized by necrosis. Calcified (L.Calx, lime and Fiere, to be- come.) A condition of deposition ol calcareous matter in tissues. Canalization (L.Canalis, a canal.) The process of formation of canals. Caries (L.Carles, rotten.) The molecular necrosis of bone, enamel, dentine, etc., corresponding to necrosis in soft tissue. Carcinoma (Gr.Karkinos, crab and Oma. tumor.) A malignant epithelial newgrowth. CatarrI) (Gr.Katarrheln. to flow down, i An Inflammatory condition of t mucous membrane In which there Is an excessive production of mucus. Caustic (Gr.Kaieln, to burn, i .\ sub- stance that destroys tissue. More violent than corrosive. 378 GLOSSARY. Cellulose (L.Cellula, a small cell and osis, a condition of.) The principal constituent of cell-membranes. Cenientuni (L.Caementum, a rough stone.) A plastic material capable of becoming hard and of binding together contiguous materials. Centrosome (Gr.Kentron, center and Soma, body.) A structural part of a cell in active mitotic cell-divi- sion. CeTumlnous (L.Cera, wax and osis, a condition of.) Of the nature of cer- umen. (The wax of the ear.) Chalicosis (Gr.Chalix, gravel and osis, a condition of.) A disease of the lungs caused by the inhalation of dust. Cliemotaxis (Gr.Chemia, chemistry and Tassein, to arrange.) The property of cell attraction or repulsion due to chemic substances. Chlamydo (Ger.Chemus, a cloak.) A cloak or mantle. (Used as a limit- ing prefix.) Cholelitliiasis (Gr.Chole, bile, Litlios, stone and osis, a condition of.) The condition In which there are cal- culi in the gall-bladder or ducts. Cholesteatoma (Gr.Chole, bile, Stear, fat and Oma, tumor.) A tumor composed of pearl-like masses of epithelial tissue mingled with more or less cholesterin. Choroid (Gr.Chorion, chorion and Eidos, like.) The vascular tunic of the eye continuous with iris and between the sclerotic coat and retina. Chromatin (Gr. Chroma, color.) The part of the protoplasm of a cell that takes up stains. Chromatolysis (Gr. Chroma, color and Luein, to loose.) The destruction of coloring matter. Chromosome (Gr.Chroma, color and Soma, body.) One of the minute bodies into which the chromatin of the cell is resolved in indirect cell- division (Mitosis.) Cicatricial (L. Cicatrix, a scar.) Of or pertaining to a cicatrix. Cicatrix (L. Cicatrix, scar.) The con- nective tissue that rep4aces a local loss of tissue. Circumscribed (L.Clrcum, around and Scribere to write.) Of limited or defined extent. Cirrhosis (Gr.Kirrhos, reddish-yellow.) An overgrowth of connective tissue in an organ usually the result of chronic inflammation. Cirsoid (Gr.Kirsos, a varix and Eidos. form.) Resembling a varix. (A di- lated and tortuous vessel. Clonic (Gr.Klonos, commotion.) Char- acterized by spasmodic and convuls- ive muscular contractions alternat- ing with relaxations. Clot (A.S.Clate, a burr.) A special soli- dification of the blood outside of a vessel. Coagulated (L.Coagulare, to curdle.) A condition in which there is a coag- ulum. Coagulum (Coagulare, to curdle.) A solidification of the blood occurring in a dead vessel. Coagulation (L.Coagulare, to curdle.) The proces.s of forming a coagu- lum. Coalesce (L.Coalescere, to grow to- gether.) The union of two or more parts of things. Coccidiosis (Gr.Kokkos. a berry and osis, a condition of.) The condition of being affected with Coccidia, a genus of unicellular protozoa. Collagen (Gr.Kolla, glue and Gennaein, to produce.) A substance of the body, especially of cartilage, that is converted into a gelatin by boiling. Collagenous (Gr.Kolla, glue and Gen- naein, to produce.) of the nature of Collagen. Collateral (L.Con, together and Latus side.) Of the nature of an acces- sory, not direct. Colliquation (L.Con, together and Li- quare, to melt.) The liquefaction or breaking down of a tissue or organ. Coma (Gr.Koma, a deep sleep.) A state of unconsciousness not influ- enced by external stimuli, control of vital functions still persisting. Compensatory (L.Compensare, to equal- ize.) Restoring a balance or defi- ciency of a part by ineans of some other part or organ. Complement (L.Cum, together and Pie- re, to fill.) That which supplies a deficiency. Complex (L.Cum, together and Plere, to fill.) The totality of a thing. A thing taken as a whole with consi- deration of Its make-up of parts. Component (L.Cum, together and Po- nere, to place. ) One of the parts that make up a body. Concentric (L. Cum, together and Cen- trum, center.) Arranged in an equidistant manner about a common point. Congenital (L.Cum, together and Gr. Gennaein, to produce.) Existing or occurring at birth. GLOSSARY. 379 fonirestion (L.Con. together and Ce- rere, to bring.) An abnormal col- lection and retention of blood in the vessels of a part. Coniflonierate (L.Cum, together and Glonnrare, to heap up.» Arranged in a mass together Indiscriminati'ly. Conidia (Gr.Konis, dust and diminutive term.) The deciduous, axial spores of certain fungi. ConjuKation (L.Cum, together and Ju- gare, to yoke.) A condition of being .|oin. Con, together and Rela- tlo, relation.) Related to. Corrosive (L.Con, together and Rodere, to gnaw.) A sub.stance that destroys tissue (less violent than a caustic.) Cortical (L.Cortex, bark.) Of or per- taining to the cortex, the surface layer. Cotyledons (Gr.Kotuledon, a socket) An enlarged vascular organ of the chorion. Croupous (A.S.Kropan, to cry aloud.) Of the nature of croup. Character- ized by a development of a mem- branous deposit or exudate on the surface of a mucous membrane. CutaneouH (L. Cutis, skin.) Pertaining lo the skin. Cycle (Gr.Kuklos, a circle.) A round of years. A period of time. Cystadenonia (Gr.Kustis, bladder, Aden, gland and Oma, tumor.) An aden- oma containing cysts. Cystic (Gr.Kustis, a bladdar. ) Pertain- ing to or resembling a cyst. Cytoplasm (Gr.Kutos, cell and Plessein, to mold.) The essential, viscid sub- stance of a living cell. — proto- plasm. Cytosis (Gr.Kutos, cell and osl.-i, a con- dition of.) Cell proliferation. Death (A..«?.Death. i The total cessation of life. Debris (L.Dis. apart and Briser, to break.) The material resulting from the destruction of anything. Deoul>Hal (L. Decubitus, a lying down.) Tile position of lying down. Degeneration (L.De, away from and Gerere, to be'jome. ) A morbid con- version of the elements of a tissue into new substance. Deleterius (L.Delere, to destroy.) Char- acterized by a hurtful or destruc- tive tendency. Denticle (L.Dens, tooth and diminutive term.) A small tooth or projecting point. Depleted (L.De, from and Plere, to fill.) Condition of diminished amount or lluid In a body or part. Dennatologio (Gr.Derma, skin and Lo- gos, study.) Pertaining to derma- tology. The study of the skin. Dessicant (L.Dessicare, to dry up.) A .substance that has the property of drying up other substances. Dessicated (L.Dessicare, to dry up.) A condition of being dried up. Detritus (L.De, away from and Terere, to rub.) Finely divided material worn off from substances by rubbing. Diabrosis (Gr.Dia, through and Blbros- kein, to eat.) A condition of having been broken through corrosive ac- tion. Diupedesis (Gr.Dia. through and Pedae- In, to leap.) The passage of blood through an unruptured vessel-wall. Dlaster (Gr.Dis, two and Aster, star.) The so-called double star or wreath In the mitoic cell division. Diastole (Gr.Dia, through and Stole, a drawing.) The period of dilatation of the chamber of the heart. DichotomoHs (Gr.Dicha, asunder and Temnein. to cut.) Regularly divid- ing into pairs from bottom to top. IHfTuse (L.Dis, apart and Fundere, to pour.) Not limited in extent. Digestion (L.Dis, apart and Gerere to carry.) The preparation of food- stuffs for absorption and assimila- tion. Diphtheritic (Gr.DiphtherIa, skin or membrane.) Pertaining to dlpthe- rla, or characterized by formation of false membrane In and upon a mucous membrane. Disintegrated (L.Dis. apart and Integer. a whole.) Broken up or decomposed. DissimUation (L.Dis, apart and Slmu- 380 GLOSSARY. lare, to make like.) To cause to appear different. Dissociated (L. Dis, apart and Sociare, to associate.) A condition of being- se- parated or broken up. Dropsy (Gr.Hudrops, dropsy.) The col- lection and retention of a non-in- flammatory lymph transudate with- in a tissue or body-cavity. Ebumated (L.Ebur. ivory.) An increased density of bone, similar to ivory. Ecchymosis (Gr.Ek, out and Chumoma, a flowing out.) An extravasation of blood into the subcutaneous tissues. Ectropia (Gr.Ek, out and Trepein, to turn.) Eversion or turning out of the edga of a part, especially of the eyelid. Effervescence (L.Effervescere, to boil up.) Giving off bubbles of gas. Effusion (L.Effundere. to pour out.) The escape of a liquid exudate into a tissue or part, especially of serum or blood. Elimination (L.Ex, out and Limen, threshold.) The expulsion of any- thing from the body, especially of waste products. Emaciation (L.Emaciare, to become lean.) A condition resulting from a general wasting away of all tis- sues of the body. Embolus (Gr.En, in and Ballein, to throw.) An obstruction in a vessel by matter from another point. Embryonal (Gr.En, In and Bruein, to grow.) Pertaining to an embyro. The foetus in the early stages of its de- velopment. Emphysema (Gr.Emphusaein, to inflate.) A condition in which there is an accumulation of gas in the inter- stices of the connective tissue. Empyema (Gr.En, in and Puon, pus.) Pus in a body cavity. Enceplialoid (Gr.Egkephalos, brain.) Of the nature of brain tissue. Endemic (Gr.En, in and Demos, people.) A disease found in a certain place more or less constantly. Endomysium (Gr. Endon, within and Mus, muscle.) The connective tissue structure separating muscle-fibre bundles. Endotlielioma (Gr.Endo, within and Thele nipple and Oma, tumor.) A tumor composed of endothelial cells. Endothelium (Gr.Endo, within and The- le, nipple.) Cells covering the inner surface of vessels not communicat- ing with the outer air. Endotoxin (Gr.Endon, within and Toxi- kon, poison.) A poisonous substance found within the cell body of a bacterium. Enterolith (Gr. Enteron, bowel and Lith- os, stone.) A concretion found in the intestines: An intestinal calcu- lus. Enterorrhagia (Gr. Enteron, bowel and Hregnunai, to burst forth.) He- morrhage into the intestines. Enucleated (L.Ex, out of xnd Nucleus, kernel.) Removed in such a way that the body comes out clean and whole from its capsule (as of a tu- mor.) Enzootic (Gr.En, in and Zoon, animal.) Pertaining to a disease of lower animals and found in a certain place more or less constantly. Enzym (Gr.En in and Zume, leaven.) A ferment formed within the body. Enzymotic (Gr.En, in and Zume, leaven.) Pertaining to leaven, (Enzym.) Eosinopliile (Gr.Eos, dawn and Philee- in to love.) Showing a peculiar af- finity for eosin or acid stains in general. Ependymal (Gr.Epi, upon and Enduma, a garment.) Pertaining to the Epen- dyma. The lining membrane of the cerebral ventricles and of the cen- tral canal. Ephemeral (Gr.Epi, upon and Hemera, day.) Lasting but a day; tempo- rary. Epidermal (Gr.Epi, upon and Derma, skin.) Pertaining to the epidermis, the outer layer of the skin. Epilepsy (Gr.Epi, upon and Lepsls, sei- zure.) Paroxysmal loss of con- sciousness with convulsions lasting but a short time. Epistaxis (Gr.Epi, upon and Stazein, to cause to drop.) Hemorrhage from the nose. Epltlieliuni (Gr.Epi, upon and Thele, nip- ple.) Cells forming the epidermis and lining vessels that communicate with the external air. Etiology CGr.Aitios, cause and Logos, study.) The study of the causes of disease. Evolutionary (L.Ex. out of Volvere, to roll.) Pertaining to evolution: The process of development from simple to complex form. Exantliematous (Gr.Ex, out of and Ant- hema, a breaking forth and ous, pertaining to.) Of the character of Exanthema: An eruption of the skin. Exciting (L.Ex, out and Citare, to stir.) Calling forth directly. Excrement (L.Ex, out and Cernere, to separate.) Matter cast out aa waste from the body (especially the feces.) Excretion (L.Ex, out and Cernere, t6 Glossary. 381 separate.) The discharge by the tis- sues of waste products. Exfoliate (L.Ex from and Foliare. to give forth leaves.) To separate In- to thin layers. Kxfoliution (L.Ex, from and Foliare to give forth leaves.) The process of separating into thin layers Exophthalmic (Gr. Ex, out and Oph- thalmos eye.) Pertaining to abnor- mal extrusion of the eye-ball. Extirpation (L.Ex. out and Stlrps stem.) Complete removal or eradi- cation of a part. Extravasation (L.Extra, outside, and Vas, vessel.) The escape of fluid from its containing cavity or ves- sel (Especially applied to tha blood.) Extra-uterine (L.Extra. outside of and Uterus, uterus.) Outside of the ute- rus. Extrinsic (Extra, without and Secus, otherwise.) Coming from the out- side: Not directly belonging to a part. Exudate (Ex, out and Sudare, to sweat.) A portion of the blood that has passed into a tissue from its vessels because of Inflammatory disturbances. Exudation (L.Ex, out and Sudare, to sweat.) The production of an exu- date. Faceted (Fr.Facette, a little face.) Provided with many small plane surfaces. Facultative (L.Facultas capability.) Capable of assuming a part or con- dition (spoken of bacteria.) Fever (L.Fibres. ) An abnormally high temperature. Fibrinopurulent (L.Fibra, fibre and Pus. pus.) Composed of fibrin and pus. Fibrinous (L.Fibra, fiber.) Of the na- ture of or consisting of fibrin. Fibrojflia (L.Fibra, thread and Gila, glue.) The glue-lilie fibres of some tumors. [Filamentous (L.Filum, a thread and ous of the nature of.) Like a small thread in structure. Filaria (L.Filum, a thread.) A genus of nematode worms, thread-like, endo- parasitlc. Filum terminale (L.Filum, a thread and Terminale, terminal.) The long, slender, thread-like termination of the spinal cord. Flagrella (L.Flagella, a whip.) .a motile whip-like process (usually applied to some bacteria.) Foci (L. Focus, a fire-place.) The prin- cipal seats of a disease. Foetus (L.Foetus, offspring.) Unborn off-spring of viviparous animals in later developmental stage. roilicle (L.FoIUs, a bellows and diminu- tive term.) A small sac or gland. Fractous (L.Frangere, to break.) Apt to become dlfilcult to control. Fracture (L.Frangere. to break.) A break in the continuity of osseous tissue (bone.) Function (L. Fungi, to perform.) The normal action or work of a part. I'uNiform (L.Fusus, a spindle and For- ma, form.) Like a spindle in form. Galaotophcrous (Gr.Gala, milk and Fer- ein, to bear.) Producing milk. Gangrene (Gr.Gangraina, a sore.) That type of necrosis characterized by putrefaction of the necrotic tissue. Gemmation (L. Gemma, bud.) The act of budding or reproduction by bud- ' ding. Gestation (L.Gestare, to bear.) The period from fertilization of the ovum to its expulsion from the uterus. Glia cells (L.Glia, glue.) Neuroglia or the supporting-stnicturft cells of nerve-ti.«sue. Glioma (Gr.Glia, glue and Oma, tumor.) A tumor composed of neuroglia cells. Gljcogen (Gr.Glukos, sweet and Gen- naein to produce.) A substance formed from carbohydrates In the body and stored up in certain structures: often called animal starch. (iranulation (L.Granula. a little grain.) The formation of new tissue in the repair of local los.s of tissue and composed of capillary vessels en- closed by groups of connective tis- sue cells. Ilaptophore (Gr.Haptein, to seize and Phorein, to carr>'.) The stable, nonpoisonou: elem?nt (of a toxin which enables it to unite with a antitoxin (Ehrllch's lateral side- chain theory.) Ilelmintli.4 (Gr.Helmlns, a worm.) A braiK h of Invertebrates known as worms. Ilematemesis (Gr.Halma, blood and Kmesis. vomiting.) The vomiting of blood. Gastric hemorrhage. Ileniatidrosis (Gr.Halma. blood and Hl- drosis, sweating.) The sweating of blood or of a blood-like substance. Ilematin (Gr.Halma, blood.) A product of decomposition of Hemoglobin. Hematocele (Gr.Halma, blood and Kele, tumor.) The extravasation of blood into a cavity, especially the tunica vaginalis testis. lleniatorenotu (Gr.Halma, blood and 382 GLOSSARY, Gennaein, to produce.) Derived from or having origin in the blood. Hematoidin (Gr.Haima, blood and Ei- dos, resemblance.) A yellowish- brown, iron-free substance obtained from hemoglobin of the blood. Hematoma (Gr.Haima blood and Oma, tumor.) A circumscribed collection of extravasated blood. Ilematometra (Gr.Haima, blood and Metra, uterus.) An accumulation of blood in the uterine cavity, ex- travasated from the mucosa. Hematuria (Gr.Haima, blood and Du- ron, urine.) Urine containing whole blood. A condition of bloody urine. Hemochromogen (Gr.Haima, blood. Chroma, color and Gennaein, to pro- duce.) A crystalline coloring mat- ter derived from the hemoglobin of the blood. Hemocoelia (Gr.Haima, blood and Kol- lia, belly.) An accumulation of blood within the peritoneal cavity. Hemogenous (Gr.Haima, blood and Gen- naein.) Derived from the blood or having origin in the blood. Hemoglobin (Gr.Haima. blood and L. Globus, globe.) The coloring matter of the red blood corpuscles. Hemoglobinuria (Gr.Haima, blood. L.- Globus, a globe and Gr.Ouron, urine.) A discharge of urine con- tainitig hemoglobin, A condition of hemoglobin in the urine. Hemolysis (Gr.Haima, blood and Luein, to loose.) Destruction of the blood or of its corpuscles. Hemoptysis (Gr.Haima, blood and Ptu- ein. to spit.) Spitting blood from the respiratory passages — pulmonary hemorrhage. Hemorrhage (Gr.Haima. blood and Hragnuni. to burst forth). The es- cape of blood through a vessel wall. Hemosiderin (Gr.Haima, blood and Sl- deros. iron.) A golden-yellow pig- ment containing iron and derived from the hemoglobin of the blood. Hemothorax (Gr.Haima. blood and Thorax, thorax.) An accumulation of blood in the thoracic cavity. Hepatogenous (Gr.Hepa, liver and Gen- naein. to produce.) Produced by or in the liver. Hermaphrodite (Hermes and Aphrodite. Greek deities.) An individual that possesses more or less completely both male and female genital or- gans. Hernia (Gr.Hernos. a sprout.) The pro- trusion of an organ through an ab- normal opening in the wall of its containing cavity. Heterogeneous (Gr.Heteros, other and Genos, kind.) Composed of different substances. Humor (L. Humor, moisture.) A fluid or semi-fluid part of the body. Hyalin (Gr.Hualos, glass.) A translu- cent substance. The chief nitrogen constitute of hydatid cysts. Hyaloplasm (Gr.Hualos, glass and Plas- sein, to mold.) The fluid portion of the cell-protoplasm. Hydrargyrosis (Gr.Hudor, water and Arguros, silver (Mercury.) A de- posit of mercury in the tissues. Hydremia (Gr.Hudor. water and Hal- ma, blood.) A condition in which the fluid of the blood is in excess of the normal proportion of cells. Hydrocele (Gr.Hudor. water and Kele, tumor.) A collection of oedematous fluid within the tunica vaginalis. Hydrocephalus (Gr.Hudor, water and Kephale, head.) A collection of oedematous fluid in the serous cav- ities of the brain or its menin.ees. 'Hydropeiricardium (Gr.Hudor, water, Peri, around and Kardia, heart.) A collection of oedematous fluid in the pericardial sac. Hydropic (Gr. Hudrops, dropsy.) Per- taining to or affected with dropsy. Hydrops (Gr.Hudrops, dropsy.) Dropsy. An abnormal collection and reten- tion of serum in the cellular tissue or in a body cavity. Hydrothorax (Gr.Hudor, water and Tho- rax, thorax.) Abnormal accumula- tion of an oedematous fluid in the pleural cavity. Hyperchromatosis (Gr.Huper, above. Chroma, color and osis, a condition of.) A condition of excessive depo- sition of pigment in the tissues. Hyperemia (Gr.Huper, above and Hai- ma, blood.) An increase in the blood supply to a part. Hypernephroma (Gr.Huper, above, Ne- phros, kidney and Oma, tumor.) A tumor composed of tissue similar to adrenal tissue. Hyperplasia (Gr.Huper, above and Plas- is. formation.) An increase in the number of cells in a part. Hyperplastic (Gr.Huper, above and Plasis, formation.) Pertaining to hyperplasia. Hypersensitive (Gr.Huper, above and L.Sensue, feeling.) A condition of increased or abnormal tendency to reaction to a stimulus. Hypertrophy (Gr.Huper, above and Tro- phe, nourishment.) An excessive GLOSSARY. 383 increase In the size of the cells of a tissue. Ilypliae (Gr Hupha, a web.) The fila- ments composing the mycelium of a fungus. Hjphoniycetes (Gr. Hupha. a web and Mukes, a fungus.) A group of fungi including the molds. Some are pathogenic. Il.vpophisia (Gr.Hupo, under and Plas- is. formation.) Defective or Incom- pUte development of a tissue. Hypothesis (Gr.Hupo, under and Tithe- nai, to put.) A proposition taken for granted in order lo draw a con- clusion to aid in explanation of certain facts. Ichorous (Gr.Ichor, serum or pus.) Of the nature of ichor: An acrid, thin, purlform discharge. lohth.vosis (Gr.Ichthus, a fish and osis. a condition of. » A condition like the scales of a fish. Icterus (Gr.Ikteros, yellow.) Jaundice, a yellow pigmentation of the tis- sues with the coloring matter of the bile. fmmunity (L.In, not and Munis, serv- ing.) A condition of exemption from a disease. Inipartetl (L.In., in and Pingere, to drive.) Driven firmly in or dis- lodged with difUculty. Inanition (L.Inanis, empty.) A wasting of the body from lack of food or from inability to assimilate It. Inbreeding: (A.S. In. and Brodan, to nourish.) The production of off- spring by closely related parents. Incorporated (L.In, and Corpus, body.) Thoroughly united with a body In a compact mass. Indurated (L.In, and Durus, hard.) Rendered hard. Inert (L.In, not and Ars, art.) Without action. Infarct (L.In, in and Farcire, to stuff.) A wedge-shaped area (hemorrhagic or anemic) in an organ produced by obstruction of a terminal vessel. Infection (L.In, in and Facere, to make.) The invasion of the body by pathogenic micro-parasites and the sum-total of the disturbances produced by their presence therein. Infectious (L. In, into and Facere, to make.) Capable of communicating a disease. Inflammation (L.In, and Flamma, flame.) The reaction of a living: animal tissue to an irritant accom- panied by circulatory disturbances and by destructive or prollf' ratlvi- tissue changes. Ingested (L.In, in and Gerere, to bring.) Taken Into the stomach or alimen- tary tract. Inherited (L.In. Into and Haerere, to ■have.) Born to or belonging to by birth. Inliibitin? (L.In, In and Habere, to hold.) Holding In check or hinder- ing from doing a thing. Inimical (L.In, not and Amicus, friend.) Having a hostile tendency. Liable to injure. Inoculating: (L.In, into and Oculus, a bud.) The introduction of a virus of a disease into a wound or abra- sion of the skin. Inosculation (L.In, into, and Os, mouth.) The joining of blood vessels by di- rect communication. Insidious' (L.Insidioe, ambush.) Coming on stealthily or imperceptlblv. Inspissated (L.In, intensive term and Spissare, to thicken.) Thickens by removal of fluid. Insusceptibility (L.In, not and Suscl- pere, to receive. ) Not having a liability to acquire a disease. Inten'ellular (L. Inter, between and Cel- la, cell, t Existing between the cells of a tissue. Interfunicular (L.Inter. between and Funiiulus, cord.) Existing between the bundles of tissue. Intermittent (L.Inter, between and .Mittere, to send.) Characterized by intervals between. Interstice (L.Inter, between and Stare, to stand.) Spaces between or to stand between. Interstitial (L.Inter. between and Sls- tere, to place.) Pertaining to struc- tures between the cells of a part. I Stroma. ) Intracellular (L.Intra. within and Cella. cell.) Existing within the cells of a tissue. Intrinsic (L.Intra, within and Secus, otherwise.) Situated entirely with- in or pertaining exclusively to a part. Intussusception (L.Intus. within and Suscipere. to receive.) A slipping of one part of an organ (usually intestine) Into the parts beyond. Invagination (L.In. within an.Moriri, to die.) In a dying londltion. MorphoIos:y (Gr.Morphe, form and Lo- gos, study.) The study of the form and structure of organized beings. .Mucus (L.Mucus.) The viscid fluid se- creted by special glands of mucous membranes. .Multiparuus (L.Multus, many and Pare- re, to produce.) Bringing forth more than one offspring at a birth. Mycelial (Gr.Mukes, a fungus and He- los, an overgrowth.) Pertaining to a mycelium. Mycelium (Gr.Mukes, a fungus and He- los. an overgrowth.) The vegetative filaments of a fungus. Mycosis (Gr. Mukes, fungus and osIs, a condition of.) A growth of fungus in the tissue. .Myeloid tCr.Muelos, marrow and Eldos, like. ) Itesemliling marrow. Myoblast (Gr. Mus, muscle and Blastos, germ.) A cell developing into a muscle fibre. -M.voma (Gr.Mus, muscle and Oma, tu- mor. ) A tumor composed of muscle tissue. Myositis (Gr.Mus, muscle and Itis, In- flammalion.) Inflammation of mus- cle tissue. My.xodema (Gr.Muxos, mucus and Olde- ma, oedema.) A condition In which tissues, especially the hands and face, are Inflltrated with a mucus- like substance. Myxoma (Gr. Muxos, mucus and Oma, tumor.) A connective-tissue tumor made up of mucin-contalning Inter- cellular substance. Nascent ( L.Nanclscor, to arise.) Just coming into existence. Just liberated from a chemical compound. Necrobiosis (Gr.Nekros, a corpse and Bios, life.) Gradual and progressive death of a cell or of a group of cells. Necrosis (Gr.Nekros, a corpse.) Death of a tissue suddenly, in mass while surrounded by living ti.ssue. Neofomiation (Gr.Neos, new and L. For- ma, form.) A circumscribed new growth of tissue of abnormal struc- ture and location and functlonless. Tumor. Neoplasm (Gr.Neos, new and Plasseln, 386 GLOSSARY. to mold.) A neoformation, a tu- mor. Neurilemma (Gr.Neuron, nerve and Lemma, a husk.) The covering- sheath of a nerve-fibre. Neuroglia (Gr.Neuron, nerve and Glia, glue.) The tissue forming the basis of the supporting framework of the central nervous tissue. Neuroma (Gr.Neuron, nerve and Oma, tumor.) A tumor composed of nerve tissue. Neuter (L.Neuter, neither.) Neither the one nor the other. Inactive. Neither acid nor alkaline. Neutrophlle (L.Neuter, neither and Gr. Phileein, to love. ) A cell or struc- ture stainable by neutral dyes. Nevus (L. Nevus, a mole.) A mole. A congenital angioma of the skin. Birthmark. Nidus (L.Nidus, a nest.) The original point of a morbid process or focus Of infection. Noxious (L. Noxious, harmful.) Having harmful properties. Nucleolus (L.Nucleus, a small nut and diminutive term.) A small body within the nucleus of a cell. Nuoleoplasni (L.Nucleus, a small nut and Gr.Plassein, to mold.) The pro- toplasm of a nucleus. Nucleus (L.Nucleus, a small nut.) The essential part of a living cell. Obligatory (L.Obligare, to bind.) Bound by conditions. Not facultative. Odontoma (Gr.Odons, tooth and Oma, tumor.) A tumor of tooth-like structure. Oedemia (Gr.Oidema, a swelling.) The accumulation and retention of lymph in lymph vessels and spaces. Dropsy. Oogenesis (Gr. Oon, egg and Gennaein, to produce. ) The origin and de- velopment of the egg. Ophthalmia (Gr.Ophthalmos, the eye.) Inflammation of the structures of the eye. Opsonin (Gr.Opsono, a dainty food.) A product of the body-cells that pre- pares bacteria for phagocytosis. Optimum (L.Optimus, best.) A condi- tion characterized by the most fa- vorable conditions. Organized (Gr.Organon, organ.) Con- verted into an organ or organ-like structure. Oscillation (L.Oscillare, to vibrate.) A regular motion back and forili within narrow limits. Osmotic (Gr.Osmos, impulse.) Pertain- ing to osmosis. The passage of li- quids and substances in solution through a membrane. Ossification (L.Ossa, bone and Facere, to make.) The formation of bone. Osteitis (Gr.Osteon, bone and Itis, in- flammation.) Inflammation of bone. Osteoblast (Gr.Osteon, bone and Blas- tos, germ.) A cell of mesoblastic origin concerned in the formation of bone. Osteoclast (Gr.Osteon, bone and Klaein, to break. ) A large multinuclear cell concerned In the removal of bone. Osteophyte (Gr.Osteon, bone and Phu- ton, plant.) A bony outgrowth, tree-like in character. Otologic (Gr.Ous, ear and Logos, study.) Pertaining to Otology: The study of tlie ear. O-x.vphile (Gr. Oxus, sharp and Phileein, to love.) Stainable with acid dyes. I'alpated (L.Palpare, to feel of.) Ex- amined with the hand to determine conditions beneath. Paracentesis (Gr.Para, near and Kente- sis, puncture.) Surgical puncture of the walls of a cavity. Paralysis (Gr.Para, near and Luein, to loose.) Loss of sensation or motion in a part. Parasite (Gr.Para, near and Sitos, food.) An organism that gains protection or sustenance or both at the ix- pense of another organism. Parencluvnia (Gr.Para, near. En, in an Causing or pro- ducing: light. Ph.vsiology (Gr.Piiusis, nature and Lo- gos, .«tudy.) The study of the func- tions of the organs of the living body. Phytoiiarasite (Gr.Phutos, plant. Para, near and Sitos, food.) A parasite vegetable organism. I'ljfmented (I--.Pingere, to paint.) A con- dition to deposition of coloring matter in the tissues. Placental (Gr.PlaliOus, a cake.) Per- taining to the placenta. The organ of the uterine •wall to which the foetus is attached and from which it obtains its nourishment. Placentoma (Gr.Plakous, a cake and Oma, a tumor, i A tumor composed of placental tissue. Pleomorphism (.Gr. Pleon. more and Orphe, form.) The state of having more llian one form. Plexiform (L.Ple.xus, braid and Porma. form.) Having the appearance or structure similar to a Plexus. (.\ network of vessels. ) * riumbosis (L. Plumbum, lead and osis, a condition of.) A condition of poi- soning by or deposition of lead In the tissues. PneumonokonioRin (Gr.Pneumon, lung and Knnia, dust, osis a condition of.) .V I'Dnilition of chronic indura- tion In the lung tissues due to the deposition of inhaled dust. Post-natal (L.Post, after and Nanslsci. to be born.) Occurring after birth. Polar (Gr. Polos, pole.) Pertaining to a pole. (Either extremity of an axis.) Poljdactyllsni (Gr. Polus, many and Oektulos, finger.) The condition of having many digits. Polygonal (Gr.Polus, many and Gonos, angle.) Having many angles or sides. (Spoken of a surface.) Pol.t hedral (Gr.Polus, many and Hedra, side.) Having many sides or sur- faces. (Spoken of a solid.) Polymeric (Gr.Polus. many and Meros. part.) .Pertaining to the existence of a large number of parts. Pol.vmorphonuclear (Gr.Polus. many. Morjihe. form and L. Nucleus, nuc- leus.) Having nuclei of many forms. Potential (UPotens. powerful.) Cap- able of doing work or of acting. Predisposition (L.Prae, before, Dis apart and Ponere, to place.) The condition of liability to acquire a disease. Primitive (L. Primus, first.) First in point of time: Original. Progreny (Gr.Pro, before and Gennaein, to produce.) Offspring or descend- ents. Progressive (L.Pro, before and Gredi. to step.) Gradually advancing or moving forward. Prolapse (L.Pro, forward and I^ahi, to slip. I The falling downward or for- ward of a part. I'roliferate (L.Pro. forwanl and Fere, to bear.) To form new tissue of the same kind (usually excessive.) Proline (L.Pro, forward and Labi, to slip.) The quality of being able to proliferate. Prophase (Gr. I'm. before and Phasis. Iihase.) The first stage in indirect cell division. (Mitosis.) Proteoses (Gr.Protos. first.) Substances formed in gastric digestion and into intermediate between a proteld and a peptone. Protoplasm (Gr. Trotos, first and Plasse- in. to mold.) The viscid, es.-ential substance of a living cell. Protot.vpe (Gr. protos, first and Tupos. type.) An original type, one after which others are copied. Protozoa (Gr.Protos. first and Zoon, ani- mal.) A class of unicellular, animal microorganisms. Pseudo (L.Pseudo, false.) False. 388 GLOSSARY. Psorospemiic (Gr.Psora, itch and Sper- ma, seed.) Of the nature of or like a Psorosperum. A protozoon. A coccidium. rtomain CGr.Ptoma, a corpse.) A pro- duct formed in the decomposition of dead animals tissues. Purulent (L.Pus, pus.) Of the nature or associated with pus. upon a sur- face. Pus (L.Pus, pus.) Liquefied, necrotic tis- sue composed of altered leucocytes, tissue shreds and usually micropar- asites, suspended in a fluid (liquor puris. ) Pustule (L.Pus, and diminutive term,) A vesicle containing pus. Pyogenic (Gr.Puon, pus and Gennaein, to produce.) Capable of producing pus. Pyorrhoea (Gr.Puon, pus and Hroia, a flow.) A persistent discharge of pus upon a surface. Pyrexia (Gr.Pur. fi. i and Hexis, a ha- bit.) An abnormal elevation of a temperature. (Fever.) Radicular (L. Radix, root and diininu- tive term.) Pertaining to or like a radicle or root. Ranula (L.Rana, frog and diminutive term.) A cystic tumor in the mouth (especially on the tongue) due to the obstruction of a gland-duct. Receptors (L.Recipere, to receive.) The "Side-chains" of a body cell (Ehr- licla's side-chain theory.) Regeneration (L.Re, again and Genar- are, to beget.) The process by which destroyed tissues are re- placed. Remittent (L.Re, back and Mittere, to send.) Characterized by abatement or subsidence or repetition. Resorbed (L.Re, again and Sorbere, to absorb.) Taken up again into the system. Spoken of a substance that has passed out and accumulated in the tissues. Reticular (L.Reticulum, a little net, Rfte). Resembling a net. Formed by a net-work. Retrogressive (L. Retro, backward and Gradus, step.) Of the nature of re- trogression. A going backward from a pre-existing condition. Rhabdomyoma (Gr.Rhabdos, a rod, llus, muscle and Oma, tumor.) A form of muscle-tumor (Myoma), characterized by the presence of striated muscle fibres. Rhe.xis (Gr.Rhexis, rupture.) The rup- ture of an organ or vessel. Rythm (Gr.Hruthmos, rythm.) The re- currence of a motion or sound at regular intervals. Rupture (L.Rumpere, to break.) A con- dition of being broken apart by vin- lence. Sacculate (L.Saccus, a sac and diminu five term.) To form small sacs. Sanies (L.Sanies. ) A thin, fetid, sero- purulent fluid discharge from an ul- cer, fistula, etc. .Sanious (L.Sanies.) Pertaining to or of tlie nature of Sanies. Sapremia (Gr.Sapros, rotten and Haima, blood.) The entrance into the blood of the products of putrefactive mi- croorganisms. Saprogenic (Gr.Sapros, putrid and Gen- naein, to produce.) Causing or pro- ducing putrefaction. Saprophytic (Gr.Sapros, rotten and Phu- tos, plant.) Pertaining to Sapro- phytes: (Vegetable organisms .iving on decaying organic matter.) Sarcolemma (Gr.Sarx, flesh and Lemma, a sheath.) The delicate sheath en- veloping a muscle fibre. Sarcoma (Gr.Sarx, flesh and Oma, tu- mor.) A tumor made up of embryo- nal connective tissue cells. Schistosis (Gr. Schistos. a cleft and osis, a condition of.) A condition of being split or cleft. Scirrhous (Gr.Skirrhos, hard.) Of the nature of a Scirrhus. (A hard tu- mor: A Carcinoma.) Sclera (Gr.Skleros, hard.) The firm outer coat of the eye-ball continuous with the cornea and optic nerve. Secretion (L.Secernere, to secrete.) The process of separating out a substance from the blood. Segmentation-cells (L.Segmentum from Secare, to cut.) One of the cells of an ovum formed by dividing into two equal parts. Senile (L.Senex, old.) Pertaining to old age. Sequel (L.Sequi, to follow.) A follow- ing upon or a resultant of. Sequestration (L.Sequestrare, to separ- ate.) The formation of a sequestrum. Sequestrum (L.Sequestrare, to separate.) A piece of dead bone that has be- come separated from the sound bone during necrosis. Siderosis (Gr.Sideros, iron and osis, a condition of.) A condition of pig- mentation by the deposit, especially in the lungs, of particles of iron. Siluroid (Gr.Siluros, a species of fish.) Pertaining to Siluroidei, an order of fishes. SimultaneouB (L.Simul. at the same GLOSSARY, 389 time.) Existing or happening at the same time. Sinusoid (Li. Sinus, a cavity and old, ot the nature of.) Like a sinus: (A hollow or cavity or tract.) Slough (M.E.Plouh, th.- skin of a snake.) A mass of soft tissue destroyed tjy necrosis. SloughinK (M.EPlouh. skin of a snake.) The process of becoming a slough. Soliped (L. Solus, alone and Pes. foot.) An animal with a single hoof or digit. Bomatlc (Gr.Soma, body.) Pertaining to the body, (-specially to the frame- work as distinguished from the vis- cera. SpeclHc (L.Species. species.) Of or per- taining to a species. Produced by a particular kind of organism. Specifltity ( 1.. Species, species and Face- re. to make.) The quality of being specific. gperniatugenesis (Gr.Sperma, semen and Gennaein, to produce.) The develop- ment of Spermatozooa. Spha4>elu8 (Gr.sphakelos, dead.) A mass of soft tissue destroyed by necro- sis. Splrem (L.Spira, a coil.) The close or mother-skein of chromatin fibrils In indirect cell division. (Mitosis.) Spongioplasni (Gr.Spoggos, a sponge and Plassein, to mold.) The fine proto- plasmic threads forming the reti- culum of a cell. Spontaneous (L.Spons. will.) Occuring witliout external Influence. Spore (Gr.Sporos. seed.) A reproductive, resting element of lower organisms. Sporulation (Gr.Sporos, seed and L.Fer- re, to mkke.) The production of spores. Stalactite (Gr.Stalazein, to drop.) A pendant cone of calcium salts like an icicle. Stasis (L. Stare to stand.) A standing still or stoppage of motion, espe- cially of blood, in a part. Stenosis (Gr.Stenos, narrow.) A narrow- ing of the lumen of a vessel. Sterile (L.Sterilis, barren.) Incapable of reproducing. Sthenic (Gr.Sthenos, strength.) Char- acterized by strength or severity. Strata (L, stratum, stratum ) A series of layers. Stroma (Gr.Stroma, a bed) The tissue forming the ground substance or framework for the essential part of an organ. Interstitial tissue. SuKKillation (L.Suggillare, to beat black and blue.) An extensive, capiUary, tissue- hemorrhage. Suppuration (L.Sub, under and Pus, pus. > The formation of pus. (Sur- face or subsurface.) Susceptible (L.Sub, under and Cipere, to take. J Having a liability to ac- quire a disease. Swelling ( A..s.Swellan, to grow larger.) An elevation or elevated area (spe- cially abnormal. J S.vmptom (Gr.Sun, together and Ptoma, a falling.) Sequential functional disturbances due to disease. S.vncytiuni (Gr.Sun. together and Kutos, Cell.) A fusion of several cells into a single cell. Syncope (Gr.Sun, together and Kop- teln, tg strike.) A partial or com- plete, temporary suspension of heart action. Synthesis (Gr.Sun, together and Tlthe- nal, to put.) The formation of a compound by putting together it« constituents. Systole (Gr.Sun. together and Stellein, to place.) The period of the heart's contraction especially of the ven- tricles. — Opposed to Diastole. Telophase (Gr.Telos, end and Phasis, phase.) The fourth and last stage In Indirect coll division. (Mitosis.) Telangiectatic (Gr.Telos, end Aggelon, a vessel and Ektasis. a dilatation.) Of or pertaining to Telangiectasis. (\ permanent dilatation of groups of capillaries aid arterioles. Tenable (L.Tenere, to hold.) Able to be held or supported. Teratoma (Gr.Teras. monster and Oma. tumor.) A tumor composed of tis- sues derived from all three germ- fay ers. Tetinic (Gr.Tetanos. tetanus) Pertain- ing to or resembling tetanus. Char- acterized by tonic muscular spasms. Thermic (Gr.Therme, heat.) Of or per- taining to heat. Thermogenic (Gr.Thermos, heat and Gennaein, to produce.) Pertaining to causing or producing heat. Thermogenesis (Gi" Therme, heat and Gennaein, to produce.) The genera- tion or production of heat. Thermolysis (Gr.Therme. heat and Lue- In. to loose.) The loss of heat. Thorarischiopaiirus fGr Thorax. thorax. Ischlon. hip and Pagos, union.) A monster with two heads but with bodies and hips united. Thrombosis (Gr.Thrombos, a clot and osis, a condition of.) A condition of the existence of a thrombus. m GLOSSAft^'. nitro- cells. Thrombus (Gr.Thrombos, a clot.) A coa- gulum formed within a living blood- vessel. Tolerance (L.Tolerare, to endure.) Abil- ity to endure the continuation of an act. Tonic (Gr.Tonikos, tone.) Pertaining to tone. Characterized by conti«uous tension or contraction, or an agent that tends to restore normal tone. Tophi (Gr.Tophos, a stone.) Hard stone- like deposits. Torsion (L.Torquere, to twist.) A twist- ing or the act of twisting. Toxin (Gr.Toxikon, a poison.) A genous product formed by Bacterial toxin. Transudate (L. Trans, through and Su- dare, to sweat.) A fluid that has passed through a membrane. Espe- cially non-inflammatoj-y blood serum that' has passed through vessel walls. Transudation (L,.Tr,^ns, through arid Sudare, to sweat.) The production of a transudate. Traumatism (Gr.Trauma, a wound and ism, a condition of.) A condition due to an injury or wound. Tricephalus (Gr.Tris, three and Kep- hale, head) A monster having three heads. Trophic (Gr. Trophic, to nutrition. Tubercle (L. Tuber, inutive term.) A Tumefied (L.Tumere, cere, to make.) In a swollen condi- tion. Tumor (L. Tumere, to swell.) A morbid enlargement. A growth of new tis- sue non-inflammatory, persistent and Independent of the surrounding structures, atypical in structure and function. Ulcer (L. Ulcus.) A denuded surface re- sulting from a continuous and some- times progressive cellular necrosis. food.) Pertaining swelling and dim- small nodule, to swell and Fa- I'lceration (L. Ulcus, an ulcer.) The for- mation of an ulcer. Vltramicroscopic (L. Ultra, beyond, Gr.- Mikros, small and Skopeein, to look at.) Too small to be seen with a microscope. Uniparous (L.Unus, one and Parere. to produce.) Bringing forth one off- spring at a birth. Vaccine (L.Vacca, cow.) An attenuated virus used for inoculation purposes. Vacuolated (L. Vacuus, empty.) A condi tion of the presence of vacuoles. Vacuole (L. Vacuus, empty.) A space or cavity in the protoplasm of a cell. Vascularization (L.Vasculum, a small vessel. ) The process of becoming vascular or of being supplied with vessels. Vehicle (L.Vehere, to carry.) A sub- stance serving to carry or hold an- other. Vesicle (L. Vesica, a bladder and dimin- utive term.) A circumscribed accu- mulation of inflammatory serous exudate in the deeper layers of the epidermis or of the mucosa, usually about pinhead size. Villus (L. Villus, a tuft of hair.) One of the minute projections of the mu- cous membrane of the intestinal .canal. Virulency (L. Virus, a poison.) Pertain- ing to extreme poisonousness, dis- ease producing power or strength. Virulent (L. Virus, a poison.) Very pow- erful or Poisonous. Vitiligo (L. Vitiligo, vitiligo.) A skln- discase characterized by disappear- ance of normal pigment in patches. Volvulus (L.Volvere, to roll.) A Twist- ing of an organ so as to occlude its lumen. Wound (A.gWund, wound.) The result of the sudden interruption of the Continuity of a tissue or tissues. Zymogenic (Zume, leaven and Genna- ein, to produce.) Causing or per- taining to fermentation. INDEX Abdomino-schisis, 95. Abscess, cold, 170. Abscess formation, 169. Abscess, hot, 170. Abscess, metastatic, 170. Absorption of necrotic tissue, 262. Acardia, 92. Acaudia, 92. Acephalus, 91. Achorion Schoenleini, 50. Achromatosis, 25,1. Acidophiles in inflammation, 152. Acme, fever, 344. Acquired diseases, 38. Acquired immunity, 79. Acromegaly, 191. Actinomycosis, 358. Avenue of entrance, 360. Differential diagnosis, 363- Distribution, 358. Etiology, 359- Extension, 363. Lesions, 361. Source of infection, 359. Susceptible animals, 359- Active and acquired immunity, 83. Acute inflammation, 173. Addison's Disease, 249. Adenoma, 329. Adenoma, clinically, 330. Adenoma, microscopic, 329. Adeno-sarcoma, 331. Adeno-sarcoma, microscopic, 332. Adipose depositories, 204. Adipose digestion, 205. Adipose tissue, 204. Adipose tissue regeneration, 181. Aerobic bacteria, 60. Agastria, 92. Agglutination test, glanders, ;i72. Agnathus, 92. Albino, 251. Alveolar-sarcoma, 311. Amboceptor, 88. Amelus, 92. Amitosis, 24. Amputation neuromata, 182, 295. Amyelus, 91. Amylin, 2,11. Amyloid changes, 211. Amyloid formation, 212. Amyloid formation, appearance, 212. Amyloid formation, cause, 212. Amyloid formation, effects, 213. Amyloid formation, tissue affected, 212. Anaphase, 27. Anasarca, 120. Anemia, 132, 198. Angioma, 295-298. Anhydremia, no. Animal parasites, 64. Anomalies, 90. Ante-natal diseases, 38. Ante-natal hypertrophy, 190. Antitoxins, 85. Anthracosis, 249. Aplasia, 91. Apnoea, 74. Apoplexy, 74. Aprosopus, 92. Apus, 93. Argyriasis, 249. Arrested development, 91. Arteriolith, 239. 391 392 INDEX. Arterioclerosis, no. Arthropoda, 66. Ascites, 119. Aspergillus fumigatus, 51. Aspergillus, niger, 52. Asthenic fever, 345. Atheroma, 340. Atheromatous degeneration, 229. Atresia, 97. Atresia anus, 98. Atresia iridis, 98. Atresia oculi, 98. Atresia oris, 98. Atresia urethra, 98. Atrichia, 91. Atrophy, 197. Atrophy, appearance, 199. Atrophy, cause, 198. Atrophy, effects, 200. Atrophy, pathologic, 198. Atrophy, physiologic, 198. Atrophy, pulmonary, 200. Atrophy, senile, 198. Autosite, 107. Avian tubercular lesion, 355. Axone, rate of growth, 182. Axone regeneration, 182. B Bacilli, 54. Bacillus necrophorus, 254-255. Bacteria, 54-56. Bacterial immunity, 88. Bacterial pigmentation, 62, Bacterial proteids, 64. Bacterial respiration, 60. Bacterial toxins, 63. Bacterium mallei, 365. Bacterium tuberculosis, 348. Basophiles, 152. Benign tumors, 276. Bile concrement, 241. Bile pigmentation, 247. Biliary calculi, 237. Birth mark, 296. Blister, 43. Blister test, 368. Blood, 178. Blood, exudation, 149. Blood flow in inflammation, 147, iz Blood oscillation, 148. Blood pressure, no. Blood quality, no. Blood, quantity, no. Blood regeneration, 178. Blood stasis, 149. Blood vessel regeneration, 178. Bovine tubercular lesions, 363. Bursattae, 252. Calcareous infiltration, 228. Calcareous infiltration, appearance, 229. Calcareous infiltration, cause, 228. Calcareous infiltration, effects, 230. Calcareous infiltration, tissue affect- ed, 230. Calculi, 231. Calculi in arteries, 239. Calculi bile ducts, 237. Calculi, cause, 231. Calculi, color, 232. Calculi, composition, 232. Calculi, lithopedia, 239. Calculi, gall bladder, 237. Calculi, intestine, 237. Calculi, kidney, pelvis, 234. Calculi, mammary ducts and sinuses, 238. Calculi, number, 231. Calculi of prepuce, 236. Calculi of salivary gland ducts, 236. Calculi, shape, 232. Calculi, size, 232. Calculi, structure, 232. Calculi, stomach, 237. Calculi, ureter, 235. Calculi, urethra, 235. Calcitli, urinary bladder, 235. Calculi, uriniferous tubules, 234. Calculi, varieties, 234. Calor, 161. Canalization, 178. INDEX. 393 Cancellated osteoma, 288. Capillaries, 166. Carcinoma, 324. Carcinoma, clinically, 326. Carcinoma, differentiation, 326. Carcinoma, encephaloid, 324. Carcinoma, metastasis, 326. Carcinoma, microscopic, 325. Carcinoma, scirrhus, 324. Caries, 252. Capillary telangiectasis, 296. Cartilage regeneration, 180. Cartilaginous tumor, 285. Caseation necrosis, 258. Castration, fatty changes, 206. Catarrhal inflammation, 174. Causes, exciting, 41, Causes, predisposing, 39-41. Cavernous hemangioma, 296. Cell, definition, 20. Cell division, maiotic, 28. Cell growth, 23. Cell motion, 29. Cell reproduction, 24. Cell rests, 277. Cell shape, 22. Cell size, 23. Cell structure, 21. Cell waste, 33. Cells in inflammation, 151-152, 133. Cementoma, 294. Centrosome, 22. Cerunienous concrements, 242. Cervical ectopia cordis, 102. Cheiloschisis, 94. Chemical causes of disease, 45. Chemical necrosis, 254. Chemical, reaction, cloudy swrlling, 201. Chemical reaction of tissue, 196. Chemotaxis, 159. Chilblains, 144. Cholelith, 237. Cholesteatoma, 33S. Chondroma, 283. Chondroma, clinically, 287. Chondroma, microscopic, 287. Chondro-sarcoma, 320. Chorio-carcinoma, 334. Chorio-epithelioma, 334. Chromosome, 27. Chronic inflammation, 173. Chylous ascites, 117. Cicatrization, 186. Cilia, 30. Circulatory disturbances, 109. Cirsoid aneurisms, 297. Cladothrix actinomyces, 359. Cloacal persistence, 102. Cloudy swelling, 201. Cloudy swelling, appearance. 203. Cloudy swelling, cause, 201. Cloudy s^velling, effects, 203. Cloudy swelling, tissue affected, 203. Coagulation necrosis, 257. Cobra, 49. Coccidium, 373. Cocci, 54. Colliquation necrosis, 257. Colloid changes, 218. Colloid formation, 218. Colloid formation, appearance, 219. Colloid formation, cause, 218. Colloid formation, effects, 221. Colloid tests, 218. Color blending, 35. Compensatory hypertrophy, 190. Complement, 89. Complement fixation, test, 372. Complete duplicates, 105. Composite odontoma, 295. Compound follicular odontoma, 294. Concentric hypertrophy, 190. Concrements, 239. Concrements, bile, 241. Concrements, cerumen, 242. Concrements, fecal matter, 240. Concrements, hair, 240. Concrements, milk, 242. Concrements, prostatic, 242. Concrements, pus, 242. Concrements, source, 239. Congenital diseases, 36. Connective tissue regeneration, 179. Contiguity, 69. Continued fever, 345. 394 INDEX. Continuity, 68. Convalescence, fever, 344. Corneal, reaction, 344. Cornification, 225. Corrosive poisoning, 45. Craniopagi, 106. Craniorrachischisis, 94. Cranioschisis, 93. Crisis, 344. Cryptorchids, 102. Cyclopia, 97. Cysts, 338. Cysts, degeneration, 340. Cysts, dermoid, 341. Cysts, extravasation, 340. Cysts, exudation, 340. Cysts, multilocular, 338. Cysts, parasitic, 340. Cystic, calculi, 235. Cystoma, 338. ID Death, yTx 263. Death, pathologic, 264. Death, physiologic, 263. Death signs, 265. Death tests, 266. Decomposition, 266. Deciduoma malignum, 334. Decline, fever, 340. Degeneration, 162. Degeneration cysts, 337. Dentigerous cysts, 2)37- Dentine regeneration, 181. Depigmentation, 251. Dermoid cysts, 336. Diabrosis, 112. Diapedesis, 112. Dicaudis, 99. Dicephalus, 106, 107. Diphtheritic inflammation, 171. Diplo-coccus, 54. Dipygusamelus, 92. Dislocation, 41. Dissolution, 176. Direct cell division, 24. Diseases, 34, 35, 38. Disease extension, 67. Disease termination, 69. Dithoracisamelus, 92, 93. Dithoracisapus, 93. Dolor, 161. Dropsy, 118. Duplicities, assymetrical, 107. Duplicities, complete, 105. Duplicities, free, 105. Duplicities, incomplete, 107. Duplicities, monochorionic, 105. Eburnated osteoma, 290. Ectopia gastrium, 95. Effusions, 113. Egagaropile, 240. Ehrlich's lateral chain theory, 83. Electric causes of disease, 45. Embolism, 128, 130. Embolism, effects, 130. Embolus, 128. Embolus air, 129. Embolus cells, 128. Embolus, composition of, 130. Embolus, location, 129. Embolus, parasitic, 128. Embolus, thrombic fragments, 128. Embryonic epithelial tumors, 324. Encapsulation of necrotic tissue, 262. Encephaloid carcinoma, 324. Endemic goitre, 219. Endothelial cells in inflammation, 152. Endothelioma, 312. Endotoxins, 62,. Enterolith, 339. Enterorrhagia, 115. Ephemeral fever, 345. Epistaxis, 114. Epithelial odontoma, 293. Epithelial pearls, 226. Epithelial regeneration, 181, 182. Epithelioma, 327. Epithelioma, clinically, 329. Epithelioma, microscopic, 328. Epithelioma, pearl, 328. Epithelioma, seritonale, 334. Epithelioma contagiosum, cause, 2>7i- INDEX. 395 Epithelioma contagiosum, lesion, T,yT„ 2,7A- Epithelium cornified, 225. Epithelization, 187. Ergot of rye, 256. Erythrocytes in inflammation, 153. Etiology of disease, 39. Exciting causes of disease, 41 to 4c. Excess food, 206. Exercise, insufficient, 206. Exfoliation, 262. Exhaustion theory of immunity, 82. Exophthalmic goitre, 218. Extension of disease, 69. Extravasate, 186. Extravasation cysts, 340. Exuberant granulation, 189. Exudate, 150, 171. Exudate, cause, determining kind, 155- Exudate, composition, 150. Eudate, effects, 155, 157. Exudate, fibrinous, 154. Exudate, hemorrhagic, 154. Exudate, purulent, 155. Exudate, serous, 154. Exudate, significance of, 156. Exudation cyst, 340. Fatty changes, 204. Fatty changes, pathologic, 208. Fatty changes, pathologic, appear- ance, 209. Fatty changes, pathologic, cause, 208. Fatty changes, physiologic, 206. Fatty changes, physiologic, appear- ance, 207. Fatty changes, physiologic, cause, 206. Fatty changes, physiologic, effects 207. Fatty degeneration, 208. Fatty infiltration, 206. Fatty necrosis, 259. Favus, 50. Fecal, concrements, 240. Fever, 342. Fever, acme, 344. Fever, asthenic, 345. Fever, continuous, 345. Fever, convalescence, 344. Fever, course, 343. Fever, decline, 344. Fever, ephemeral, 344. Fever, intermittent, 345. Fever, onset, 343. Fever, sthenic, 345. Fibrinous exudate, 154. Fibroblasts, 165, 179. Fibroma, 279. Fibroma, clinically, 282. Fibroma, differentiation, 282. Fibroma, hard, 281. Fibroma, soft, 281. Fibro-sarcoma, 315. Fibrous connective tissue regenera- tion, 179. Fibrous hyperplasia, 192. Fibrous odontomata, 293. Fission, 58. Fistulous tracts, 170. Flagella, 55. Follicular odontoma, 293. Focal necrosis, 260. Foramen ovale, 102. Fracture, repair, 180-184. Freckles, 249. Functio laeso, 161. Galactoliths, 238. Gangrene, 258. Gastric calculi, 22,7. Gastroliths, 237. General diseases, 39. Giant cells, 153. Giant cell sarcoma, 308. Giantism, 190. Glanders, 364. Glanders, agglutination test, 372. Glanders, avenue of infection, 365. Glanders, cause, 365. Glanders, diagnosis, 371, 2>7~- Glanders, lesions, 366. 395 INDEX. Glanders, mallein test, 371. Glanders, course of infection, 365. Glioma, 291. Glycogen, 222. Glycogen composition, 222. Glycogen tests, 222. Glycogenic infiltration, 222. Glycogenic infiltration, appearance, 223. Glycogenic infiltration, cause, 223. Glycogenic infiltration, effects, 223. Goitre, 218. Grafting, 182. Granulation, healing by, 187. Granulation, exuberant, 189. Growth of tumors, 273. H Hair balls, 240. Hair lip, 94. Hair sore, 360. Haptophores, 88, 89. Health, 35- Healing by primary union, 185. Healing by granulation, 187. Heart anatomical changes, 109. Heart diminished action, 109. Heart increased action, 109. Helminthes, 65. Helminthes response to stimuli, 140. Hemaglobinuria, 245. Hemangioma, 296. Hemangioma cavernosum,. 296. Hemangioma cirsoid, 297. Hemangioma hypertrophicum, 297. Hemangioma simplex, 296. Hemangiosarcoma, 321. Hematemesis, 114. Hematidrosis, 112-115. Hematocele, 115. Hematogenous pigmentation, 244. Hematoidin, 246. Hematoma, 113. Hematometra, 115. Hematuria, 114. Hemic, poisons, 46. Hemocoelia, 115. Hemoglobin in pigmentation, 244. Hemolysis, 346. Hemophilia, iii. Hemoptysis, 114. Hemorrhage, 74, 112. Hemorrhage, cause, iii. Hemorrhage, diabrotic, 112. Hemorrhage, diapedetic, 112. Hemorrhage, ecchymotic, 114. Hemorrhage, epistaxis, 114. Hemorrhage, effects, 115. Hemorrhage, petechial, 113. Hemorrhage, rhexis, 112. Hemorrhage, suggillation, 114. Hemorrhagic infarction, 113. Hemorrhagic exudate, 154. Hemosiderin, 246. Hemothorax, 115. Heredity, 35. Heredity in fatty changes, 206. Hermaphroditism, 103. Hermaphrodite, bilateral, 103. Hermaphrodite, lateral, 103. Hermaphrodite, pseudo or false, 103. Hermaphrodite, true, 103. Hermaphrodite, unilateral, 103. Hernia, 41. Histoid tumor, 270. Holoschisis, 94. Humoral theory of immunity, 83. Hyalin, 213. Hyalin, chemical composition, 214. Hyaline formation, 213. Hyaline formation, appearance, 214. Hyaline formation, cause, 214. Hyaline formation, effects, 215. Hydrargirosis, 250. Hydrops, 118. Hydrothorax, 119. Hydropericardium, 119. Hydrocele, 119. Hydrocephalus, 120. Hymen persistence, 102. Hyperchromatosis, 244. Hyperemia, 133-142. Hyperemia, active, 135. Hyperemia, arterial, 135. Hyperemia, arterial, appearance, 136. INDEX. 397 Hyperemia, arterial, cause, 135. Hyperemia, arterial, effects, 136. Hyperemia, arterial, pathologic, 137. Hyperemia, arterial, physiologic, 137. Hyperemia, arterial therapeutic, 137. Hyperemia, passive, 133. Hyperemia, venous, 133. Hyperemia, venous, pathologic, 134. Hyperemia, venous, therapeutic, 134. Hypernephroma, s^^j. Hyperplasia, 190, 192. Hyperplasia, appearance, 193. Hyperplasia, cause, 192. Hyperplasia, effects, 193. Hyperplasia, fibrous, 192. Hyperplasia, interstitial, 192. Hyperplasia, parenchymatous, 192. Hypertrophy, 189. Hypertrophy, ante natal, 190. Hypertrophy, appearance, 191. Hypertrophy, cause, 191. Hypertrophy, compensatory, 190. Hypertrophy, concentric, 190. Hypertrophy, effects, 192. Hypertrophy, general, 190. Hypertrophy, inherited, 190. Hypertrophy, post natal, 190. Hypertrophy, false, 190. Hyphomycetes, 50. Hypochromatosis, 250. Hypoplasia, 93. Hypospadias, 95. Icterus, 249. Immediate uniim, 185. Tnnnunity, 75. Immunity, acquired, 79-81. Immunity, bacterial, 81. Immunity, inherited, 80. Immunity, opsonic, 81. Immunity, passive, 81. Immunity, natural, yj. Immunity, toxic, 80. Impaired function, 161. Inanition, necrosis, 257. Incision test, 266. Increased transudation, 118. Indirect cell division, 25. Infarct, 131. Infarct, anemic, 131. Infarct, hemorrhagic, 131. Infarction, 131. Infective granulomata, 344. Inflammation, 138. Iiitlannnation, acute, 173. hitlammation, catarrhal, 174. inflammation, causes, 143-155. Inflammation, cliemic, 144. Inflammation, chronic, 173. Inflannnation, croupous, 171. Inflammation, diphtheritic, 171. Inflammation, electric, 144. Inflammation, effects, i6r. Inflammation, factors concerned in, 146. Inflammation, hemorrhagic. 172. Inflammation, infective, 167. Inflammation, interstitial, 173. Inflammation, mechanic, 143. Inflannnation, non-infectious. 143. Inflammation, non-suppurative, 167. Inflammation, parenchymatous, 173. Inflannnation, phlegmonous, 170. Inflammation, proliferative, 174. Inflammation, purulent, 169, 174. Inflammation, pustular, 174. Inflannnation, signs, 160. Inflannnation, simple, 166. Inflammation, specific, 174. Inflammation, suppurative, 167. Inflammation, termination, 174. 175. Inflannnation, thermic. 143. Inflannnation, traumatic, 143. Inflannnation, types of, 166. Inflammation, ulcerative. 174. Inflammation, vascular changes, T46, 147. 148. Inflannnation, vesicular, 174. Inflannnatory exudate, 150. Inflammatory exudation, 149. Inherited diseases, 3^. Inherited epilepsy, 37. Inherited immunity, 77. Inherited malformations, 7,7. 398 INDEX. Inherited ophthalmia, 38. Inherited tumors, 2>'}- Inspissated bile, 241. Inspissated pus, 242. Intermittent fever, 345. Interstitial hyperplasia, 192, 193. Interstitial inflammation, 173. Interstitial expansion, tumor, 274. Intestinal calculi, 237. Involucre, 262. lodothyreoglobulin, 218. Irritability, t^^)- Irritant, 139. Ischemia, 132. Ischiopagus, 106. Ischiopagus parasiticus, 106. Jack sores, 261. Karyolysis, 302. Karyokinesis, 25. Katabolism, 32. Keloid, 283. Keratosis, 225. Keratosis, appearance, 226. Keratosis, cause, 225. Keratosis, effects, 226. Lactation a factor in fatty changes, 206. Lacteal calculi, 238. Lacteal concrements, 242. Lamellae formation, 181. Larkspur, 46. Leiomyoma, 299. Lesion, 19. Leucocytes in inflammation, 151. Leucocytes in tumors, 271. Leucocytes, basophilic, 152. Leucocytes, eosinophylic, 151. Leucocytes, neutrophylic, 151. Leucocytes, polymorphonuclear, 151. Leucocytic margination, 159. Leucoderma, 251. Leucomains, 49. Leucoprotase, 154. Lipoma, 287. Lipoma, clinically, 289. Lipoma, microscopically, 289. Liquor, puris, 155. Lithopedia, 239. Local disease, 38. . Loco, 48. Luxation, 41. Lymphangioma, 298. Lymphorrhagia, 117. Lymphorrliagia, cause, 117. Lymphorrhagia, effects, 117. Lymphosarcoma, 305. Lysis, 344. M Malformations, 90. Malformations, atypical, 91. Malformations, multiple, 105. Malformations, single, 91. Malformations, typical, 91. ]\Ialign tumor, 276. Mallein, 371. Mammalian cornea, 141. Margination, leucocytic, 150. Mechanic causes of diseases, 41. Melanin, 248. Melano-sarcoma, 318. Melanosis, 248. Membrane, cell, 22. Meningocele, 93. Meroschisis, 94. Metabolism, 32. Metaphase, 27. Metaplasia, 194. Metastases, carcinoma, 326. Metastatic tumor, 273. Metorrhagia, 115. Microcardia, 93. Microcephalus, 93. Micrococcus, 54. Micrognathy, 93. Micromelus, 93. Microophthalmia, 93. Miliar tubercle, 352. TNDEX. 399 Miliary tumors, 272. Mirror test, 266. Mitosis, 25. Mixed cell sarcoma, 310. Mole, 91. Monopygusamclus, 93. Monopygusapus, 93. Monothoracisamelus, 93. Monothoracisapus, 93. Moribund stage fever, 344. Mosaic coloring, 36. Moulds, 50. Movement, amoeboid, 29. Movement, ciliary, 30. Movement, intracellular, 29. Mucoid changes, 215. Mucoid changes, appearance, 216. Mucoid changes, causes, 216. Mucoid changes, effects, 217. Mucoid changes, pathologic, 216. Mucoid changes, physiologic, 215. Mucoid tissue regeneration, 179. Mucus, 215. Multilocular cysts, 338. Alultiplicity, 99-108. ^lummifying necrosis, 258. Muscular tissue regeneration, 182. Mycelia, 359. Myeloid sarcoma, 3aS. Myelomeningocele, 94. Myocarditis, 109. Myoma, 298. Myositis ossificans, ii"]. Myxoedeiiia, 216. Myxoma, 284. Myxoma clinically, 285. Myxoma miscropically, 284. Myxosarcoma, 319. N Necrobiosis, 252. Necrosis, 164, 254. Necrosis caseation, 258. Necrosis chemical, 254. • Necrosis, coagulation, 257. Necrosis colliquation, 257. Necrosis fatty, 259. Necrosis focal, 260. Necrosis inanition, 255. Necrosis mummifying, 258. Necrosis putrefying, 258. Necrosis senile, 259. Necrosis subsurface, 257. Necrosis surface, 257. Necrosis thermic, 255. Necrotic stomatitis, 251. Necrotic tissue, disposal of, 175. Nephritis, 172. Neoplasms, 268. Nerve cell regeneration, 182. Neuroma, 295. Neuromata amputation, 182-295. Neurotoxic poison, 46. Nevus, 296. Nucleus, 22. Numerical hypertrophy, 192. Nutritive disturl)ances in atrophy, 198. Obstructed nutrition, 253. Obstructed outflow of Lymph, 119. Ochronosis, 245. Odontoma, 291. Odontoma composite, 295. Odontoma compound follicular, 294. Odontoma, epithelial, 293. Odontoma fibrous, 293. Odontoma follicular, 293. Odontoma, radicular, 295. Oedema, 118, 221. Oedema appearance, 120. Oedema cause, 118. Oedema eflfects. 121. Oedema varieties, t 19. Olein, 204. Onset fever, 343. Ospora porrigines, 50. Ophthalmic tubercular, 358. Opsonins, 82. Organoid tumor, 270. Osseous regeneration, 180. Ossification, 227. Ossification appearance, 227. Ossification cause, 227. Ossification eflfects, 227. 400 INDEX. Osteoblasts, i8o. Osteoclasts, i8o. Osteoma, 290. Osteoma cancellated, 290. Osteoma clinically, 291. Osteoma eburnated, 290. Osteo-cystoma capsular dentiferum, Osteophytes, 227. Osteo sarcoma, 321. Palatoschisis, 94. Palmatin, 204. Pancreatic calculi, 238. Papilloma, 321. Parasites vegetable, 49. Parasites in embolism, 128. Parasitic causes of disease, 49. Parasitic cysts, 340. Parasitic theory of tumors, 278. Parenchymatous degeneration, 201. Parenchymatous hyperplasia, 192. Parenchymatous inflammation, 173. Parenchymatous poisons, 46. Partial recovery, 69. Pathogenesis, 19. Pathology definition, 19. Pathology comparative, 19. Pathology general, 19. Pathology human, 19. Pathology special, 19. Pathology veterinary, 19. Pathologic anatomy, 19. Pathologic atrophy, 198. Pathologic death, 264. Pathologic physiology, 19. Pearl cell epithelioma, 328. Persistent foetal structures, loi. Phagocyte, 159. Phagocytosis theory, 82. Phlebolith, 239. Phlegmonous inflammation, 170. Phosphorescence, 62. Photic cause of disease, 44. Physic cause of disease, 43. Phyto-bezoars, 241. Phyto-parasites, 49. Phyto-toxin, 79. Pigmentary changes, 242. Pigmentary infiltration, 244. Pigmentation bile, 247. Pigmentation carbon, 249. Pigmentation cells, 248. Pigmentation diminished, 250. Pigmentation excessive, 244. Pigmentation effects, 250. Pigmentation hemoglobin, 244. Pigmentation hemosiderin, 246. Pigmentation hemotoidin, 246. Pigmentation iron, 250. Pigmentation lead, 250. Pigmentation mercury, 250. Pigmentation silver, 249. Placentoma, 334. Plumbosis, 250. Pneumonia groupus, 172. Pneumomycosis aspergillosis, 51. Porcine tubercular lesion, 354. Polydactylism, 98. Polymeluspygus, 99. Polymelusthoracicus, 98. Poisons, 45. Post mortem staining, 265. Post natal diseases, 38. Post natal hypertrophy, 191. Predisposing causes of disease, 39-41. Predisposing causes of age, 39. Predisposing causes of breed, 40. Predisposing causes of climate, 40. Predisposing causes of color, 40. Predisposing causes of food and water, 41. Predisposing causes of genus, 40. Predisposing causes of imitation, 40. Predisposing causes of location, 40. Predisposing causes of occupation, 41. Predisposing causes of overwork, 41. Predisposing causes of previous dis- ease, 41. Predisposing causes of season, 40. Predisposing causes of sex, 40. Preputial calculi, 236. Pressure atrophy, 199. Primary tumors, 273. INDEX. 401 Prognathism, loo. Progressive tissue changes, 177. Proliferation tissue, 175. Proliferative inflammation. 174. Prophase, 26. Prostatic concrements, 242. Protoplasm, 20. Protozoa, 64. Protozoa response to stimuli. 140. Proud flesh, 189. Psammo sarcoma, 314. Pseudo-hermaphrodite, 103. Pseudo-hypertropliy, 190. Ptomains, 63. Purulent inflammation, 169-174. Putrefaction, 62. Pus, 15s, 167-168. Pus concrements, 242. Pustule, 170. Pustular inflammation, 174. Pygopagus, 105. Pyorrhoea, 169. Pyrexia, 342. Regeneration wliitc fibrous tissue, 179. Renegcration yellow elastic tissue, 180. Regenerative inflammation, 175. Regenerative power, 177. Remittent fever, 345. Reinnervation, 182. Renal adeno-sarcoma, 331. Renal tubular calculi, 234. Renal pelvic calculi, 234. Resistance to tumors, 275. Resolution, 174. Retention cyst, 340. Retention theory of immunity, 82. Retrogressive tissue changes, 196-197. Retrogressive tissue in tumors, 275. Rhabdomyoma, 299. Rhexis, 112. Rigor mortis, 265. Ringworm, 51. Round cell sarcoma, 304. Rubor, 160. Rupture, 41-184. Rachischisis, 94. Ranulae, 340. Rattlesnake, 49. Ray fungus, 359. Reaction aseptic injury, 142. Reaction, septic injury, T42. Receptor, 85-86-87. Recovery, 69. Redness, 160. Regeneration, 164-177. Regeneration adipose tissue, 181. Regeneration blood, 178. Regeneration blood vessels, 178. Regeneration cartilage, 180. Regeneration connective tissue, 179. Regeneration degenerated tissue, 175 Regeneration dentine, 181. Regeneration epithelium, 181. Regeneration mucoid tissue, 179. Regeneration muscular tissue, 182. Regeneration nerve cells, 182. Regeneration osseous tissue, 180. s Saccharomyces, 52. Saccharomyces cerevisiae, 52. Saccharomyces farciminosus, 53. Salivary calculi, 236. Saponification of fat, 259. Sarcinae, 54. Sarcoma, 300. Sarcoma alveolar, 311. Sarcoma cells, 302. Sarcoma, chondro, 320. Sarcoma, fibro, 315. Sarcoma, grape, 317. Sarcoma, hemangio, 321. Sarcoma, melano, 318. Sarcoma mixed cell, 310. Sarcoma myeloid cell, 308. Sarcoma, myxo, 319. Sarcoma, psammo, 314. Sarcoma round cell, 304. Sarcoma structure, 303. Scar, 211. 402 INDEX. Schistosis, 93. Schizomycetes, 54. Scirrhous carcinoma, 324. Sebaceous cyst, 340. Secondary tumors, 273. Senile atrophy, 198. Senile necrosis, 259. Sequestration, 262. Sequestrum, 262. Serous exudate, 154. Serous infiltration, 221. Serous infiltration appearance, 221. Serous infiltration cause, 221. Serous infiltration effects, 222. Siderosis, 250. Significance of inflammatory exudate, 156. Signs of death, 265. Signs of inflammation, 160. Situs viscerum inversus, 100. Sodium urate, 224. Specific inflammation, 174. Spina bifida, 94. Spindle cell sarcoma, 307. Spirilla, 55. Sporotrichium audouini, 51. Stadium decrementi, 344. Stadium incrementi, 343. Staining, post mortem, 265. Stearin, 204. Sternopagus, 106. Sthenic fever, 345. Still birth, 267. Stimulus, 139. Stocking, 161. Substitution, 186. Sub-surface necrosis, 257. Suppuration, 167. Suppuration sub-surface, 170. Suppuration surface, 167-169. Suppurative osteitis, 169. Surface necrosis, 257. Swelling, 160. Symmetrical duplicity, 105. Synactosis, 93-97. Syncephali, 107. Syncope, 73. ' Syncytium, 153. Syncytioma malignum, 334. Syndactylus, 97. Synmelus, 97. Synmelusapus, 97. Synmelusdipus, 97. Synmelusmonopus, 97. Synorchism, 97. Synophthalmia, 97. Tattooing, 250. Temperature, 161. Temperature, cause of cloudy swell- ing, 202. Temperature, cause of degenerations^ 197. Telophase, 28. Teratoid tumors, 270. Teratoma, 335. Termination of disease, 69, 174. Tests for death, 266. Thermic causes of disease, 43. Thermic necrosis, 255. Thermogenesis, 343. Thermolysis, 343. Thoracisischiopagus, 106. . Thoracopagus, 106. Thoracoschisis, 95. Thrombosis, 122. Thrombosis, cause, 123. Thrombosis, effects, 127. Thrombus, 122. Thrombus annular, 124. Thrombus appearance, 124. Thrombus calcification, 127. Thrombus complete, 124. Thrombus decolorization, 125. Thrombus, extension, 124. Thormbus infective softening, 126. Thrombus location, 124. Thrombus, mixed, 124. Thrombus organization, 126. Thrombus partial, 124. Thrombus red, 124. Thrombus simple softening, 125. Thrombus white, 124. Tinea tonsurans, 51. Tissue, 173. INDEX. 403 Tophi, 224. Toxic immunity, 80. Toxopliore, 88-89. Transplantation, 182. Transportation of visceral organs, 100. Traumatic wounds, 185. Tncephalus, 108. Trichobezoars, 240. Tricophylon tonsurans, 51. Tubercle, 352. Tuberculin, 357. Tuberculin test, 357. Tuberculosis, 347. Tuberculosis extent, 347. Tuberculosis etiology, 348. Tuberculosis avenue of infection, 349. Tuberculosis source of infection, 349. Tuberculosis lesions, 350. Tuberculosis extension, 35O. Tuberculosis elimination, 357. Tumor, 160. Tumors, 268. Tumors benign, 27^. Tumors body resistance, 275. Tumors cause, 276. Tumors cells, 277. Tumors clinically, 276. Tumors color, 272. Tumors consistency, 273. Tumors extension, 274- Tumors frequency, 269. Tumors growth, 27^. Tumors histoid, 270. Tumors intercellular substance, 270. Tumors malign, 273. Tumors metastasis, 273. Tumors miliary, 272. Tumors mottled, 273. Tumors number, 273. Tumors organoid, 270. Tumors primary, 273. Tumors retrogressive changes, 275. Tumors secondary, 273. Tumors shape, 272. Tumors size, 272. Tumors structure, 270. Tumors teratoid. 270. Tumors varieties, 278. Twins, 105. u Ulcer, 164. Ulceration, 164. Ulcerative intlamniation, 174. Union dorsal, 105. Union posterior, 105. Union ventral, 105. Urates, 224. Uratic infiltration, 224. Uratic infiltration appearance, 224. Uratic infiltration cause, 224. Uratic infiltration effects, 225. Ureter calculi, 235. Uretheral calculi, 235. Uric acid, 224. Valvular insufficiency, 109. Valvular stenosis, 109. Varieties of tumors, 278. Vascular constriction, inflammation, 146. Vascular disturbances, 146. Vascular permeability, no. Vascular regeneration, 178. Vascular variations, no. Vascularization, 178-186. Vegetable parasites, 49. Venesection in fatty changes, 206. Venom, 49. Vesicle, 43. Vesicular inflammation, 174. Viper, 49. Vitiligo, 251. w Wall-eyed horses, 251. Wandering cells, 152. Wart. 321. White fibrous regeneration, 179. Wound, 41. Wound cause, 185. Wound healing, 185. Wound sub-surface, 185. 404 INDEX. Wound surface, 185. Wound traumatic, i s^^^'r"> '^°\o> % <^'^"" A-^- .\'^ ■ VX'^- » 1 \ ■> \"^ ^^. ,^V '^C^O' x^" "'^^^ \^ , \ 1 x^^ ■% \^' \ . 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