.i^'^i^')^#^ Wmrir Class __u_[l_ll_5 Book G)pyright}^'^ CDPXRIGHT DEPOSIT. DISEASES OF DOMESTICATED BIRDS ^^^^ THE MACMILLAN COMPAKY NEW YORK • BOSTON • CHICAGO • DALLAS ATLANTA • SAN FRANCISCO MACMILLAN & CO., Limited LONDON • BOMBAY • CALCUTTA MELBOURNE THE MACMILLAN CO. OF CANADA, Ltd. TORONTO ^ DISEASES OF DOMESTICATED BIRDS BY ARCHIBALD ROBINSON WARD, B.S.A.. D.V.M. Director, Research Department, The Jensen-S^lsbcry Laboratories, Kansas City, Missouri AND BERNARD A. GALLAGHER, D.V.M. Bacteriologist. Bureau of Animal Industry, United States Department of Agriculture, Washington, D. C. WITH INTRODUCTION BY VERANUS ALVA MOORE, B.S., M.D., V.M.D. Professor of Comparative Pathology, Bacteriology and Meat Inspection, New York State Veterinary College at Cornell University, and Director of the College s^txo gotfe THE MACMILLAN COMPANY 1920 All rights reserved Copyright, 1920, By the MACMILLAN COMPANY Set up and electrotyped. Published, January, 1920 n^ -3 1920 ©CI.A559G85 ^x^ " 1 PEEFACE The writing of this book has been prompted by a conviction held by the authors, regarding the magnitude of the losses experienced by poultry producers as a result of preventable infectious diseases and parasitic infestations. It is believed that the importance of these losses warrants the effort expended in presenting the essential facts concerning poultry diseases to meet the needs of veterinary practitioners, veterinary stu- dents and poultrjTuen. The title of the book indicates a slight broadening of scope beyond the field of a work on diseases of poultry. Material included deals with the ostrich, cage birds and wild birds in semi-domestication in zoological gardens. Chapters dealing with anatomy of birds, and killing of poultry have been included. The peculiarities of diseases of birds are indicated by the emphasis laid on certain features of the subject matter. In general, skill in diagnosing diseases of birds by observing symptoms is of less impor- tance than ability to recognize the identity of disease at autopsy. Symptoms are slightly characteristic, but autopsy material is freely available. Consequently more facts concerning details of gross lesions are given than those relating to symptoms. In many cases, particularly in the septicemias, symptoms and lesions are not dis- tinctive, and fine distinctions of etiology must be made by a bacteri- ologist. On this account considerable material useful to a bacteri- ologist alone has been included. Available sources of information are indicated in the references appended to each chapter and by specific references to authors in the text. Special acknowledgment is made for assistance obtained from IsTeumann's " Parasites et Maladies Parasitaires des Oiseaux Do- mestiques " in the preparation of the chapters on parasites. Much material concerning the less common parasites has been dravni from this book and l^eumann's zoological nomenclature has been largely followed. s, \ ^ A. R. W. B. A. G. introductio:n' The statement is accepted that diseases are the greatest hindrance to the development of animal and poultry husbandry. Measures for the prevention, successful treatment or control of these maladies must come from those who understand their nature. It is grati- fying, therefore, that veterinarians, and others interested in the subject, are to have access to a volume dealing with the diseases of poultry, prepared by men of long experience in the study of the phenomena of disease. Likewise, poultry raisers will appreciate a treatise setting forth the known facts concerning the maladies which sooner or later may affect their flocks. A book of this kind will be of indispensable value in eliminating many of the miscon- ceptions regarding the diseases of poultry and in pointing out the things that are known and the precautions that must be observed in maintaining healthy flocks. The extent of the poultry industry in the United States is little appreciated by veterinarians. There is no other species in the animal kingdom that contributes to the material support of so large a number of people as the domesticated fowl. In addition turkeys, geese, ducks and pigeons are significant factors in food production while the ostrich and other birds play an important part in orna- mentation. In the Hartz Mountains, the raising of canary birds for the amusement and entertainment of people is an important in- dustry. The barnyard fowl plays a large part in the food supply of the country. The extent of the poultry business can be approximated from the fact that in 1910 there were 5,578,525 farms in the United States that reported a total of 280,350,000 fowls with a value of $140,205,000. With the prices at the present time, their value would be treble that of 1910. In 1915, the United States exported 20,784,000 dozen eggs but it imported over 3,000,000 dozen and over 8,000,000 pounds of egg yolks and frozen eggs. These figures indicate the large number of people who are financially interested in the poultry business. The raising of turkeys and other species is also sig-nificant. In 1910 there were in the United States 3,688,000 turkeys with a value viii mTEODUCTION of $6,605,000; 2,906,000 ducks valued at $1,567,000; 4,431,000 geese valued at $3,194,000 ; 1,765,000 guinea fowls valued at $613,000 ; 2,730,000 pigeons with a value of $762,000 ; 6,458 pea fowls estimated at $18,000 ; and 5,361 ostriches valued at $1,- 696,000, In 1915, this country imported ostrich and other feathers to the value of $2,500,000. Besides, there is a large business in song and other birds maintained as pets. In certain localities, the raising of one or more species of poultry- constitutes the essential occupation of many of the people. The pro- ductivity of domestic fowls is greater than that of any other species of animals in proportion to their value. The price of the annual products from a flock of ducks, hens or turkeys may be many times larger than the cost of the original flock. There is no other form of animal life that suffers more from the ravages of disease than fowls. The losses from the general maladies are heavy and those from the infectious ones are sometimes appal- ling. Various estimates have been made of the annual losses occa- sioned by these causes. They vary from 10 to 30 per cent. Hens in particular suffer from a wide range of diseases and parasitisms. Some of these are veritable plagues and at times are the cause of serious losses. In 1903, while studying poultry diseases in a lo- cality where eggs and chickens were the cliief articles of commerce, it was not unusual to learn of individual losses ranging from a few hundred to several thousand dollars due to roup or diphtheria. Other large flocks were decimated by tuberculosis. While it is easy to understand that heavy losses may occur in localities where fowls are kept in large numbers, it should be recognized that they are proportionately heavy in smaller flocks. In such circumstances, the death of a few hens is often the cause of much privation if not actual suffering among their owners who are dependent upon the products of their fowls for the necessities of life. The general diseases of poultry present many points of interest, although they have received relatively little attention. The general pathology of the feathered tribes is not well understood. Little seems to be known of their tissue reactions to injury. Their resist- ance to ordinary wound infections differs strikingly from that of mammals. Pasteur suggested that this might be due to their higher body temperature. On the other hand, the infectious diseases and parasitisms have been more carefully studied. The findings of many valuable researches are recorded on the nature of the more serious ones. Certain of them, such as bacillary white diarrhea and INTKODUCTION ix the parasitisms, have been elucidated sufficiently to enable veterin- arians or poultry owners to prevent them. Others that cause heavy losses, such as roup or diphtheria and tuberculosis, can be controlled. When this is done, millions of dollars worth of poultry that is now lost will be saved. This can be done as soon as the technical knowl- edge, now available, is utilized to its full extent. It is believed that veterinarians can render a valuable service to this heretofore professionally neglected, yet important industry, es- pecially in localities conspicuous for the raising of poultry. Be- cause of the relatively small value of the individual, and the large numbers to be dealt with, methods for preventing disease must be applied to the flock. With the exception of the more Valuable birds, individual treatment may not be practicable, but the princi- ples of sanitation and the preventive measures are as helpful here as elsewhere in the raising of animals. Veterinarians should re- alize that the treatment, prevention or control of diseases in poultry, as well as in quadrupeds, is primarily an economic question and that a score of dollars saved by preventing or treating diseases in fowls is just as essential as the saving of a like amount in sheep or calves. This book, dealing with the diseases and the parasites of poultry, will be of much aid to veterinarians who wish to render full service to their communities. V. A. Moore. TABLE OF CONTENTS CHAPTER I PAGE Anatomy of Birds 1 CHAPTER II Hygiene and Sanitation 20 CHAPTER III Apoplectiform Septicemia and Sleeping Disease 28 CHAPTER IV EowL Cholera 34 CHAPTER V Fowl Typhoid and Similar Infections 50 CHAPTER VI Bacillary White Durrhea 68 CHAPTER VII Fowl Plague 81 CHAPTER VIII Avian Tuberculosis 88 CHAPTER IX Avian Diphtheria and Bird Pox 96 CHAPTER X Aspergillosis and Favus Ill CHAPTER XI Infectious Entero-Hepatitis of Turkeys 120 CHAPTER XII Coccidiosis 127 CHAPTER XIII Spirochetosis and Rare Infectious Diseases 135 xi xii CONTENTS CHAPTER XIV PAGE Leukemia and Pseudo Leukemia 146 CHAPTER XV General Diseases 150 CHAPTER XVI Internal Parasites 178 CHAPTER XVII External Parasites 208 CHAPTER XVIII Infectious Diseases and Parasites of the Ostrich 226 CHAPTER XIX Infectious Diseases of Geese and Ducks 242 CHAPTER XX Infectious Diseases of Canary Birds 252 CHAPTER XXI Tumors in Fowls 261 CHAPTER XXII Toxicology 276 CHAPTER XXIII Surgical Diseases 295 CHAPTER XXIV Caponizing 302 CHAPTER XXV Killing Poultry 314 DISEASES OF DOMESTICATED BIRDS CHAPTER I ANATOMY OF BIRDS The structure of birds differs in many respects from that of mammals and deserves a special description. The aim of the authors is to brino; to the attention of the veterinarian the more important differences which are observed in the structure of domesticated birds as compared with that of domesticated mammals. The subject will be considered under the following; sub-divisions. 1. Skeleton, 2. Musculature, 3. Circulatory system, 4. ISTervous system, 5. Ali- mentary system, 6. Respiratory system, 7. Urinary system, 8. Generative system, and 0, The skin and its appendages. SKELETON Skull. The bones of the skull become united shortly after hatch- ing and lose their individual identity except in the case of the as- cending processes of the premaxillary and nasal bones which are not rigidly joined to the frontal bone but through their cartilaginous attachment permit the elevation of the superior mandible. The in- ferior processes of the premaxillary bone, the supermaxillaries and the palatine bones which form the roof of the palate do not meet in the median line, with the result that the palate presents an elongated opening or cleft. Vertebral column. The cervical vertebrae vary in number in the different species. Statements of anatomists differ concerning the number, because of difficulties experienced in defining cervical and thoracic vertebra. The atlas or first cervical vertebra is ring-like in form and articulates with the occipital bone of the skull by means of a deep concavity into which the condyle of the occipital bone is re- ceived. This articular arrangement and that of the other cervical vertebras gives the head and neck great mobility. The articular sur- face is concave from side to side and convex in a dorso-ventral direc- tion on the anterior extremity of each vertebra, presenting a saddle shaped appearance. The posterior extremity is the reverse, that is, concave dorso-ventrally and convex from side to side. 1 DISEASES OF DOMESTICATED BIRDS Nasal 45S13I Incisive Quadrate /> ou . ^ ^.Occipital /^ Pf^^'anges //^■■"Metacarpus ,/\tlas ./V^ -Carpus Ulna Pygostyle Metatarsus Fig. 1. The skeleton of the fowl. (Bradley) The thoracic vertebrae are nearly al"wajs fused together by the con- solidation of their spinous and transverse processes. The first may be free and the last may be fused -with the lumbar vertebrae. The lumbar and sacral regions of the vertebral column show no special line of demarcation. The fourteen vertebrae are consoli- dated into one bony mass which carries ridges on its ventral surface representing the transverse processes of the original independent vertebrae. The coccygeal vertebrae are seven in number. The last is the largest, is flattened on both sides and curves in a dorsal direction ANATOMY OF BIRDS d at the end. It is known as the pygostyle. The coccygeal vertebrse are movable upon each other. Ribs. These bones articulate dorsally with the thoracic vertebrse, and ventrally with the sternum by means of the inferior ribs, except in the case of the first two which do not reach the sternum. The last rib is often united to the one adjoining and does not connect with the sternum. Some of the ribs have flat uncinate processes which extend from the posterior border and lie over the external face of the following rib near its middle. The sternum is highly developed in birds and forms the floor of the thoracic cavity and to some extent, of the abdominal cavity. It is concave on its dorsal or internal face and convex on its ventral or external face. In fowls and pigeons a deep ridge extends along the median line of the ventral face. This is known as the brisket or keel. It serves to increase the area of attachment for the powerful breast muscles. The sternum of the duck and goose does not present as large a keel as that of the fowl and pigeon, but owing to the greater breadth of the sternum and more solid construction the area for muscular attachment is as great. In the fowl two long slender lateral processes are formed on each side as a result of deep notches which extend anteriorly into the body of the sternum. The lateral external process is shorter than the lateral internal process and covers the last two ribs with a broadened terminal bony plate. The lateral borders of the body of the sternum support articular facets for the reception of the inferior ribs. The anterior border presents an eminence, the episternal process to which the furculum (wishbone) is attached by a ligament. The articular surfaces for the coracoids are located on each side of the episternal process on the anterior border. Tlie internal surface of the sternum exhibits several openings through which air is passed to the interior of the bony structure. Bones of the wing. These comprise the scapula, coracoid, and clavicle in the shoulder region ; the humerus in the arm ; the radius and ulna in the forearm ; two carpal bones, the radio-carpal bone and ulno-carpal bone; one carpo-metacarpal bone, and three digits the second of which has two phalanges. The scapula is long, narrow, thin and curved like a sabre. It extends caudad over the ribs to near the pelvis. Anteriorly it is united with the coracoid with which it forms an articular cavity for the reception of the head of the humerus. The coracoid also articulates with the sternum by its ventral extremity. It is rod 4 DISEASES OF DOMESTICATED BIEDS shaped and extends in a posterior direction obliquely ventrad from scapular to sternum. The coracoid at its ventral extremity presents an opening for the passage of air to the internal air space. The clavicle is attached to the coracoid at its superior end. It extends ventrad and caudad and curves in to the median line at the point of the sternum where the two clavicles unite in a flattened plate and become attached to the episternal process by a ligament. The united clavicles form a V or U shaped bone termed the fork or furculum. This bone represents an elastic spring and serves to prevent the wings from approaching each other during contraction of the de- pressor muscles. The humerus is long in palmipeds and the gallinse, and short in the pigeon. It is stout, slightly curved and presents a pneumatic foramen near its articular head. The ulna is much larger than the radius and is separated from it except at the extremities, where the two are united by ligamentous bands. The olecranon process of the ulna is only slightly developed. The two carpal bones represent fusions in embryonic life, of the four bones of the proximal row. The distal carpal row of three bones fuse with the metacarpal bones. Bones of the leg. These are the pelvic or hip bone; the femur or thigh bone; the patella, tibio-tarsus and fibula in the lower leg region ; a tarso-metatarsal bone, and four digits. The pelvic bone is made up of three bones as in mammals, the ilium, ischium and pubis. It differs from the mammalian bone in that the pelvic girdle is not complete on the ventral floor, the two pubic bones failing to meet in the center to form the pubic sym- physis. This arrangement facilitates the passing of the egg through the cavity. The ilium is the largest segment and extends along the vertebral column in the lumbar and sacral regions. It is consoli- dated with the last two thoracic vertebrae and the lumbar and sacral vertebrse, this extensive fusion giving the pelvis a rigidity which compensates for the lack of a pubic union. The ischium partly forms the side of the pelvic cavity. The pubis is mainly attached to the ischium along the lower border and bends inward to form the incomplete floor of the pelvic cavity. The ilium, ischium and pubis are united at the acetabulum or articular cavity for the reception of the head of the femur. The femur articulates at its distal extremity with the patella, tibia and fibula. The latter bone is united to the tibia, but does not ex- tend to its distal articulation. The tibia is comparatively long. ANATOMY OF BIKDS 5 It has two articular surfaces on its distal extremity which articulate with the tarso-metatarsal bone. The tarsus is absent in birds. In males the tarso-metatarsus exhibits a slightly curved conical projec- tion near the distal third for the support of the spur. Four digits articulate with the distal extremity of the tarso-meta- tarsus. Three are directed radially cephalad. The internal digit has three phalanges; the middle, four and the external, five. The fourth digit is directed caudad and has two phalanges succeeding a rudimentary first metatarsal bone attached to the metatarsus by fibro-cartilaginous tissue. The distal bone of each digit is covered by a horny claw. MUSCULAR SYSTEM In general the muscles of birds correspond to those of mammals, with such modifications as are most suited to the mechanism of avian structure. The tendency, especially in turkeys and fowls, is to- ward extensive ossification of the muscle tendons. This is partic- ularly noticeable in the tendons of the legs but may also be observed in the wing and neck in some cases. The fowl and turkey also present a marked contrast in the appearance of the muscles of the breast and wings as compared with those of the legs. The breast and wing muscles are white, due to the relatively small amount of sarcoplasm in the muscle fibers. The red muscles are rich' in sarco- plasm. White muscles are more powerful but have less endurance than red ones. Free flying birds have red pectoral or breast muscles. The pectoral muscles are two in number, the superficial or great and the deep or small pectoral. The former depresses the wing and the latter elevates it. These muscles are very massive. The great pectoral muscle is attached to the clavicle, to the sternal crest near its border, to the posterior lateral process of the sternum and to the last ribs. It is inserted into the lateral tuberosity near the head of the humerus. It is this muscle that propels the bird in flight. The small pectoral muscle originates from the portion of the ventral face of the sternum not occupied by the great pectoral and also from the clavicle and membrane between the latter and the sternum. Its tendon is inserted into the humerus opposite that of the great pectoral muscle after passing through the foramen trios^ seum which acts as a pulley. This foramen is formed by the union of the scapula, coracoid and furculum. The diaphragm does not exhibit the muscular development of that 6 DISEASES OF DOMESTICATED BIEDS of mammals. It is principally membranous with fine muscular bundles attached to the ribs. Two thin, delicate membranes com- pose the diaphragm and divide it into two planes, a pulmonary and a thoracic-abdominal plane. The former is spread over the in- ferior face of the lungs and is attached to the ribs on its border. It assists in respiration. The thoracic-abdominal plane has its origin on the dorsal spine in common with the pulmonary plane. It is convex anteriorly and extends to the sternum, dividing the body cavity into a thoracic and an abdominal cavity. It also assists in respiration and is particularly concerned with the abdominal air sacs. The pectineus muscle assists in the mechanical flexion of the toes in the act of perching on the roost. It originates on a tuberosity of the hip bone in front of the acetabulum and is continued by a long thin tendon to a short distance distad from the head of the tibia where it joins the flexor perforatus of the three anterior digits. CIRCULATORY SYSTEM The heart of birds is cone shaped, short and wide in the ostrich, elongated and possessing a more acute apex in the common fowl. It is placed in the anterior extremity of the thoracic cavity. Three veins, two anterior venae cavse and one posterior vena cava, terminate in the sinus of the right auricle. A peculiarity of the heart of birds is the absence of a tricuspid valve at the right auriculo-ven- tricular opening. Instead, a strong muscular fold which becomes closely applied to the ventricular septum during systole prevents re- gurgitation of blood into the auricular cavity. Two pulmonary veins empty into the left auricle. The left auriculo-ventricular opening is provided with a bi-cuspid or mitral valve. The pulmonary artery and aorta each has a semilunar valve. Arteries. The aorta gives off two innominate arteries, right and left brachio-cephalic, on leaving the heart and then passes over the right bronchus to become the descending or dorsal aorta. It con- tinues along the spine, giving off numerous branches, to the coccygeal region where it separates into three terminal arteries. The two carotids leave the innominate arteries and curve toward the ventral median line of the neck where they ascend in close prox- imity to each other to near the head. At the angle of the jaw each carotid divides into the external and internal carotid arteries. The arteries, especially those of the head and viscera, are distinguished ANATOMY OF BIRDS 7 by their frequent anastomoses. This is also true of the veins of birds. Veins. The blood is returned to the heart by three trunks, the two anterior vense cavse and the posterior vena cava. The right jugular exceeds the left in size. The two communicate with each other by means of a cross branch at the base of the cranium. Lymphatics. The lymphatics of birds do not form two strata, a superficial and a deep seated, as in mammals. The latter only is observed. Lymphatic glands are few. The most conspicuous are located at the base of the neck and in the anterior thoracic cavity. They are replaced by plexuses of IjTiiphatic vessels surrounding the principal blood vessels. From the aortic plexus arise tw^o thoracic duets which pass cephalad on the ventral surface of the lungs and terminate respectively in the jugular vein of the same side. NOEMAL AVIAN BLOOD In birds as in mammals the blood is composed of a straw colored fluid or plasma in which float several types of blood corpuscles. One important difference between avian and mammalian blood, excepting the camel, is the presence of nuclei in the red corpuscles of the former. The formed elements or corpuscles are divided into two main divisions, the red cells or erythrocytes and the white cells or leucocytes. These elements vary greatly in number in different birds, and even in the same bird at different ages. Each cubic millimeter of an adult fowl's blood contains approximately 3,250,000 red cells and 26,000 white cells, giving a percentage relation of 125 to 1. In certain pathologic conditions this relation is markedly changed, the red cells rapidly decreasing and the white cells increas- ing in numbers. Red blood corpuscles or erythrocytes are straw colored, nucle- ated, oval, flattened discs, about 12 microns in length and 7.3 mi- crons in width. The nuclei take a deep blue stain with methylene blue, or Giemsa. The surrounding protoplasm takes a light yellow with methylene blue and a pink color with Giemsa's stain. White blood corpuscles or leucocytes are nucleated, colorless cells, rounded or irregular in form. They exhibit ameboid movement in the blood stream, some being more actively motile than others. The variations in their size, character of the nuclei, pres- ence of granules and character of the inclosed granules dift'erentiate these cells into five varieties. These varieties with their percentage ratio are as follows : 8 DISEASES OF DOMESTICATED BIEDS Small mononuclear leucocytes (lyraphocytes) 40 Large mononuclear leucocytes 18 Polymorphonuclear leucocytes 35 Eosinophiles 4 Mast cells 3 Lymphocytes. In these blood cells the nucleus is rounded or oval and almost completely fills the cell. It stains a deep blue with Giemsa. The narrow band of cell body stains a lighter blue and is not readily differentiated from the nucleus by ordinary staining. The lymphocytes are from 5 to 7 microns in diameter. Large mononuclears have a round or oval nucleus surrounded by a well defined border of cell protoplasm. The nucleus takes a deep blue stain, the cell body a pale blue. The cell diameter is 10 to 15 microns. Polymorphonuclears have the appearance of having several nu- clei held together by threads or nuclear bands. They contain con- siderable protoplasm inclosing rod shaped or rounded granules. The nucleus stains blue, the protoplasm, a lighter color and the granules violet or brownish red with Giemsa's stain. Diameter, 10 to 15 microns. Eosinophiles have an irregular nucleus. The cell protoplasm is filled with rounded granules which stain a bright red with Giemsa's stain. The nucleus takes a blue stain and the cell body a pale blue. Diameter, 12 microns. Mast cells have a lobulated nucleus which stains a deep blue. The cell protoplasm takes a pale stain. The granules are small and rounded and stain a dull violet with Giemsa and a deep blue with methylene blue. Diameter, 8 to 10 microns. Other blood cells of less importance which may be observed are as follows : Blood platelets are small colorless discs with granular centers. They are 3 to 4 microns in diameter and are usually found in small heaps of 6 to 8 cells. Shadow cells contain a rounded or broad oval nucleus which takes a deep blue stain. The cell body is colorless and not well de- fined or irregular in outline. These apparently represent red blood corpuscles undergoing degeneration. The stroma of the corpuscle loses its pigment, becomes colorless and gradually disappears leaving the nucleus partially or wholly separated. They are especially nu- merous in pathologic blood. Microblasts and macroblasts are found in the blood of voung ANATOMY OF BIRDS 9 fowls. These represent red corpuscles which are smaller and larger respectively than the average red corpuscle. Myelogenous leucocytes appear frequently in young fowls. They are like mast cells except that their protoplasm is vacuolated. NERVOUS SYSTEM The nervous system of birds, with few exceptions, corresponds with that of mammals. However, there are several modifications which are of considerable interest. The cerebral hemispheres of the brain are well developed but have a smooth surface in contrast to the convoluted surface observed in the cerebrum of mammals. The cerebellum is conspicuous by the smallness of its lateral lobes. The optic lobes are placed in a lateral inferior position at the sides of the cerebellum. The large size of the optic chiasma and nerves indicates the paramount importance of the visual apparatus. The diameter of an optic nerve is equal to that of the spinal cord in its dorsal region. The olfactory lobes are relatively small. The hippocampi are absent in the cerebrum of birds. An important fea- ture of the nervous system of birds is the absence of nervous tracts leading to the spinal cord from the cerebrum. The cerebrum does however exert an influence over the rest of the nervous system through its nervous tracts connecting it with the other divisions of the brain. The anatomical evidence of the absence of nervous tracts between the cerebral hemispheres and the spinal cord is supported bv the absence of any marked defects of movement succeeding the removal of the cerebrum. The fowl so treated, on recovery from the operation, is not sensitive to light or sound. It fails to pick up grains and must be fed. Movement is not interfered with as the bird constantly walks about aimlessly. Its avoidance of obstacles shows that it is giiided by some obscure means. Ability to perch and to maintain its balance is not lost. The weight of the brain of a medium sized fowl is ten grams. The spinal cord of birds extends into the coccygeal vertebrae. It is cylindrical throughout its length except in the sacral and cervico- dorsal regions where two expansions are noted. The dorsal columns of the cord diverge from each other in the sacrum to form the cavity kno^ni as the sinus rhomboidalis which represents a ventricular dilatation of the spinal canal. The brachial plexus is formed by the last cervical and first two dorsal spinal nerves in ducks and geese and 10 DISEASES OF DOMESTICATED BIEDS by the last three cervical and first thoracic spinal nerves in fowls, turkeys and pigeons. It furnishes branches to the pectoral region and wing. The pelvic region and legs are supplied by the lumbo- sacral plexus which is formed by two lumbar and four sacral spinal nerves. The spinal nerves vary in number according to the number of vertebrse present in each species. They arise from the spinal cord by two roots. The anterior or ventral root is motory, the posterior or dorsal, sensory in function. The ganglia on the latter are propor- tionately large. ALIMENTARY SYSTEM The alimentary system of birds differs to a considerable degree from that of other animals. There is no provision for mastication of food in the mouth owing to the absence of teeth. The food is taken up by the beak and is immediately passed by the tongue into the pharynx. From there it enters the esophagus and is carried to the crop where it is stored, partially softened, and slowly passed on to the proventriculus or glandular stomach. The gall bladder is absent in the pigeon and ostrich and occasionally in the guinea fowl. Mouth. The mouth is triangular in shape in such birds as the chicken, turkey, pigeon and canary. In the duck, goose and ostrich the mouth is comparatively long, with parallel borders and rounded anterior extremity. The roof of the mouth or hard palate is di- vided in the median line from near its anterior extremity to the pharynx, thus allowing free communication with the nasal passages. The soft palate observed in mammals is absent. The pharynx is relatively voluminous and permits the passage of large grains, or food masses. On its floor is the entrance to the larynx. The esoph- agus lacks the well developed muscular wall of mammals but rela- tively has a much greater diameter. Crop. Gallinaceous birds possess a crop or ingluvies which rep- resents a dilatation of the esophagus near its entrance to the thoracic cavity. Its wall, like that of the esophagus, consists of an outer membrane, a longitudinal muscular layer, a circular muscular layer, and an inner mucous membrane. Passage of its contents to the first stomach is aided by a wide circular muscle in the subcutaneous tissue surrounding the crop. Palmipeds, such as ducks and geese, are not provided with a distinct crop. Instead, the cervical portion of the esophagTis may become greatly distended in such a manner as to form a lone; fusiform reservoir. Fig. 2. Diagrammatic representation of the principal internal organs of the fowl. 1, tongue; 2, pharynx; 3, up- per portion of esophagus; 4, crop; 5, lower portion of esophagus ; G, proven- triculus; 7, gizzard; 8, origin of duo- denum ; 9, first branch of duodenum ; 10, second branch of duodenum; 11, origin of floating portion of small in- 29.. testine; 12, small intestine; 12', ter- minal portion of small intc'^tine; 13, free ends of ceca; 14, origin of ceca; 15, rectum; 16, cloaca; 17. vent; IS. mesentery; 19, left lobe of liver; 20, right lobe of liver; 21, gall bladder; 22, spleen; 23, pancreas; 24, lung; (Heart not shown but located approxi- mately here) ; 25, ovary; 2(), o\iduct; 27, kidney; 28, ureter; 29, up])oi larynx; 30, trachea; 31, lower larynx or syrinx ; 32, bronchus; 33, cleft palate; 34, common ori- ¥• . fice of eustachian tubes. (Redrawn from Chauveau, with sliglit additions) ■/3. 12 DISEASES OF DOMESTICATED BIEDS In pigeons the crop is divided into two lateral pouches. In both male and female, marked changes take place in the mucous mem brane shortly before the young are hatched. The membrane becomes thickened, epithelial cells are rapidly proliferated, undergo fatty degeneration and lead to the formation of a milky fluid which accu- mulates in the depressions between the ridges of the mucosa. This fluid is used to feed the young during the first days of life. A certain amount of fluid is secreted by the alveolar glands of the esophagus which together with the water consumed serves to soften grains to some extent and also to produce a slight fermentation of the crop contents. The crop has no secretory glands other than mucous glands. It is connected with the proventriculus or first stomach by a continuation of the esophagus which passes into the thoracic cavity and along the ventral face of the left lung. Proventriculus. The proventriculus is small and fusiform in shape. Its walls are thick and contain numerous secretory glands which pour out gastric juice. The food is not held in the proven- triculus to be digested but after becoming saturated with the gastric secretion is forced into the gizzard where it is triturated by the powerful muscles of this organ with the aid of pebbles picked up by the bird. Gizzard. The gizzard or ventriculus bulbosus is a dense, mus- cular organ, flattened on two surfaces, with rounded border. In- ternally it is lined by a thick, tough, corrugated membrane which incloses a cavity of considerable volume, in which may be found food in various stages of disintegration and numerous pebbles, or bits of stone. Secretion of gastric juice also takes place in the gizzard according to Jobert. However, this organ acts principally in a mechanical way to grind the food and serves as a substitute for teeth. It is more highly developed in grain eating birds than in those subsisting principally on fish or animal food. In strictly carnivorous birds such as eagles, or hawks, the dense muscular wall is absent, or is limited to a portion of the organ, the remainder consisting of a membranous cul-de-sac. When reduced to a semi- fluid mass the food is released into the duodenum or first portion of the intestine, which joins the gizzard at a point near the entrance of the proventriculus. Intestines. On leaving the gizzard the duodenum extends pos- teriorly, bends on itself and returns to near its origin. Between its two parallel branches rests the pancreas which gives off its secretion into the lumen of the duodenum near its termination. ANATOMY OF BIRDS 13 The pancreatic juice acts on the starchy material while the secre- tion of the proventriculus acts on the proteins in the food. Suc- ceeding the duodenum are, according to some writers, the other two divisions of the small intestine, the jejunum and ileum. These form several convolutions and are continued by the rectum to the cloaca. At the point of juncture of the small intestine and rectum, in certain species of birds, are found two elongated diverticula lead- ing from the intestine. These are the ceca or blind pouches. In grown fowls and turkeys they are from 4 to 7 inches in length and may be distended to a diameter of ^ to % of an inch. Especial importance is attached to them because of the fact that they are the seat of marked lesions in coccidiosis of chickens, and of turkeys, and in infectious entero-hepatitis of turkeys. In some species of wild birds, the ceca may reach a length of 10 inches while in others they are absent or merely rudimentary. Their function is apparently the retention of food material which has not been absorbed in passage through the small intestine. The cloaca serves as a common cavity for the entrance of the intestine, ureters, oviduct in the female, and vasa deferentise in the male. It is divided into three parts. The rectum enters the first part, the ureters and genital canals open on the lateral faces of the second and the bursa of Fabricus, a blind sac or glandular cavity, opens on the dorsal wall of the third or outer division. The bursa of Fabricus may disappear in adults. The one oviduct in the female opens on the left side of the second division. The material from the intestine and ureters is held in the cloaca to form the character- istic droppings and is then passed out through the anus or vent. Mucosa of the alimentary canal. The alimentary canal is lined internally by a mucous membrane which is thick, and com- posed of many layers of cells in the mouth, pharynx, esophagiis and crop. The mucosa is thin, and composed of one layer of columnar epithelial cells in the proventriculus, gizzard and intestine. In the gizzard the membrane is covered by a homy surface layer. In the submucous tissue of the mouth and pharynx are found several pairs of glands. These, however, are not considered as true salivary glands but produce a mucous secretion. The esoph- agus exhibits numerous alveolar secretory glands in the submucous tissue. The glandular stomach is conspicuous for the layer of tubular secretory glands which are set perpendicularly to the mu- cous membrane and which pour their secretion of gastric juice into the interior of the stomach. Over the mucous membrane of the 14 DISEASES OF DOMESTICATED BIRDS gizzard is a tough horn-like covering formed by the hardening of the products secreted by the underlying simple glands. The mucous membrane of the intestine presents innumerable cylindrical elevations known as villi. It is through these that the digested food is assimilated and carried by means of the chyle- vessels or lacteals to the portal vein and thence to the liver. !N^u- merous goblet cells for the secretion of mucin are present in the villi. Liver. This organ is dark brown in color and composed of a right and left lobe, the former being the larger. The right lobe has a gall bladder on its ventral surface, while the bile from the left lobe is poured directly into the duodenum through a separate bile duct, the hepatic or choledic duct, which empties a short dis- tance behind the two pancreatic ducts. The cystic duct opens caudad of the hepatic duct and drains the gall bladder. Pancreas. This organ is long, narrow and lobulated. In color it is pale red. It is highly developed in birds and occupies the space between the two branches of the duodenum. Two or some- times three ducts carry its secretion into the ascending arm of the duodenum near its extremity and just anterior to the hepatic duct. RESPIRATORY SYSTEM The organs of respiration in birds differ markedly from those of mammals. They resemble more nearly the reptilian type of formation. Air passages. The nostrils are represented by two narrow openings at the base of the upper mandible of the beak. The nasal chambers are short and narrow and are separated by a septum which is partly bony and partly cartilaginous. The turbinated bones of mammals are represented by three cartilaginous structures. The nasal cavities open into the mouth by a common, elongated slit in the median line of the hard palate. Cavities known as the sub- orbital or infraorbital sinuses occupy a position on either side of the head. They commiinicate with the nasal cavity by narrow passages which extend from a comparatively low level in the sinus, upward into the nasal cavity. The arrangement prevents natural drainage of the sinuses. Birds possess an upper and a lower larynx. The former cor- responds to the larynx of mammals but serves only as an opening for the passage of air. An epiglottis is absent but its function is ANATOMY OF BIEDS 15 assumed bj two lateral lips which close the laryngeal opening dur- ing the passage of food through the pharynx. The inferior larynx, or syrinx, is the voice organ. It is located in the anterior thorax at the division of the trachea into two bronchi. The end of the trachea, in fowls, is compressed from side to side and forms the wall of the syrinx. In certain birds the syrinx is complicated in structure and may be formed of a number of tracheal rings ex- panded to form large bony cavities. Sound is produced by the vibration of membranes within the walls of the lower larynx. The trachea is long in birds and its cartilaginous rings are com- plete. In the bronchi the cartilaginous rings are incomplete, a portion of the wall being formed by a membrane. The bronchi enter the lungs at the anterior extremities, become membranous and give off branches to these organs and to the air cells of the thorax and abdomen. The lungs are pale or bright red in color and of a spongy tex- ture. They are closely applied to the dorsal surface of the thorax and present several deep indentations into which the ribs fit. The ventral surface is smooth and is covered by a fold of the diaphragm. Only a small portion of the thoracic cavity is occupied by the lungs. Air sacs. These are membranous receptacles into which the air is carried bv terminal branches of the bronchi. Through these branches the cells are in direct communication with the lungs. They also, with certain exceptions, communicate with canals or spaces in the various bones, to which they supply air. The membranous wall is composed of two delicate layers, an external serous and an in- ternal mucous layer. The latter is a continuation of the mucosa of the bronchi, the former is regarded as a reflection of the peritoneum and pleura. Nine air sacs are found in the thoracic and abdominal cavities. The single anterior thoracic air sac surrounds the inferior larynx, bronchi and large blood vessels of the region. It receives air from the anterior part of the lungs by two openings and com- municates with deep seated air cells of the neck and with the cla- vicle, coracoid, scapula and sternum. Two lateral thoracic sacs receive air from the internal edge of each lung opposite the base of the heart. They transmit air currents to the air cells of the axillary region, vertebrae, ribs and humerus. The diaphragmatic air cells are four in number, two anterior and two posterior. They are inclosed between the two diaphragmatic folds. Air is received from the lungs but is not communicated to bony structures from these. Two abdominal air sacs each receive a long voluminous bron- 16 DISEASES OF DOMESTICATED BIEDS chial branch which leaves the respective lung on its posterior in- ferior surface. These sacs extend from the lungs to the cloaca and are the largest in the body. They supply the bones of the pelvic region and femur in those species in which these bones are aeri- ferous. The femur of the pigeon and the humerus of the ostrich have no air spaces but retain their marrow. UEINAEY SYSTEM The urinary tract is composed of two kidneys each drained by a ureter lying along its ventral face and proceeding caudad to empty into the cloaca posterior to the terminus of the rectum. The kid- neys are elongated, reddish brown bodies divided into three prin- cipal lobes. They are closely applied to cavities in the pelvis on each side of the spinal column. These organs are not divided into macroscopically visible cortical and medullary zones as in mammals but have a homogeneous structure. In texture they are quite soft and rupture easily when pressed by the finger. The ureter does not originate in a renal pelvis but is formed by the union of several uriniferous tubules along the ventral face of the kidney. Its course may be traced by the white color of the urates which it carries, a material corresponding to the urine of mammals. GENEKATIVE SYSTEM The male generative organs consist of two testicles each provided with a vas deferens or excretory duct. The testicles are oval shaped organs situated in the sub-lumbar region at the anterior extremities of the kidneys. They vary greatly in size at different seasons, but show a remarkable development during the breeding season. The two vasa deferentise pass along the kidneys by the side of the ureters, exhibiting transverse convolutions along their course. Each opens on a small papilla situated in the uro-genital division of the cloaca. The base of each papilla is surrounded by a plexus of blood vessels which serve the purpose of an erectile tissue during coitus. In the drake and gander a long single penis is developed. The female generative organs consist of a single ovary and an oviduct situated on the left side of the abdominal cavity. The right ovary and oviduct usually fail to develop. Occasionally a rudi- mentary right oviduct is present. In one actively laying hen Gal- lagher observed a right oviduct which was nearly as long as the ANATOMY OF BIEDS 17 left oviduct and equally voluminous. Its anterior extremity ex- hibited an infundibular membrane in contact with the ovary. Pos- teriorly it opened into the cloaca opposite the left oviduct. The appearance of its mucous membrane suggested that it was capable of functionating. The ovary is placed in the left sub-lumbar region, opposed on its superior surface to the ribs. In fowls it contains from twelve to fifteen hundred germ cells in various stages of development from microscopic granules to fully formed yolks in functionating ovaries. The oviduct terminates in the urogenital division of the cloaca just anterior to the left ureter. It is divided into five regions, each of which has a specific function. The first region, the infundibulum, is a delicate membrane of a funnel-like form which receives the ovum. Succeeding this is the part secreting albumen followed by the isthmus which secretes the shell membrane. The uterus or fourth region forms the shell. The last region, the vagina, is short and is provided with a sphincter muscle at its entrance to the cloaca. SKIN AND ITS APPENDAGES The skin of birds is without sweat glands. There are some small glands in the exterior passage of the ear, which secrete an unctious fluid. There is also a protruding glandular organ located above the coccyx between the tail feathers and known as the uropygium or rump gland, an organ peculiar to birds. It is round or oval in form and is divided into two halves by a medial septum. The exit passage is through a teat-like cone which projects above the level of the skin. Two external orifices are observed in the gland of the duck. In hens the gland is about the size of a pea, in geese about as large as a hazel nut and in the swan about an inch and one half in length. Its function is to secrete an oily fluid for water-proofing and dressing the feathers. The secretion is taken up by the beak and spread over the plumage. The feathers are complicated modifications of epidermic struc- ture. Each feather is composed of a quill, a shaft and a vane. The quill is embedded in a feather follicle of the skin and extends outwardly to the point where the barbs of the vane arise. It has an opening at its base for the reception of the dermal papilla and another opening at its point of junction with the vane. The shaft continues the quill to the extremity of the feather. The vane con- sists of two rows of barbs which arise on opposite sides of the shaft. 18 DISEASES OF DOMESTICATED BIEDS These barbs each carry two rows of barbules which interlock with those of adjoining barbs. The feather is elevated by a small muscle located in the skin at the root of the quill. The comb and wattles of fowls and the caruncle of turkeys are developed from the skin. INCUBATING PERIODS The length of time necessary for hatching eggs by natural incu- bation shows some variation. The normal period for the common hen is 21 days but this period may be shortened to 19 or 20 days by warm weather and unusually constant brooding by the hen. On the other hand, if the eggs have been abandoned and allowed to cool for a time, hatching may be delayed for several days. These varia- tions doubtless occur in the case of other birds. The incubation periods of various birds, subject to variations as explained are as follows. Table I. — Incubatixg Periods Hen 21 days Pheasant 25 days Duck 28 days Peafowl 28 days Guinea-fowl 25 days Goose 30 days Turkey 28 days Pigeon 18 days PULSE, TEMPERATURE AND RESPIRATION" Loer has made an extensive series of observations on the tempera- ture, frequency of pulse and respiration in domestic birds. His re- sults are summarized as follows. Frequency of heart beat as determined by digital palpation after opening the thoracic cavity was 128 to 140 per minute in the hen and 141 to 149 per minute in the pigeon. The heart beat of the duck as determined by auscultation varied from 150 to 180 per minute. ANATOMY OF BIKDS 19 Table II. — Eespiration Frequency and Normal Temperatures of Birds Species Respiration frequency Centigrade degrees Fahrenheit degrees Min. Max. Min. Max. Min. Max. Hen Turkey Pheasant Pigeon Duck Goose 12 12 16 16 12 28 16 36 28 20 40.5 40.0 41.0 41.0 41.0 40.0 42.0 41.5 44.0 43.0 43.0 41.0 104.9 104.0 105.8 105.8 105.8 104.0 107.6 106.7 111.2 109.4 109.4 105.8 REFERENCES 1. Boyce and "Warrington. Observations on the anatomy, physiology and degenerations of the nervous system of the bird. Tr. Boy. Soc, Vol. 191, 1899. 2. Bradley. The structure of the fowl. London : A. & C. Black, Ltd., 1915. 3. Burnett. Clinical pathology of the blood of domesticated animals. New York: The Macmillan Cbmpany, 1918. 4. Chauveau. Comparative anatomy of the domesticated animals. New York: D. Appleton and Company, 1905. 5. Ellenberger. Handbuch der vergleichenden mikroskopischen Anat- omic der Haustiere. Erster Band. Berlin : Paul Parey, 1906. 6. Ellenberger u. Baum. Handbuch der vergleichenden Anatomic der Haiistiere. Berlin: August Hirschwald, 1900. 7. Kaupp. The anatomy of the domestic fowl. Philadelphia : W. B. Saunders Co. 8. Loer. Vergleichend physiologische Untersuchungen liber die normal Rektal temperature, Atem und Pulzfrequenz der Vogel. Inaug. Diss. Bern, 1909. 9. Owen. Comparative anatomy and physiology of vertebrates. Birds and mammals, Vol. H. London: Longmans Green & Co., 1866. 10. Steen. Blutuntersuchungen bei gesunden Hiihnern. Inaug. Diss. Leipzig, 1913. CHAPTER II HYGIENE AND SANITATION SECURING HEALTHY STOCK In establishing a flock of poultry it is highly important that pre- cautions be taken to prevent the introduction of disease with the original stock. It is a common desire among beginners, to con- sider purchasing adult birds, in order to secure speedy returns. It should be borne in mind that the number of instances in which healthy young pullets may be purchased is comparatively rare. Too often hens are sold because they are old and past the best laying period, or because the flock has become unprofitable because of some disease. Fowl cholera, avian tuberculosis and diphtheria are com- monly introduced by the purchase of adult stock. Starting a flock from hatching eggs or day old chickens is the least dangerous method of introducing stock but there remains the danger of introducing white diarrhea. RELATION OF SOIL TO HEALTH "Well drained soil is desirable in that the presence of moisture and mud is minimized. A wet soil favors parasites. Least desir- able for poultry yards is sticky clay or adobe. In wet weather the latter soil collects on the toes of chickens in the form of balls so large as to impede walking. Chickens kept on such soil require individual treatment to free the toes, and in doing this they are liable to be injured. The continued use of a given area of soil for poultry, results in its becoming excessively infested with the eggs of various para- sites and consequently a source of danger to the birds kept thereon. Therefore, it is highly desirable that chickens be not kept on the same soil year after year. The problem of securing fresh areas for chickens is solved in various ways. Where the chicken house is a permanent, immov- able structure, yards may be fenced off on either side and used in alternate years. When birds are kept under the colony system, the structures necessary for the fowls are built on skids. A team may 20 HYGIENE AND SANITATION 21 be hitched to the building to move it as desired. A very desirable method of securing fresh soil is to move chicken houses in harmony with a crop rotation system. In this manner a given area is cropped for three or four years after chickens have occupied it, before the land is used for birds again. When quarters are so cramped that no change can be made in the chicken yards, deep plowing is of some advantage in turning up fresh earth and covering contaminated soil. Small areas may be sprinkled with lime, or be thoroughly soaked to some depth by the liberal application of a disinfectant. LOCATION AND CONSTRUCTION OF POULTRY HOUSES Dampness is very injurious to fowls, and consequently the build- ings should be located with reference to securing good drainage after rains. Where choice is possible, sandy soil should be chosen on account of its permeability to water. Provision should be made to secure free ventilation without drafts of air. 'No especial effort need be made to secure warmth in a poultry house in the daytime even in a severe climate. The building should be so located as to permit the unobstructed illumination of the interior by sunlight. The frequency with which poultry houses must be cleaned and sprayed with parasiticides should be borne in mind when they are being constructed. Any structural detail which interferes with the free access to any part of a house by a man, should be avoided for it will interfere with routine cleaning. The habit displayed by mites, of collecting in cracks, should be recognized in providing buildings with a minimum of such places where vermin may col- lect. ]^est boxes, perches and similar fittings should not be per- manently attached to the building, but should be readily removable for cleaning and spraying. Certain details of construction will at least constitute impedi- ments to the dissemination of parasites and infective material from bird to bird. Thus, stretching chicken wire under the roosts will largely prevent birds from coming in contact with droppings in the roosting quarters. In houses designed for laying hens in a cold climate, each bird should be provided with from three to four square feet. Exercise, which is absokitely essential to health, will be provided by mixing some of the feed with clean litter on the floor. 22 DISEASES OF DOMESTICATED BIEDS CLEANING AND DISINFECTING BUILDINGS Previous to applying a disinfectant to a building it is essential that all dirt and filth be removed by sweeping, scraping or washing. This is necessary in order to expose the woodwork to the unob- structed action of the disinfectant. A considerable range of choice of disinfectants is possible. Selec- tion of a disinfectant will be made on the basis of relative cheap- ness, availability and suitability to the requirements imposed by the article to be disinfected. Compound solution of cresol. This substance also kno^vn as liquor cresolis compositus, consists of a mixture of equal parts of cresol with a linseed oil-potash soap. It mixes well with soft water, but is less satisfactory in this respect when hard water is used. This disinfectant may be obtained at any drug store and on account of cheaper price is to be preferred to carbolic acid. It is employed for general disinfection in the proportion of four ounces to a gal- lon of water. Formaldehyde gas. Formaldehyde is ordinarily obtainable in a forty per cent solution in water, a product which is known as formalin. Formaldehyde is a strong non-poisonous disinfectant, is not hindered in its action by albuminous material and in general is not harmful to metals. The gas is a good surface disinfectant and may be employed in disinfecting incubators and such rooms as may be easily made air tight. Ordinary poultry houses are not constructed tightly enough to warrant the trouble of sealing all cracks. Under conditions warranting its use, the room in which the gas is to be used is carefully examined and all cracks are sealed with strips of paper applied with paste. The gas is liberated from the watery solution by mixing formalin with needle crystals of potassium permanganate. For each 1,000 cubic feet of air space there should be used 20 ounces of formalin and 16% ounces of potassium permanganate. The permanganate is placed in a shallow pan with flaring sides and the proper amount of formalin is poured in the pan. Provision should be made to protect the floor as the ingredients of the mixture may splash during the violent reaction that ensues. Splashing will be minimized by using a bucket, but in this case considerable formaldehyde gas may con- dense on the walls of the vessel. After mixing the chemicals, the operator should leave the room promptly to avoid inhaling the irri- tating fumes. The room should be kept sealed for eight hours. HYGIENE AND SANITATION 23 This method of fumigation is not applicable when the temperature falls below 05° F. for the gas condenses under such conditions. Disinfection may be accomplished by spraying objects with a mixture of 5 parts of formalin to 95 parts of water. Carbolic acid or phenol. Pure carbolic acid exists at ordinary temperatures as needle-like crystals. This substance is frequently used in the form of liquefied carbolic acid which consists of 9 parts of the crystals mixed with 1 part of water. Carbolic acid is ordi- narily emj^loyed as a disinfectant in a five per cent solution of the crystals. As the crystals dissolve slowly, solution is hastened by the use of hot water. The fluid may be applied liberally to surfaces as a spray, or fabrics and implements may be immersed in the fluid for an hour. Carbolic acid is somewhat expensive, and on this account some other cheaper agent may be employed. The substance in ques- tion should not be confused with " crude carbolic acid " which is quite diiferent in composition. Crude carbolic acid. Commercial crude carbolic acid is a by- product of the distillation of coal tar. It contains certain insoluble oils and a mixture of cresols and similar substances which possess disinfectant value. AVhen the content of these is known, an effective disinfectant may be made by including these substances in two per cent solution. The disinfectant in question should not be confused with true carbolic acid (phenol). Chloride of lime. Chloride of lime or chlorinated lime consists of slaked lime which has been exposed to the action of chlorine. It is a white powder which deteriorates in strength rapidly after opening the hermetically sealed container in which it is supplied. This disinfectant is particularly useful where the action of a de- odorant is desired besides a disinfectant. It is commonly employed diluted with water in the proportion of six ounces to a gallon of water. The presence of organic matter interferes with the effective- ness of this agent. Various coal-tar creosote disinfectants. Mixtures of various coal-tar products, principally creosote oil, with soap in the form of emulsions are on the market under a large variety of trade names. The disinfecting value of these products varies greatly, but when the carbolic acid coefiicient is stated, one of these products may be used with assurance as to its efficiency. The expression carbolic acid coefiicient, refers to the relative germicidal value of a product as compared with carbolic acid. Bichloride of mercury or corrosive sublimate. This agent is 2-1: DISEASES OF DOMESTICATED BIRDS usually employed in the strength of 1 part to 1000 parts of water. It is available in the form of tablets mixed with ammonium chloride to facilitate solution in water. A tablet may be added to a certain specified amount of water to make a disinfectant of a definite strene:th. Bichloride of mercury has the disadvantage of attacking metals and its activity is seriously impaired by contact with albu- minoid substances. Its poisonous nature is some disadvantage. Whitewash. Whitewash is made by adding about one pint of water to each two pounds of freshly burned lime. The vessel con- taining the mixture is covered and allowed to stand for about an hour while slaking occurs. Water is then added to the mixture until it is thinned to such a consistency that it may be readily applied. Weather proof whitewash may be made as follows: Slake one bushel of quicklime in twelve gallons of hot water. Dissolve two pounds of common salt and one pound of zinc sulphate in two gal- lons of boiling water. Pour this mixture into the slaked lime and add two gallons of skim milk, mixing thoroughly. Whitewash has feeble disinfectant powers, but is useful in im- proving the illumination of interiors. To a certain extent it covers up infective material and fills up the smaller cracks which might harbor parasites. The value of scattering air slaked lime about poultry houses is questioned in view of the irritation of the eyes and air passages induced by the dust. Application of disinfectants. The frequency with which poul- try houses are disinfected warrants investment in some form of pump. For the smaller establishments, a pump built to be used in a pail may suffice. In larger poultry farms a pressure spray pump mounted in a barrel on wheels forms a very convenient outfit. CLEANLINESS OF FOOD AND DRINKING WATER Feeding troughs may be provided with a cover of slats in the form of a peaked roof. Birds will be compelled to reach through the slats to eat mash, and cannot walk in the feed. Sanitary water fountains entirely prevent birds from walking in the drinking water. Further protection of the drinking water by the use of potassium permanganate is very generally practiced. A saturated solution of this substance is prepared in a large bottle or jar and is kept con- veniently near the drinking fountain. When water is drawn for the birds, enough of the stock solution is added to impart a deep wine color to the water. HYGIENE AND SANITATION 25 POST-MORTEM EXAMINATION The first step in making an autopsy on a bird is to examine carefully the exterior of the carcass for lesions of the diseases which exhibit external manifestations. The skin may show the presence of lice, mites or epithelial tumors. The head may be the seat of bird pox nodules, favus, or swelling due to roup. The skin of the head may present a pale appearance as in infectious leu- kemia, fowl typhoid, coccidiosis and tuberculosis or a congested or darkened appearance as in cholera, enteritis, pneumonia and in- fectious entero-hepatitis. Exudates of diphtheria may be observed in the mouth. Swellings of the joints of the wing or legs may in- dicate tuberculosis or gout. Evidence of diarrhea should be looked for on the feathers surrounding the vent. The general condition of nourishment of the bird is determined by palpation, especially in the breast region. In preparation for the examination of the internal organs it is best to pluck the feathers from the under surface of the body from the base of the neck to the vent and well up on each side of the body beneath the wings. The carcass is then stretched back downward over a table or board and held in position by cords attached to each leg and to the neck near the head. The other ends of the three cords are tied at the sides and one end of the table or board. An- other method of holding the carcass in position is to nail each foot and the neck to the board. Those who have occasion to make frequent autopsies find it convenient to lay the bird out on a shal- low, rectangTilar, flat bottomed tin pan fitted with eyelets on the sides and ends for the reception of cords tied to the feet and neck of the carcass. The pan serves to retain fluids, intestinal contents, etc., which may escape during the autopsy, and also is easily cleaned and disinfected. The internal organs are exposed by making an incision through the skin and body wall on either side of the breast near the base of the wing and continuing it along the side to the vent and then forward to a point opposite the beginning of the incision. The ribs may be cut through with a knife at the cartilaginous articula- tion between the superior and inferior ribs or they may be severed by means of a pair of scissors or bone forceps. The breast bone and abdominal wall can be removed by cutting through the b(mes of the shoulder girdle at the entrance to the chest with bone forceps. 26 DISEASES OF DOMESTICATED BIEDS Peritoneal and other attachments are cleared away with the knife as the inferior body wall is being removed. Before removing any of the organs a general survey of the parts may reveal one of the following conditions : The presence of fluid in the abdominal cavity, which would be suggestive of peritonitis or enteritis; the presence of blood clots in either cavity indicating internal hemorrhage; yolk concretions or other egg material free in the abdominal cavity of females ; tubercular masses on the intestine, liver or spleen ; tumors in the various organs ; or moldy growths in the air sacs, indicating aspergillosis. The liver is then examined. It may be congested or show small necrotic spots in cholera and several bacillarv septicemias or be pale and enlarged in infectious leukemia and fowl typhoid. In tuberculosis fat-like nodules with yellowish centers would be found. In entero-hepatitis the areas of necrosis would be yellowish or greenish. Various sorts of tumors may be present on the surface of the liver. The alimentary tract requires a careful examination since many of the diseases are manifested by lesions at some point along its course. Frequently the congested areas of the mucosa may be de- tected through the serous membrane before the intestine is opened. It is advisable, however, to lay the whole tract open from the crop to the vent. The crop and proventriculus may show congested or inflamed areas as a result of the ingestion of strong irritants or poisons. The gizzard is relatively free of disease but may contain parasitic worms in its wall. The duodenum is often the seat of intense inflammation especially in the septicemic diseases such as cholera and fowl plagiTC. Coccidia also cause congestion of the duodenal mucosa. In infectious entero-hepatitis and coccidiosis the ceca are usually distended with necrotic material and the cecal walls are ulcerated or desquamated. In enteritis the inflammation may involve a considerable portion of the intestinal mucosa and may be observed in any part of the small intestine or in the ceca or rectum. The cloaca is to be inspected for evidence of vent gleet. Intestinal worms may be present in any portion of the intestinal tract. Unless present in comparatively large numbers they should not receive special consideration. Round worms may be found gathered into large masses which tend to obstruct the passage of the contents of the intestine. Wlien numerous they may also produce a catarrhal condition of the intestinal mucosa. Some tapeworms HYGIENE AND SANITATION 27 when numerous cause nodular formations on the intestinal wall which resemble the lesions of intestinal tuberculosis. An enlarged, congested spleen may be associated with the acute bacterial septicemias. An enlarged, firm, mottled appearing spleen would suggest infectious leukemia. In the latter disease the kid- neys are also enlarged and of firmer consistency. Tubercular nod- ules may be present. A gangrenous or cystic ovary or an ovary exhibiting hard, angular, shrunken ova, in the case of the fowl, is practically diagnostic of B. puUorum infection. Occasionally gangrene of the ovary may be due to some other microorganism. In such cases peritonitis is apt to be present. The oviduct should be opened and examined for inflammatory changes, constrictions, tumors or the condition known as egg bound. JSTormally the lungs are found deflated and closely applied to the breast wall. In acute congestion and pneumonia the lungs are distended and stand out in a firm position surrounding the heart. The pneumonic lung is solidified and will sink in water. N^odular growths in the lungs may represent tuberculosis or aspergillosis. The former is much less frequently found involving the lungs of birds than the abdominal organs. Aspergillar nodules are usually accompanied by moldy growths on the mucosa of the bronchioles or air sacs. In young chickens the trachea and larger bronchi are slit open to discover the presence of the red worm, Syngamus trachealis, or of aspergillar growths. Pericarditis, thickened pericardial fluid or hemorrhagic points on the heart indicate a septicemia such as cholera or fowl typhoid. The pericardium and also the liver may be covered by a fine white deposit consisting of urate of soda crystals in visceral gout, or as a result of disturbances of metabolism due to a diseased condition. REFERENCES 1. Kaupp. Poultry diseases and their treatment. Chicago : American Journal of Veterinary Medicine, 1919. 2. Pearl, Surface and Curtis. Diseases of poultry. New York: The Macmillan Company, 1918. 3. Salmon. Diseases of poultry. Washington: George E. Howard & Co. 4. Salmon. Important poultry diseases. Revised by Gallagher and Foster. U. 8. Dep. Agr., Farmers Bull. 957, 1918. CHAPTER III APOPLECTIFORM SEPTICEMIA AND SLEEPING DISEASE APOPLECTIFORM SEPTICEMIA Characterization. The disease is a liigUy fatal septicemic in- fection of chickens caused by a streptococcus. History. The disease was first described by JSTorgaard and Mohler in the United States and later was observed by Magnussen in Sweden. Etiology. The causative organism is a streptococcus, the in- dividual elements being .6 to .8 microns in diameter. There is great diversity in the length of chains. In tissues they are short and in cultures, long. The organism is Gram positive, non-motile, and no capsule for- mation has been observed. It is an aerobe and a facultative an- aerobe. Growth occurs on common solid and liquid media most abundantly at 37° C, and less rapidly at room temperature. In alkaline bouillon growth occurs within 24 hours at 37° C. Long chains develop which form skeins or balls of flocculent ap- pearance which are deposited on the sides and bottom of the tube. After three days the growth settles to the bottom in the form of a white non-viscid deposit. This upon agitation breaks up into nu- merous small particles. After a sparse seeding on agar, growth is visible after 24 hours in the form of small shiny, grayish colonies about 1.5 mm. in diameter. By transmitted light these appear to have a brown center surrounded by an irregular pale bluish border. The max- imum size is attained on the third day. In agar stab cultures, mi- nute spherical grayish white colonies with fimbriated borders, appear along the line of puncture. They do not coalesce, and very slight growth is observed on the surface. The surface colonies on agar plates are very similar to those developing on a sparsely seeded slant culture. The colonies in the depths of the medium are seen as minute pearly points of granular appearance. With the aid of a hand lens the outline ap- 28 APOPLECTIFORM SEPTICEMIA AND SLEEPING DISEASE 29 pears ciliated. Similar but more profuse growth occurs on glycer- ine agar, and serum-gelatin-agar. In stab cultures on gelatin, growth is not observed until the fourth or fifth day. It consists of a finely granular line of minute spherical colonies, grayish white in color. The colonies have a fimbriated border and do not exceed a pinhead in size. The growth is not abundant nor characteristic and does not spread on the sur- face. 'No liquefaction occurs. Colonies on gelatin plates resemble those on agar, but are slightly more opalescent. Growth on blood serum appears within 24 hours in the form of small whitish colonies .6 to .8 mm. in diameter. Sometimes the color has a yellowish tint. The colonies do not coalesce. The water of condensation becomes turbid by reason of the presence of small gray clusters of the streptococci. Growth in milk occurs without causing visible change. In old cultures there is observed a solidification of the lower stratum, vis- ible when the tube is turned upside down. In litmus milk, the blue color is changed to a pale madder pink, indicating acid formation. No gi'owth occurs on potato. No indol is formed. Bouillon containing one per cent of glucose, lactose and saccha- rose, in fermentation tubes, forms a favorable medium. Growth is more profuse than in plain bouillon and extends into the closed arm. Gas is not produced in these sugars, but acid formation oc- curs. Similar results are obtained with galactose, maltose and the alcohols mannite, dulcite and sorbite. No hemolytic effect occurs in Conradi-Drigalski plate cultures. Acid formation occurs on litmus-lactose-agar plates. Morbid anatomy. The skin displays hemorrhagic discolora- tion on the breast and neck, due to diffuse hemorrhages in the sub- cutaneous and muscular tissues. The abdominal cavity contains an abundance of sero-sanguinous exudate. Similar exudate some- times is present in the pericardial sac. The veins of the mesentery are engorged. The liver is greatly enlarged, paler in color than normal and the entire surface is covered wath a semi-organized plastic exudate. The spleen may be similarly swollen. The gall bladder is distended with bile, while the kidneys are hyperemic and swollen. The intestines, especially the duodenum, are observed from the peritoneal surface to be congested in patches. On opening the intestines, the mucosa corresponding to the discolored areas is considerably swollen. The contents of the intestine consist of 30 DISEASES OE DOMESTICATED BIEDS blood stained feces and mucus. The lungs show circumscribed areas of congestion. On opening the cranium a profuse subdural exudate is observed. The meninges are injected and the ventricles contain an abnormal amount of discolored serum. Symptoms. Information regarding symptoms is limited to ob- servations made on the behavior of inoculated cases only. A short time after inoculation, birds display evidence of depression. There is staggering gait with effort to balance with the aid of the wings. If the birds are not disturbed they will lie in one place until death occurs in coma. Sometimes diarrhea occurs immediately before death. Pathogenesis. Fowls are susceptible to intravenous or subcu- taneous inoculation and by the feeding of cultures. The mortality is heavy among fowls when the disease is spreading under natural conditions. Pigeons, rabbits and mice are susceptible. Intravenous inoculation of the duck may cause loss of coordination and death with endocarditis. Sparrows are more resistant than pigeons and chickens but succumb to large intramuscular and intraperitoneal doses. In the dog, intravenous inoculation causes rise of tempera- ture and lameness apparently due to a transitory arthritis. Ab- scesses may occur in the dog, a point of interest in that suppuration has not been observed in other animals. Guinea pigs, swine and sheep prove refractory. Cats may succumb to intraperitoneal in- oculation. Horses exhibit a disturbance of health following intra- venous inoculation. Immunization. It is possible to immunize a fowl by intra- venous inoculation of killed culture so that the bird will tolerate an otherwise fatal dose of virulent culture. Successive injections of virulent culture cause the blood serum to take on protective prop- erties, l^orgaard and Mohler have found this serum administered intravenously in a .5 c.c. dose, protective against a .1 c.c. intra- venous inoculation of culture. SLEEPING DISEASE Synonym. Schlafkrankheit, Schlafsucht, (German) ; maladie du somneil, (French). Characterization. The disease is a septicemic infection of fowls characterized by sjonptoms of sleepiness and caused by an encapsulated streptococcus. History. The disease was first described by Dammann and APOPLECTIFOEM SEPTICEMIA AND SLEEPING DISEASE 31 Maneg'old in Germany and later by Greve in the same country. Symptoms. The symptom most frequently occurring is a more or less marked desire to sleep. The hen sits for hours at a time with closed eyes and ruffled feathers, with the head bent backward in the feathers of the neck. At interv^als the bird awakens and opens the beak wide as if panting. The conjunctiva, usually of one eye only, becomes reddened and markedly swollen. Secretion from the conjunctival sac dries on the edges of the lids. Except when the dis- ease has a very short duration, the comb and wattles gradually become pale. Commonly diarrhea exists for several days and the bird dies in a highly emaciated condition. Birds may die suddenly after showing sjTiiptoms for only a day or less. Morbid anatomy. The carcass exhibits the appearances com- mon in hemorrhagic septicemia, such as distention of the subcu- taneous veins with dark red blood, infiltration of portions of the musculature with bloody, watery fluid. There is bloody, shiny, viscid fluid in the abdominal cavity and the peritoneum is swollen and diffusely reddened. The mucosa of the proventriculus and of the intestine is swollen while that of the latter is diffusely red- dened. The liver is enlarged, brownish yellow in color and is fri- able in texture. It is studded irregularly with dark red hem- orrhages. The spleen is enlarged and the capsule is distended while the pulp is fragile in texture. The kidneys are swollen and dirty yellow in color. The lungs are congested and permeated with nu- merous small, dark red hemorrhages and may be edematous. Fi- brinous exudate may occur on the costal surfaces of the lungs. Punctiform hemorrhages may occur under the epicardium. The heart is distended with coagulated blood. The pericardium is often distended with pale serous fluid and a tough, fibrous layer of ex- udate frequently forms on the pericardium. Smears from the heart blood stained with carbol fuchsin are seen to contain chains of streptococci. The capsules are also seen distinctly enveloping single cocci as well as diplococci. Etiology, The streptococcus causing the disease is designated Streptococcus capsulaius gallinarum. It differs in the length of the chains and in the size of the elements according to the sort of animal in which it appears as a natural disease or into which it is inocu- lated. These differences occur also in artificial cultivation. In animal blood and in fluid media, chains of up to 30 elements are ob- served and in sugar bouillon as many as 100 elements may occur. The size of the single elements varies between .3 and .5 micron. 32 DISEASES OF DOMESTICATED BIKDS The individuals in the chains occur as diplococci. ISTo motility is present. The streptococci are stained by all of the common anilin dyes and are Gram positive. With Kiihn's carbol methylene blue the capsules appear greenish in color. With a modification of Klett's anthrax capsule stain the cocci appear dark blue while the capsules are pale red or pink, with dark red undulating contours. The cap- sules are seen distinctly only in material from the animal body. The streptococci gi-own on the various culture media show them very poorly or not at all. The organism grows aerobically and anaerobically and its optimum growth temperature is that of the body. It thrives best on solid blood serum, and grows well in milk. It can also be grown on meat extract bouillon, gelatin, agar, agar gelatin and grows least well on po- tato. In order to cause rich gTowth an addition of 4 to 6 per cent of glycerin or one per cent of sugar is necessary. Acid is formed in saccharose bouillon and indol in limited amount. Gelatin is not liquefied. It is very sensitive to drying and also to heat. In bouillon cul- tures which have been warmed to 80° C, for five minutes it is killed. At 100° C. it is killed in % minute. One per cent solution of carbolic acid kills in 2 minutes, while a similar solution of liquor cresoli saponatus, lysol, and creolin renders it inactive in three minutes. Pathogenesis. The disease is transmitted to hens by inocula- tion of blood or pieces of organs as well as by inoculation with cul- ture. Infection with the latter succeeds through subcutaneous in- oculation or when finely dissipated bouillon culture is inhaled. In carcasses of birds dead after subcutaneous inoculation, evidence of coagulation necrosis is seen frequently, accompanied by infiltration of the surrounding tissues with bloody or purulent fluid. The time of appearance of symptoms in hens after artificial in- fection varies greatly. Sometimes sickness is noted after six days, with death occurring after seven days more. Again, it is possible for 30 to 70 days to elapse between the time of inoculation and death. The disease is transmissible by subcutaneous inoculation to pigeons, rabbits, white mice, gray mice, and lambs. The course of the disease is more acute in pigeons than in hens, but the lesions are similar. Dogs, ducks and guinea pigs do not succumb to artificial infec- tion. Differential diagnosis. The observation of capsules surround- APOPLECTIFOEM SEPTICEMIA AND SLEEPING DISEASE 33 ing the streptococci in smears from tissues will differentiate the af- fection from apoplectiform septicemia, a very similar infection. Prevention. Measures similar to those recommended in the discussion of fowl cholera are indicated. Treatment. 'No medicinal treatment is available. REFERENCES 1. Dammann n. Manegold. Die Schlafkranklieit der Hiiliner, Deutsche tierdrztl. Wchnschr., Bd. 13, 1905, S. 57Y. 2. Greve. Beitrasr zur Kenntniss der Streptokokken-Krankheit (Schlaf- krankheit) der Hiihner. Deutsche tierdrztl. Wchnschr,, Bd. 16, 1908, S. 213. 3. Magnnssen. Ueber Eine fiir Europa neue Hiibnerseucbe. Centralhl. f. BaMeriol (Etc.), Oriq., 1, Alt., Bd. 56, 1910, S. 411. 4. Norgaard and Moliler. Apoplectiform septicemia in chickens. TJ. S. Dep. Agr. Bureau. Animal Indust. Bull. 36, 1902. CHAPTER IV FOWL CHOLERA Synonyms. Chicken cholera, pasteiirellosis avium, cholera gal- linarum, hemorrhagic septicemia of fowls; Hiihnercholera, (Ger- man) ; cholera des ponies, (French). Characterization. Fowl cholera is an acute contagious septi- cemic disease affecting domesticated birds, which is accompanied by febrile temperature and causes heavy mortality. The popular desig- nation " cholera " is frequently used to indicate any highly destruc- tive disease of poultry. Etiology. The causative organism is a member of the septi- cemia hemorrhagica group and has been designated by various names, among them, Bacillus avisepticus, B. hipolaris septicus, B. avicida, B. cholerce gallvtiamm, and Pasteurella avium. A strain isolated by Ward possessed the following characteristics : "Morphology. The individual cells are short, non-motile rods, with rounded ends. They usually occur singly, but a few are seen in pairs. Spherical forms are numerous in actively growing cultures. The size varies from .4 to .6 micron broad and from 1 to 2 microns long. A bipolar arrangement of the protoplasm is demonstrated when carbol fuchsin and alkaline methylene blue stains are used. The bipolar staining is notice- able freqiTently in smear preparations from tissues. The presence of a capsule is suggested by an unstained area surrounding each organism when a background of stain is deposited upon the cover glass. The same appear- ance is noticeable in smear preparations from tissues. The organism re- tains the stain but faintly when treated after Gram's method. "Biologic Characters. The organism is aerobic and facultative anaero- bic. It grows readily at 37.5° C, and with much less rapidity at room temperature. "Agar. The colonies on one per cent agar, after forty-eight hours incii- bation at 37.5° C, appear as round, smooth, thin, shiny disks, with entire border and measuring about 2 mm. in diameter. Under a two-thirds ob- jective they appear coarsely granular and show concentric circular markings. They appear smoky brown in color by directly transmitted light, and gray by reflected light. Colonies beneath the surface are usually lenticular in shape, and the granular appearance is more marked under a two-thirds objective than in the surface colonies. After twenty-four hours the growth on the agar slant culture is flat, smooth, shining, translucent, grayish white by reflected light, and smoky brown by transmitted light, with un- 34 FOWL CHOLERA 35 dulate border. The condensation water becomes decidedly turbid. After the first week of growth the liquid clears somewhat with the deposition of a viscous sediment. No pellicle has been observed on the condensation water. " Ulyccrine Agar. Growth upon this medium presents no features dis- tinguishable from that upon agar slant. " Gelatin. Surface colonies, after about two weeks' growth at room tem- perature, are round, vitreous masses, with entire border and smooth shiny- surface. A large proportion of the colonies are raised, forming a conical mass not exceeding 1 mm. in diameter. Such colonies appear highly re- fractive by directly transmitted light. Under a two-thirds objective the colonies have a finely granular appearance and show concentric circular markings. Sub-surface colonies are lenticular in shape and granular. " After three days' growth under similar conditions the growth in gelatin stab cultures is noticeable as a mass of closely aggregated colonies near the surface. After about two weeks the surface growth appears as a round, thin gray mass, with contoured surface and undulate border. At the same time the growth along the whole length of the path of the inoculating needle appears as a mass of closely aggregated distinct colonies. "Potato. Implantations on this medium have not resulted in visible growth. "Alkaline Bo}(illon. After forty-eight hours at 37.5° C. the fluid becomes slightly clouded and does not clear up on standing, even after four months. In cultures two or three days old no sediment is deposited, but in older cultures a viscous sediment accumulates. The reaction is alkaline to litmus and markedly so in old cultvires. No pellicle is formed, but occa- sionally a circular bluish band of growth adheres to the tube at the level of the surface of the fluid. "Sugar-free Bouillon. Growth is similar to that in alkaline bouillon. "Acid Bouillon. The growth is similar in appearance to that in alkaline, except that the turbidity is less marked and no accumulations have been noticed at either surface or bottom of liquid. Reaction becomes alkaline in old ciiltures. " MVl'. No change occurs in this medium during the length of time that it is ordinarily kept under observation. "Fermentation Tubes. (1) One per cent glucose bouillon: The liquid throughout the tube becomes uniformly slightly clouded in twenty-four hours at 37.5°C., and remains so. The reaction becomes acid in two days. No gas is formed. A slight amount of viscous sediment collects. " (2) One per cent lactose bouillon : The character of growth is similar to that in glucose. The reaction remains alkaline. " CS) One per cent saccharose bouillon : The growth is similar to that of the two preceding. The reaction becomes acid in two days, but eventually becomes alkaline in cultures several weeks old. "Dog Blood Serum. After twenty-four hours at ^7.^° C. the path of the needle is occupied by a smooth, shiny, raised growth of a color determined by that of the serum. The condensation water is markedly turbid. Six dnys later the growth, as well as the surface of a pellicle on the condensa- tion water, has a coppery lustre. 36 DISEASES OF DOMESTICATED BIRDS " LofPer's Blood Serum. After twenty-four hours' growth at 37.5° C, the path of the needle is marked by a white, raised growth, with shiny, con- toured or smooth surface and undulate border. The condensation liquid becomes decidedly turbid. After several days the surface of the growth becomes dull. The liquid is then observed to contain a viscous sediment and to have patches of pellicle floating upon the surface. " Indol. A positive reaction is obtained in sugar-free bouillon cultures. "Animal Inoculation. Subcutaneous or intravenous injection of fowls with 1 c.c. of a 24-hour bouillon culture resulted in death in about fifteen hours. Doses as small as 0.05 c.c. killed in about three days. A young rabbit inoculated with 0.5 c.c. in an ear vein was found dead fourteen hours later. A guinea pig inoculated with 1 c.c. svibcvitem was found dead in fourteen hours. Another receiving 0.5 c.c. subcutem survived thirty-six hours. A pigeon swallowing 1 c.c. died in twenty-one hours, and another receiving 0.12 c.c. subcutem was found dead fourteen hours later." Pathogenicity. Besides common fowls, geese, ducks, turkeys, pheasants, pigeons and a large number of wild birds are susceptible to infection. Hemorrhagic septicemia in geese is discussed in Chap- ter XIX. The virulence of the fowl cholera organism varies greatly. Had- ley has shown that the minimum lethal dose for fowls may lie at any point between 10 c.c. and 0.000,000,000,000,001 c.c. of a 48 hour bouillon culture. Hadley states that infection results from the inoculation into the breast muscle of less than fifty organisms and probably by the inoculation of no more than four. To test the infectiveness of the carcasses of fowls dead of the disease in a natural outbreak, "Ward fed such material to ten healthy cockerels. On the first day following the exposure by feeding, three birds were dead ; on the second day, three; on the third, fourth, fifth and sixth days, one bird each died. The incubation period may vary from eighteen hours to as many days. The blood and all discharges of a sick bird are infective. Eggs have been demonstrated to contain the virus. Infection may be induced in very small doses in a large variety of ways such as ingestion, subcutaneous, intravenous or intramus- cular injection, introduction of culture into the conjunctival sac, or into the scarified skin. Repeated passage of the virus through birds or through guinea pigs results in an increase of virulence of a strain. On the other hand diminution of virulence occurs under conditions not well un- derstood. Doubtless there are also variations of virulence with re- spect to the species attacked during various outbreaks. FOWL CHOLERA 37 In the case of infection by ingestion the organisms are believed to penetrate the uninjured mucosa of the intestines and gain access to the lymph and thence to the blood. Death is undoubtedly caused by toxins. There is however, lack of unanimity of opinion as to whether the toxic effect is due to intracellular or to extracellular toxins. Prognosis. Prognosis is serious, for 90 to 95 per cent of acute cases succumb. Symptoms. In the pcracute form, the bird either drops dead suddenly or more often dies on the roost at night. In the acute form the first noticeable symptom in the fowl is the yellow color of the droppings. The yellow material consists of urates and is usually found on the feathers near the vent. Di- arrhea follows later. The discharge varies considerably in color and consistency. It may be a greenish mass of pasty consistency, a brownish red mucus or a viscous transparent fluid. The yellow color of the urates is the most constant character. Evidence of sickness is afforded by the unnatural attitude of the feathers and by disinclination of the bird to move about. During the later stages, no food is taken, but very sick fowls may drink copiously. Drowsiness is marked in the later stages. Frequently a mucous discharge drips from the mouth. The temperature varies from 109° to 112° F. Death usually occurs within three days from exposure to infec- tion but has been observed to occur within eighteen hours after in- gestion of material from the carcass of another bird dead of the disease. During an acute outbreak, sickness is seldom noticed more than twenty-four hours before death. The chronic form of the disease generally appears at the end of an outbreak. The birds are dull, depressed and show persistent or intermittent diarrhea. The mucosae are pale and emaciation is marked. Arthritis may develop in one or more joints, and leads to ankylosis. Morbid anatomy. A reddening of the skin of the breast and abdomen is frequently observed. The comb often is dark red in color, but may be pale. There is a general congestion of the blood vessels of the visceral organs. The heart, in almost every case, is studded with punctiform hemorrhages. Less frequently are observed a fibrinous or a gelatinous exudate in the pericardium. One of the lesions occurring most frequently consists of hemorrhages in the first and second duodenal flexures. They may be so deep seated as to be 38 DISEASES OF DOMESTICATED BIKDS visible from the peritoneal surface. Under sucli conditions the con- tents of the duodenum consist of a pasty mass permeated with blood clots. The contents of the intestines sometimes consist of a cream- colored pasty mass, or may be green or brownish-red in color. In many cases the liver is permeated with whitish punctiform areas of necrosis. The oral, nasal, and pharyngeal cavities frequently con- tain a viscid mucous fluid. The lungs may show congestion and catarrhal or hemorrhagic pneumonia. More rarely caseous foci are present. Sero-fibrinous exudate may occur in the air sacs. Hemorrhages are usually restricted to the heart and duodenum, and occur else- where in the intestines rarely. Still less frequent- ly are they observed to be abundant throughout the skeletal muscles. Microscopic examination of stained smears from heart blood and organs will reveal numerous bipolar staining rods. Differential diagnosis. Avian plague can be dif- ferentiated by the fact that no organisms are present in the blood as demonstrated by cultures or by the mi- croscopic examination of smears. Further, inoculation of pigeons and rabbits with ma- terial from a case of plague will not produce infection in these ani- mals. Fowl cholera has features in common with fowl typhoid. How- ever, diarrhea is not usual in the latter and at autopsy the intes- tines are found to be pale, and the contents are normal in con- sistency. In fowl typhoid the heart is pale and dotted with grayish points due to cell infiltration. A bacteriological examination is necessary for differentiating the various cholera-like septicemias. This is not necessary in practice for no information is available to Fig. 3. Blood smear from blood of a pigeon infected with fowl cholern. a, red blood cells; b, fowl cholera bacteria. (Klee) FOWL CHOLEKA 39 warrant handling such outbreaks bj methods other than those used to combat cholera unless biologic products are used. Treatment. The treatment of individual sick birds is not rec- ommended, and their immediate slaughter is advised. Immunization. Pasteur in his memorable studies on immuni- zation against disease first worked with the fowl cholera organism in an attempt to produce an immunity against the disease caused by this organism. He utilized in his experiments cultures of the fowl cholera bacterium which he believed had become attenuated by exposure to air for a period of several months. His favorable results laid the foundation for the further study of the control of disease by the utilization of the specific causative organism as an agency of prevention. Kitt, Cogny, Vages and others working along the lines pursued by Pasteur have failed to substantiate his findings. However, it is quite possible that Pasteur worked with a strain of the fowl cholera organism which had immunizing value. Such an inference may be drawn through the researches of Hadley who demonstrated that a particular strain of the fowl cholera or- ganism designated strain 52, although practically avirulent, had the power, when injected in the live state, of conferring immunity to rabbits against the subsequent injection of a highly virulent strain. These findings were, to a considerable degree, confirmed by Gal- lagher who also found that fowls acquired a marked resistance to comparatively large amounts of a virulent culture following the injection of immunizing strain 52. At the same time the latter's experiments with killed cultures of several strains of the fowl cholera organism, including strain 52, as immunizing agents gave negative results. In each case fowls injected Avith bouillon cul- tures of organisms killed by heating at 60° C. for 1 hour, by car- bolizing to .5 per cent or by mixing with ether in equal parts, failed to show resistance to a subsequent injection of .000,000,001 c.c. of a virulent strain. Mack failed to produce immunity by the use of killed organisms against artificial infection but claims successful results in a num- ber of natural outbreaks. The use of an avirulent living organism with immunizing properties offers the most promising method of prevention. One c.c. of a 24 to 48 hour bouillon culture grown at 37° C is injected subcutaneously. The point most convenient for injection is the unfeathered area of the breast beneath the wing. It is possible to produce an antiserum by injecting a horse re- 40 DISEASES OF DOMESTICATED BIKDS peatedly with cultures of the fowl cholera organism. The passive immunity induced by its injection into fowls is short, and its use- fulness is limited to flocks already infected or in grave danger of becoming so. Immunization with an aggressin has been accomplished in an experimental way by Weil. He produces a pleural exudate in a rabbit by injecting with fowl cholera bacilli. This exudate is car- bolized and heated for three hours at 44° C. A dose of 5 c.c. is said to immunize against subsequent injection of a lethal dose. Prevention. Sanitation with reference to known methods of dissemination should be the basis of combating the disease. The chief sources of infection within an infected flock are dead birds eaten by members of the flock, and contamination of food and water by droppings. On large poultry farms, measures to secure isola- tion of the center of infection should be enforced promptl3^ This may involve temporary fencing, or moving the buildings, if portable. Daily inspection of the roosting houses at daybreak should be made to remove dead birds and to secure sick ones before they have opportunity to go afield. Constant watch during the day will reveal droopy birds which should be killed. Feeding troughs may be so arranged that the birds can only put in the head and do not have opportunity to contaminate the feed with their feet. The drinking water may be rendered safe by adding to it mercuric chloride in the proportion of one part to six thousand parts of water. Earthenware containers should be used. Disinfection of houses and adjacent areas should be carried out daily. Since the floor of the roosting house is highly contaminated by droppings, it should be disinfected if possible, before the birds leave the roost. At any rate, the birds should be excluded from the roosting house until it is possible to disinfect. Poultrymen, familiar with the ravages of cholera, have been knowTi to ship sick and exposed birds to market, as the simplest way to avoid financial loss. Apart from the obvious effect in re- moving a center of infection, it has another effect in further spread- ing infection. Birds dying during the trip to the shipping point are thrown by the roadside, where they are liable to be partially eaten by any fowls encountering them. The disease may be intro- duced into a flock in a large number of ways such as introducing birds in the incubation period of the disease, the carrying in of infection on the shoes, by water, by animals, by pigeons or wild FOWL CHOLERA 41 birds. All these possibilities, except perhaps the last two, suggest appropriate defensive measures. EDEMA OF THE WATTLES OF FOWLS Characterization. Edema of the wattles is an infectious dis- ease involving the w^attles and which usually runs a chronic course. History. The disease has been described by Seddon who ob- served it among fowls in the suburbs of Melbourne, Australia. Etiology. From all acute cases it is possible to isolate a short rod indistingTiishable from the one causing fowl cholera. In view of this fact and since fowl cholera is very common in the region in question it is likely that the wattle lesion merely represents a localized chronic form of disease caused by the fowl cholera bac- terium. Pathogenicity. Scarification of the wattle of fowls and rubbing in of culture in one case resulted in general illness, conjunctivitis, edema of wattle, diarrhea and formation of necrotic material. The bird when killed showed little change beyond the head lesion which was found to contain the organism that was inoculated. Another fowl inoculated in the same way showed edema and necrosis at the point of inoculation. The bird subsequently displayed immunity to infection through scarification or by subcutaneous injection of virulent culture. A hen receiving one fourth c.c. of culture intra- muscvilarly died in 24 hours and showed septicemic lesions at au- topsy. The disease occurred spontaneously among White Leghorns pos- sessing large wattles. These brushed on the ground during feeding, which offered an opportunity for injury and infection. Wounds re- ceived during fighting offer another opportunity for entrance of virus. The pigeon is killed by intramuscular inoculation of culture. Eabbits succumb to the infection with lesions of hemorrhagic sep- ticemia. Symptoms. There is sudden enlargement of the wattles due to more or less distention with fluid. In the beginning stage the wat- tles are hot, dark red in color and upon incision a clear fluid exudes. The birds manifest symptoms of general illness, loss of appetite, etc. Sometimes there is conjunctivitis. Subsequently there is gi'adual absorption of fluid accompanied by thickening of the wattle by fibrous tissue. ISTodules sometimes form in the tissues beneath the 42 DISEASES OF DOMESTICATED BIEDS mandible or under the scars of wounds acquired during fighting. The morbid process leads to disfigurement of the wattles by swell- ings and bj their assmning a crinkly form. In a small percentage of cases of the disease fatal septicemia occurs. Morbid anatomy. The more highly thickened areas in the wat- tles consist of masses of caseous material. In some cases the ne- crotic mass is surrounded by fibrous tissue, yellowish brown in color and hard, almost horny in texture. Treatment. Cropping the wattles offers the most satisfactory means for dealing with the infection. The operation is described on page 298. Prophylaxis. Preventive measures must be essentially those employed against fowl cholera. CHOLERA-LIKE SEPTICEMIAS The literature contains descriptions of a considerable number of acute infections occurring among fowls, turkeys, geese, ducks, swans and other birds. In a number of instances the diseases have been shown not to be fowl cholera by bacteriological evidence that is convincing today. In other instances the features differentiat- ing the disease from fowl cholera do not appear convincing at the present time. The reports cover a considerable period of time during which many changes have occurred in methods of identify- ing cultures. Thus the old bacteriological descriptions are inade- quate for making an accurate classification of these infections. There is little practical need for a close examination of the etiology of these septicemias. The general methods of prophylaxis are identical with those necessary in combating fowl cholera. DISEASES IDENTICAL WITH FOWL CHOLERA There are examples of diseases substantially identical with fowl cholera which have been described under different names or without assignment of name. Lisi described a fatal septicemia occurring in fowls which caused the death of all the birds in the flocks in- vaded. J^ocard and Leclainche agree with Lignieres that the dis- ease was fowl cholera. Eabieaux observed a disease which he des- ignates as a hemorrhagic septicemia of the duck and fowl. Lig- nieres as well as Hutyra and Marek agree that Eabieaux does not show that the disease described by him is different from fowl cholera. FOWL CHOLERA 43 EPIZOOTIC DYSENTERY OF FOWLS AND TUKKEYS Lucet describes a septicemic disease of fowls and turkeys. He differentiates the disease from fowl cholera by the insusceptibility of the rabbit to subcutaneous inoculation and other peculiarities even less convincing. Etiology. The organism causing the infection is a short, slightly motile rod which does not stain by the Gram method. It does not grow on potato and gelatin is not liquefied. Pathogenicity. The disease is inoculable from fowl to fowl, from the fowl to the turkey, from turkey to turkey and reciprocally. It is also transmissible between the two species by ingestion. The pigeon is insusceptible to subcutaneous inoculation. The gTiinea pig is not affected by subcutaneous or intraperitoneal injection. The rabbit is insusceptible to injections in the same way, but succumbs to intravenous inoculation. Symptoms and lesions. There is nothing distinctive in the symptoms displayed while the lesions are those of fowl cholera. EPIZOOTIC PNEUMO-PERICAKDITIS IN THE TURKEY Characterization. The disease is an infection of the turkey characterized by lesions of the lung and pericardium. History. M'Fadyean first described the infection in England, while Jowett encountered it near Cape Town. Etiology. The organism causing the disease is a small ovoid rod closely resembling that causing fowl cholera. M'Fadyean notes that it possesses motility, while Jowett is silent on the point. It is Gram negative and is readily stained by the ordinary dyes. No lique- faction is produced in gelatin, no gas is formed in agar shake cul- tures, no acid formation nor coagulation occurs in milk and no vis- ible growth is observed on potato. Growth occurs equally well under aerobic or anaerobic conditions. 'No unusual or striking character- istics are presented by the growth on agar slant or bouillon cultures. Pathogenicity. In the natural outbreak observed by Jowett, turkeys only succumbed, while fowls, geese and pigeons in close contact with them escaped infection. Subcutaneous inoculation of the turkey with cultures caused symptoms of dullness, stiffness and mouth breathing followed by death in a few days. Guinea pigs and rabbits succumb to inoculation. Fowls are only slightly sus- ceptible while pigeons succumb to intraperitoneal inoculation. 44 DISEASES OF DOMESTICATED BIEDS White rats die after intraperitoneal inoculation, but subcutaneous inoculation may fail. Morbid anatomy. Severe pericarditis is one of the most no- ticeable characteristics observed at autopsy. The pericardium may show extensive adhesions to the heart wall, and the latter may be covered with a layer of yellow colored fibrinous exudate. The peri- cardial sac may contain sero-fibrinous exudate. The lungs show pneumonic changes and are frequently completely hepatized. Be- yond possible fatty changes in the liver and paleness and swelling of the kidneys, changes in other organs are not marked. Microscopic examination of blood smears from heart blood, peri- cardial exudate, lung and various organs, reveals the presence of a bipolar rod. Relation of disease to fowl cholera. MTadyean believes that the effects produced on various animals by the organism described by him, warrant the differentiation of the disease from fowl cholera. He notes that pericarditis and pneumonia occur in fowl cholera, but not with such constancy as they occur in the disease described by him. AN EPIZOOTIC AMONG FOWLS Mazza reported upon a disease that caused heavy mortality in various parts of upper Italy. Etiology. Cultures from various organs almost always yield growth of a motile rod, while culture media seeded from exudate, blood and brain are more often sterile. Mazza concludes that the organism differs from that of fowl cholera in several particulars. It is larger than B. avisepticus, does not usually exhibit bipolar staining, is motile, is not very pathogenic for rabbits and is rarely observed in the blood. Pathogenicity. Hens and pigeons succumb to the infection without exception. Guinea pigs are completely insusceptible while rabbits are very slightly susceptible. Symptoms. In general the hens die suddenly during the night without having previously shown distinct symptoms of disease. In other cases, symptoms like those occurring in fowl cholera are ob- served. Morbid anatomy. In external appearance the fowls usually show no signs of emaciation. The only abnormal conditions en- countered are darkening of the comb and large red areas on the skin of the abdomen and of the breast. The subcutaneous cellular tissue FOWL CHOLEEA 45 appears scanty and occasionally hemorrhages are observ^ed in this locality. Quite constant lesions are encountered in the chest and in- volve one or both lungs. There is a serous exudate in the chest cavity sometimes with other signs of inflammation. More rarely there is observed serous bloody fluid in the pericardium and red- dening of the mucosa of the duodenum. In the cranial cavity there is rarely observed a reddening of the pia mater and of the brain substance. HEMOKRHAGIC SEPTICEMIA OF THE RING DOVE Leclainche reports the occurrence of a septicemic disease of ring doves from which he isolated an organism regarded as belonging to the hemorrhagic septicemia gi'oup. Etiology. The causative organism is an ovoid rod identical in shape with that causing fowl cholera, but somewhat larger. The organism shows bipolar staining and is Gram negative. Growth occurs on potato and gelatin is not liquefied. Pathogenicity. The infection is transmissible to the ring dove by inoculation and by ingestion. The domestic pigeon is much more resistant. The fowl is absolutely refractory while the rabbit and guinea pig are susceptible. Symptoms. The symptoms are those usually presented by birds affected with a septicemia. Morbid anatomy. Lesions consist chiefly of hemorrhagic in- flammation of the small intestine. CHOLERA OF COSCOROBA SWANS Tretrop observed a septicemia among swans in the zoological gar- den of Antwerp to which he has given the above designation. The species involved was Coscoroha Candida. About fifty birds were in the flock, of which the majority died. A large number of other species of swans and other waterfowl were in contact with the dis- eased ones but escaped infection. Etiology. There is found constantly in the organs of the dis- eased birds, a microorganism designated Bacillus coscoroba. It is an ovoid motile rod 1.5 to 2.5 microns long and 1 to 1.4 microns broad. Bipolar staining is observed and the organism is Gram negative. The organism grows equally well in bouillon, milk, gel- 46 DISEASES OF DOMESTICATED BIRDS atin and not on potato. Milk is coagulated and indol formed. Gel- atin is not liquefied. Pathogenicity. The mouse is very susceptible to inoculation but the white mouse will not contract the infection by ingestion. Birds of the order passer es succumb rapidly to intramuscular injection of culture. The duck and fowl are insusceptible. Numerous spe- cies of swans, geese and ducks in contact with the diseased birds, escaped infection. Symptoms. The birds remain in a squatting position, and show the usual manifestations of sickness exhibited by those affected with a septicemia. Morbid anatomy. The subjects are generally in good condi- tion. The muscles offer nothing special and the heart appears nor- mal. Commonly, active congestion is observed in the lungs. Some- times one or two caseous foci are present, which are easily enucle- ated. The liver is enlarged, dark in color and frequently shows small whitish spots. The spleen is sometimes slightly engorged, sometimes slightly increased in size. The intestine always shows diarrhea with contents yellowish or yellowish gi-een in color. The intestines do not show marked injection of the blood vessels. No- dules the size of a small pea are frequently found in the abdominal cavity in the vicinity of the vertebral column. HEMOKRHAGIC SEPTICEMIA OF THE SWAN Fiorentini observed a septicemic infection among swans in the zoological gardens of Milan. Morbid anatomy. In young birds that have died quickly there is an edematous infiltration of the lungs with ecchymoses on the serous membranes. There is also a slight hyperemia of the intes- tinal mucosa, dark blood clots in the heart cavity and cloudy degen- eration of the liver cells. In older birds that have died after several days sickness there are more severe lesions. The lungs show fibrous pneumonia in the stage of gray hepatization. The upper lobes of the liver show a grayish yellow exudate composed mostly of lym- phoid elements, besides marked thickening of Glisson's capsule. The hepatic tissue shows a marked infiltration with red blood cells in the spaces between the liver cells. In numerous places in the liver there are yellowish zones caused by the fatty degeneration of the cellular elements. In the intestine there is slight hyperemia but no exudate nor swelling. On the serous membranes there are numer- FOWL CHOLEKA 47 ous confluent ecchymoses, especially along the course of the coronary arteries. Etiology. The blood of dead swans yields cultures of a short rod with rounded ends and which shows bipolar staining. The shape of the organism is very similar to that of the fowl cholera bacterium, but it is somewhat larger. The organism has some characteristics in common with that of fowl cholera. Both stain alike by the Gram method and do not give an indol reaction. However, they differ in other characteristics as the swan organism is motile. It also forms rods as long as 4 microns. Growth in bouillon, agar and gel- atin furnishes no distinguishing characteristic. Copious brown col- ored growth occurs on potato accompanied by a bad odor. Pathogenicity. The organism is virulent for the swan and a goose (A'iiser aegyptiacus) while various aquatic and other birds escaped infection. Rabbits, guinea pigs, ducks, geese, hens and pigeons succumb to intramuscular inoculation of culture. INFECTIOUS ENTERITIS OF PHEASANTS Fiorontini observed an epizootic among pheasants in the public gardens of Milan which occurred a short time after an epizootic of the same nature among swans. The disease was slightly con- tagious for after many months the greater part of the birds escaped infection. Etiology. The organism causing the disease resembles that of fowl cholera. It measures .7 micron in diameter and 1 to 2 mi- crons in length. In cultures the organism forms chains which are sometimes very long. Growth in bouillon is rapid at 22° to 24° C. Indol is produced. On gelatin in 48 hours, a gray layer of gro^\i;h develops. On potato the color varies according to the development of the growth. After 48 hours, the color is pale yellow, which changes to brown while the borders are rose brown. The culture has the appearance of honey. Pathogenicity. Pheasants alone are attacked and a preference for males is exhibited. The infection is transmitted by inoculation of cultures subcutaneously or intravenously in small amounts. In- gestion of culture induces disease identical with that occurring natu- rally. Hens are not affected by receiving 2 to 3 c.c. of virulent culture and such inoculation does not assure immunity to fowl cholera. Eabbits and gxiinea pigs are immune. t' 48 DISEASES OF DOMESTICATED BIRDS Symptoms. The birds display depression and the gait is uncer- tain. The appetite is poor. Late in the disease an abundant di- arrhea occurs, with the passage of gTayish yellow or greenish colored material. The state of coma and somnolence seen in fowl cholera does not occur. The attack lasts five to eight days. Morbid anatomy. Lesions occur throughout the intestine. The mucosa is congested, is reddish brown in color and is covered with a viscid layer or by a croupous exudate. Ecchymoses are not found on the serous membranes. The liver is friable and the spleen is swollen but not hemorrhagic. REFERENCES 1. Fiorentini. Enterite infettiva del fagiani. Atti della Societa iialiana di scenze naturali, 1896, p. 89. 2. Fiorentini. Hamorrhagische Septikamie der Scliwane. Centralhl. f. Balteriol. {Etc.), 1. Alt. Orig., Bd. 19, 1896, S. 932. 3. Gallagher. Fowl cholera and other hemorrhagic septicemia immuni- zation experiments. J. Am. Vet. M. Ass., Vol. 50, (n.s. Vol. 3), 1917, p. 708. 4. Hadley. Fowl cholera and methods of combating it. Rhode Island Agr. Exp. 8ta. Bull. lU, 1910. 5. Hadley. A biological study of eleven pathogenic organisms from cholera like diseases in poultry. Rhode Island Agr. Exp. Sta. Bull. 146, 1910. 6. Higgins. Notes upon an epidemic of fowl cholera and upon the com- parative production of acid by allied bacteria. Jour. Exper. Med., Vol. 3, 1898, p. 651. 7. Jowett. Epizootic pneumo-pericarditis in the turkey. J. Comp. Path, and Therap., Vol. 21, 1908, p. 324. 8. Kitt. Die Serumimpfung gegen Gefliigelcholera. Monatshefte f. praU. Tierh., Bd. 16, 1904, S. 1. 9. Leelainche. Sur une nouvelle septicemic bemorrhagique. La maladie des palombes. Ann. de V Inst. Pasteur, T. 8, 1894, p. 490. 10. Lucet. Dysenteric epizootique des poules et des dindes. Ann. de V Inst. Pasteur, T. 5, 1891, p. 312. 11. Mazza. Bakteriologische Untersuchungen liber eine neuerdings auf getretene Hiihnerepizootie. Centralhl. f. Bdkteriol. (Etc), 1. Aht. Orig., Bd. 26, 1899, S. 181. 12. Mack and Records. The use of bacterins in the control of fowl cholera. Univ. Agr. Exp. Sta. Bull. 85, 1916. 13. M'Fadyean. Epizootic pneumo-pericarditis in the turkey. J. Comp. Path, and Therap., Vol. 6, 1893, p. 334. 14. Nocard and Leelainche. Les maladies microhiennes des animaux. Paris : Masson et Cie. 1903. 15. Pasteur. De 1' attenuation du virus du cholera des poules. Compt. Rend. Acad. Sci. Paris, T. 91, 1880, p. 673. FOWL CHOLERA 49 16. Pasteur. Sur les maladies virulentes, et en particular sur la maladie appelee vulgairement cholera des poules. Compt. Rend. Acad. Sci. Paris, T. 90, 1880, p. 239. 17. Rabieaux. Sur une septicemie hemorrhagique du canard et de la poule. J. de med. vet. et de zootech., T. 51, 1900, p. 129. 18. Seddon. Oedema of the wattles of fowls due to an organism of the pasteurella group. Vet. J., Vol. 21, 1914, p. 24. 19. Seddon. A diseases of the wattles of the fowl. J. Agr. Victoria, Vol. 12, 1914, p. 426. 20. Tretrop. La maladie des cygnes coscoroba. Ann. de V Inst. Pasteur, T. 14, 1900, p. 224. 21. Ward. Fowl cholera. Uiiiv. of Cat. Agr. Exp. Sta. Bull. 156, 1904. CHAPTER V FOWL TYPHOID AND SIMILAR INFECTIONS FOWL TYPHOID Synonym. Hiibner typhus (German). Characterization. Fowl typhoid is a specific infectious disease of fowls, having the general characteristics of a septicemia and is caused by Bacterium sanguinarium (Bacillus gallinarum). History. The disease seems to have been first described by Klein in England in 1889 under the name of infectious enteritis of fowls. The organism was designated by him, Bacillus gallinat^m. Had- ley states that a culture of this organism has been preserved since its isolation by Klein, and that a study recently made by him re- veals the organism to be identical with Bacterium sanguinarium. The disease and its causative agent were described by Moore in 1895. Other outbreaks in the United States have been described by Dawson, Curtice and by Taylor. Pfeiler and Eehse observed the same disease in 1912, gave it the name " Hiihner typhus," and described the organism under the name Bacterium typhi gallinarum alcalifaciens. A second outbreak oc- curring in 1915 has been described by Pfeiler and Roepke, Etiology. The characteristics of the organism are described by Moore as follows: " Morpliology. Bacterium sanguinarium varies somewhat in size ac- cording to the medium in which it has developed. In tissues of fowls or rabbits it is from 1.2 to 1.8 microns long and from 1 to 1.3 microns broad. The ends are tapering or rounded in cultures ; in the short forms it could easily be mistaken for a micrococcus. In tissue it frequently appears in small clumps, but usually in pairs imited end to end. Spores or vacvioles have not been discovered. Involution forms are common. In cultures on agar it is more slender than in tissues. When examined in a hanging drop preparation, especially at the edge, it frequently shows a marked polar arrangement of the cellular protoplasm. In these preparations there is observed a marked dancing motion of the organism. In old bouillon cultures short chains composed of these organisms united end to end are sometimes observed. " Staining. It stains with the aniline dyes ordinarily used, btit retains the coloring matter very feebly, or not at all, when treated after the Gram method. 50 FOWL TYPHOID AND SIMILAR INFECTIONS 51 " Cultivation. This organism is readily cultivated on the ordinary media. It is obtained in pure cultures from the heart blood or liver of a fowl just dead from the disease. "Agar. On this medium, at 37° C, the growth is moderately vigorous. It has a grayish glistening appearance. Isolated colonies are from 1 to 2 mm. in diameter, convex, and with sharply defined borders. Agar plates emit a peculiar penetrating odor, which differs decidedly from the pungent odor given off by Bacterium suisepticum. The growth on this medium resembles very closely that of B. suipestifer. " Gelatin. In this medium the growth is less vigorous. In stick cul- tures it is more abundant along the line of inoculation than on the svirface. Isolated colonies are about 0.25 mm. in diameter, appearing to the un- aided eye as homogeneous bodies, but slightly granular under low mag- nification. On the surface of the gelatin the colonies are granular and slightly spreading. They are not characterized by any distinctive mark- ings. There is no liquefaction or softening of the medium. " Potato. On the surface of potatoes a delicate grayish yellow growth appears after forty-eight hours when kept at a temperature of 35° C. Frequently there is no development, owing, presumably, to the acids in the potato. " BotiUlon. In alkaline peptone bouillon at 36° O. the growth imparts a uniform cloudiness to the liquid within twenty-four hours. If the bouillon contains much sugar the reaction becomes acid, otherwise it re- mains alkaline. A grayish friable sediment forms in the bottom of the tube. After several days' standing the growth settles, leaving a clear supernatant fluid. In a simple peptone solution containing one-half of 1 per cent sodium chloride the growth is less vigorous than in the one con- taining the meat juice. In meat extract bouillon the growth is likewise feeble. In acid peptone bouillon there is a very faint cloudiness imparted to the liquid. " Alkaline bouillon containing 1 per cent dextrose in the fermentation tube becomes cloudy within twenty-four hours afteir inoculating' and strongly acid in reaction. Similar tubes of bouillon containing saccharose and lactose become clouded throughout but they remain alkaline in reac- tion. The degree of alkalinity increases with age. Gas is not produced during the growth in bouillon containing these sugars. "Life condition.s and properties. This organism develops at a temnera- ture from 20 to 41° C. It does not grow well in acid media. It produces indol. "Resistance. It is destroyed at 50° C. in fifteen minutes. A 1 per cent solution of carbolic acid was fatal to it in 5 minutes. It resists drying when in films on cover-glasses for from 7 to 15 days. "Pathogenesis. This organism is fatal to fowls, pigeons, rabbits, guinea pigs, and mice. Other animals have not been tested. Excepting in in- travenous injections, comparatively large quantities of a pure culture were required to produce fatal results. Fowls inoculated in the wing vein with 0.3 c.c. of a fresh bouillon culture died in from three to thirteen days; usually on the fifth or sixth day. The temperature begins to rise on the second day after inoculation. It reaches 109 to 111° F. a few days 52 DISEASES OF DOMESTICATED BIEDS before death occurs. In cases vphere the fowls live from five to six days they appear perfectly well for at least three days, when the feathers begin to have a slightly ruffled appearance. Pigeons inoculated with 0.2 c.c. of a bouillon culture die in from four to five days. In rabbits the lesions re- semble very closely those produced by attenuated hog cholera bacteria (B. suipestifer). Guinea pigs inoculated in the abdominal cavity with from 0.2 to 0.3 c.c. of a bouillon culture die in from five to eight days." Differences from B. puUorum. The two causative organisms differ materially in their action on sugar media. B. pulloimm pro- duces gas in dextrose, mannite and levulose, while B. sanguinarium does not produce gas in any of the sugars in common use. Milk is rendered acid by B. pullorum and alkaline by B. sanguinarium with or without saponification in the latter instance. B. pullorum is neg- ative to the methyl red test when grown in 1 per cent maltose bouil- lon, while B. sanguinarium gives a positive reaction. Symptoms. These are quite similar to those of other acute septicemic diseases. Drowsiness and indifference to surroundings are marked. There is loss of appetite and general weakness. The head may be drawn in close to the body or may hang limp. The mucosae of the head are pale. Diarrhea is present in the majority of cases. The droppings are yellowish and may be tinged with green. The comb and wattles are usually paler than normal but may be darkened with venous congestion. The blood is pale red in color and presents a marked decrease in red cells and great in- crease of white cells. The period of incubation is four to six days and the duration of symptoms in fatal cases from four to twelve days. A temperature elevation of three to five degrees is noted. Morbid anatomy. There is a general anemic appearance of the serous membranes. The mucous membrane of the intestine is usu- ally pale. At times it may show slight areas of congestion, or hem- orrhagic points. The most marked changes observed on post mortem examination are in the liver, spleen, kidneys and blood. The liver is greatly enlarged and generally dotted with grayish necrotic spots. It may, at times, be congested throughout or show spots or bands of congestion. It has a tendency to become friable. Microscopic ex- amination of sections of the organ reveals an engorgement of the blood vessels and a breaking down of the parenchymatous tissue. The hepatic cells present different stages of degeneration from cloudy swelling to complete necrosis. The necrotic areas vary in size from that of a few cells to macroscopic lesions. The spleen is sometimes FOWL TYPHOID AND SIMILAR INFECTIONS 53 enlarged, dark colored and pulpy. It may show necrotic points. The kidneys are somewhat enlarged, may be lighter in color and slightly injected with blood. The vascular system shows the most constant changes. The heart appears normal or else pale with grayish spots of necrosis. The blood is lighter in color and does not clot readily. Microscopic ex- amination reveals a great disproportion between the number of red and white cells present. The red cells decrease in numbers to a marked degree as the disease advances while the white cells become greatly increased in numbers. This increase is confined principally to the polymorphonuclear leucocytes. The following table from Moore will illustrate the proportionate relationship between the red and white cells during the course of the disease. Table III. — Blood Changes in Fowl Fed Culture March 26. Date Temper- ature ° F Number of red corpiis- cles per c. mm. Number of white corpuscles per c. mm. Remarks. Mar. 26 106.2 3,535,000 18,940 Well. Mar. 28 110.0 2,430,000 70,000 Fowl eats very little. Apr. 2 110.6 1,684,210 80,000 Blood very pale; fowl weak; refuses food. Apr. 3 106.0 1,745,000 245,000 Very weak; many red corpuscles attacked by leucocytes. Apr. 4 Found dead. In stained preparations of the blood numerous red corpuscles are observed undergoing degeneration. This is manifested by the fail- ure of the cellular protoplasm surrounding the nucleus to stain reg- ularly or at all, and also by vacuolization of the protoplasm of the cell. Bacterium sanguinarium may be recovered in pure culture on arti- ficial culture media from the blood, liver, spleen and kidneys of fowls recently dead of the disease. Differential diagnosis. Fowl typhoid is distinguished from fowl cholera by the absence of severe congestion of the mucous mem- brane of the intestine especially the duodenum, by the absence of hemorrhagic spots on the heart, by the failure to find bipolar stain- ing bacteria in the blood, and by the finding and isolation of B. 54 DISEASES OE DOMESTICATED BIEDS sanguinarium. Also, the duration of symptoms is apt to be mucli shorter in the case of cholera. Fowl typhoid is differentiated from fowl pest by the absence of severe intestinal congestion, failure to find petechise in the mucosa of the proventriculus and by the fact that fowl pest is caused by a filterable virus and no organisms can be detected in the blood stream, or isolated on artificial culture media. Infectious leukemia has somewhat similar lesions and also shows a greatly changed condition of the blood. However, in this disease the loss of red cells and increase of white cells is much more marked than in fowl typhoid. Also, it is the mononuclear cells, instead of the polymorphonuclears, which show the principal increase in numbers in infectious leukemia. Unlike fowl typhoid, infectious leukemia is caused by a filterable virus and no microorganism can be grown, from the blood or organs on artificial culture media. Fowl typhoid and acute Bacterium pullorum infection of grown fowls have symptoms and lesions which are somewhat similar. The causative organisms also closely resemble each other both morpho- logically and in their cultural characteristics. In B. pullorum in- fection, however, the ovary is congested and nearly always presents several hard irregular ova. It is the principal seat of predilection for the pullorum bacterium. PSITTACOSIS OF PAEEOTS Synonyms. Septic fever of the parrot, parrot septicemia, (Eng- lish) ; septicemic des perruches, mycose des perroquets, (French) ; Psittacosis, (German). Characterization. The disease is a contagious septicemia in- volving parrots and parrakeets and causing fever, weakness, stupor and diarrhea. Transmission to man. The disease has received considerable attention because suspicion has been aroused that the infection may be transmitted to man. A number of outbreaks of infectious pneu- monia in man have been observed to occur simultaneously with the bird disease. Leichtenstern sums up the question of the transmission of the dis- ease to man as follows : " 1. Epidemiological, clinical and especially bacteriological evidence is not disclosed to prove that the infection of house epidemics of pneumonia suspected of being psittacosis, did originate from sick parrots. " 2. It is proven that bacterial diseases, especially enteritis, occur fre- FOWL TYPHOID AND SIMILAR INFECTIONS 55 quently in parrots, particularly those freshly imported, and inflict sporadic and also excessive mortality. " 3. No one will doubt that the streptococci, staphylococci, pneumococei, coli and proteus varieties occurring in these fatal parrot diseases may under certain circumstances also become dangerous for man. " 4. The disease of man designated psittacosis is in clinical and ana- tomical features an atypical pneumonia coupled with tyi^hoid symptoms and the disease has the same character in all epidemics. " 5. The same house epidemics of pneumonia occur not rarely, without the intervention of parrots and one may from this draw the conclusion that all the former psittacosis epidemics were nothing more than atjioical pneumonia in which the sick parrot, accidentally present in the house, played no etiological role. " 6. The above conclusions under 5 are contradicted in some measure by the no small number of former so-called psittacosis house epidemics. Especially contradictory to these conclusions is the Paris epidemic of 1892 in which the transmission of the disease from the sick parrots to man must be considered on the basis of epidemiological facts as, at the least, apparently wholly indicated." Etiology. An organism belonging to the hog cholera group has been isolated from cases of the disease in parrots, by IsTocard and by Palamidessa. It is an actively motile, Gram negative rod which grows equally well under aerobic or anaerobic conditions. The gro^vtll in bouillon and on agar presents no characteristic features. Growth on gelatin at first consists of a shiny, transparent, iridescent streak which develops into a porcelain-white growth. 'No liquefac- tion of gelatin occurs, and milk is not coagulated. Growth on potato resembles that of B. coli. The organism may be isolated from the blood, bone marrow, spleen and other organs of infected birds. It has been isolated from the intestinal contents of parrakeets which were in apparent good health. Pathogenesis. The causative organism is pathogenic for the parrot, parrakeet, pigeon, fowl, mouse, rabbit and giiinea pig. All discharges of an infected bird are infective and in view of the close contact between birds there is every opportunity for transmission of infection. The disease occurs most frequently among birds dur- ing shipment from the tropics and shortly after landing. Contribu- tory factors to its occurrence seem to be the unusual restraint, crowd- ing, filthy cage conditions, climatic conditions and general hard- ships suffered during shipment. Symptoms. The disease is manifested by shivering, inappe- tence, diarrhea with frothy greenish droppings which are sometimes blocdv. The bird exhibits gTcat thirst, drowsiness and disinclination 56 DISEASES OF DOMESTICATED BIEDS to move. The wings droop, the eyes are closed, the feathers are ruffled and the head is turned on the shoulder. When attempt is made to move, great weakness is evident. The bird usually avoids the perch. Convulsions precede death by a short period. In more chronic eases there is a discharge from the nostrils and eyelids, coughing, snuffling and difficult, panting respiration. Emaciation is evidenced by prominent breast bone and loss of weight. Vomiting is occasionally observed. The disease is usually fatal and hope of recovery may be enter- tained only in cases which survive for eight or nine days and which display some appetite. Most die in from three to five days after sickness is noted. The incubation period in natural exposure varies from three days to several weeks. Morbid anatomy. The organs of the abdominal cavity show intense congestion and ecchymoses are present in the peritoneum. Small grayish spots may be observed in the liver, spleen and kid- neys. The spleen is usually enlarged and soft in texture. The intestines show general congestion, or catarrh and often contain ulcers on the mucosa. The muscles often present a striated and spotted appearance. The heart muscle is often dark or hemor- rhagic. Ecchymoses may be present in the endocardium and peri- cardium. The lungs may present various conditions such as total consolidation, yellowish pneumonic patches, areas of atelectasis or of congestion. The air sacs may contain fibrinous or fluid exudate. Treatment. The patient sliould be kept in a room having a temperature of from 90° to 100° F. continuously. Gray advises that aspirin or cyllin may be given in the drinking water. In cases showing improvement, the aspirin may be replaced by aromatic sul- phuric acid and quinine sulphate. Food may consist of bread and milk, banana, sponge cake soaked in sherry, etc. Prevention. The most effective prevention would consist of improvement of methods of isolation of individuals and of general conditions on shipboard. Prophylaxis on shore involves perfect segregation of birds and the application of disinfection. DISEASE OF PIGEONS CAUSED BY A BACILLUS OF THE HOG CHOLERA GROUP Moore observed an infection in pigeons in ISTew Jersey caused by an organism closely related to Bacillus suipestifer. FOWL TYPHOID AND SIMILAR INFECTIONS 57 Symptoms. The disease is characterized by emaciation and a peculiar turning of the head from one side to the other. Occasion- ally there are paroxysms of aimless flying about. The disease is popularly designated " megrims." Etiology. The organism belongs to the hog cholera group of bacteria but differs in several particulars from the specific organism isolated from affected hogs. The organism from the pigeon is ap- preciably larger. In bouillon a delicate pellicle develops on the surface of the fluid, and in old cultures, a deposit is formed on the sides of the tube. A marked indol reaction occurs. The pigeon culture is less rapidly fatal for experimental animals than B. sui- pestifer. Morbid anatomy. Autopsy of a bird that had slio^vn the pe- culiar head movement for several days revealed no lesions in the thoracic or abdominal cavities. There was a friable exudate about 1 mm. in thickness, in the subarachnoid space over the cerebellum and the posterior lobes of the cerebrum. It was grayish yellow in color and easily removed. The subjacent brain tissue was reddened but otherwise the brain was normal in appearance. The organism in question was recovered in pure culture from the brain lesion but not from the heart blood. Another pigeon found dead, showed great emaciation but few other changes beyond pale, fatty heart nmscle. The same organism was recovered in pure culture from the liver and blood. AX INFECTION IN PIGEONS CAUSED BY BACILLUS PARATYPHOSUS B. Zingle observed an infection in pigeons apparently caused by B. jxira typhosus B. Morbid anatomy. The external appearance of the carcass, be- yond marked emaciation, presents nothing suspicious. The oral cavity in all cases is free from lesions. Upon skinning, the breast muscle is seen to be colored yellow in some places and permeated with bright yellow knots like oat gi-ains. The liver frequently has a yellowish gray color, and on closer observation it is seen to be cov- ered over the whole surface with countless hyperemic areas, which are sharply defined from the surroundings. In more cases the liver is permeated with yellow, round, compact knots varying in size from that of a grain of wheat to that of a bean, which give the surface a roughened appearance. The spleen is generally small without par- ticular macroscopic changes. The intestine appears somewhat hem- 58 DISEASES OF DOMESTICATED BIRDS orrhagic. The most marked lesions are shown by the kidneys. These are extraordinarily large, and the borders of the several lobules have completely disappeared. The color of the kidneys is mostly gray-yellow. They appear to be sprinkled through with numerous speck-like foci and they are very fragile in consistency. The lungs appear free from lesions in many cases. Frequently, however, the lungs contain numerous opaque, gray-white foci the size of a hemp seed which are uniformly distributed. Lesions are not ob- served in the trachea, but the mucous membrane of the crop in iso- lated cases contains yellow crumbly, button-like areas of exudate. Etiology. In the bacteriological examination of blood, muscu- lature and organs a bacillus was found which agreed with paraty- phoid B in cultural, morphological and serological characters. The culture agglutinated in a dilution of 1 : 15,000 completely and par- tially at 1 : 25,000 wath B. parody phosus B serum of a titre of 1:30,000. All the strains showed the same characteristics as B. paratyphosus B in litmus milk, glucose, Endo agar, malachite green agar, gelatin, Barsiekow solution 1 and 2, neutral red agar, orzein agar as well as milk, potato and bouillon. Pathogenicity. White mice succumbed to subcutaneous injec- tion in two days. It was especially noticeable that the organism occurred in great numbers, and was never observed mixed with other organisms. Pathological histology. In microscopic sections of the kidneys there are found inflammatory foci somewhat larger than a millet seed with round cell infiltration of the interstitial area. Also parenchymatous degeneration of the epithelium of the convoluted tubules in that the nuclei of the same in part are poorly stained and the protoplasm appears to be granular. The lumina of the tubules are filled with masses of desquamated epithelial tissue. When stained with Sudan they show fatty degeneration of medium degree in the epithelium of the labyrinths. The investigation of the liver shows that the organ is permeated with numerous abscesses. The knots in the musculature present themselves microscopically as abscesses varying in size from that of an oat grain to that of a pepper seed, with distinct lymphocyte walls which mingle with the neighboring muscle fibers. In the center of the abscesses there is much fibrin and also pus cells. FOWL TYPHOID AND SIMILAR INFECTIONS 59 In the lungs there are numerous abscesses analogous in structure to those in the muscle. Relation to bird pox. Because of a suspicion that bird pox virus was present, inoculation experiments were undertaken. By rubbing of pus from liver, kidneys, lungs, etc., as well as blood and musculature, skin, muscle nodules, and crop exudate, into scarified breast skin of pigeons, there appeared after 2 to 3 days, yellowish swellings which looked exactly like pox. After a week they reached the maximum size of a pea. During this time the breast muscle fell away very markedly. These swellings began to shrink and dry up, while as a rule no fresh swellings appeared. Some of the pigeons died within 2 to 4 weeks after inoculation. By that time the pox- like swellings on the breast skin were totally dried up or had fallen off. The musculature was atrophied, flecked with yellow and in some cases contained numerous knots shaped like an oat grain with section findings like those in the original pigeons. Other pigeons lived. After some time the pox scabs fell off, the breast muscle filled out, so that the bird appeared clinically healthy. These results were obtained easily through inoculation of gener- ation after generation, also with dried out material, and the B. para- typliosus B could be recovered each time. The question arose as to whether these organisms were the pri- mary cause of this pigeon disease or whether like hog cholera, the paratyphoid bacillus played a part of a leader. There was the pos- sibility of a mixed infection with bird pox, and on this account ex- periments were started with contamination free filtrates of cultures and organs. Also inoculation experiments were undertaken with cultures that had been grown for many generations in fluid and solid media. While the filtrate experiments gave no positive result, inoculations with pigeon paratyphosus culture always gave pox-like appearances in two days. AVIAN SALMONELLOSIS Lignieres and Zabala describe an infection in fowls caused by an organism which they regard as showing all the specific characters of the hog cholera bacillus. The authors note that their organism is non-motile, while the hog cholera organism of Salmon and Smith is motile. However, they conclude that this difference is not sufiicient to differentiate the organisms. Consequently they propose the name avian salmonellosis for the disease observed. 60 DISEASES OF DOMESTICATED BIRDS Etiology. The organism isolated is a non-motile rod wliicli is Gram negative. Whether a precipitation of casein occurs in milk or not, the medium becomes liquid again in 5 to 8 days. The color is grayish and the reaction is strongly alkaline. Indol is not pro- duced and gelatin is not liquefied. Growth occurs on potato. There is nothing distinctive about growth on other media. Pathogenicity. It is possible to inoculate healthy hens and rab- bits with several drops of infected blood without killing them. Sub- cutaneous inoculation with culture does not always kill hens but intravenous injection of 1 to 2 c.c. of culture has a fatal result. The pigeon is easily killed by intravenous and subcutaneous inoculation. Ducks and geese are resistant to the infection. The rabbit inocu- lated intravenously with 1 c.c. of culture is killed, while subcutaneous inoculation merely causes tumefaction at the point of inoculation. Symptoms. 'No symptoms characteristic of the infection in question are displayed. Morbid anatomy. The comb is black, and sometimes dark ecchymoses are observed on the skin. There is a clear fluid in the pericardium. The liver and the kidneys are congested. The spleen is enlarged and much more so than in fowl cholera. The mucosa of the digestive tract is reddened in places, but hemorrhages are rarely found. PATHOGENICITY OF B. ENTEEITIDIS AND B. PAEATYPHOSUS B TO BIRDS Reinholdt has found that introduction of either B. enteritidis or B. parafyphosus B into hens, pigeons, geese and ducks, sometimes causes a transitory disease and sometimes a fatal disease. This is true of a wide variety of methods of inoculation such as intravenous, intraperitoneal, subcutaneous and intramuscular injection, as well as administration by the stomach. Pigeons are most susceptible to in- fection, followed in order by geese and hens. Administration of the organisms per os under normal conditions of feeding is of least influence. A very large number of organisms is necessary to induce infection. The organisms are always recovered when the bird dies, but this is not always true when a bird is slaughtered while healthy. Agglutinins are detected six days after infection. FOWL TYPHOID AND SIMILAR INFECTIOXS 61 SEPTICEMIAS CAUSED BY COLON BACILLI Fowls. Outbreaks of septicemic infections in fowls caused by B. coJi have been reported by Lignieres, Martel, Claussen, Zeiss and Sclilegel. The symptoms are practically indistinguishable from those of fowl cholera. The birds show somnolence, depression, diarrhea and inappetence. In the late stages, the comb may be dark colored as in cholera. At autopsy, there is inflammation of the intestines with hemor- rhages in places. There may be a small amount of serous exudate in the abdominal cavity. The spleen is softened and hypertrophied. There is pericarditis manifested either by the presence of hemor- rhages, solid exudate or fluid exudate. Microscopic examination of stained smears from the blood and organs shows numerous bipolar staining rods. However, the organisms average twice as large as those of fowl cholera. In inoculation experiments made by Lignieres, hens resisted sub- cutaneous and intramuscular injection of 1 to 2 c.c. of culture. On the other hand the pigeon succumbed to a dose of 1 c.c. The same dose injected subcutaneously into the rabbit and guinea pig caused only a local abscess, while intrapleural or intraperitoneal injection killed. Martel killed hens by intramuscular injection of small amounts of culture. Failure resulted from attempts to cause infection by intravenous injection or by ingestion of cultures, excrement and virulent products. The giiinea pig, rabbit, white rat and white mouse w^ere found to be susceptible to injections. Claussen isolated a strain that was uniformly fatal to canary birds, white mice and guinea pigs. Pigeons, hens and ducks became sick only exceptionally. The infection led to the death of only 50 per cent of the inoculated birds, while the remainder recovered after three to six days. The incubation period was on an average, twelve hours long. Rabbits were very refractory to inoculation. Claussen concludes that colon organisms occurring in the intes- tines of healthy hens possess the ability of becoming virulent under certain conditions and cause a cholera-like infection. These spe- cial conditions are believed to be furnished by the harmful influ- ence exerted by shipment for long distances with resulting hunger, thirst, cold and lack of ventilation. Zeiss reports a case in which two hens in a healthy flock sud- 62 DISEASES OF DOMESTICATED BIEDS denly displayed lack of appetite with depression and died soon. Autopsy revealed extraordinary softness of the spleen and liver to- gether with limited subcutaneous hemorrhages. Preparations from the blood revealed bipolar rods. The organism isolated from the cases showed the morphology and biologic characteristics of B. coli. The organism was pathogenic for canaries. On the other hand, guinea pigs could not be infected by either subcutaneous nor intra- venous injection with 2 c.c. doses of 24 hour bouillon culture. Pigeons. Sanfelice observed an outbreak of a disease among pigeons caused by B. coli. Most of the birds appeared at autopsy as follows: On opening the abdominal cavity a sero-fibrinous exu- date is noted on the whole surface of the intestines. The abdominal fluid is increased in amount. The spleen is swollen. There are adhesions of the intestines, the heart and the liver. The exudate appears in the form of a pseudomembrane in that when grasped with tweezers, it pulls off completely. In some pigeons besides the peritonitis described, there is inflammation of the mucosa of the oviduct, which is covered with a purulent exudate. Often eggs are found in the oviduct, which could not be laid on account of the inflammation. An organism identified as B. coli was observed in smears and was recovered in culture from the oro-ans. Pigeons inoculated subcutaneously with one to one and one half c.c. of cul- ture, developed an abscess at the point of inoculation but did not die. Larger doses injected into the abdominal cavity caused death. Pheasants. Klein described an organism isolated from young pheasants dead of an infectious disease. The organism was motile, somewhat shorter than B. coli and did not coagulate milk. He concludes that the organism, though belonging to the same family as B. coli, was a different species. GEOUSE DISEASE Under the name of grouse disease, Klein has described a pneu- monia caused by a member of the B. coli gi*oup. Subsequent inves- tigation by a committee of inquiry on grouse disease revealed the fact that the condition of the lungs described by Klein represents post-mortem changes. The supposed etiological agent is regarded by the committee as a post-mortem invader. It was noted that Klein had opportunity to study only birds that had been dead sev- eral days. The cause of mortality among grouse was watched by the committee very closely for six years and in no instance was FOWL TYPHOID AND SIMILAR INFECTIONS 63 there observed an epizootic like that described by Klein. A large number of agencies are responsible for the death of grouse, and probably the most important is infestation with Trichostrongylus pergracilis as pointed out first by Cobbold. QUAIL DISEASE Synonym. Colibacillosis tetraonidarum. Characterization. Quail disease is an infectious disease which according to Morse is caused by a member of the colon group and characterized by congestion of the lungs, focal necrosis of the liver and ulceration of the intestine. It has been recognized only among birds in captivity. Species affected. The disease has been observed in the bob- white (Colinus virginidnus) , the California quail (Lophortyx cali- fornicus vaUicola), the Gambel quail (Lophortyx gamheli), the mountain quail (Oreortyx pidus), the scaled quail (Callipepla squamata) and the sharp-tailed grouse (Pediocaetes phasianellus canipestris) . History. The disease for many years has been observed among quail shipped for stocking areas of land and appears during trans- portation, or immediately after. It seems evident that the unusual conditions and hardships endured during the shipment constitute an important factor predisposing to the occurrence of the infection. Many outbreaks occur among quail which have been recently cap- tured in Mexico. Morse has written an article summing up the available information regarding the characteristics of the disease. Etiology. Morse reports finding a bacillus of the B. coli group present in diseased birds, with striking constancy. Cultures are readily isolated from the liver and intestines. It cannot always be cultivated from the heart blood of birds dead of the disease, nor always from the lungs. Pathogenesis. The organism is not pathogenic for chickens, pigeons nor rabbits but kills mice and guinea pigs with characteristic lesions. Experiments with quail are hindered by the difficulty in obtaining birds that have not been exposed to infection. Symptoms. The symptoms first become manifest by dullness, inappetence and ruffling of the feathers. Death may occur within two or three days after the appearance of symptoms. In chronic cases emaciation becomes extreme. Morbid anatomy. As a rule, the carcass is in good condition. 64 DISEASES OF DOMESTICATED BIRDS There is slight congestion of the lungs, and of the liver. The sur- face of the latter organ presents a few areas of necrosis. Some- times the liver contains no necrotic spots and is merely congested, but in some cases the necrosis involves a large area. The intestinal wall contains numerous small yellowish areas of necrosis which may be seen through the peritoneal surface. These may be exceedingly minute, or reach the size of a pinhead. In some cases the necrotic process appears in the form of ulcers, some of which may perforate the intestinal wall. In other cases the intestinal lesions may con- sist of mere reddened areas. Prophylaxis. It is likely that the removal of birds from the natural wild environment, interference with natural food supply, crowding in cages and shipment are the fundamental factors pre- disposing birds to infection. These undesirable conditions of \\n- natural crowding are difficult to correct. The cleaning and disinfection of shipping cages should be carried out very thoroughly. So far as possible, birds should be isolated in small lots during shipment. All possible precautions to prevent the contamination of feed and water should be carried out. Treatment. The nature of the disease and subjects are such as to prevent successful treatment. asthenia in fowls (going light) Characterization. The affection is characterized by extreme emaciation associated with reddening of the walls of the duodenum. History. Dawson described the disease as occurring in the vi- cinity of Washington, D. C. Etiology. The organism isolated from the duodenum of af- fected birds is designated Bacterium aMheniece and is regarded as a variety of the colon species. Pathogenicity. Dawson was imable to induce disease in chick- ens by feeding organs or cultures, or by inoculating them intra- abdominally, subcutaneously and intravenously. ISTevertheless he was inclined to believe that the organism in question was the cause of the disease. Dawson considers that the presence of the organism in the part of the alimentary canal where the digestive process is most active FOWL TYPHOID AND SIMILAR INFECTIONS 65 interferes with nutrition. Pigeons, mice and rats proved equally refractory. A guinea pig inoculated subcutaneously with duodenal contents succumbed to the infection. Rabbits inoculated subcutane- ously with culture and fed the same, proved refractory. Intra- abdominal inoculation of half a cubic centimeter of culture proved fatal to a rabbit. Symptoms. Extreme emaciation is the most noticeable symp- tom. The appetite is voracious. There is no evidence of diarrhea and no increase of temperature. The comb and wattles are slightly more pale than normal. Morbid anatomy. Autopsy of affected fowls reveals extreme emaciation of the muscular system and viscera with almost complete absence of fat. There is reddening of the walls of the duodenum and the contents are mucoid in appearance. Treatment. Dawson recommends purgation to remove the or- ganisms in the duodenum. For this purpose he administers castor oil in a dcse of two teaspoonfuls or calomel in one fourth grain doses repeated frequently. He suggests that purgation be followed by a stimulating tonic recommended by Megiiin as follows : Powdered fennel, anise, coriander seed, cinchona, each 30 grains ; powdered gentian and ginger, of each 1 dram; powdered sulphate of iron, 15 gTains. Mix. Add from 2 to 4 grains of this mixture for each fowl to the food twice a day. REFERENCES 1. Claussen. L^eber Kolibakterienseptikamie bei Hiihnern als Trans- portkrankheit. Ztschr. f. Ir^fehtionshr. d. Haustiere, Bd. 3, 1907, S. 69. 2. Committee of inquiry on grouse disease. The grouse in health and disease. London : Smith, Elder & Co., 1911. 3. Curtice. Fowl typhoid. Rhode Island Agr. Exp. Sta. Bull 87. 1002. 4. Diipuy. De la psittacose au point de vue epidemiologique. Prog. Med.. 1897, p. 225. 5. Hadley. Infections caused by bacterium ptdlorum. Rhode Island Agr. Exp. Sta. Bull. 172. 6. Klein. Ueber eine akute infektiiise Krankheit des schottiscben Moor- huhnes (Lagopus scoticus). Centralhl. f. BaMeriol, Bd. 6, 1889, S. 36. 7. Klein. Ein weiterer Beitrag zur Kenntniss des Bacillus der Grouse- disease, Cenfrolhl. f. Bal-ferioL, Bd. G. 1889, S. .593. 8. Klein. T^eber eine epidemisclie Krankheit der Hiihner, verursacht durch einen Bacillus-Bacillus Gallinarum. Centralhl. f. Bal-teriol., Bd. 5, 1889. S. 689. 9. Leiehtenstern. Ueber infektiose Lungenentzundungen und den 66 DISEASES OF DOMESTICATED BIEDS heutigen Stand der Psittacosis-Frage. — Werden durcli spezifish erkrankte Papageien bosartige Lungeneiitzundungen beim Menschen herv'orgerufen ? Centralhl. allgem. Gesundheitspfl., Bd. 18, 1899, S. 241. Abs. in Centralhl. f. Bakteriol {Etc.), 1. AU., Orig., Bd. 26, 1899, S. 651. 10. Lignieres. Septicemie a coli-bacille chez la poule Compt. rend. Soc. de Uol., T. 46, 1894, p. 135. 11. Lignieres and Zabala. Sur tine nouvelle maladie des poules. Bull. Soc. Cent, de Med. Vet., T. 59, 1905, p. 453. 12. IVIartel. Maladie a coli-bacille de la poule et de la dinde. Compt. rend. Soc. de boil, T. 49, 1897, p. 500. 13. Moore. On a pathogenic bacillus of the hog-cholera group associ- ated with a fatal disease in pigeons. U. S. Dep. Agr. Bur. Animal In- dust. Bull. 8, 1895. 14. Moore. A study of a bacillus obtained from three outbreaks of fowl cholera. U. S. Dep. Agr. Bureau, Animal Indust. Bull. 8, 1895. 15. Moore. Infectious leukemia in fowla — 'A bacterial disease fre- quently mistaken for fowl cholera. U. S. Dep. Agr. Bureau Animal In- dust. 12th and 13th Ann. Kep., 1895-96. 16. Morse. Quail disease in the United States. TJ. S. Dep. Agr. Bureau Animal Indust. Circ. 109, 1907. 17. Palamidessi. Di una infectione nell' womo transmesso probabilmenti dai pappagalli. Policlinico, 1895. Abs. in Centralhl. f. Bakteriol. (Etc.), 1. AU., Orig., Bd. 20, 1896, S. 316. 18. Pfeiler imd Rehse. Bacillus typhi gallinarum alcalifaciens und die durch ihn verursachte Hiihnerseuche. Mitteil. a. d. Kaiser Wilhelm In- stitnt f. Landwirthschaft in Bromherg, Bd. 5, 1913, S. 306; Abs. in Cen. train, f. BaUeriol. (Etc.), 1 AU. Ref., Bd. 58, 1913, S. 575. 19. Pfeiler and Roepke. Zweite Mitteilung iiber das Auftreten des Hiihnertyphus und die Eigenschaften seines Erregers. Centralhl. f. Bak- teriol. (Etc.), 1 AU. Orig., Bd. 79, 1917, S. 125. 20. Reinholdt. Infektionsversuche mit den " Fleischvergiftern " (Bacil- lus enteritidis Gartner und Bacillus paratyphosus B) beim Geflugel. Cen- tralhl. f. Bakteriol. (Etc.), 1. AU. Orig., Bd. 62, 1912, S. 312. 21. Rettger and Koser. A comparative study of Bacterium pnllorum (Rettger) and Bacterium sanguinarium (Moore). J. Med. Research, Vol. 35, 1917, p. 443. 22. Sanfelice. Eine Seuche dei Tauben durch Bacterium coli verur- sacht. Ztsclir. f. Hyg. v. Infektionskr., Bd. 20, 1895, S. 23. 23. Smith and Ten Broeck. Agglutination affinities of a pathogenic bacillus from fowls (fowl tyiihoid). (Bacterium sanguinarium, Moore.) /. Med. Research, Vol. 31, 1915, p. 503. 24. Smith and Ten Broeck. The pathogenic action of the fowl typhoid bacillus with special reference to certain toxins. J. Med. Research, Vol. 31, 1915, p. 523. 25. Smith and Ten Broeck. A note on the relation between B. pul- lorum (Rettsrer) and the fowl typhoid bacillus (Moore). J. Med. Re- search. Vol. 31, 1915, p. 547. 26. Taylor. A report upon an outbreak of fowl tj^phoid. J. Am. Vet. M. Ass., n. s. Vol. 2, 1916, p. 35. FOWL TYPHOID AND SIMILAR INFECTIONS 67 27. Zeiss. Ivoliseptikiimie bei ITuhnern. Archiv f. Hyg., Bd. 82, 1914, S. 27. 28. Zingle. Untersuchungen iiber eine Taubenseuche mit Paratyphus-B- Bazillenbefund. Zeitschr. Infehtionshr. d. Haustiere, Bd. 15, 1914, S. 269. CHAPTEK VI BACILLARY WHITE DIARRHEA Characterization. Bacillary white diarrhea is an acute, highly fatal septicemic disease of young chicks caused by Bacterium pul- lorum. The infection also exists in adult hens in a chronic, rarely fatal form, usually confined to the ovary. The disease as it occurs in hens bears no specific name and is merely referred to as B. pul- lomm infection. Etiology. Rettger and Harvey describe the characteristics of the organism substantially as follows : "Morphology, staining properties, etc. I'he organism is a long, slender bacillus (.3-5 micron x 1-2.5 microns) with slightly rounded ends. It usually occurs single, chains of more than two bacilli being rarely found. It is non-motile, non-liquefying, non-chromogenic, aerobic and facultatively anaerobic. In its microscopic appearances it resembles the bacillus of typhoid fever. It is stained readily by the ordinary basic anilin dyes. It does not stain by the Gram method; neither does it retain its color when treated with dilute acetic and mineral acids. The organism does not produce spores, or at least they have never been observed. " The maximum temperature tolerated is 56 to 57° C. (moist) for an exposure of fifteen minutes. The optimum temperature is 35 to 37° C. "Cultural characters: Agar plates. Small white colonies make their appearance within twenty-four hours. They increase in size slowly and seldom attain more than one millimeter in diameter, even after three or four days' incubation. Under themicroscope they appear yellow and vary in form from oval and spindle-shaped to round. The surface is usually marked with a rosette figure or what seems to be a lobed nucleus. Occa- sionally two or even three of these markings may be seen. " Slant agar. Growth is quite visible in twenty-four hours, and re- sembles that of the tyi^hoid bacillus. It spreads little and remains deli- cate, even after prolonged incubation. On glycerine agar the growth is practically the same. " Gelatin plates. Small white colonies may be seen in forty-eight hours. They remain small for several days, and only under exceptional conditions do they develop into characteristic surface colonies which to a certain ex- tent resemble the grape-leaf colony of B. typhosus. " Gelatin stah. A delicate growth occurs in forty-eight hours along the whole line of inoculation. It is of distinctly granular appearance and spreads very little on the surface. The gelatin is not liquefied. " On potato development is very slow. A narrow, almost invisible 68 BACILLAKY WHITE DIAKRHEA 69 streak is produced along the line of inoculation. In litmus milk little or no apparent change occurs within the first forty-eight hours, after which the milk becomes slightly acidified without any signs of coagulation of the casein. " Gas production in sugar houillon. Negative results were obtained with maltose, lactose, saccharose, inulin, and dextrin bouillon. Dextrose and mannite were attacked, however, with both acid and gas production. In the dextrose fermentation tubes about twenty per cent of the closed arm was filled with gas, and the mannite tubes averaged about the same. The gas consisted of Co., and H in the ratio of 1 : 3. " Indol and nitrite production. Neither indol nor nitrite could be de- tected in Dunham's peptone solution at the end of one week's growth in the incubator." Toxin production. B. pullorum lias been shown by Smith and Ten Broeek to prodnce a toxin fatal to rabbits. Filtrates of bonillon cultures when injected intravenously may cause death Avithin two hours, or marked dyspnea followed by death over night, or cause loss of weight followed by recovery. The lesions induced, include con- gestion of various organs such as liver, spleen, kidneys, adrenals, lungs and mesenteric lymph glands together with hemorrhage into the gastric mucosa. Source of infection. Infection may occur in several ways. The most common source is through infected eggs. It has been demonstrated that affected chicks which survive the disease fre- quently retain the causative organisms in the system and later, in the event that the ovaiy becomes infected, pass them off in the eggs. Many infected eggs fail to hatch, the embryos dying in the shell at an early or late stage of development. Should one or more chicks be hatched, harboring the disease, the others of the lot are exposed early and nearly all become affected. The chicks are especially susceptible during the first 48 hours of life, but are practically in- susceptible after the third day. Another source of infection is through brooders and incubators that have previously held infected chicks. Day-old chicks frequently carry the disease to other points and contaminate brooders or infect other chicks with which they come in contact. However, the largest percentage of outbreaks is traced directly to the presence of infected hens in the flock from which the eggs for hatching were derived. There is a well defined cycle through which the bacterium passes ; namely, from the in- fected ovary of the hen through the egg to the chick and back to the ovary of the pullet which has survived the disease as a chick. Pathogenicity. Susceptibility to infection bears a remarkable 70 DISEASES OF DOMESTICATED BIRDS relation to age. During the first fortv-eigiit hours the baby chick is most susceptible to Bacterium pullorum and at this period of life, has practically no resistant forces to combat the infection. In the succeeding twenty-four hours, more resistance is shown bv those not BACILLARY WHITE DIARRHEA 71 previously affected. At the end of four days, the unattacked chicks have generally acquired a resistance to acute infection. The re- sistance at this age, while very apparent in broods of young chicks, is not absolute, since fatal outbreaks in old fowls are recorded in the literature on the disease. Half grown guinea pigs are killed in from 24 to 48 hours when injected subcutaneously. The chief lesion is a large edematous area beneath the skin of the abdomen. Rabbits are killed in three to seven days by subcutaneous injection of one to two c.c. of 48 hour bouillon culture. In the case of all experimental inoculations, the organism may be recovered in pure culture from all the internal organs. Mortality. Baeillary white diarrhea is, without doubt, the most fatal disease of young chickens. i\jnong those broods affected, the death rate varies between 40 and 90 per cent. The high percentage is UK^-e often registered than the low one. Symptoms. The external symptoms of baeillary white diar- rhea are similar to those of coccidial and aspergillar white diarrhea. The presence of soft, whitish droppings and similar symptoms in each case caused these three diseases to be grouped under the com- mon term " white diarrhea." The position of each as an important specific disease requires that they should be treated separately, espe- cially since they are not confined to young chicks but affect gro\vn fowls as well. The affected bird is drowsy, and dejected in appearance. The feathers are rufiled, the wings droop and the chick sways back and forth in a standing position. The appetite is diminished. The irritation of the droppings when being voided often causes the chick pain as evidenced by a peculiar cry at the time. The drop- pings may adhere to the down about the vent, blocking the opening. This gives rise to the expression " pasting up behind." In acute cases the chick soon falls to the floor and death occurs after a short period of coma. In more chronic cases the chick remains standing in a dull inattentive position a good portion of the time while not under the hover or hen. It acquires the appearance of having a short back and a large abdomen. Often one or both feet swell. The chick stands on one leg with the toes of the elevated foot just touching the floor. Lameness is shown in attempts to w^alk. The disease may show itself within two or three days after the chicks are hatched and spread rapidly through the brood. The period of incubation is four to ten days. Deaths begin to occur 72 DISEASES OF DOMESTICATED BIRDS soon after hatching and continue to the third or fourth week. Chicks which survive, remain stunted and unthrifty for some time. Morbid anatomy. The lesions observed on autopsy are not clearly distinctive for this disease which is purely septicemic in nature. The early, rapid development of the disease, in a host unprepared to combat it, prevents the formation of many distinctive lesions. The failure of the yolk to be absorbed is the principal abnormal condition that is apparent. However, this condition is observed in very young chicks which have died through other causes, such as weak constitution, faulty incubation, and brooder defects. The liver usually shows an ochre color, with bands or streaks of congestion. This appearance is not constant as in some cases an apparently normal mahogany or chocolate colored liver is observed. In some instances the liver has the normal appearance, and the yolk sac has been absorbed. This is especially common in less acute cases. The lungs may show minute necrotic areas and, as a rule, congestion. Diagnosis. Diagnostic features of the disease are its early appearance, the high mortality within the first month, the occurrence of deaths within a few days after hatching, and the absence of inter- nal lesions other than unabsorbed yolk or striations on the surface of the liver. Confirmatory positive evidence is obtained by examina- tion of stained smears of the blood, liver or yolk with discovery of the causative organism. Further evidence is yielded by feeding or in- oculation experiments with young chicks. Artificial cultural methods are more precise. The causative or- ganism may be readily isolated in a pure culture from the heart blood, liver, spleen, kidneys or unabsorbed yolk. It may be differ- entiated from other organisms of a similar type by its cultural and biochemic characteristics, and by its agglutinating properties against a homologous serum. Differential diagnosis. Bacillarv white diarrhea is differenti- ated from the other diseases commonly classed as white diarrhea by its early occurrence, the exceptional mortality, and the absence of the characteristic lesions of coccidiosis, or of aspergillosis. Coccidi- osis is slower in its development and usually affects chicks at a later period. It is manifested by hemorrhagic areas in the ceca, dilatation of these organs, and the presence of necrotic casts in their lumina. In the event that this disease is present, the coccidial cysts may be readily demonstrated on microscopic examination of the cecal con- tents. BACILLARY WHITE DIARRHEA 73 Aspergillosis is comparatively rare in young chicks. Its charac- teristic growth may be found in the air passages, and the mycelia, or spores of the fungais can be observed by microscopic study of the moldy gTowth. Treatment. Attempts to cure bacillary white diarrhea are fu- tile. Some recover, owing to natural resistance, or other reasons. The so-called treatments recommended by some advisers are not to be relied upon. Once the disease has become established in the sys- tem, the causative microorganisms are distributed through the vari- ous organs by way of the blood stream and a septicemia has developed which is beyond the reach of any antiseptic treatment which has yet been discovered. By careful nursing, certain individuals might be assisted in surviving ; however, this is inadvisable because of the fact that the monetary value of the baby chick does not justify the ex- penditure of the time devoted to its treatment. Furthermore, the fact that those which recover are likely to serve as reservoirs for the causative organisms and constitute the sources of future outbreaks would speak against the policy of treatment. Where the disease is known to exist in a flock of breeding fowls and is anticipated in the hatch of baby chicks, precautions may be taken to lessen its attack by advanced treatment of the chicks. ^ Per- manganate of potash may be placed in the drinking water in sufficient quantity to give the latter a deep red color.^ This corresponds to dilu- tion of approximately 1 to 10,000. In such dilution, the antiseptic is non-irritating to the sensitive mucous membranes of the chick and may serve to inhibit the growth of the pullorum bacterium in contami- nated drinking water, and in the digestive tract of the chicks. But- termilk may be used as a food, as it combats the development of the bacterium in the intestine, due to the lactic acid which it carries. Prevention. The first principle of prevention is the eradication of carriers in the breeding stock, or the use of eggs for hatching which come from flocks known to be free of pullorum infection. Certain tests which are later discussed may be depended upon to detect the presence of the disease in a large percentage, if not all, of the infected hens of a flock. These birds may be discarded for breeding purposes or disposed of as the owner may desire. In this connection, it has come to our attention indirectly that in rare in- stances normal hatches have succeeded ones in which high mortality has occurred, the eggs in each case being derived from flocks in which a number of infected hens have been detected but retained as breeders. 7-t DISEASES OF DOMESTICATED BIEDS The significance of this is not apparent, but opens an interesting field for study, if the observations are accurate. If it is desired to breed from an infected flock for the purpose of perpetuating the particular strain of fowl, or for other reasons, pre- caution may be taken to minimize the losses by the following pro- cedure. Incubator trays, or shelves, of the pedigree type which are partitioned oft" into compartments capable of inclosing a few chicks, say from six to ten as the owner may decide, are to be used. The partitions are to be sufiiciently high to prevent the chicks in adjacent compartments from coming in contact. This also means that the partitions should be of solid structure to prevent picking back and forth. It is only necessary to use such trays a day or two before the hatch is expected to come oft', and for three daj's after it is com- pleted. The chicks are to be retained in their respective compart- ments and need not be fed for 48 or even 72 hours, since they are provided with food material during this period through the yolk which is drawn into the abdominal cavity previous to hatching. Should symptoms of disease develop, the chicks in the particular compartment are to be removed and disposed of. The attendant should then disinfect his hands before watering or caring for the others. As the disease is contracted principally during the first 48 hours of life, and only to a slight extent during the succeeding 24, this method of procedure will prevent a general spread to the hatch. The temperature and air requirements may be regulated to suit the needs of the chicks. Humidity, due to close confinement and lack of air circulation, is to be gTiarded against. The trays may be re- moved to the brooders, or similar structures may be placed in the latter and the chicks transferred to them, with care to avoid mixing the segregated lots. After three days, the danger of infection is re- duced to a minimum, and all of the hatch may be allowed to run together. BACTERIUM PULLORUM INFECTION OF GROWN FOWLS Occurrence. Infection of hens by the organism in question is not marked by external changes nor is it regarded as a common cause of death. Jones reports one outbreak due to B. pullorum in- fection which assumed an acute character with marked symptoms and considerable mortality. In this case the fowls were infected through the feeding of eggs which had failed to hatch and which came from an infected flock. About 50 birds died durino- the outbreak. The BACILLARY WHITE DIARRHEA VO present writers have encountered at autopsy a naturally infected fowl which had developed fatal B. pullorum septicemia from primary ovarian infection. Symptoms. In the chronic form, no symptoms are apparent to the observer. The fowls continue to lay, although from the number of retained and undeveloped ova, it is evident that laying is retarded. In the acute cases reported by Jones, within a period varying from two to six weeks after exposure by feeding, the affected birds showed a loss of appetite and energy. They appeared droopy and somnolent, with ruffled feathers and retracted heads. The combs and wattles were pale and more or less diarrhea was present. In the fatal cases, death ensued in from one to several days after the onset of symptoms. Morbid anatomy. In the acute cases autopsied by Jones the most constant lesions were the presence of small necrotic foci in the liver, spleen, pancreas and heart. The capsule of the liver, the peri- cardium and the heart were in many instances covered by a fibrinous exudate. In the majority of chronic cases, autopsy will show^ the lesions to be confined to the ovary. This organ usually presents an appear- ance quite characteristic. The diseased ova which have partially or wholly developed are hard, shrunken and angular. The natural yolk color has changed to a dark brown or greenish color. On cut section the ova are of a tough cheesy consistency, with a yellowish red, or greenish tinge. The condition of the ova closely resembles " gan- grene of the ovary " of earlier writers. The morbid ova may also appear as cysts, with darkened fluid contents. Occasionally only small cysts are present in the ovary and it is through cultural meth- ods alone that the presence of pullorum infection may be detected. Small foci consisting of sac-like structures with yellowish colored solid or fluid contents may occur in almost any portion of the ab- dominal or pleural cavities. Involvement of the pericardial sac is not uncommon. The causative bacterium may be readily isolated from the angular ova or cysts and grown on artificial culture media. In some cases where ovarian lesions are not pronounced, it is necessary to remove the ovary and disintegrate aseptically. The mass is placed in a flask of houillon, from which cultures may be plated on agar and the organism isolated in pure culture. Diagnosis. Several methods of diagnosing the presence of B. pullorum in fowls are available and are more or less satisfactory. The presence of bacillary white diarrhea in a brood of chicks which 76 DISEASES OF DOMESTICATED BIRDS Fig. 5. Xormal ovary. (Redrawn from Eettger, Kirkpatrick and Jones) has been batched from eggs from a particular flock of bens is proof enough of infection in the flock, providing that there is a reasonable certainty that contamination has not been introduced by outside sources or from infected incubators or brooders. Detection of the characteristic pullorum-infected ovaries, on post mortem examina- tion, is definite proof that the disease is prevalent in the flock. Bac- FiG. 6. Ovary infected with B. pulloriim. (RedrawTi from Rettger, Kirkpatrick and Jones) BACILLAEY WHITE DIAREHEA 77 teriological examination of eggs from a suspected flock also leads to a diagnosis. However, this method is impractical because of the fact that an infected hen only occasionally drops an infected egg and considerable laboratory work is necessary to establish the presence of the disease. For the detection of individual carriers among hens held for breeders, two other methods which give positive proof of the presence of infection in the flock and pick out the infected individuals with a high degree of accuracy have been developed. These are the agglutination test applied first by Jones, and the intradermal test developed by the authors. Agglutination test. This test is based on the fact that the blood serum of an animal which has experienced the attack of a given species of bacteria will in some instances cause the organisms to agglutinate or form into clumps when a suspension of the bacteria is mixed with the serum of the animal in proper dilution. The wing vein is severed at the point where it passes over the elbow joint and 3 to 5 c.c. of blood collected in a sterile test-tube or vial. The flow of blood is then stopped by momentary pressure over the cut, or by the application of a small pledget of cotton. Usually no effort is necessary to stop the flow of blood, as chicken blood clots readily. Blood may be drawn more rapidly by severing the promi- nent vein visible on the ventral surface of the wing near the shoul- der. The collected sample is set aside and allowed to clot. It should not be agitated while the clot is forming, as this tends to prevent the collection of a clear serum. After the clot has formed, the sample may be placed in a refrigerator or other cool place. In a few hours the serum will have been pressed out by the contraction of the fibrin and can be drawn off as a clear fluid, free of blood cor- puscles or hemoglobin. If the test is not to be made immediately, the serum may be preserved by the addition of carbolic acid in suf- ficient quantity to form a .5 per cent solution. For this purpose, it is convenient to use a 5 per cent solution of carbolic acid as a standard, .1 c.c. being added to .9 c.c. of serum, or 1 drop to 9 drops. For the test a standardized suspension of B. puUorum is prepared. This may be heated at 60° C. for one hour, to kill the organisms, or used in the live state. The latter has been the practice of the au- thors. However, there appears to be no marked advantage in the use of live antigen, and killing by heat or .5 per cent carbolization has the advantage that the organisms are dead and hence absolutely harmless. In the test, the bacterial suspension is placed in the test tubes 78 DISEASES OF DOMESTICATED BIRDS in the quantity of 1 c.c. to each tube. A series of tubes is em- ployed for each serum, depending on the number of serum dilu- tions to be made. In practice, a serum which causes agglutination in a dilution of .01 or even .02 is sufficient to establish a positive diagnosis. Using 1 c.c. as the standard amount of bacterial sus- pension, sera which have been diluted by the addition of normal salt solution to the extent of .04, .02, and .01 per cent of the original, are distributed in their respective tubes in quantities of 1 c.c. each. The tubes are labeled to show the identity of the various sera and the dilutions. In practice, it is found convenient to dilute the serum to 10 per cent of its original volume and add .4, .2, and .1 of a c.c. to the 1 c.c. of bacterial suspension. The tubes are shaken to insure a thorough mixture of the contents and may be set aside at a tem- perature of 37° C. for from twenty-four to forty-eight hours, when readings may be made. Instead, when rapid diagnosis is desired, they may be placed in an incubator at 37° C. for ^ hour and then centrifuged at the rate of 1500 to 1800 revolutions to the minute for several minutes. Either course gives similar results. In positive cases the organisms in the fluid collect in flocculent masses which have a tendency to form a diffuse coating over the bottom of the tube, while in the negative cases the organisms are deposited in a small circular mass in the center of the bottom of the tube. This is par- ticularly apparent where centrifugalization has been employed. On shaking the tubes the clearly positive ones will show a clear fluid containing flocculent masses while the negative ones are uniformly clouded. The agglutinating serum dilution which will establish a diagnosis has not been definitely fixed. It is a well known fact that normal blood serum is capable of agglutinating organisms to a greater or less degree. In B. pullorum infection tests, a serum which in the amount of .02 c.c. or less causes agglutination, undoubtedly indicates a positive case. Intradermal test. This test depends for its results upon the principle underlying allergic reactions. It is very similar in char- acter to the intradermal tuberculin test, especially as used to detect tuberculosis in fowls. A culture of several strains of B. puUorum from widely separated sources is growm in bouillon at a temperature of 37.5° C. for a period of thirty days to three months. Whether these time limits are necessary has not been determined. The product is then steril- ized at a temperature of 60° C. for a period of one hour and carbolic BACILLAEY WHITE DIARRHEA 79 acid is added in sufficient quantity to form a .5 per cent solution for preserving purposes. In the earlier experiments of the authors, the product was passed through a Berkefeld filter and concentrated to onc-tonth of its original volume. Later it was found that the original sterilized product concentrated to Vs its volume gave as satisfactory results. The material is injected into either wattle of the fowl in the amount of approximately .2 .^a^^?'?'*!;" c.c. The injection is made with a hypodermic syringe graduated in tenths of a c.c, and a needle of fine caliber is used to avoid causing traumatic swellings. The injection is made at a point near the lower border of the wattle. Where the flock is apparently free of infec- tious disease, no disinfect- ants are employed at the point of injection since the natural resistance of birds to ordinary wound infection is sufficient to giiard against infection. In the ab- sence of a graduated syringe, the amount to be injected may be gauged by injecting enough to cause a perceptible swelling at the point of inoculation. During the first three hours after injection the wattle shows an edematous condition which rapidly disappears in non-reacting birds. Ecadings are taken at twenty-four to thirty hours after injection. The wattle may be swollen to several times its natural thickness and may be readily observed at a distance, or the swelling may be so slight that palpation, or comparison with the uninjected wattle will be necessary. Any swelling other than that due to traumatism as a result of faulty technique, should be consid- ered significant. REFERENCES <;;;5gVti-V Fig. 7. Edematous swelling of wattle in- dicating positive reaction to the intrader- mal test for B. pullorum infection. (Original) 1. Bushnell and Maiirer. The use of milk cultures of B. bulgarieus in the prevention and treatment of bacillary white diarrhea of young chicks. Am. Vet. Rev., Vol. 44, 191.3, p. 195. 2. Gage and Martin. Notes on the histo-patholog>^ of the intestines in young chicks infected with bacterium pullorum. J. Med. Besearch, Vol. 34, 191G, p. 149. 3. Gage and Hyland. On the diagnosis of infection with bacterium 80 DISEASES OF DOMESTICATED BIRDS pullorum in the domestic fowl. Mass. Agr. Exp. Sta. Bull. US, 1914. 4. Gage and Paige. Bacillary white diarrhea (Bacterium pullorum in- fection) in young chicks in Massachusetts. Mass. Agr. Exp. Sta. Bull. 16S. 1915. 5. Jones. The value of the microscopic agglutination test in detecting fowls that are harboring Bact. pullorum. J. Med. Research, Vol. 27, 1913, p. 481. 6. Jones. Further studies on bacillary white diarrhea in young chickens. Rept. N. Y. State Vet. Col. 1910-1911, p. 69. 7. Jones. An outbreak of an acute disease in adult fowls, due to Bact. pullorum. J. Med. Research, Vol. 27, 1913, p. 471. 8. Rettger. Septicemia among young chickens. N. York M. J.. Vol. 71, 1900, p. 802. 9. Rettger. Septicemia in young chickens. N. Yorh M. J., Vol. 73, 1901, p. 267. 10. Rettger. Further studies on fatal septicemia in young chickens or " white diarrhea." J. Med. Research, Vol. 21, 1909, p. 115. 11. Rettger. Ovarian infection in the domestic fowl and direct trans- mission of the disease to the offspring. J. Exper. M., Vol. 19, 1914, p. 552. 12. Rettger and Harvey. Fatal septicemia in young chickens, or " white diarrhea." /. Med. Research, Vol. 18, 1908, p. 277. 13. Rettger, Hull and Sturges. Feeding experiments with Bacterium pullorum. The toxicity of infected eggs. J. Exper. M., Vol. 23, 1916, p. 475. 14. Rettger, Kirkpatrick and Card. Chickens: Milk feeding and its influence on growth and mortality. Comparative study of the value of sweet and sour milk. Storrs Agr. Exp. Sta. Bull. 80, 1915. 15. Rettger, Kirkpatrick and Stonebiirn. Bacillary white diarrhea of young chicks. Third report. Storrs Agr. Exp. Sta. Bull. 7^. 1912. 16. Rettger, Kirkpatrick and Jones. Bacillary white diarrhea of young chicks. Fourth report. Storrs Agr. Exp. Sta. Bull. 77, 1914. 17. Rettger, Kirkpatrick and Jones. Bacillary white diarrhea of young chicks. Storrs Agr. Exp. Sta. Bull. 85, 1915. 18. Rettger, Kirkpatrick and Jones. Bacillary white diarrhea of young chicks — VI. Storrs Agr. Exp. Sta. Bull. 88. 1916. 19. Rettger and Stoneburn. Bacillary white diarrhea of young chicks. Storrs Agr. Exp. Sta. Bull. 60. 20. Scherago and Benson. Experiments on the intradermal test for Bacterium pullorum. Cornell Yet., Vol. 9, 1919, p. 111. 21. Ward and Gallagher. An intradermal test for Bacterium pullorum infection in fowls. TJ. S. Dep. Agr. Bull. 517. CHAPTER VII FOWL PLAGUE Synonyms. Bird plague, fowl pest, bird pest, infectious peri- tonitis of birds, exudative typhus of birds, Brunswick bird plague ; Peste aviarire, Peste des oiseaux (French) ; Geflilgelpest, Huhner- seuche, Huhnerpest, Vogelpest, Geflugelseuche, Kyanolophiea gallin- arum, Putenseuche (German) ; Peste aviaria, Epizoozia tifoide dell pollame, Tifo essudativo del gallinacei (Italian). Characterization. Fowl plagiie is an acute infectious disease of birds, caused by an ultra microscopic virus. It runs a rapid course and causes high mortality. Geographical distribution. The disease has been reported in Italy, Germany, France and Belgium. Etiology. The virus is ultra microscopic, passes through porce- lain filters, and is believed to be a protozoan. The presence of the virus has been demonstrated in the blood, the nervous system, nasal and oral discharges, serous exudates and feces. The virus is believed to be largely localized in the red blood cor- puscles. The virulence of the red corpuscles is such that death has been produced by a dose of .000,000,000,163,84 c.c. Dessication is not rapidly fatal to the virus for it has been ob- served to remain active for several weeks. It has been rendered inactive by exposure to direct sunlight or to a temperature of 65° to 70° C. for a few minutes. The activity of the virus is destroyed rapidly by whitewash and the common disinfectants. Certain granules have been observed in the brain of geese, hens and pigeons dead of the disease. Ottolenghi believes that they are derived from the nuclei of the cells. Certain peculiarities suggest to him the supposition that they contain the virus of fowl plague. Other granules in the brains of geese and hens are differentiated from the former by the fact that the cytoplasm of the cell is involved in their formation. Pathogenicity. The disease has been observed in fowls, turkeys, peafowls, giiinea-fowls, geese, pheasants, pigeons, ducks, and a large number of wild birds. Wild ducks when placed under conditions of semi-domestication contract the infection. 81 82 DISEASES OF DOMESTICATED BIRDS The virus is believed to be transmitted naturally by nasal and oral secretions, by the droppings of diseased birds or by eating carcasses of dead birds. Wounds of the skin when contaminated with virus readily result in infection. Mites (Dennanyssus avium) have been tested as to their ability to transmit the disease, with nega- tive results. Likewise ticks have given negative results. The disease is most frequent in early spring, declines in preva- lence in the summer and does not occur during the winter. In arti- ficial transmission, fowls succumb to subcutaneous or intramuscular injection or to application of the virus to the scarified skin. They likewise become infected by ingestion. After the subcutaneous or intramuscular injection of moderate amounts of heart blood and pieces of spleen or kidney the size of a pea the inoculated hens die as a rule within 36 to 48 hours, often in 3 to 4 days, and quite rarely only after 5 to 7 days. Feeding of larger amounts of pieces of organs causes death after about the same length of time or a few hours longer than in the case of subcutane- ous injection. Filtrates of nasal mucus, contents of the small in- testine, bile, brain, blood and internal organs are infective for hens. Many authors have failed to transmit the disease to old and young ducks or to young pigeons. Young geese are susceptible to sub- cutaneous and intramuscular inoculation or by the mouth, and die as a rule after about seven days. On the other hand, old geese are very slightly susceptible to ordinary methods of inoculation. Subdural inoculation of these has succeeded, and caused the nervous type of the disease. The disease exhibits peculiarities in showing a preference at dif- ferent times for different species of birds all in contact with one another, such as fowls, pigeons, geese and ducks. Mammals are immune to infection. In young geese and in pigeons the disease assumes the nervous type, which runs a much less rapid course. In these the virus at first localized in the blood corpuscles seems to disappear therefrom, and becomes established in the central nervous system. However, the virus may reappear in the blood shortly before death. Cominotti has obser\'ed the nervous type of the disease in wild ducks in confinement under conditions resembling those under which domesticated birds are kept. The virus was found always in the central nervous system and was never demonstrated in the blood or the internal organs even when large quantities of inoculating mate- rial were used. Transmission of the infection from w^ild ducks to FOWL PLAGUE 83 fowls was possible bv subcutaneous injection of portions of cerebral svibstance. It was not possible to infect domesticated ducks with wild duck virus in doses however large, and administered by intra- venous inoculation, ingestion, intracerebral inoculation or instilla- tion into the conjunctivae. Symptoms. The incubation period is usually 3 to .5 days, but exceptionally 2 days or even 1 days. It is much shorter when birds are inoculated. The symptoms greatly resemble those of fowl chol- era. Death may occur while the bird is on the roost or on the nest without its having previously exhibited symptoms. There is an acute type of the disease in which the bird lives at the most three or four days. In a subacute form the birds survive 7 or 8 days. Recovery practically never occurs. In the acute type, the first noticeable symptom is inappetence. Then the bird declines into a condition of weakness and somnolence, hides in corners, becomes indifferent to surroundings, with half closed eyes, drooping comb, and ruffled feathers. The temperature rises to 110° or 112° F., but may drop to subnormal before death. The comb commonly takes on a violet color which proceeds from the borders, or spots form on the sides, but it soon appears black. In some cases the comb is covered with white scales. The bird gen- erally dies quietly in a somnolent condition, which is only occa- sionally interrupted by spasms. In the subacute form which occurs quite frequently in cases of natural infection, the bird ceases to eat and drink, and goes on the nest for protection from the light. The general appearance is deceptive as indicative of the diseased condition. Upon investiga- tion and when an effort is made to see the bird walk, it may not rise to the feet, or moves the feet with difficulty, staggers, with the head wabbling and turned backwards which attitude appears to be involuntary. With the development of the disease, paresis occurs and stupor becomes deeper. In some cases in this stage a viscid secretion flows from the nostrils and mouth or the material may be squeezed from the nostrils. A diphtheritic type has been observed, in which fibrinous exudate occurs in the nasal, oral and phar\Tigeal cavities. Conjunctivitis and lachrymation may occur. As a rule there is no diarrhea. The feces are quite solid, often green in color and of the usual amount. In the later stages of the disease some birds discharge hardly any feces. At death and after, a fluid is discharg(>d from the cloaca and beak. Morbid anatomy. Freese has conducted numerous autopsies 84 DISEASES OF DOMESTICATED BIKDS of naturally infected birds and describes the lesions as follows: Hemorrhages in the mucous membrane of the passage between the proventriculus and gizzard are highly characteristic of the disease. They also occur in the mucosa of the true proventriculus between the conical elevations or very seldom they are limited only to these elevations. It is possible for the hemorrhages to occur in both places in the same fowl. The hemorrhages of the mucosa between the papillse or in the opening between the two stomachs may be superficial, in the mucosa or in the tissues lying beneath. They vary gTeatly in size and may be barely visible or several centimeters in diameter. They are red or dark red in color and often are not sharply circumscribed. If the conical papillae are involved, either the whole mass is reddened or only the upper border about the mouth of the gland. The hemorrhages in the proventriculus in many cases are very small and are often quite separated, so that their presence might not be obsei'\'ed on superficial examination. This is all the more likely unless the viscid, gTay, white, cloudy mucus is removed. Small hemorrhages are frequently found in the fatty tissue sur- rounding the gizzard, on the mesentery of the small intestine and superficially under the cuticle of the gizzard. More rarely, fine subepicardial hemorrhages are observed in the pericardium, espe- cially in the heart fat, and in the tracheal, laryngeal and pharyngeal mucosae. They are rarely found in the pulmonary pleurge. The kidneys are swollen to an extraordinary extent. They are either grayish brown in color and clouded or in the acute cases, dark brown on account of the presence of an excessive amount of blood. In the functional ovary, there is a marked congestion of the vessels of the yolk capsules. Occasionally hemorrhages are ob- served under the serosa in the yolk mass. In acute cases a certain degree of swelling of the spleen is ob- served. As a rule, however, lesions of this organ do not occur. The liver does not show important lesions, but some writers describe congestion in acute cases. Inflammation of the small intestine is at the most limited to the first portion of its length. In some cases there is observed only a slight catarrhal inflammation, while in other cases there is a marked inflammation with hemorrhages. The ceca and the remaining large intestine are very rarely inflamed. Inflammation of the intestine occurs in about half of the cases. FOWL PLAGUE 85 Exudate in the abdominal cavity is either serous or sero-fibrinous. The fibrin as a rule is in suspension in the serous fluid in the form of flakes, or is deposited loose on the peritoneum in the form of threads or sheets. The peritoneum is not inflamed but is smooth, shiny and trans- parent. Exudate occurs in the abdominal cavity in about a quarter of the cases. Exudate occurs in the pericardium in the form of a serous or sero-fibrinous fluid, which on opening of the pericardial sac often coagulates into a gelatinous mass. The presence of exudate in the pericardium occurs somewhat less often than in the. abdominal cavity. A bluish red coloration of the comb occurs very often. There is nothing characteristic about it as compared with a number of other diseases. Some authors emphasize the significance of catarrh of the upper air passages and of the phar^oix. They note the occurrence of viscid gTay white mucus in the beak, throat and nasal cavity, but it is considered to be a normal secretion which remains in its place of production for some time before death. In wild ducks dying of the nervous type it has been noted that autopsy reveals no characteristic gross changes. Diagnosis. The presence of hemorrhages in the proventriculus, the swelling of the kidneys and the severe injection of the blood vessels in the yolk capsules of the ovary, occasionally associated with the presence of hemorrhages, in birds dying of a pest-like disease, are most significant. The autopsy findings alone will not always suffice for making a diagnosis. In some cases as in other infectious diseases, the lesions may be so slight as not to warrant drawing conclusions. A diagnosis of fowl plague can be established most certainly by successful transmission to a hen with absence of a causative agent recogTiizable in tissues or in cultures from the blood and organs. Differential diagnosis. Phosphorus poisoning causes lesions having the greatest similarity to those of fowl pest and also causes a high mortality. In general the hemorrhages in the proventriculus occurring in phosphorus poisoning extend deeper than in fowl pest, also in the poisoning, erosions occur in the hemorrhagic mucosa. In phosphorus poisoning there is also a marked inflammation of the upper part of the intestine. N'otwithstanding the great similarity of the lesions the two conditions can be diftcrentiated at autopsy by 86 DISEASES OF DOMESTICATED BIRDS the escape of the so-called phosphorus vapor from an opening in the gizzard or crop and by the characteristic smell. ISText in similarity is fowl cholera. This is characterized by the occurrence of subepicardial hemorrhages, an exudate in the peri- cardium, a marked inflammation of the intestine and by the in- flammation frequently occurring in the lungs. In only a few cases would these lesions be confounded with those of fowl pest. Rabbit inoculation is valuable, for this animal is immune to fowl pest and susceptible to fowl cholera. Spirochetosis will be suggested by the drowsiness and paralytic symptoms and must be difterentiated by microscopic examination of blood taken during an early stage. In spirochetosis such blood will be found to contain spirochetes, but such an examination will be misleading, if the sample be dra\\Ti after the crisis has occurred. Preventive measures. Treatment is unavailing. The general sanitary measures such as recommended for cholera, should be em- ployed. Attempts to immunize by vaccination with diluted red corpuscles have failed. A slight measure of success by vaccination with virus killed by ether, has been obtained. Birds after two vaccinations were protected to a slight extent in that death was delayed. The agency of poultry exhibitions in rapidly disseminating the infection should be borne in mind. The disease apparently gained a wide distribution in Germany as a result of a show held in Bruns- wick in 1901. REFERENCES 1. Belfanti and Ascoli. Spigolature nella Peste Aviaria e nell' Afta. Clin. Vet., Vol. 39, 1916, p. 577. 2. Centanni. Die Vogelpest; Beitrag zu dem durch Kerzen filtrirbaren Virus. Centralhl. f. BaUeriol. {Etc.), 1 Alt. Orig., Bd. 31, 1902, S. 145. 3. Cominotti. Peste aviaria nella anitre. Clin. Vet., Vol. 39, 1916, p. 129. 4. Dubois. Une maladie infectiense des poules a microbes invisibles. Compt. rend. Soc. de hiol. Vol. 54, 1902, p. 1162. 5. Freese. Ueber Hlihnerpest mit besonderer Beriicksichtung der pathologischen Anatomie. Deutsche tier'drztl. Wchenschr., Bd. 16, 1908, S. 173. 6. Hertel. Ueber Geflug(!l-cholera imd Hiihnerpest. Arb. a. d. Tc. Gsndhtsamte., Bd. 20, 1904. S. 453. 7. Joest. Beitrag zur Kenntnis der Bakterienflora des Hiihnerdarmes nebst einigen Bermerkungen iiber eine neue Huhnerseuche. Berl. tierdrztl. ^Ycllnschr., 1902, S. 241. FOWL PLAGUE 87 8. Kleine und Moellers. Ueber Hiihnerpest bei Gansen. Centralhl. f. BahterioL, Bd. 39, 1905, S. 545. 9. Ivraus iind Schiffmann. Studien liber Immunisierung gegen das Virus der Hiihnerpest. Centralhl. f. Bahteriol. {Etc.), 1. Abt. Orig., Bd. 43, 1907, S. 825. 10. Landsteiner u. Berliner. Ueber die Kultivierung des Virus der Hiihnerpest. CeniraJhl. f. Bahteriol. {Etc.), 1 AM. Orig., Bd. 67, 1912, S. 1G5. 11. Leclainche. La Peste Aviaire. Revue Gen. de. Med. Vet., T. 3, 1904, p. 49. 12. Lijisehiitz. L'eber mikroskopisch sichtbare filtierbare Virusarten. Centralhl. f. BaUeriol., Bd. 48, S. 77. 13. Lode und Gruber. Bakteriologische Studien iiber die Aetiologie einer epidemischen Erkrankungen der Hiihner in Tirol. Centralhl. f. Bah- teriol. (Etc.), 1 Alt., Orig., Bd. 30, 1901, S. 593. 14. Maggiora und Valenti. Ueber eine Seuche von exudativen Tyi^hus bei Hiihnern. Zeit. f. Hyg., Bd. 42, 1903, S. 185. 15. Mane. Immunizierungsversuche bei Hiihnerpest. Arh. a. d. h. Gsndhtsamte, Bd. 21, 1904, S. 537. 16. Ostertag und Bugge. "Weitere Untersuchungen iiber die Hiihner- pest. Zeitschr. f. Infehtionshr. d. Hanstiere, Bd. 2, 1906, S. 1. 17. Ostertag und Wolffhiigel. Untersuchungen iiber die " Hiihnerpest," die neue Geflugelseuche. Monatschr. f. praht. Tierh., Bd. 14, 1903, S. 49. 18. Ottolenghi. Ueber einen besonderen Befund bei der Gefliigelpest. Centralhl. f. Bahteriol. {Etc.), 1 Aht. Orig., Bd. 67, S. 510. 19. Buss. Beobaehtungen iiber das Virus der Hiihnerpest. Airh. f. Hyg., Bd. 59, 1906, S. 286. CHAPTER VIII AVIAN TUBERCULOSIS Characterization. Avian tuberculosis constitutes an affection closely related to the same disease in mammals, characterized by the development of tubercles principally in the visceral organs. Poultr^anen refer to the disease as spotted liver, liver complaint, rheumatism, or describe the birds as going light. Species affected. A considerable number of domesticated and wild birds are affected. The disease has been observed in the fowl, guinea-fowl, peafowl, turkey, duck, goose, swan, pigeon, os- trich, parrot, canary, pheasant, sparrow, and in a large number of species of wild birds kept in zoological gardens. Etiology. Typical strains of the avian variety of B. tuhercu- losis possess characteristics enabling them to be differentiated from the human and bovine varieties. Avian bacilli are more readily isolated and cultivated in pure culture, than are the mammalian varieties. The avian organisms are somewhat shorter and stain more evenly than those of the mammalian variety. While the guinea pig is most susceptible to mammalian strains, inoculation with avian material may result in emaciation with no visible lesions, or in relatively slight lesions of a non-progressive character. When lesions are not visible after inoculation, it does not preclude the possibility that tubercle bacilli may be present and demonstrable microscopically, or culturally, or by further inoculation of the tis- sue into other guinea pigs. The transmissibility of avian tuberculosis to mammals and vice versa is of interest in connection with the control of the disease. As a general rule, fowls are not susceptible to the human and bo- vine varieties. Experimental evidence exists to show that calves may be infected by injections of avian tubercle bacilli, and that fowls have been artificially infected with tubercle bacilli of mam- malian origin. The majority of experiments to test this trans- mission have given negative results. In view of these findings, the simultaneous occurrence of tuberculosis in cattle or man, and in fowls exposed to infection from them, has slight value as evi- dence of transmission. All three varieties of the disease are so 88 AVIAN TUBERCULOSIS 89 common that coincidences may occur. The literature of tuber- culosis reveals comparatively few instances in which avian tubercle bacilli have been found naturally in cattle or in man. "With the exception of the intertransmissibility of avian tuber- culosis between pigs and fowls, the disease in fowls stands by itself as an economic and hygienic problem. There is considerable evi- dence that parrots and canaries may be infected from a mammalian source. While pigs undoubtedly contract tuberculosis most frequently from bovine sources, they do to a lesser extent acquire it from avian sources. The possibility of the transmission of tuberculosis between pigs and fowls should not be overlooked in connection with hygienic measures against the disease in either. Outbreaks of avian tuber- culosis in pigs in contact with infected fowls have been observed both in Denmark and in the United States. Eastwood and Grif- fith made cultures from a series of seventy-eight pigs exhibiting only localized tuberculosis. The avian tubercle bacillus was found alone in twenty-six of these pigs, or thirty-four per cent. Of the remainder, the avian organism was found to be present along with bovine bacilli in two cases. Symptoms. Until the disease has developed sufficiently to cause emaciation, there are no characteristic s;)Tiiptoms, except in the rare cases when the skin or joints are involved. In the latter case poul- trymen describe the condition as rheumatism. This term as applied to a disease in birds is practically synon^^nous with arthritis. An- emia and emaciation are constant in advanced cases, the latter be- coming extremely marked. The loss of weight is very noticeable ; the bird becomes weak and moves about very little. This disin- clination to move may be due either to extreme weakness or, more rarely, to involvement of the joints. Under such conditions, the bird spends much of the time in a crouching position. An unnatural character of the gait is noticeable. The eyes are bright and appetite remains markedly good in ad- vanced cases. The skin and visible mucosae are pale, and the feathers are ruffled. The temperature is usually within the normal range, and rarely is subnormal. Young birds affected with the dis- ease enough to show symptoms are not encountered, doubtless due to the time necessary for tlie development of serious lesions. The separation of deaths from one another in point of time is a characteristic feature of the disease. Morbid anatomy. Emaciation is striking in most cases that 90 DISEASES OF DOMESTICATED BIEDS die of the disease. The muscles of the breast may be represented by barely a trace. Avian tubercles do not differ greatly in gross appearance from those of the mammalian type. The smallest ones consist of nodules of tissue in which central caseation has not yet begun. In larger ones varying degree of caseation is illustrated, but calcification is not frequently observed. Avian tuberculosis differs from mam- malian tuberculosis markedly in that the visceral organs primarily are involved and lesions of Ijaiiph nodes are of subordinate im- portance. The liver is usually studded throughout with nodules which are easily separated from the hepatic tissue. There may be several sizes of nodules, suggesting that several corresponding invasions of bac- teria have occurred. The smaller tubercles are white or grayish white, while the larger, older ones are more yellow in color. The presence of the tubercles brings about secondary degenerative changes in the liver, as a result of which the tissue becomes pale and friable. As a consequence, fatal hemorrhages may occur. The or- gan is enlarged in advanced cases, and in exceptional cases may con- stitute one-fourth of the weight of the bird. The spleen, like the liver, is found involved in practically all advanced cases. The relative enlargement is greater, for this organ may attain the size of a walnut. The small amount of functional tissue remaining is often striking. The smallest tubercles of the intestine are located in the deeper layers of the mucous membrane. Slightly larger ones are in inti- mate contact with the intestinal wall but project somewhat. Still larger ones, as much as an inch in diameter, are pedunculated and in most cases the interior of such tubercles communicates with the lumen of the intestine. Lesions of the intestine also occur in the form of numerous but isolated ulcers on the mucous membrane. The kidneys, ovary, mesentery, and lungs are involved less often, while cases of tuberculosis of the pancreas, gizzard, and skin are rare in fowls. In the kidneys, the tubercles are discrete, hard, and glassy. These organs alone may be affected. Small tubercles are observed on the mesentery associated with tubercles on the intestine. Involvement of the lung apparently is associated Avith advanced de- velopment of the disease and then it occurs comparatively rarely. The tubercles may be isolated or aggregated into extensive areas. Skin lesions may consist of single spherical masses, each surround- ing the root of a feather, or more often, consist of larger masses. AVIAN TUBERCULOSIS 91 A form of nodular disease of the skin lias been observed in which tubercle-like organisms are found, and efforts to cultivate them give negative results. Another point of difference is that the organisms are decolorized by acidulated alcohol, which does not occur in the case of true avian tubercle bacilli. Unquestionable tuberculous le- sions of the skin occur in pigeons. A tuberculous lesion consisting of a cutaneous horn is relatively common in parrots. Bone lesions have been observed particularly on the breast bone and ribs. Lesions occur in the knee, back, digital and shoulder joints. The extremities of the bones enlarge with accumulation of cheesy material, or may discharge a semi-fluid substance. Differential diagnosis. A diagnosis of tuberculosis by physical examination of the living bird is hardly possible in most cases, nor is this important. Emaciation creates a strong presumption of the existence of tuberculosis but is not conclusive, for it occurs in as- thenia, in serious infestation with air sac mites and in other condi- tions less well understood. At autopsy of fowls, the possibility of the occurrence of tumors of the liver, and nodular tseniasis of the intestines should be borne in mind. ^Nodular lesions not involving the liver and spleen, may quite safely be considered as not tuberculosis. In the turkey the more highly colored areas occurring in infectious entero hepatitis are not likely to mislead one familiar with these lesions. Gouty arthritis and bumblefoot in the fowl are suggestive of tuberculosis. JSTodules in the lung caused by aspergillosis may be differentiated from tuberculosis by microscopic examination. Microscopic examination of smears for tubercle bacilli is available as a means of diagnosis, especially since organisms are unusually abundant in lesions of avian tuberculosis. Tuberculin test. ISTumerous efforts have been made to apply the subcutaneous tuberculin test to fowls, using tuberculin prepared from both avian and mammalian cultures, but without success. Better results have attended trials with the intradermal (intra- cutaneous) form of the test in manner similar to that in which it is applied to cattle. The wattle is chosen as the site of injection and a very fine needle of 'No. 26 or 27 gauge is employed. The aim is to deposit the tuberculin not in the deeper layers, but in the stratum Malpighii. It should not be injected so superficially that the tuberculin will be lost by rupture of the epithelium. The tuberculin employed is prepared in the usual manner from an avian tubercle culture, and is diluted fifty per cent for use. The 92 DISEASES OF DOMESTICATED BIRDS dose varies from one-twentieth to one-tliirtietli of a cubic centimeter. After short experience, attention to the graduations on the syringe will be abandoned and the dose judged by the appearance of the tis- sues at the point of injection. The head of the fowl should be held with considerable firmness by an assistant during the injection, in order to obviate the. necessity for inflicting unnecessary damage to the tissues, which would interfere with observing the results. Care must be taken to avoid injury of the wattle by rough handling. A positive reaction to the test consists of a swelling of the in- jected wattle. Perhaps ten per cent of the swellings will be so slight as to be doubtful. Observations made by Van Es and Schalk indicate that among the reactions considered by them as doubtful, about one-half were found on slaughter, to contain lesions, and half to be free from lesions. The majority of reactions will leave no doubt as to the existence of a pronounced edematous swelling, which may increase the thickness of the wattle to several times normal. Of 90 birds tested by Van Es and Schalk, showing typical" reac- tions, 88 were found tuberculous at slaughter and 2 showed no vis- ible lesions. Of 130 birds slaughtered and found without lesions, 120 or 91.5 per cent had failed to react to the test. About 8.5 per cent of the non-reacting fowls were found to have lesions. Thus the results shown indicate that the intradermal tuberculin test for fowls is about as accurate as the same test or the subcutaneous test in cattle. The test surely furnishes information regarding the extent to which infection has spread in a flock and consequently provides in- formation regarding which birds should be eliminated. Of three and four year old birds in an infected flock, as high as 86 per cent may react. Of two year olds, 2-1 per cent and of pullets, 3 per cent have reacted. It may further be of use in determining whether or not tuberculosis exists in a flock from which it is contemplated to purchase birds. Transmission. The tendencv of lesions involving the intestine to perforate the wall and discharge into the lumen, provides the main channel for the dissemination of tubercle bacilli. Microscopic examination of such lesions reveals enormous numbers of the or- ganisms. In view of the rarity of pulmonary lesions and the rela- tive frequency with which intestinal lesions occur, the feces must be regarded as the chief channel of elimination of infection. Tubercle bacilli have been demonstrated to be present in the feces of infected AVIAN TUBERCULOSIS 93 birds but are not found in the feces of a very large percentage of such birds. Tubercle bacilli have been demonstrated in eggs laid bv tubercu- lous hens but it has not been demonstrated that such a channel of dissemination of the infection is an important one. It seems quite certain that the disease is not observed in young birds as might be expected if transmission through the egg were common. Tubercle bacilli, when directly exposed, are sensitive to sunlight, but the conditions about poultry establishments are such as to war- rant belief that they may persist alive for months. Feeding experiments leave no doubt but that the alimentary tract is the chief portal for entrance of infective material. Exposure of healthy birds by contact with infected birds sets up disease Avhich may persist for a year before important lesions develop. The eat- ino- of carcasses of birds dead of the disease undoubtedlv contributes to dissemination of infection. In some cases, exposure by feeding infected droppings has induced disease that was fatal in six months. Wliile the introduction of tuberculous fowls must be regarded as the most common means of infecting a flock, there exists the possi- bility of its being accomplished by infected pigeons, among which the disease is not uncommon, or by pigs. Economic importance. Tuberculosis is capable under favor- able conditions of causing a very heavy death rate during the course of a year. Comparatively few accurate observations have been made in this country, but annual losses up to nearly 50 per cent have been reported. Enough reports are available from the northern half of the United States, the Pacific Coast, and Canada to indicate that the disease is prevalent in the area mentioned. The insidious nature of the disease contributes to the unconcern of the owner of an infected flock. Deaths will not occur until the flock has been extensively infected and when they occur, are so scattered in point of time that they do not cause the same concern on the part of the owner as would be occasioned by the same num- ber occurring in a short time. Consequently there is lack of in- centive to take up repressive measures. Prevention. The problem of the control of tuberculosis in fowls presents several features that render it much simpler than the corresponding problem in cattle. The productive usefulness of hens is ended at three years of age, when it is the common practice 94 DISEASES OF DOMESTICATED BIEDS to market the birds for table use, if this indeed is not done after two years. Thus total replacement of stock is possible in a short period. The extensive use of incubators and brooders assures the isolation of the young from infected old birds. Where the business is conducted on an intensive scale on a small area, isolation of birds of various ages is quite often practiced. Thus ideal conditions for combating the disease already exist in certain plants, if indeed the disease does ever make considerable progress under such conditions. It is undoubtedly true that the disease only becomes serious v^hen there is unlimited opportunity for mingling of birds of various ages as exists where poultry are kept without restraint. This is the con- dition in the average small poultry yard, or in an extensive poultry business where the system of using unfenced colonies is practiced. In attempting to control the disease among unfenced birds, the end sought is to secure isolation of young birds and maintain it throughout life. In every extensively infected flock there will be a certain number of badly diseased, worthless birds, which may be recognized by physical means, and destroyed. The intradermal test may be ap- plied to determine the extent of the infection. The results of this test, the age of the birds and egg yield, will aid in reaching a de- cision as to whether all or part should be marketed at once. Many reacting birds will be found at autopsy, to contain very minute lesions and there should be no prejudice against killing such for food. Appropriate disinfection of contaminated buildings, and tempo- rary abandonment of areas of soil too large to disinfect, will natur- ally suggest themselves. Van Es reports upon results of testing a flock of 249 birds, of which 43.37 per cent were tuberculous. All reacting and undesir- able birds were eliminated, leaving 56 non-reacting birds. These, together with 47 birds purchased after the test, increased the next year to 249. One bird died of tuberculosis after the first test and had undoubtedly failed to react on account of severe lesions. A second test made a year after the first one revealed 2.41 per cent of reactors. These were regarded as having contracted the disease from the one non-reactor of the first test. Mention of hygienic measures such as good ventilation, sunlight, and warm quarters has no place in a discussion of the control of tuberculosis in fowls. The disease is a veritable scourge in parts of California where such hygienic conditions are most favorable. AVIAN TUBERCULOSIS 95 Wild birds. Deaths from tuberculosis are frequent among wild birds kept in captivity. Out of 459 birds dying in the Berlin Zoological Gardens during a given period, 118 or 25.7 per cent were tuberculous. The disease was present in specimens belonging to 10 of the 15 orders of birds represented. The other five orders were represented by few specimens, and the observers, Koch and Rabin- owitsch, believe that all orders of birds are susceptible. A similar examination of 500 birds from the London Zoological Garden re- vealed tuberculosis in 30 per cent of the birds dying. REFERENCES 1. Hastings and Halpin. Avian tuberculosis. Univ. of Wis. Ag7: Exp. Sta. Research Bull. 28, 1913. 2. Moore. The morbid anatomy and etiology of avian tubercvdosis. J. Med. Research, n. s. Vol. 6, 1904, p. 521. 3. Van Es and Schalk. Avian tubercvdosis. North Dal-ota Agr. Exp. Sta. Bull. 108. 4. Ward. Tuberculosis in fowls. Univ. of Cal. Agr. Exp. Sta. Bull. 161, 1904. CHAPTEE IX AVIAN DIPHTHERIA AND BIRD POX General discussion. The group of pathological conditions re- ferred to by various authors under such designations as simple ca- tarrh, colds, contagious catarrh, influenza, coryza, roup, canker, diphtheria and bird pox present a complicated subject for discussion. The pathological features presented by the lesions of the mucosa of the fowl's head in the conditions described as roup or diphtheria, have been concisely summarized by Moore. He studied the disease in the eastern United States and has described three stages or va- rieties of lesions as follows : " (1) An exudate of a serous or muco-purulent character in the con- junctiva or nasal cavities. Ordinarily this condition cannot be recognized in the mouth. The mucosa in these cases is apparently but slightly altered. " (2) The mucosa over a small or larger area is covered with a spreading exudate of a grayish or yellow color. It is firmly attached to the mucous membrane and when removed leaves a raw, bleeding surface. Sections through this exudate and the subadjacent tissues show that the epithelial layer is destroyed, and the underlying tissue infiltrated with cells. The extent of the infiltration varies in different individuals. " (3) The mucosa is covered with a thick mass of exudate, varying in color from, a milky white to a lemon yellow or brown. It is easily re- moved, leaving a more or less granular and healed surface. This sloughed mass is frequently dried at its margins to the adjacent tissue. It emits a strong putrid odor, due to decomposition. The drying of the margins prevents the fowl from expelling the exudate after it becomes separated from the underlying tissue." In the far West and South, the lesions described will commonly be found accompanied by the tumor-like lesions known as chicken pox or epithelioma contagiosum. The earlier studies of the etiology of the diphtheritic lesions of fowls extending over a long period have resulted in a mass of con- clusions, in the main contradictory and confusing. Various authors have ascribed the lesions as due to gregarina, chlamdyozoa, coccidia and numerous species of bacteria. The discovery that the filterable virus of chicken pox is capable of causing diphtheritic lesions has now received abundant confirma- 96 AVIAN DIPHTHERIA AND BIRD POX 97 tion and furnishes a basis for clearing up the confusion. Among writers who have studied both avian diphtheria and pox and who agree on this point are Uhlenhuth and Manteufel, Schmid, Bertegh, and Sigwart. Whether there are other specific infectious diseases of fowls char- acterized by diphtheritic lesions not due to pox virus, remains to be determined by further investigation. The idea has been advanced that diphtheritic lesions of the mucosa of the head of the fowl may result from invasion by various bacteria. There is gTOund for questioning the validity of differentiating into separate disease entities such conditions as simple catarrh, com- mon colds, contagious catarrh, influenza and coryza. In large in- fected flocks, birds with catarrhal lesions alone, diphtheritic lesions alone, and pox lesions alone will be found in close association with others perhaps exhibiting all these lesions. Clinical evidence in such flocks points very strongly to the conclusion that the cases characterized by the presence of serous exudate in the nostrils are but the early stages of avian diphtheria. Insufficient etiological ev- idence is available to justify recognizing such conditions as specific infectious diseases. Characterization. Avian diphtheria is an infectious disease, manifested by the formation of catarrhal exudate in the nasal cavity, eyes, and sinuses associated with pseudo-membranes in the mouth and wart-like nodules on the external surface of the head. Until recent years, the term diphtheria or roup was applied to cases showing the internal exudative lesions, while those with external growths were designated bird pox, chicken pox or epithelioma con- tagiosum. The discovery that a single causative agent can produce both types has resulted in the two conditions being classed as simply external and internal lesions of one disease. Etiology. Diphtheria and bird pox are caused by a virus the nature of which is not well known. The organism has not been cer- tainly identified microscopically and is so small that it will pass through a Berkefcld filter. However, according to Marx and Sticker, it will not pass through a porcelain filter. Widely diverging opinions concerning the nature of the virus have been expressed by the various writers who have studied the dis- ease. Friedberger and Frohner assigned protozoa of the class gre- garina as the cause. Borrel described certain cell inclusions for which Lipschiitz has suggested the name StrongyJo plasma avium. Halasi believes the etiological agent to be a chlamydozoon. 98 DISEASES OF DOMESTICATED BIEDS Tenacity of virus. Burnet observes that finely powdered virus in physiological salt solution placed in sealed ampoules in a water bath at 60° C. is killed in about 8 minutes. At 56° C. the finely powdered virus does not resist longer than half an hour. In sus- pension in water at 37° C. it has been found inactive after 8 days; active after 3 days; active after 30 days at 22° C. ; active after 6 days at 25° C. Marx and Sticker found virus active after 3 hours at 60° C, but the material probably was not as finely powdered as in the experiment conducted by Burnett. The same authors found that desiccated virus in ampoules deprived of air remained active after an hour at 100° C. Scabs exposed to the sunlight in a Petri dish were still virulent after two months. Reischauer observes that the virus resists dry heat at 80° C. for 15 to 30 minutes and moist heat 5 minutes at 100° C. Marx and Sticker found a suspension of crusts virulent after 1^ hours in a 1 per cent solution of carbolic acid. In solutions of 2 and 2^/2 per cent it lost its virulence. Reischauer notes that the virus is killed in 5 minutes by 1 per cent solution of potash, acetic acid or carbolic acid. Burnett kept a sus- pension of virus in ordinary water in a refrigerator at 6° C. for 60 days and found it virulent after that length of time. Finely pow- dered virus mixed with glycerine was found to be virulent after 120 days. Haring and Kofoid tested the effect of various germicides upon powdered pox virus. The virus was saturated with the germicide and after the lapse of a certain amount of time, the virus was in- oculated into a fowl by scarification. Five per cent carbolic acid failed to kill in 20 minutes ; 2 per cent liquor cresolis compositus failed to kill in 20 minutes ; 2 per cent potassium permanganate failed to kill in 20 minutes ; 2 per cent copper sulphate failed to kill in 20 minutes ; tincture of iodine failed to kill in 10 minutes ; mer- curic chloride in 1 : 1000 solution failed to kill in 20 minutes; steam heat at 100° C. failed to kill the virus in 5 minutes but did do so in 30 minutes; dry heat at 200° C. killed the virus in 30 minutes. Powdered pox scabs saturated with physiologic salt solution and al- lowed to decompose for 10 days in a warm place proved non-virulent. Dry powdered pox scabs kept in a test tube from May, 1906, to Sep- tember, 1911, proved virulent. Pathogenicity. Diphtheria and pox are especially prevalent in chickens and pigeons, and are also common in turkeys, geese, ducks and guinea-fowl. Pheasants, quail and various wild birds are susceptible. AVIAN DIPHTHERIA AND BIRD POX 99 Natural infection. ^Natural infection occurs under conditions which are not yet well understood. Apparently, the virus pene- trates through a slight lesion of the skin or mucous membranes and reaches the skin or the mucous membranes of the mouth by way of the blood stream. Infection by ingestion probably occurs. An in- stance of infection by a biting fly, Stomoxysis calritrans, has been reported. Experimental transmission. The infection may be readily passed from the infected to susceptible birds by rubbing infective material into the skin or mucous membrane of the latter, especially if the parts be slightly scarified. In the pigeon the disease occurs on feathered portions of the body. To secure infection it is only necessary to pull out the feathers and rub in the virus lightly. After five or six days the skin shows a characteristic swelling. The follicles are greatly enlarged and upon pressure, whitish plugs are forced out. The virus is readily transmitted from the pigeon to the fowl but is transmitted from the fowl to the pigeon with great difiiculty, if at all. Passage through the fowl appears to lower the virulence of the virus for the pigeon. Intravenous injection of the fowl with pox virus as a rule causes only diphtheritic lesions of the mucosa of the head, with no changes of the skin. This is true whether the virus which was injected, originated from the skin or the mucous membrane lesions. Inoculation of the comb with material from mucous membrane lesions does not always result in the occurrence of pox lesions. Some observers interpret these negative results as proving the ab- sence of pox virus in the diphtheritic material. Others regard the results as mere failures of pox virus to take. The virus is present in the circulating blood and internal organs in acute cases, as demonstrated by inoculation experiments. In some cases injection of liver and blood of birds affected with chronic lesions of the mucous membranes of the head, will reproduce the disease. When positive results occur, the incubation period is long and the cases induced are mild. In chronic cases, the virus in the blood appears to be weakened or lessened in amount. The virus from either skin or mucous membrane lesions, when filtered, will give positive results in most cases. Even if the material filtered is of high virulence, it will only produce mild cases of mucous mem- brane infection. The incubation period for both diphtheritic and pox lesions varies 100 DISEASES OF DOMESTICATED BIEDS from 3 to 12 days, depending upon the virulence of the virus and the method of inoculation. After injection of filtered virus, the period varies from 6 to 15 davs. Isolated instances of incubation jDeriods to 25 days have been observed. Mortality. The fatalities occurring in an infected flock vary within a wide range depending upon individual circumstances. Under favorable conditions, the disease may not spread to more than 10 per cent of exposed birds, with the death rate proportionately low, while in other cases 80 per cent of the exposed may become in- fected, with deaths relatively numerous, approaching in some in- stances 50 jDcr cent of those affected. The virulence of the virus is variable and constitutes the main element for consideration in each outbreak. The mortality depends, to a large extent, on climatic conditions. Fowls are more severely affected during the fall and winter months and it is during this period that the heaviest losses are encountered. Course of disease. Avian diphtheria may follow an extremely acute course, affected birds dying without showing noticeable ex- ternal symptoms which would attract the casual observer. In less acute cases the disease may be resisted for several days after symp- toms are apparent, the fowl finally succumbing apparently as a re- sult of toxemia, or of starvation due to eye affection which inhibits feeding. In" the milder, and especially in the more chronic cases, marked symptoms may persist for several weeks and finally result in recovery, in so far as outward appearances are indicative. Symptoms. The disease is manifested by three clinical forms : (1) a pure mucous membrane disease, (2) a pure skin disease, and (3) a combination of skin and mucous membrane affection. The disease usually first manifests itself in a discharge from the nostrils which soon becomes viscid and plugs the nasal passages. In some individuals the first evidence of disease presents itself in the eye. One or both eyes may show a sticky discharge that tends to gTun the eyelids and obstruct vision. The exudate continues to form in the conjunctival sac, causing a swollen appearance of the eye and as- suming a cheesy character. This, through pressure and the accom- panying inflammation, may produce panophthalmia and loss of the eye. The exudate in the nostrils also becomes cheesy in consistency and causes a pressure on the cleft palate and distortion of the bony structures of the adjacent parts. The affected bird early shows ex- treme dullness and loss of vitality. The tendency is to mope around AVIAN DIPIITHEKIA AND BIED POX 101 indifferent to its mates, surroundings, or to a person's approach. The head feels warm to the touch and there may be a rise of tem- perature. Diarrhea is often present. Death may result within two or three days in severe outbreaks or the bird may linger for a week or more with progTessively increasing debility and more marked lesions. The head in many cases shows a pronounced swel- ling on one or both sides below and in front of the eye due to the accumulation of a cheesy mass within the suborbital sinus. Sneez- ing, which has been apparent in the early stages, gives way to a whistling or rattling in the throat. The inflammation in the nos- trils may spread to the mouth and pharynx, or even to the larynx and trachea, where exudates are formed which are principally of the croupous type. Breathing is entirely carried on through the mouth and the continual passage of air over the tongTie tends to dry the tip with the result that its surface becomes hard and contracted. This condition is commonly termed " Pip " and may occur in any affection which closes the nostrils, and compels breathing through the mouth. Death may be caused by dyspnea from the presence of massive accumulations in or upon the larynx, from toxins absorbed from the primary causative agents and secondary invading organ- isms, or from starvation, owing to inappetence, or the failure to dis- cover food in blind cases. JSTo doubt the combination of causes act- ing together are responsible for the heavy mortality, amounting to 90 per cent in some instances, among young birds. Before death, the subject becomes emaciated, sleepy, and finally unconscious for a period of several hours. Mild cases show less marked disturbances and may go on exhibit- ing s_\anptoms for several weeks, finally apparently recovering their normal condition. Certain individuals retain the disease in a chronic state and serve as carriers for future outbreaks. Oftentimes the bird shows no external manifestations of illness. The comb and wattles have a deep red appearance and the hen con- tinues to lay. She dies quite suddenly and, on examination, the only lesion apparent is the formation of a false membrane on the border of the larynx or just inside that organ. This exudate has occluded the air passage and caused death by suffocation. Fre- quently the condition is discovered in time to save the fowl through the owner's attention being attracted by a peculiar noise which ac- companies the effort of the bird to breathe. It will be observed to open its mouth widely and attempt to dislodge the exudate by a spas- modic movement of the respiratory apparatus. The resulting ef- 101 DISEASES OF DOMESTICATED BIRDS feet may be termed a " bird cough." Prompt attention in such cases nearly always saves the life of the fowl. The disease spreads rapidly through a flock affecting a large per- centage of the birds and causing the death of a variable percentage according to the virulence of the virus. Young birds are especially susceptible, adults less so, and a few exhibit complete resist- ance. Morbid anatomy. The external lesions have the appearance of wart-like growths prominently raised from the surface of the skin. The size may vary to a considerable degree according to location, or through combination of several nodules. General- ly they have a diameter of Yg to ^/4 of an inch. These pox tumors occur chiefly on the unfeathered or lightly feathered por- tions of the body, and par- ticularly on the comb, wat- tles, eyelids and at the commissures of the beak. They may also be found at Fig. 8. Head of a Plymouth Rock cock affected times on the under surface with epithelioma contagiosum (bird pox). . ,• i i (j^lgg) of the wings, particularly if there has been an abrasion or bruise at this point They may be rarely observed around the vent. The nodules first appear as small w^hitish points which rapidly increase in size, reaching their maxi- mum size in four to six days. They form an integral part of the epithelium, being in reality an extrusion of enlarged epithelial cells. If the superficial scale of exudate is removed, the tumor will be seen to consist of whitish cylindrical masses arranged perpendicularly to the skin. The mass assumes a yellowish color which later changes to a dark bro^vn or black as the tuberosity degenerates and develops AVIAN DIPIITIIEEIA AND BIRD POX 103 into a hard dry scab. After seven to nine days this scab may be easily removed leaving a whitish area only slightly elevated above the surface and usually pitted. The scabs retain the virus of the disease and Avhen rubbed on the scarified skin or mucous membrane Fig. 9. Head of a turkey affected with epithelioma contagiosum (bird pox). (Klee) of the mouth, even after a period of five years, may reproduce typical lesions. Haring and Kofoid describe the microscopic structure of chicken pox tissue as follows : " The epithelial tumors are produced by a hyperplasia of the epithelium due to an increase both in the size and number of cells. The zone of growth is in the stratum of Malpighii, the principal region of prolifera- tion being in the outer edges from which the cells increase in both direc- tions. A proliferating epithelium forms cell nests surrounded by thick bands of connective tissue, which contain blood vessels with thickened walls. The rapidly proliferating peripheral cells of the Malpighian layer are seen thickly studded with granules. The nucleus contains deeply staining chromatin bodies which are in an active process of proliferation. Ivaryokinetic figures are common in this region. More deeply in the epithelial tumor mass the cells are greatly increased in size and haA^e rela- tively fewer granules. The nuclei are nale and show little evidence of cell division. In these cells, are large cell inclusions which are very strik- ing in appearance, and which Eeischauer and others have thought to be protozoa. There is usually but one of these bodies in each cell. They vary in size from five to twenty microns, most of them are round, al- though some of them are quite irregular in shape. They are evidently fatty in structure as they stain black with osmic acid. When eosin and methylene blue are iised, they stain a faint pink, resembling somewhat the Negri bodies found in the brain tissue of rabid animals, although they are 104 DISEASES OF DOMESTICATED BIRDS usually much larger. They seem to have no definite internal structure, being- usually homogeneous in appearance. Deeper in the epithelial mass the cells are very large and show evidence of degeneration, here the cyto- plasm stains poorly and has but few granules. Burnett has called this con- dition hydropic. In the center of the older epithelial cell masses, the cells are so degenerated that they form a necrotic mass. The nucleus, of the cell first degenerates. The cause of this degeneration is probably due to the fact that the cell nests increase in size by multiplication at the peri- phery. The outside cells consume all the nutriment at the expense of the central ones and cause their degeneration. The central necrosis rapidly extends, involving the greater part of the tumor mass." The cell inclusions characteristic of pox have been studied ex- tensively and the interpretation of their nature and significance has been the subject of much discussion. Some observers see in them, stages in the life of a protozoan, while others regard them as products of degeneration of the cell. In the early stage of false membrane formation, the external layer of the mucosa is principally involved. There is an exfoliation of the cells, which become swollen and amorphous. The cell proto- plasm early loses its identity, while the nuclei disintegrate more slowly and appear as independent bodies showing different degrees of degeneration. ]\rucous exudates which have undergone coagula- tion, together with the epithelial cells, enclose leucocytes in various stages of degeneration. An edematous area is formed around the membrane, and wandering leucocytes are observed in the ^Malpiiihian layer of the mucosa. During this stage there is a well marked line of differentiation between the morbid area and the comparatively unaffected base. As the pseudo membranes are extended, the under- lying tissues are more deeply involved. The deeper epithelial cells become infiltrated and exhibit cloudy swelling. A fibrinous exudate accumulates which holds the cell elements in a compact tenacious mass. In this may be observed numerous organisms, principally of the bacterial type, which are to be considered as secondary invaders. Protozoal organisms may also be present including flagellates, amebas, coccidia and other forms. Some investigators have attributed the origin of avian diphtheria to certain of these protozoa. However, the evidence brought out has not been sufficient to establish these organ- isms as specific causes. The course of development of filterable viruses in the animal system is a problem which has not been satis- factorily solved, and until this is accomplished, it is unsafe to give etiologic sigTiificance to organisms or cell inclusions which may be found associated with certain morbid conditions. AVIAN DIPHTHEEIA AND BIRD POX 105 The gross lesions of the mucous membranes are not characteristic of infection with pox virus alone. Ilaring and Kofoid have pro- duced similar lesions by mechanical injuiy or by the injection of pyogenic bacteria. However, in diphtheritic lesions not due to pox virus, the cell inclusions characteristic of pox infection are not present. Diagnosis, In typical outbreaks, the disease is readily recog- nized by the closely adherent pseudo membranes on the mucosa of the mouth and pharynx, and by the characteristic nodules on the comb and wattles. When the latter are present, the diagnosis is estab- lished. Treatment. This, to a certain extent, must be individual and according to the stage of the disease. When the excretions are watery or viscid they may be partially removed from the nostrils by pressing on both sides with the fingers in a manner which will force the ma- terial through the openings. The nasal channels are then flushed out with an antiseptic solution such as permanganate of potash in 2 per cent solution, or boracic acid in 3 per cent solution. This can be ac- complished by means of a syringe or medicine dropper. The most eft'cctive method, however, is to submerge the head in the antiseptic solution for a period of 30 seconds, keeping the mouth open and the beak elevated to permit the air to escape from the nostrils and be replaced by the fluid. The treatment should preferably be repeated . twice daily. Certain features of the structure of the fowl's head interfere with natural drainage in diseased conditions, and likewise, interfere with medication. The sub-orbital sinuses so often involved, have no nat- ural drainage. The passages connecting them with the nasal cavity lead upward, with the result that fluids cannot escape. The tur- binated bones also impede the exit of tenacious exudate. The pres- ence of exudate in both the turbinated bones and in the sub-orbital sinuses prevents access of fluid to the aft'ected mucosa. When patches are present in the mouth, they should be carefully removed mechanically before treating as above ; or the aft'ected areas may be swabbed with tincture of iodine, 2 per cent carbolic acid, 70 per cent alcohol or argyrol in 20 per cent solution. Swellings of the sides of the head are to be freely opened and the contents removed. The eyes should be kept free of exudate and a mild antiseptic instilled between the eyelids. For this purpose argyrol in 20 per cent solu- tion has given the best results. Two drops are placed beneath the eyelid twice daily. The lachrymal duct and nostrils are also bene- 106 DISEASES OF DOMESTICATED BIRDS fited by the eye injection since the solution passes into them from the eye. In the case of severe eye involvement it may be necessary to feed the fowl artifically because of the difficulty encountered by the bird in finding its food. The question of whether it is profitable to treat all cases rests with the individual owner. Since the pox tumors disappear in the natural course of the dis- ease, the value of medicinal agents in hastening this end is ques- tioned. Among the remedies that have been recommended are tinc- ture of iodine, an ointment of glycerine, vaseline or lard containing 2 per cent of carbolic acid and 70 per cent alcohol. Prevention. In some instances infection is brought to a flock by new birds from infected flocks, or by exposure at shows. It is possible that infection is carried on the clothing of persons who have been among infected birds, or by materials on w^hich the excretions of diseased birds have been deposited. Free flying birds may also serve as carriers although it is quite likely that they are rarely re- sponsible for outbreaks. Newly purchased fowls and those which have been exhibited at shows should be quarantined on their arrival for a period of two weeks and carefully examined before being set free among others. When a fowl is observed to be ill with sym]j- toms of diphtheria, it should be isolated immediately. Often it is good policy to destroy the patient because of the danger of the attendant who is treating the bird carrying the virus to healthy fowls. Those handling diseased fowls should disinfect their hands before feeding or caring for others. It would also be advisable to wear rubbers in the hospital and remove them on leaving in order to gTiard against carrying infection on the shoes. When infection has broken out in a flock particular care should be exercised in keeping the houses as clean as possible. They should be disinfected by spraying or washing with carbolic acid in 5 per cent solution, compound cresol in 2 per cent solution, or formaldehyde in 2 per cent solution. The yards may be spread with unslaked lime or chloride of lime, or the soil should be plowed imder. All birds that die should be burned or buried deep. Those which have re- covered, if retaining any evidence of the disease, should be destroyed, as certain ones may serve as carriers and furnish the source of a future outbreak. The drinking water may be medicated with per- manganate of potash. A sufficient amount of the latter should be employed to give the water a deep purple color. Immunization. An attack of the disease confers an immunity complete in from 12 days to 3 weeks but which varies in duration AVIAN DIPHTHEKIA AND BIRD POX 107 and degree according to the severity of the infection. Thus, chronic mild infection of the mucous membrane does not always produce ab- solute immunity. Infection of the mucous membranes alone will induce an absolute immunity against inoculation of the skin. Vari- ous authors have demonstrated immunity in fowls for periods vary- ing from 2 months to 2 years. Live virus only has been shown to confer immunity and the injection of killed virus has no immunizing effect. A number of Avorkers have attempted the immunization of fowls against diphtheria and chicken pox and treatment of the same conditions by means of a vaccine prepared from the exudates and pox nodules of affected fowls. The material is ground up in a suf- ficient amount of normal salt solution to form a suspension and is filtered through cotton to remove large particles. It is then diluted until it appears moderately cloudy and heated at 55° C. for 1 hour. Doses of 1 c.c. are injected subcutaneously on two or three occasions with intervals of 5 to Y days. A product prepared by this method has been favorably reported upon as an immunizing and curative agent by several workers. Ex- periments by the present writers have not sustained the claims made for the immunizing value of a vaccine prepared by this method. Fowls which have been vaccinated and later artificially inoculated with virulent material have developed characteristic internal and ex- ternal lesions of diphtheria with accompanying fatalities. Bacteriology of avian diphtheria. Many investigations of the bacteriology of avian diphtheria w^ere made previous to the recogni- tion of the role of pox virus in causing diphtheritic lesions, so it is not possible to determine whether the lesions were primarily due to pox virus, or were due to bacteria alone. Other reports of in- vestigations conducted more recently do not contain evidence that pox virus was not concerned in the causation of the lesions. Extensive investigations of the bacteriology of avian diphtheria have been made by Harrison and Streit, Bordet and Fally and by Hausser. Moore first reported finding a member of the hemorrhagic septi- cemia group in diphtheritic lesions in fowls, which observation has been confirmed by a large number of investigators. Sig\vart has observed the spontaneous appearance of fowl cholera in birds af- fected with diphtheritic lesions of the mucous membranes. In these cases the primary cause of the diphtheritic lesions was considered to be pox virus. He explains the occurrence by assuming that the 108 DISEASES OF DOMESTICATED BIRDS pox lesions favored the increase of virulence of saprophytic hem- orrhagic septicemia organisms commonly present in the mouth. Jackley has worked on the bacteriology of roup, reaching the fol- lowing conclusions : " 1. A bacterium, designated culture ' 33A,' having all of the morplio- logical, cultural and biochemic characters of the pasteurella group, ap- parently deserves recognition as the etiological factor in roup. " 2. The organism has been recognized by smears in all cases of roup examined. " 3. It has been isolated and grown upon artificial culture media and the characteristic local lesions of the disease again reproduced. " 4. Finally, an absolute protection has been shown against the natural disease after immunization with a pure culture bacterin of this organism." Beach, Lother and Halpin isolated from roup lesions an organism probably belonging to the hemorrhagic septicemia group. Injection of killed culture was shown to produce immunity against injection with virulent culture. The organism was regarded as a secondary in- vader, as it did not produce lesions of roup or chicken pox. It was regarded as of importance as a secondary invader in wound infection. The identity in name and similarity of lesions of diphtheria in man and in birds has attracted attention to the possible relationship between the two diseases. There is no doubt that the two diseases are quite distinct in etiology even though rare cases of infection of birds with Bacterium diphtheria? have been reported. SIMPLE CATARRH OR COLD This condition is a mild inflammation of the nasal passages and is common to all species of domesticated birds. It cannot be differ- entiated from the early stage of avian diphtheria. Etiology. No definite cause may be assigned to this affection. It has been asserted that weak or improperly nourished birds are more likely to be attacked than strong, vigorous, well nourished in- dividuals. Exposure to unfavorable conditions in which rain or dampness accompanied by cold draughts tend to so aifect the mucous membranes of the nostrils that the various organisms which are nor- mally present in this region become pathogenic, has been held to be the primary contributing cause. Symptoms. The aft'ected fowl is more or less dull in appearance, according to the severity of the attack. The appetite is diminished, breathing becomes difficult, and a watery discharge from one or both nostrils is early in evidence. This discharge may disappear in the AVIAN DIPHTHERIA AND BIRD POX 109 course of two to four days, or it may take on a viscid consistency, closing the nasal openiniis and necessitating breathing through the mouth. The discharge may also escape through the mouth. This is rendered easy by the cleft palate peculiar to birds. Morbid anatomy. The mucous membrane of the nasal passages becomes swollen and congested and an excessive secretion of mucous fluid is poured out. Treatment. As the disease is of short duration, it is usually only necessary to place the patient under more favorable conditions to bring about recovery. In the more severe cases, the nostrils should be washed out twice daily with boracic acid in 3 per cent solution, or creolin in 1 per cent solution. REFERENCES 1. Beach. Suggestions to poultrymen concerning chicken pox. Univ. of Calif. Coll. of Agr. Circ. No. 1^5, 1915. 2. Beach, Lothe and Halpin. An outbreak of roup and chicken-pox in which the high mortality was apparently caused by a secondary invader. J. Agr. Research, Vol. 17, 1915, p. 554. 3. Bertegh. Ueber die Beziehungen zwischen Geflugeldiphtherie und Gefiiigelpocken. Centralhl. f. Bakteriol. (Etc.), 1. AM., Grig., Bd. 67, 1912, S. 43. 4. Bordet and Fally. Le microbe de la diphtheric des poules. Ann. de r Inst. Pasteur, T. 24, 1910, p. 563. 5. Burnet. Contribution a I'epithelioma contagieux des oiseaux. Ann. de v. Inst. Pasteur, T. 20, 1906, p. 742. 6. Gallagher. Epithelioma contagiosum of quail. /. Am. Vet. Med. Ass., Vol. 3, 1916, p. 366. 7. Hadley and Beach. Controlling chicken-pox, sore-head or contagious epithelioma by vaccination. Proc. Am. Vet. Med. Ass., 1913, p. 704. 8. Ilalasi. Beitrage zur Kenntniss de Geflugelpocke luid der Geflugel diphtheric. Inaug. Diss. Kozl. 9. Haring and Kofoid. Observations concerning the pathology of roup and chicken pox. P^^oc. Am. Vet. Med. Ass., 1911, p. 413. 10. Harrison and Streit. Roup. Ontario Agr. College. Bulls. 125 and 132. 11. Hausser. Bacteriologische Untersuchungei) iiber Geflugeldiphtherie. Centralhl. f. Bahteriol. {Etc.), 1 AM. Orig., Bd. 48, 1909, S. 535. 12. Jackley. A study of the etiology of roup in birds. Kansas Agr. Exp. Sta. Tech. Bull. U. 1917. 13. Mack. Tbe etiology and morbid anatomy of diphtheria in chickens. Am. Vet. Bev.. Vol. 28, 1905, p. 919. 14. Mack and Records. The control of epithelioma in chickens by vac- cination. Nevada Agr. Exp. Sta. Bulls. 82 and 8k. 15. ]\''qnteufel. Beitrage zur Kenntniss der Tmmunitatserscheinungen I"i dert pogennannten Gefliigelpocken. Arh. a. d. k. Gsndhtsamte., Bd. 33, 1909-10, S. 305. 110 DISEASES OF DOMESTICATED BIRDS 16. Marx u.' Sticker. Untersuchungen iiber das Epithelioma contag- iosum des Gefliigels. Deutsche Med. Woch., Bd. 28, 1902, S. 893. 17. Moore. A preliminary investigation of diphtheria in fowls. U. 8. Dep. Agr. Bureau Animal Indust., Bull. No. 8, 1904. 18. Miiller. Zur Aetiologie der Gefliigeldiphtherie. Centralhl. f. Bak- teriol. (Etc.) 1 Alt. Orig., Bd. 41, 1906, S. 423. 19. Reischauer. Tiber die Pocken der Vogel, ihre Beziehungen zu den echten Pocken und ihren Erreger. Centralhl. f. BaMeriol. {Etc.), 1 Aht. Orig., Bd. 40, S. 356. 20. Schmid. Untersuchungen iiber der Beziehungen zwischen Gefliigel- diphtherie und Epithelioma contagiosum. Centralhl. f. BaMeriol. {Etc.), 1 Aht. Orig., Bd. 52, 1909, S. 200. 21. Sig-wart. Experimentelle Beitrage zur Frage der Identitat von Gefliigeldiphtherie und Gefliigepocken. Cenlralhl. f. BaMeriol. {Etc.), 1 Aht. Orig., Bd. 56, 1910, S. 428. 22. Sweet. A study of epithelioma contagiosum of the common fowl. Univ. of Calif. Puhs. in Zoology, Vol. 71, 1913, p. 29. 23. Uhlenhuth imd Manteufel. Neue Untersuchungen iiber die atiologischen Beziehungen zwischen Gefliigeldiphtherie (Diphtheria avium) und Gefliigelpocken (Epithelioma contagiosum). Arh. a. d. Jc. Gsndhtsamte, Bd. 23, 1909-10, S. 288. 24. Ward. Poultry diseases in California. Proc. Am. Vet. Med. Ass., 1904, p. 164. 25. "Ward. Observations on roup in chickens. Proc. Am. Yet. Med. Ass., 1905, p. 198. CHAPTER X ASPERGILLOSIS AND FAVUS ASPERGILLOSIS Synonyms. Pneumo-mycosis, brooder pneumonia. Characterization. Aspergillosis is a disease of the pulmonary region due to infection with fungi. It is characterized by the forai- ation of an exudate, usually of a moldy appearance, on the mucous membrane of the air passages, principally the air sacs of the ab- dominal cavity. Etiology. The disease is almost invariably introduced by fungi of the genus Aspergillus, Aspergillus fumigatus being the most con- stant causative agent. Other members of the aspergillus group have been identified in the morbid processes. These, however, are of slight sigTiificance as they have not been associated with the incidence of pulmonary mj'cosis to any great extent. Aspergillus fumigatus is widely distributed in nature and is often observed on vegetable matter of all kinds which has been exposed to dampness. Birds scratching among moldy grains or in moldy litter may inhale the spores. These find a favorable place for propagation on the mucosiie of the bronchi, or of the air sacs. The fungus may be readily grown on potato, rye bread or plain agar which is acid in reac- tion. The most suitable temper- ature is between 35° and 40° C. The growth appears after 24- hours incubation as a whitish downy layer over the surface of the medium. This is composed of an interwoven mass of trans- parent mycelial threads which later give off branches capped by fruit heads. Each of the latter is composed of a mass of small rounded ]ll FiG. 10. Aspergillus fumigatus. (Kedrawn from jMoliler and Buck- ley ) 112 DISEASES OF DOMESTICATED BIRDS bodies closely associated in the form of a ball, the outer area of which shows radiating- lines of spores. These are clear and hig-hly refrac- tile. Their diameter varies from 2.5 to 3.5 microns. The color of the growth olianges with age, succeeding from white to greenish and later, in old cultures, to a bro^vnish color. The spores are quite re- sistant. They are not destroyed by heating at 05° C. for a period of seven hours and require an exposure of 12 hours to a 5 per cent solution of carbolic acid for their destruction. In the dried state, they are very resistant and may germinate after several months or even several years when conditions are favorable. Pathogenicity. Of the aspergillus group, A. fumigatus is the most pathogenic to birds. A. nigressens, A. glaucus and A. candidus are less pathogenic in the order named. All species of birds are apparently susceptible to infection. Do- mesticated ones, especially those confined in large flocks and exposed to moldy organic matter, are most often affected. These include chickens and pigeons. Young chicks frequently are attacked by an acute form known as brooder pneumonia. Cage birds, particularly those in zoological gardens, are often fatally affected. In France thousands of pigeons are fed by men in a manner similar to the method used by parent pigeons in feeding their young; viz., loading the mouth with grain and fluid and passing it directly to the mouth of the pigeon. Among these men severe cases of pulmonary aspergil- losis occur as a result of their exposure to contaminated gTain. The disease may be transmitted artificially to animals and birds by inoculation or by causing the organism to be inhaled. Inocula- tion of small quantities of spores into the veins or peritoneal cavity of rabbits, guinea pigs, fowls, or pigeons causes death from septi- cemia in from 24 hours to 1 or 2 weeks. In the older cases necrotic areas are present in the visceral organs and the aspergillus fungus is readily isolated from these. Lesions resulting from inhalation infection are usually confined to the air passages. Fowls and ani- mals exposed in rooms to dust or rye flour containing aspergillus spores, have contracted the disease and died as a result. Aspergillosis in the ostrich is discussed on pp. 228 and 229. Mortality. Fatalities may be high in broods of chicks that^have been extensively exposed to infection. Those attacked apparently all succumb. Older birds are quite resistant. Evidence points to the conclusion that once the disease is established in the system a fatal termination follows. Symptoms. Considerable variation in the external signs of as- ASPERGILLOSIS 113 pergillosis may be expected. As a rule the morbid condition has existed for some time before symptoms are noticed. When the le- sions are located in the trachea or bronchi, hoarseness of breathing, or a rattle in the throat may be the only indication of infection in the early stages. In air sac involvement alone no respiratory symptoms are shown. It is doubtful if external symptoms of infection of the air channels of the bones of the wing are manifested. As the disease progresses the bird becomes dull and less active. There is a noticeable decrease in w^cight accompanied by emaciation. The term " going light " is frequently applied to this condition. Di- arrhea is not a constant symptom but is usually present in the later stages. Temperature elevation is not constant in the more chronic form. Difficult respiration, sleepiness, extreme weakness and marked emaciation precede death. The appetite decreases as the disease pro- gresses. Death results from asphyxia and toxemia. In baby chicks the symptoms are apparent early and are similar to those of bacillary white diarrhea and intestinal coccidiosis. In both young and old birds the lesions observed at post mortem readily reveal the nature of the disease. Morbid anatomy. The lesions are principally confined to the respiratory system. This system is complicated in birds for in addi- tion to the lungs it includes several air sacs in the peritoneal cavity and air channels in certain of the bones. In some instances through penetration of the walls of blood vessels by the mycelia, new areas of infection may be established in other organs as a result of meta- stasis. The mold may develop at any point on the respiratory mucous membrane or may be spread over a large portion of its surface. Our observations at numerous autopsies place the abdominal air sacs as the most severely involved region. The morbid process is manifested by the presence of a membrane of greater or less thickness depend- ing on its location on the mucosa, or at times by nodules in the parenchyma of the lungs. In the trachea and bronchi the false membrane is comparatively thin while in the air sacs it may be much thicker and give a rigid contour to these organs. Frequently the sacs are filled with fungoid growth and cellular exudate, the whole forming a solid mass. The bronchioles may also be plugged with mycelia, spores and cellular exudate consisting of exfoliated epithelial cells, leucocytes and occasionally red blood corpuscles. The surface of the membrane may be grayish or gTeenish in color. The latter color is nearly always in evidence at some point. It is in 114 DISEASES OF DOMESTICATED BIRDS this area that numerous spores may be demonstrated on microscopic examination. The mycelial threads penetrate the mucosa to the submucosa or may enter the adjacent blood vessels forming thrombi and establishing an area of necrosis resulting in a nodular formation similar to that of tuberculosis. In the abdominal region the organs in contact with the air sacs are often involved through adhesions or direct passage of the fungus into their interior. In the main, the pathologic condition progresses by direct contact. Organs affected through the blood stream reveal small areas of ne- crosis in which the mycelial threads may be detected. The kidneys are more often affected in this manner than the liver. Artificial inoculation through hypodermic injection, intraperitoneally or in- travenously, produces extensive lesions in these organs. The mycelia may be demonstrated microscopically in necrotic areas or in nodules in the earlier stages of development. Mycelia may also be observed in the mucous membrane lesions, and espe- cially in greenish colored areas are spores readily discovered. The tissues surrounding the growths are found infiltrated with small round cells, leucocytes and connective tissue cells, indicating an at- tempt on the part of the system to build a protective wall against the spread of the parasite. This attempt is usually abortive although evidence of regenerative changes are apparent in some lesions. Giant cells are also occasionally present in the tubercle forma- tions. Course of disease. Among older birds the disease has a tend- ency to occur sporadically, more or less extensive intervals elapsing between deaths from this cause in a particular flock. Where the ex- posure is great, outbreaks of considerable importance may result. The resistance of vigorous individuals, however, is high and epi- zootics such as are associated with certain other diseases are rarely encountered. In gi-own birds aspergillosis follows a semi-acute or chronic course. Death may occur in from 1 to 8 weeks. In brooder chicks resistance is less pronounced and acute outbreaks often follow exposure to moldy food or material. The disease runs a rapid course with fatal termination in 2 to 7 days. Birds confined to limited areas as is the case in zoological gardens, show a high percentage of fatalities from this cause. Diagnosis. Tuberculosis, coccidiosis and aspergillosis are not readily differentiated sjnnptomatically in grown fowls. On autopsy the lesions are quite distinctive. Tuberculosis principally affects the ASPERGILLOSIS 115 liver, intestine and spleen, being less of a pulmonary disease in birds than is the case in other animals. The tubercles are of a fleshy type on cross section and show small yellowish points. Coc- cidiosis is practically confined to the intestinal tract. Its lesions are of a necrotic type involving principally the duodenum and ceca. Aspergillosis tends to localize on the walls of the air passages and forms a moldy growth generally exhibiting a greenish tinge, at least in spots. Microscopic examination of the morbid material furnishes a spe- cific diagnosis since the causative organisms in each case are usually numerous and very different in morphology. The disease in young chicks called brooder pneumonia, shows symptoms similar to those of bacillary white diarrhea and cocci- diosis. In all three the chicks have a droopy appearance associated with diarrhea and loss of appetite. In general it may be said that bacillary white diarrhea is more highly fatal, with deaths occurring shortly after hatching. Coccidiosis usually appears at a later period and is also apt to result in heavy losses. Autopsy is necessary, how- ever, for positive diagnosis. The lesions in the air passages are not as extensive as in older fowls because of the acuteness of the af- fection, but may be discerned by careful examination. Bacillary white diarrhea is a purely septicemic disease, while coccidiosis usu- ally shows intestinal lesions with accumulation of necrotic or blood stained material in the ceca. Microscopic or cultural methods may be resorted to in obscure cases. Treatment. It is inadvisable to attempt treatment because of the deep seated position of the parasitic fungiTS, its resistance to remedial agents and the advanced stage of the attack when symptoms are observed. Prevention. The widespread distribution of Aspergillus fiimi- gatus renders absolute prevention difficult. Care in the selection of grain and litter will minimize to a great degree the chances of in- fection. Good housing arrangements which guard against dampness will prevent the propagation of molds if present to a slight extent in feed or litter. When the disease is discovered in a flock the source of infection should be located. The feed may have a musty odor or a greenish appearance in places, or straw litter may be moldy. In the former instance cooking will destroy the fungus. Moldy litter should be discarded. Experiments have shown the possibility of infection being carried to newly hatched chicks through the egg.. The mycelia of the fungus 116 DISEASES OF DOMESTICATED BIRDS are known to be capable of penetrating the egg shell and developing in the albuminons material with consequent destruction of the em- bryo. The aspergillus colony may be observed as a dark spot on the internal membrane of the air chamber. Infection through this source is no doubt rare. It may be giiarded against by using clean straw or chaif in nests for laying or sitting hens, and by dipping eggs for hatching in grain or wood alcohol before incubating. Feed- ing discarded eggs to young chicks is dangerous since these may carry the causative organisms of several diseases. FAVUS Syno)itj]ns. White comb; favus de la poule (French); Weisser Kannn (German). Characterization. Favus is a contagious, chronic disease of the skin characterized by the presence of white areas most commonly localized on the head and is caused by a fungiis. Etiology. The fungiis causing the disease is designated Loplio- pliyton gaUi)ia\ It grows readily on agar containing 1 per cent peptone and 4 per cent of glucose or maltose at room temperature when the medium is seeded with material from the diseased patches. Growth first appears as a small, round, pure white, downy colony. As it enlarges it takes the form of a button which is slightly cup shaped. The culture ordinarily remains white if kept at a low temperature. At 27° to 37° C. the colony takes on a delicate rose color, becomes umbilicated, wrinkled and divided into sectors by lines radiating from the center. At 30° C. the culture is wholly rose colored, but more or less deep depending upon the culture. Sometimes the color varies in the same culture tube. The diffusion of the raspberry color in the medium is said to be an exclusive char- acter of the species in question. Pathogenicity. The infection is readily transmitted to a fowl by rubbing the comb with scales from a diseased bird. The disease is unmistakably present on the fifteenth day after inoculation and persists for months. Similar results are obtained with cultures. Mice, rabbits, guinea pigs and man are susceptible. Infection may occur through direct or indirect contact. Symptoms and morbid anatomy. The disease first appears on the head and its appendages such as the comb, wattles and barbs. ISTearly always the initial lesion is in the vicinity of the beak, in the form of numerous small white points. Under a magnifying glass ASPERGILLOSIS 117 they are seen to be covered with a fine, short down which later disappears quickly and does not return again. The white point en- larges and forms a layer 1 or 2 mm. thick adhering to the epidermis underneath. The color is generally white or gray. In time the thickness of the crusts increases as do the surface dimensions. Finally the small patches origi- nally isolated, coalesce. The ex- tension is regular. A white patch may reach the dimensions of the comb itself. Sometimes the di- mensions of a patch remain small but it is not rare to observe patches 7 or 8 cm. long and 3 or 4 cm. broad on large combs. The diseased area examined closely presents for study thin places and thick places. Those which form small hard eminences of a grayish white color or slight- ly reddened at the top, are irregu- larly disseminated over the area of the plaque. Between these elevations the patch is merely a thin membrane of a pearly white color. Wherever the white area is thickened, the scratching detaches small fragments like a white powder, of which certain pieces resem- ble mica flakes. When the lesion in extending, encounters the feathers, its appear- ance changes slightly. A deposit of whitish crusts accumulates at the base of each feather. Some feathers fall out spontaneously, and all those which have this squamous collar at the base, have little re- sistance against being plucked. If a feather is pulled it comes out entire with its yellow root part, but it bears with it, like a collar, the whitish deposit which surrounds the point where the feather emerges from the skin. Course of disease. The disease is benign. Instances in which affected birds become cachectic and die, are exceedingly rare. Ee- covery may occur in three months spontaneously, or the disease may last for years. Long duration may be considered as an example of a succession of infections, rather than the persistence of one infec- tion. The disease persists in subjects associating with other infected Fig. 11. Favus, involvino; tlie head. (Drawn from photograph by Sabour- aud, Suis and Suffran) 118 DISEASES OF DOMESTICATED BIKDS Fig. 12. Deposit of crusts on quills of feathers occurring in favus involving feathered areas. (Drawn from photograph by Sabouraud, Suis and Suffran ) birds, in infected quarters, while there is a tendency to recovery when affected birds are isolated. Treatment. Isolation of affected birds from the flock and from other infected individuals in some cases is sufficient to cause the disappearance of the disease. Previous to the application of any remedy the affected areas should be softened with soap and warm water, after which as much of the deposit as possible should be re- moved. The comb lesions may be treated with carbolized vaseline or green soap containing five per cent of carbolic acid. A mixture of glycerine 6 parts and iodine 1 part has been employed on the comb as have salicylic acid ointment (1 : 10) ; tincture of iodine diluted with equal parts or more of alcohol ; five per cent formalin ointment or solution ; and an ointment made of red oxide of mercury 1 part, to 8 parts of lard. A 1—500 solution of bichloride of mercury may be used among the feathers. Prophylaxis. In an infected flock, the closest examination of the exposed birds should be made, so that those slightly infected may be isolated and treated. Otherwise they will perpetuate the infec- tion in the flock. Care should be exercised to prevent the introduc- tion of birds from flocks not positively known to be free from the disease. In an infected flock, thorough cleaning and disinfection of the quarters should be carried out. REFERENCES 1. Balfour. Aspergillary pneumokoniosis in the lung of a turkey. Fourth Rep. Wellcovie Research Lab., 1911. 2. Beach and Halnin. Observations on an outbreak of favus. J. Agric. Research, Vol 15, 1918, p. 415. ASPEEGILLOSIS 119 3. Lignieres et Petit. Peritonite aspergillaire des dindon. Rec. de Med. Vet, T. 75, 1898, p. 145. 4. Lucet De V Aspergillus fumigatus chez animaux domestiques et dans les oefs en incubation. Paris, 1897. 5. Matruehot et Dassonville. Recherches experimentales sur une der- matomyeose des poules et sur son parasite. Rev. Gen. de Bot., T. XI, 1899, p. 430. 6. Mohler and Buckley. Pulmonary mycosis of birds. U. S. Dep. Agr. Bureau Animal Indust. Circ. 58, 1904. 7. Neumann. Aspergillosis in domesticated birds. J. Comp. Path, and Therap., Vol. 21, 1908, p. 260. 8. Sabouraud. Le trichophyton de la poule et la maladie humaine qu'il determine. Arch, de Med. Experim., Mai 1909. 9. Sabouraud, Suis et Suffran. La " crete blanche " (favus) de la poule et son parasite. Rev. Vet., T. 34, 1909, p. 601. CHAPTER XI INFECTIOUS ENTERO-HEPATITIS OF TURKEYS Si/)ionym. Blackhead. Characterization. Entero-hepatitis is an infectious disease of turkeys and fowls, characterized by distention of the ceca with ne- crotic material and the formation of yellowish or yellowish-green ne- crotic areas in the liver. Geographic distribution. It is widely distributed over the United States, and has also been reported from Canada, Europe, Aus- tralia and Africa. Etiology. The causative organism as described by Smith belongs to the genus ameba and has been designated by him Ameha mele- agridis. Through the researches of Hadley, the rule of an ameba in the causation is disputed. The latter investigator asserts that a fla- gellated protozoal organism, Tricliomonas, is the causative agent and that the organism described by Smith merely represents a transitory stage in the life cycle of the flagellate. The difticulties to be met with in establishing the etiologic factor of this disease are far greater than is the case in bacterial affections. In routine examination of entero-hepatitis cases by the present writers, it has been observed that flagellate forms are frequently present in the cecal exudate of tur- keys dead of entero-hepatitis while more often protozoal organisms of the ameba type are seen in comparatively large numbers. Fur- ther and more extensive investigation appears to be necessary in order to establish firmly the specific etiology of this disease. The organism described by Smith is round or oval in form with a single contoured outline. The structure appears homogeneous throughout with the exception of a small granular area eccentrically located and representing the nucleus. This encloses a smaller rounded body distinguished as the nucleolus. The protozoa in fixed or hardened tissue are from 6 to 10 microns in diameter, in fresh smears from 8 to 15 microns in diameter. The organism attributed by Hadley as the causative agent is a flagellate. This is most easily recognized in the motile stage. In this form it presents an irregular outline. It may be pear shaped, ovoid, triangi^ilar or elliptical in form. It has three anterior fla- 120 INFECTIOUS ENTERO-HEPATITIS OF TUKKEYS 121 gella, a vibratory membrane and one posterior flagellnm. The nu- cleus is placed anteriorly. One or more food vacuoles may be ob- served. The average length of this form is about 10 microns. Pathogenicity. Young turkeys are especially susceptible, al- though there appears to be no period of immunity to primary in- fection during the life of the bird. The greatest losses occur during the first two or three months of life. Practically all of the exposed poults contract the disease at this time. Young chickens are only slightly susceptible but may serve as carriers of the organism. Source of infection. The disease is principally spread through exposure to infested ground. Once the causative agent has been brought on the premises, it is apt to continue its activity year after year. Whether this is wholly due to the resistance of the encysted stage of the parasite, to climatic or other external influ- ences or whether it is perpetuated in the intestinal tract of compara- tively resistant turkeys or chickens is open to speculation. From the fact that mature turkeys may show symptoms of entero-hepatitis during all seasons of the year, it is reasonable to assume that they constantly harbor the organism in a saprophytic form and only de- velop the disease as a result of adverse conditions or weakened con- stitution from other causes. Curtice states that chickens though rarely infected may serve as carriers. In any case, the disease is contracted by the poults ranging on ground infested by the droppings of carriers of the parasite. The parasite passes from the intestine in the encysted or resistant stage. In this form when not exposed to the direct rays of the sun or to considerable drying it may retain its vitality for a long period, possibly one to two years. Earth worms may play some part as mechanical carriers of cysts which have sur- vived in the soil under favorable conditions. When these encysted forms are taken into the alimentary tract by poults in feeding, they undergo changes which renew their activity. The tough resistant covering is discarded and forms developed from the central granular mass or nucleus penetrate the mucosa of the intestine, especially the ceca and may be carried by the blood stream to the liver. The para- sites multiply rapidly in the intestine and are passed out in enormous numbers in the droppings. By this means, other susceptible birds in the flock are directly infected through coming in contact with the contaminated material in feeding. Symptoms. The symptoms of entero-hepatitis become apparent within a period of four weeks after exposure. Young birds show less resistance and develop manifestations earlier than grown ones. 122 DISEASES OF DOMESTICATED BIKDS The disease runs a rapid course in the former and deaths may follow in a few days. Older turkeys, fatally affected, usually suc- cumb within four weeks after the onset of symptoms. The mortality approaches 90 per cent in poults and 10 per cent or more in the gro^vn birds, according to the extent of exposure. Affected poults exhibit a drowsy attitude with constantly increasing lack of vigor. They are unable to keep up with the flock in its daily travel over large areas. The appetite is diminished, the feathers ruffled, wings are pendant, and a general air of debility is manifested. Diarrhea is nearly always present and quite characteristic. The droppings are soft and yellowish in color or may be mixed with brownish ex- crement. During the later stages the head may present a darkened or purple appearance due to impaired circulation of the blood. This symptom has led to the disease being termed " blackhead." However, this term is misleading since the darkened appearance of the head is not a constant svmptom and may also be observed in other diseases which lead to a weakened heart action. In older turkeys the symptoms are less pronounced and may be of much longer duration. They show loss of appetite, unthrifty appearance, lessened activity, progressive emaciation and diarrhea, with soft yellowish droppings. The disease may persist for a period of two weeks to two months and result fatally or the bird may regain its normal condition. Relapses frequently occur during the following year. The disease is more prevalent during the late summer or fall in young poults but may occur at any season and is frequently reported among grown turkeys during the winter and spring. Morbid anatomy. The lesions of entero-hepatitis are confined to the intestine and liver. In the intestinal tract the ceca are the principal seat of infection. In many cases only one cecum exhibits macroscopic alterations but quite frequently both ceca are equally involved. The walls become greatly thickened and covered by a necrotic exudate which completely fills the cavity or leaves but a small central space. The accumulation of exudate gives rise to a marked distention of these blind pouches plainly apparent when the intestine is exposed at autopsy. The exudate is dull gray in color and of a friable or cheesy consistency. The entire length of the cecum may be involved or only a limited area, depending on the severity or duration of the morbid process. In the majority of cases the liver is found infected to a greater or less degree. The lesions are characteristic. Areas of degeneration appear on the sur- face in circular form and of varying size. They are usually about INFECTIOUS ENTERO-HEPATITIS OF TURKEYS 123 Ys to % of an inch in diameter and may be isolated and few in num- ber or numerous and closely associated, even coalescent. Their color varies from a yellowish to a yellowish-green. These areas of ne- crosis extend more or less deeply into the structure of the liver and result from plugging of the smaller arterioles with the parasites and cellular debris. They are not always of a homogeneous color, but may appear mottled with small areas of approximately normal liver tissue. No elevation above the liver surface is in evidence as may be the case in tuberculosis or sarcomatosis of the liver and the tend- ency is rather to a slight depression beneath the capsule. The liver is often enlarged to a considerable degree and congested. In very acute cases the ceca show slight evidence of exudate but are more or less inflamed while the liver is free of lesions. Other areas of the intestine, especially the duodenum and rectum, harbor the causative parasite and may exhibit congestion of the mucous membrane, hemorrhagic points or even spots of necrosis. However, the ceca and liver are the main seats of disease and more to be relied upon for diagnostic evidence. Infrequently the morbid process within the lumen of the cecum extends through the mucosa, sub- mucosa, muscular layers and serous coat causing perforation and exu- dation into the peritoneal cavity leading to peritonitis or extensive adhesions of the cecum to the surrounding loops of intestine. This condition is apparently due to the action of invading bacteria since the protozoal organisms have not been demonstrated in these sec- ondary lesions. Microscopically the cecal exudate is found to be composed of protozoal bodies, exfoliated mucosa cells in various stages of degen- eration, connective tissue shreds, blood cells and an amorphous de- tritus. The cecal wall is greatly thickened due to infiltration and connective tissue hypertrophy. The mucosa shows extensive de- generative changes or is absent in areas. Depending on the depth of the ulceration, the circular or longitudinal muscular layers show more or less infiltration with small round cells and congestion, which may extend to the serosa. In the liver the necrotic foci show vary- ing stages of cell degeneration and are surrounded by a congested area. Walling off of the affected spots is not well marked or is totally absent. Small round cells, protozoal organisms and nuclear remnants are distingiiished in the amorphous necrotic material. In both the intestinal membrane and in the liver the protozoa occur either singly or in groups between the epithelial, or parenchymatous cells where they may be enclosed in a connective tissue network. 124 DISEASES OF DOMESTICATED BIKDS Thej have also been observed in the interior of giant cells (Smith), and epithelial and endothelial cells (Hadlej). Diagnosis. Entero-hepatitis is readily differentiated from other diseases bv the definite character of its internal manifestations. The presence of yellowish or yellowish-green spots on the surface of the liver is specific. Turkeys are much less frequently alfected with tuberculosis, or malignant tumors than fowls and these dis- eases may be eliminated where several birds in a flock become in- fected at the same time, especially in the case of poults. The lesions of tuberculosis, on cut section, present a fleshy appearance whitish in color with yellowish points and usually extend to the spleen, intestine and mesentery where they appear as rounded nodules. Tumor formations vary greatly in size, are fleshy in character and are usu- ally found on the serous membrane. They are of a chronic cliar- acter and occur sporadically. In tuberculous infection, tubercle ba- cilli will be found in large numbers on microscopic examination of smears from the nodules. Treatment. Extensive experiments looking to the treatment of entero-hepatitis have so far failed to develop a satisfactory method. The insidious nature of the affection and the deep seated location of its parasite in the wall of the intestine and in the liver render it practically immune from interference by curative agents. . Eme- tin hydrochlorid, a derivative of ipecac, by repeated hypodermic injection has given more or less satisfactory results in the treat- ment of amebic dysentery in man, a disease somewhat analogous to entero-hepatitis of turkeys. However, the above disease of man is- of a chronic nature and lends itself to a more prolonged course of treatment than is permitted in the case of the comparatively acute disease under consideration. Also the value of young turkeys does not justify the time and expense which would be involved even were the treatment fairly successful. Giving ipecac in small doses might prove beneficial. The most promising and economical treatment is the administration of crude catechu by means of the drinking water. This has been recommended by Fantham for coccidiosis of fowls and has given good results in our experience. One-third teaspoon- ful of crushed crude catechu is added to each gallon of water. It is quite possible that the use of catechu in this manner during the first three months would bring the exposed poults safely through the most dangerous period. Should signs of constipation develop as a result of this treatment, the entire flock may be given Epsom salts in the proportion of one teaspoonful to every ten poults. The salts can INFECTIOUS ENTERO-HEPATITIS OF TURKEYS 125 be dissolved in water and the solution mixed with a feed to be given early in the morning. Turkeys on range would require special at- tention for the successful operation of the above measures. Isola- tion or disposal of birds showing symptoms of disease is of the first importance in guarding against a further spread of the malady. Thorough cleaning and disinfection of quarters and yards will tend to keep the outbreaks in check. Carbolic acid in 5 per cent solution, or compound cresol in 3 per cent solution are efficient disinfectants. Prevention. Prevention of entero-hepatitis in infected com- munities is more difficult than the prevention of other diseases of domesticated birds, because of the fact that turkeys range over an area of several miles in diameter when allowed to rvm at large as is the usual custom in this country. The possibility of healthy flocks becoming infected by feeding on ground contaminated by diseased flocks is very apparent and renders preventive measures under such conditions rather difficult of execution. Where turkeys are con- fined to a limited area or do not come in contact with other flocks which harbor the parasite, simple precautionary measures may in- sure freedom from the disease. The main channel of entrance is through the introduction of birds which come from infected flocks. Particular care in selecting purchased birds should be exercised. The fact should be established beyond doubt that they are of a flock which has shown no symptoms of disease and have not been associated with neighboring diseased flocks. A period of quarantine extending over 30 days is also advisable before newly acquired tur- keys are placed with the home flock. Where the disease has been prevalent on premises to such an ex- tent as to make the raising of turkeys unprofitable, it is advisable to dispose of the entire lot and allow a period of approximately twn:) years to elapse before restocking. Local conditions may modify or suggest preventive measures. Limeing or plowing the runs or home feeding yards is indicated. The principal fact to be considered is that the disease must first be introduced, either by infected birds (almost invariably the turkey) or by mechanical carriers, such as persons coming from infected farms and carrying the causative par- asite on their shoes. Wild birds may possibly serve as carriers. Other agencies could be mentioned by means of which the organism of entero-hepatitis might be carried from infected farms ; however, these are of minor importance and cannot easily be guarded against. Eggs for hatching, from infected turkeys may be dipped in 95 per cent alcohol to destroy any parasites which may have become at- 126 DISEASES OF DOMESTICATED BIEDS tached to the shell. Practically the only danger in using eggs from infected flocks is that the shells may have come in contact with drop- pings harboring the infectious parasite. On first indication of the presence of entero-hepatitis the affected birds should be destroyed and their carcasses burned or deeply buried. The quarters should be thoroughly cleaned and disinfected with 5 per cent carbolic acid or compound cresol in 3 per cent solu- tion. The runs or local feeding ground should be cleaned and limed or plowed under as the chance for infection is greatest at the points where the flock congregates most often. The confinement of turkeys to inclosed yards has been tried with apparently favorable results. By this method of rearing, entero-hepatitis could be more easily controlled. Hadley regards the prevention of Trichomonas infection in tur- keys as presenting a somewhat different problem from that involved in the prophylaxis of many diseases. The parasites are found nor- mally present in the intestines of all poultry. Their pathogenic activity in turkeys, in his opinion, depends upon factors present in the host which are probably quite unrelated to virulence on the part of the infecting organism. This view would suggest the exer- cise of great care in feeding in order to preserve health even though the flagellates are present in the intestine. REFERENCES 1. Curtice. Notes on experiments with blackhead of turkeys. U. 8. Dep. Agr. Bureau Animal Indust. Circ. 119, 1907. 2. Curtice. The rearing and management of turkeys with special refer- ence to the "blackhead" disease. Rhode Island Agr. Exp. Sta. Bull. 123. 3. Curtice. Further experiments in connection with the blackhead dis- ease of turkeys. Rhode Island Agr. Exp. Sta. Bull. 12^. 4. Cushman. Nature of blackhead in turkeys. Rep. Rhode Island Agr. Exp. Sta. 1894. 5. Hadley. Blackhead in turkeys. A study in avian coccidiosis. Rhode Isla77d Agr. Exp. Sta. Bidl. Ul. 6. Hadley. The role of the flagellated protozoa in infective processes of the intestines and liver. Rhode Island Agr. Exp. Sta. Bull. 166. 7. Milks. A preliminary report on some diseases of chickens. Louisi- ana Agr. Exp. Sta. Bull. 108. 8. Moore. The direct transmission of infectious entero-hepatitis in turkeys. TJ. S. Dep. Agr. Bureau Animal Indust. Circ. 5, 1896. 9. Smith. Infectious entero-hepatitis in turkeys. U. 8. Dep. Agr. Bureau Animal Indust. Bull. 8, 1895. 10. Smith. Further investigations into the etiology of the protozoan disease of turkeys known as blackhead, entero-hepatitis, typhlitis, etc. J. Med. Res., Vol. 33, 1915, p. 243. CHAPTEK XII COCCIDIOSIS Characterization. Coccidiosis is primarily a disease of the in- testinal tract. In young chicks it may also affect the liver and in geese, the causative organism may be localized in the kidneys. It is one of the greatest scourges of fowls, pigeons and turkeys. Etiology. The organism causing coccidiosis is designated Ei- meria (Coccidium) avium and belongs to a class of protozoan para- sites known as sporozoa. The organism is included in the animal kingdom and reproduces by both sexual and asexual processes. The parasite was long known as Coccidium a u mm but owing to the rules of priority in zoological nomenclature, the familiar name of the genus C occidium has been replaced by Eimeria. In the oocyst or resistant stage, the one most easily recognized on microscopic examination of the intestinal contents, the protozoan generally appears as an oval body containing a central granular mass surrounded by a highly refractile zone with a double con- toured border. The size varies from 25 microns to 35 microns in length and from 15 microns to 20 microns in breadth. Life history of Eimeria avium. The life history has been ad- mirably worked out by Fantham. There are two principal stages in the life cycle, a stage of asexual multiplication, termed schizogony, and a stage of sexual reproduction in which male and female elements unite to form resistant bodies for life outside the animal cells. In the asexual stage the newly formed parasites pass from one cell to another, and it is during this cycle that the great destruction of in- testinal mucosa occurs. (a) The young, growing parasite. The oocyst reaches the duo- denum of the bird through the medium of the food or water. Here the tough cyst wall is softened and four small oval bodies or spores are released. From each of these are given off two actively motile vermiform bodies with one end more pointed than the other, which vary from 7 to 10 microns in length. These are the primary infect- ing germs or sporozoites (fig. 13 A). The sporozoite passes into an epithelial cell lining the first portion of the intestine where it curls on itself (fig. 13 B), takes on a spherical outline (fig. 13 C) and be- 127 Fig. 13. Diagram of life cycle of Eimeria (cocci- dium) avium. (Fantham) B-H. Illustrate the asex- ual reproduction (scliizog- ony) of E. avium. Epithe- lial host cells diagrammat- ically outlined. I-L. Illustrate the pro- duction of sexual forms ( gametogony ) . N-T. Illustrate spore formation ( sporogony ) . A. Sporozoite or primary infecting germ wliicli pene- trates the epithelial cell of the duodenum of the host. B. Sporozoite curving on itself before becoming rounded within the host cell. C. Young, growing para- site. D. Fully grown parasite (Trophozoite) . E. Schizont, with numer- ous daughter nuclei peri- pherally arranged. ( Seen in transverse section.) F. Schizont, showing far- ther differentiation of mero- zoites. G. Merozoites arranged " en barillet," about to issue from the host cell. H. Free merozoites. I ? . Young macrogame- tocyte with coarse granules. Id. Young microgametocyte with fine granules. J9. Growing female mother cell, showing chromatoid and plastinoid granules. ^ JcT. Microgrametocyte with nucleus divided to form a number of bent, rod- like portions, the future microgametes. K?. Macrogamete which has formed a cyst wall for itself but left a thin spot for the entry of the microgamete. Kef. Microgametocyte with many biflagellate microgametes about to separate from it. L. Fertilization. One microgamete is shown penetrating the macrogamete, while other male cells are near the micropyle but will be excluded. M. Fertilization. The male pronucleus is lying above the female chromatin. Degenerating microgametes are shown outside the oocyst. N. Oocyst (encysted zygote) with contents filling it completely. 0. Oocyst with contents concentrated, forming a central, spherical mass. Many such cysts seen in infected cecal droppings. P. Oocyst with four nuclei. Q. Oocyst with contents segmented to form four rounded sporoblasts. (As seen in fresh preparations.) R. Oocyst with four sporoblasts which have grown oval and are becoming sporocysts. S. Oocyst with four sporocysts, in each of which two sporozoites have dif- ferentiated. T. Free sporocyst in which the sporozoites have assumed the most suitable position for emergence. 128 COCCIDIOSIS 129 gins to grow in size at tlie expense of the host celh This is known as the trophozoite stage (fig. 13 D). (b) Asexnal multiplication or schizogony. When fully developed the trophozoite has a diameter of 10 to 12 microns. In preparation for propagation the nucleus divides into a number of daughter nuclei which arrange themselves in a zone at the periphery. This consti- tutes the schizont stage and represents the beginning of asexual mul- tiplication or schizogony (fig. 13 E). Each nucleus becomes sur- rounded with protoplasm and assumes a long narrow form with pointed ends. The length ranges from 6 to 10 microns (fig. 13 F G). These bodies, known as merozoites, differ from sporozoites in that their nuclei contain a small particle of chromatin, the karyosome. From 8 to 20 merozoites are formed from 1 schizont. On separation from one another (fig. 13 H), the merozoites work their way into other cells, lining the intestinal tract and may repeat the process of development just outlined, or differentiation into sexual forms may take place within the newly invaded cells. This process is termed gametogony. (c) Sexual reproduction or gametogony. Two forms of the or- ganism are now produced, the macrogametocyte or female mother cell (fig. 13 I J) and the microgametocyte or male mother cell (fig. 13 I J). Both forms are oval in shape, the former being somewhat larger and more granular than the latter. Also the former gives rise to only one daughter cell or macrogamete (fig. 13 K) while the latter produces a large number of minute, biflagellate, actively motile male cells or microgametes (fig. 13 K). The macrogametes are from 11.8 to 17.5 microns in length and 6 to 11 microns in breadth, in sections. The microgametes are 3 to 4 microns in length, in sections. (d) Fertilization. Fertilization takes place through the entrance of the microgamete or male cell into the structure of the female cell or macrogamete at the thin spot at one end known as the mi- cropyle (fig. 13 L). After the entrance of the male cell the macro- gamete secretes protoplasm which plugs the opening and prevents the entrance of other microgametes. On union of the nuclei of the two gametes, a zygote is formed which proceeds to spore formation or sporogony (fig. 13 M IST). (e) Sporogcmy. The zygote is surrounded by a tough double con- toured membrane which is extremely resistant. This stage is kntiwn as the escii; stage, or oocyst. The contents arc at first granular and grayish in appearance (fig. 13 'N). Later the granular material is 130 DISEASES OF DOMESTICATED BIRDS gathered into a compact circular mass approximately in the center of the oocyst (fig, 13 0). The nucleus imbedded in the central mat- ter now undergoes division into two and these in turn divide, form- ing four daughter nuclei (fig. 13 P). These are surrounded by cyto- plasm and separated from each other. As a result four rounded bodies are formed within the cyst. These are sporoblasts (fig, 13 Q). Later the sporoblast loses its rounded form, becomes oval and is inclosed in a cell wall (fig. 13 R). In this form it is termed a sporocyst and from it develops a spore which contains two young infective parasites or sporozoites. The life cycle is completed by the rupture of the oocyst wall in the intestinal tract of the host, which releases the spores and the primary infecting sporozoites. From experiments made by feeding fowl chicks with coccidian oocysts, Fantham concUides that the period for the total life cycle of the parasite is from eight to ten days. Pathogenicity. Apparently coccidiosis is infectious to all do- mesticated and wild birds which are exposed to its causative organ- ism. It has been observed in a wide variety of these birds and its incidence has been marked by high mortality, especially in those con- fined to limited areas. It is highly destructive to young chickens and frequently affects baby chicks. Its gTeatest ravages are seen in chickens which have passed the brooder stage and are exposed to the infective agent in infected houses or grounds. Limited range, as is customary in the rearing of domesticated birds, and especially in the case of chickens closely confined in large fiocks, is conducive to heavy infection and high mortality in the event that coccidia are present. Next to chickens, pigeons are no doubt most severely af- fected. Outbreaks among ducks and geese occur less often as an epizootic unless the birds are closely confined, but individual infec- tion commonly occurs. Birds of all ages are susceptible. Mature birds exhibit a fair de- gree of resistance. They may harbor the coccidia and appear nor- mal until they become grossly infected, or become weakened through other causes to such an extent that their power of resistance is lost. Mortality. In chicks affected at the age of two to ten weeks, the disease runs a rapid course and the mortality may reach 100 per cent in closely confined flocks. In older fowls, the fatalities, while not so great, are usually very heavy in those surrounded by unsan- itary conditions. Mature hens have a greater power of resistance but even among these, severe losses may be observed. The mortality is governed by the degree of exposure. COCCIDIOSIS 131 Course of the disease. The coccidium when once introduced into a flock develops rapidly in the cells of the intestinal mucosa^ giving rise to a great number of sexual and asexual forms which are passed out in the droppings and are ingested by healthy birds. Accumu- lation of infected droppings naturally tends to increase the number of these organisms ingested and results in gross infection. Where fairly good sanitary conditions are maintained, the spread of the disease is less general and the amount of infectious material con- sumed is proportionally lessened. As a result, birds which have a degree of normal resistance are protected against heavy infection. Symptoms. The outward manifestations of coccidiosis depend to a considerable degree upon the age of the birds attacked. In young chicks, the disease develops rapidly and the mortality is high. The affected ones display the usual appearance associated with de- bilitating internal disorders, such as weakness, disordered feathers, droopy wings, bunched appearance, loss of appetite, and somnolence. The droppings are semi-fluid and usually whitish in color, but may be of a fluid nature with brownish tinge. In very acute cases in young chicks the droppings are deeply stained with blood. Affected chicks of an age of three weeks or less to two months seldom survive in a severe outbreak and those that recover are stunted and worthless. Chicks affected fatally succumb in from one to several days after out- ward symptoms are apparent, depending upon their age. The older ones show a stronger resistance, but in these too, the fatalities are extremely heavy. In grown fowls, the disease usually assumes a more chronic type, although acute outbreaks are not infrequent. In these acute out- breaks, the affected birds show the droopy appearance which is more or less characteristic of all infectious diseases of fowls, and which, in itself, has comparatively little value as a diagnostic feature. In semi-acute cases, the fowl develops a progressively increasing list- lessness and loss of activity. The comb becomes pale and periods of dejection, during which the bird stands in an isolated position, in- crease as the disease progresses. The appetite may remain normal and is frequently ravenous when the fowl is aroused at feeding time. During intervals between regailar feeding, there is little effort to scratch for food with the others of the flock. The symptoms may be apparent for from one to three weeks, death occurring quite sud- denly or after a short period of coma. In the more chronic form, the fowl retains a pale appearance of the comb and wattles for several weeks, the appetite appears nonnal while the bird is eating, 132 DISEASES OF DOMESTICATED BIRDS but the amount of food consumed is less than usual, owing to the general indifference to food during prolonged intervals. Emacia- tion is marked both in semi-acute and chronic cases, principally due to the fact that the destruction of the lining membrane of portions cf the intestine prevents normal assimilation of the food. Leg weakness and paralysis are frequently observed. Affected geese become gi-eatly weakened and emaciated. After walking a few steps they will fall and after a struggle roll on their backs, a position which is frequently assumed. Morbid anatomy. The lesions are principally confined to the intestinal tract and are most noticeable in the ceca, in chickens and turkeys. In young chicks in which the disease assumes an acute course, the ceca are filled with a bloody semi-solid mass which shows through the intact tubes and gives them a distended contour. This mass consists of blood cells, exfoliated mucosa, fecal matter, and ex- tremely numerous coccidial forms of which the oocysts or egg forms are especially apparent on microscopic examination. In older fowls, the ceca may be distended to a greater or less degree. In the ma- jority of eases, the distention is marked and the tubes are firm to the touch over a considerable extent of their length. Hemorrhagic areas may show through the serous membrane, or the affected parts may ap- pear pale and deadened. One cecum only may give evidence of mor- bid changes, but as a rule both are equally affected. On incision, the lumina are found packed with a solid necrotic mass of a grayish color and cheesy consistency. The mucous membrane is completely degenerated and forms a part of the caseatcd mass. On microscopic examination, the necrotic material appears as an amorphous mass in wdiich mucus, cells in various stages of degeneration, food material and numerous coccidial cysts are incorporated. The mucous lining of the duodenum is invariably the seat of pathologic changes and is the portion of the intestine first affected. In many instances, this is the only part which shows lesions on post-mortem examination. The lining membrane is deeply congested, or hemorrhagic. Diagnosis. Coccidiosis is readily diagnosed by a microscopic examination of the droppings of infected birds, or of the intestinal contents at autopsy. A small amount of the material is broken up in several drops of a 1 per cent potassium hydrate solution, normal salt solution, or water and about two drops of the mixture are placed on a glass slide and a cover glass applied. The coccidia usually are very numerous in advanced cases and are easily recognized in the oocyst or resistant stage. They have an oval appearance with COCCIDIOSIS 133 a central, rounded, darkened area surrounded by a wide, clear', transparent zone with double contoured border. Other stages of de- velopment may be observed, however, the oocyst form is most easily recognized. Symptomatically the disease may be confused with ba- cillary white diarrhea and aspergillosis in young chicks, and with tuberculosis, aspergillosis, and infectious leukemia in older fowls. It is differentiated from bacillary white diarrhea by the fact that deaths from the latter occur principally within the first three weeks of life, while coccidiosis usually appears at a later period. As- pergillosis occurs more rarely and is generally restricted to a rela- tively small number of the flock. It is easily differentiated from coccidiosis on post-mortem examination by the localization of its lesions in the air passages, especially in the air sacs of the abdomen. Tuberculosis is readily distinguished by its characteristic nodular formations in the liver and intestines, or by microscopic examina- tion. In infectious leukemia, the liver is enlarged and usually studded with small necrotic spots while the ceca are free of masses of caseated material. Treatment. Attempts at treatment have not given very satis- factory results owing to the highly resistant powers of the organism during certain stages of its life cycle and to the position which it occupies in the intestinal membranes. Crude catechu, recommended by Fantham, has, in our experience, proved more effective than other preparations which have been recommended. The most convenient method of administration is by means of the drinking water. The lumps should be broken up by grinding or pounding into a coarse powder and added to the water in the proportion of Vs teaspoonful to each gallon of water. This solution is to be kept constantly avail- able to the flock while the disease is prevalent. Should signs of constipation develop, the entire flock may be given a dose of Epsom salts in the proportion of Vs teaspoonful to each adult fowl. The salts can be dissolved in water and mixed in a mash. The purgative effect is greatest if the mash is fed in the morning when the crop contains a minimum amount of food. It is advisable when s\anp- toms of coccidiosis are first noticed to give the flock a dose of Epsom salts before the crude catechu treatment is started. Where catechu is not available, bichloride of mercury may be substituted. It is given in the drinking water in the strength of 1 to 6000. Perman- ganate of potash 1 part in 500 parts of drinking water has also proved effective. Prevention. Once this disease has been introduced, the most sat- 134 DISEASES OF DOMESTICATED BIRDS isfactorj method of combating it is through preventive measures against its spread. Birds showing symptoms should be isolated im- mediately, the houses thoroughly cleaned, and the floors, dropping boards and roosts soaked with carbolic acid in 5 per cent solution, or crude carbolic acid, or compound cresol, in 2 per cent solution. Other disinfectants, especially the coal tar prodvicts, may be substi- tuted, provided sufficiently strong solutions are applied. The dis- infectant may be spread by means of a spray pump or brush, but it is important that the places exposed to droppings should be covered by the fluid. During the course of an outbreak the droppings are to be removed frequently as it is through these that the infection is passed to healthy birds while feeding in contaminated pens. Runs to which diseased fowls have had access are highly dangerous to the non-infected and should be abandoned for a year at least if possible. These may be plowed and seeded, or if their use as runs is impera- tive the soil may be limed and plowed under. Since earth worms are credited with serving as hosts of the coccidium, stringent measures are necessary on badly infected premises, to accomplish complete eradi- cation of the disease. Covering the ground with chloride of lime or unslacked lime at intervals may prove sufficient, especially where preventive measures have been adopted early and a minimum ex- posure to infested droppings is indicated. Fowls received from out- side sources, unless known to be unexposed, should be quarantined for a period of three to four weeks before being placed in the flock. REFERENCES 1. Fantham. Experimental studies in avian coccidiosis. Proc. Zool. Soc. London, Vol. 3, 1910, p. 708. 2. Fantham. Coccidiosis in British game birds and poultry. /. Econ. Biol, Vol. 6, 1911, p. 75. 3. Jowett. Coccidiosis of the fowl and calf. J. Comp. Path, and Therap., Vol. 24, 1911, p. 207. 4. Meyer and Crocker. Some experiments on medical treatment of coccidiosis in chickens. Am. Vet. Rev., Vol. 43, 1913, p. 497. CHAPTEE XIII SPIROCHETOSIS AND RARE INFECTIOUS DISEASES SPIROCHETOSIS Synonyms. Fowl fever, spirillosis of fowls, spirillose des poules, Hiihnerspirillose. Characterization. Spirochetosis is an acute, highly fatal, fe- brile, septicemic disease of birds caused by spirochetes and trans- mitted by fowl ticks. Geographical distribution. The disease has been reported in ISTorth and South Africa, India, Australia, Russia, Hungary, Rou- mania, Bulgaria, Cyprus, South America and the West Indies. The existence of the disease in the United States within the area of distribution of the fowl tick (See Fig. 53, p. 221) has been suspected by various writers, but so far as known its presence has not been definitely proven. Symptoms ascribed to excessive tick infesta- tion, such as paralysis, drooping of wings, ruffled feathers, loss of ap- petite and even death have suggested the idea that spirochetosis may be present. Etiology. 8 pirochceta (Treponema) gallinarum (S. march- ouxi) causes the disease in fowls, while 8pirochceta anserina has been identified as the cause of a similar infection in geese. Some consider 8. anserina as identical with 8. gallinarum. The general shape of a fully developed spirochete is that of a nar- row sinuous thread, in some cases reaching nearly 20 microns in length. The cells possess active motility. Spirochetes are generally regarded as protozoan organisms, although the belief that they are bacteria has many adherents. The organisms may be stained in blood films by fixing with osraic acid vapor, after which the films are hardened in absolute alcohol and stained with Giemsa or one of the modifications of that stain. Carbol fuchsin may be employed as a stain. ISToguchi has cultivated 8. gallinarum in a special medium de- vised to provide suitable conditions. An infected bird is placed under ether anesthesia and blood is drawn aseptically from the heart. To prevent coagulation the blood is mixed with an equal amount of 135 136 DISEASES OF DOMESTICATED BIRDS 1.5 per cent solution of sodium citrate in a .9 per cent solution of sodium chlorid. A piece of kidney of a normal rabbit or a piece of pectoral muscle of a fowl is placed in a test tube. Ascitic fluid is added to make the column of fluid 10 cm. high or about 10 to 15 c.c. To this is added a few drops of the infected blood. The fluid is covered with a layer of paraffin oil that has been autoclaved twice. Ascitic fluid is not always suitable and it may be necessary to try many lots. The maximum growth is reached at about the fifth day, the cells being fully developed typical spirochetes. After the fifth day de- generation of the cells begins and proceeds slowly. The organism has been demonstrated to remain virulent for chickens through 13 gen- erations of culture. However, under certain cultural conditions it may lose its virulence. The inoculation of birds with such aviru- lent strains induces a resistance to subsequent infection with a viru- lent strain. Pathogenicity. Fowls, geese, ducks, guinea-fowls, turtle doves and sparrows have been reported as susceptible. Animals com- monly employed in laboratory work are immune, but Levaditi re- ports that he produced a transitory spirochetosis in a rabbit lasting three or four days. Poultrymen, when spirochetosis occurs, are apt to attribute losses to excessive tick infestation and to the resulting loss of blood with- out recognizing that an infectious disease is the cause of the losses. The prevalence of the disease will coincide with the season that is most favorable to the multiplication of ticks, but deaths will oc- cur at any time when susceptible stock is introduced, providing ticks are at all active. Bevan notes that birds in infected flocks become immune. How- ever, the birds previously immune will succumb after the introduc- tion of newly arrived susceptible birds starts the infection anew. It is possible that the passage through susceptible birds increases the virulence of the virus. Upon introduction of infection into a flock hitherto uninfected, spirochetosis may be exceedingly fatal and exterminate a flock in a few days. Young birds are particularly susceptible. The course of the experimentally produced disease varies accord- ing to the method of the introduction of the virus, the activity of the spirochetes and the receptivity of the bird. When the inocu- lation is made by means of the tick, after 6 to 8 days and sometimes more, the spirochetes are encountered in the circulation. If inocu- SPIROCHETOSIS AND RARE INFECTIOUS DISEASES 137 lation is made with virulent blood through the skin, the period of incubation is reduced to a period varying from 48 to 72 hours. The period of incubation is longer when the virus is placed on the skin superficially. The disease is acquired easily through the mouth, especially if the virulence of the parasite has been raised by a number of passages. Symptoms. Very commonly the disease occurs in such an acute form that birds apparently healthy at night are found dead under the roost in the morning. In the less rapidly fatal form there is dullness, ruffling of the feathers, somnolence and diarrhea. The comb becomes pale as a result of anemia. The temperature reaches 110° or 112° F. but drops abruptly at the crisis, which coincides with the disappearance of the spirochetes from the circulating blood. During the course of the disease^ there is a marked decrease in the number of red corpuscles and a leucocytosis characterized by increase in the number of polynuclear leucocytes. After the crisis, the poly- nuclear cells diminish and the mononuclear cells increase in num- ber. The acute type of disease may be terminated by death in from four to five days- after the onset of symptoms. Death often occurs during convulsions. The chronic type may follow the acute phase or appear inde- pendently. Death may not occur for fifteen days. Paralytic symp- toms are noted. The wings may droop^ or the head be twisted back, or the legs may be involved. Inability to use the claws is an early sjTiiptom of leg paralysis. There may be disturbances of gait, and the bird may appear knock kneed or bowlegged. Emaciation and anemia are also particularly characteristic of the chronic type. Morbid anatomy. In birds dead of an acute attack, the spleen is found to be enlarged to several times normal. The liver also is greatly enlarged, shows fatty degeneration and sometimes focal ne- crosis. The other organs do not usually show marked lesions beyond the paleness of muscles, lungs and kidneys resulting from the ane- mia. The intestines sometimes are congested, and show punctiform hemorrhages. In chronic cases on the other hand, the liver and spleen are smaller than normal. The skin shows evidence of tick bites in the form of subcutaneous hemorrhagic areas. Microscopic examination of the blood of a bird dead of the disease, or during life after the crisis, will not reveal spirochetes. Life cycle of spirochetes. After the spirochete in the blood reaches a length of 16 to 19 microns it divides by a transverse divi- 138 DISEASES OF DOMESTICATED BIKDS Fig. 14. Various stages in the flexions and transverse divisions of Treponema ( Spirochoeta gallinarum ) . ( Hindle ) sion. This is accomplished only after a series of movements con- sisting of doubling back on itself, coiling of the two portions, un- coiling and eventual separation. The process is illustrated in Fig. 14, the successive stages of the process being indicated by the let- ters a to h. Sometimes the separation occurs as illustrated in e, but usually takes place after the position h is reached. Whether or not transverse division takes place directly without previous flexion has not been definitely determined. The act of uncoiling and sep- aration as illustrated in d, f, and g of Fig. 14 very closely sim- ulates a process of longitudinal division and has been erroneously so interpreted by some observers. The process of transverse division doubtless occurs repeatedly in the blood. Penetration of red blood cells and invasion by spirochetes has been observed but seems to be uncommon. At the time of the crisis of the disease, which is synchronous with the disappearance of spirochetes from the circulating blood, some spirochetes break up into a number of coccoid bodies in a manner analogous to the formation of spores within a bacterial cell. It is not certain that these coccoid bodies formed under the conditions in question redevelop into spirochetes within the blood of the fowl. Some of the spirochetes taken into the tick with a feeding of fowl blood, penetrate the wall of the gut and gain access to the coelomie fluid which occupies the body cavity of ticks. After a short time SPIROCHETOSIS AND RARE INFECTIOUS DISEASES 139 MULTIPLICATION OF — COOCOIO BODIES IN CELLS OF ARQAS FORMATION OF COCCOID BODIES IN CELLS OF ARQAS Fig. 15. The life-cycle of Treponema {SpirocJueta) galUnaruni illustrated dia- grammatically. (Hindle) the spirochetes further penetrate into various organs of the tick, including the ovary and Malpighian tubules where they multiply by ordinary fission. In the cells of these organs the spirochetes break up into coccoid bodies. Other spirochetes remaining in the lumen of the- gut also form coccoid bodies. These circumstances re- 140 DISEASES OF DOMESTICATED BIRDS suit in the infection of the Malpighian secretion and excrement with coccoid bodies. While the salivary gland has been considered with reference to the part played by saliva in introducing infection into fowls, the obser- vations tend to show that contamination of the tick-bite wound by coccoid bodies in excrement and coxal fluid, is responsible. Coccoid bodies are capable of development into the typical spiro- chete by a process of gi-adual lengthening. This has been observed in the ticks but not in the blood of a fowl. The eggs of an infected tick contain coccoid bodies and the progeny of such a tick is infective either by feeding on a fowl or when in- gested by a fowl. Ticks after feeding on infected blood are most liable to be in- fective when kept at a temperature of 30-35° C. When ticks are kept at 15-18° C, the spirochetes disappear from the alimentary tract, and such ticks do not transmit the infection. Differential diagnosis. The various septicemias of fowls, more particularly fowl cholera, might readily cause symptoms and lesions simulating spirochetosis. Microscopic examination of stained blood smears should furnish conclusive evidence by showing whether the septicemia is caused by spirochetes or by bacteria. The limited area of the United States in which ticks occur, see p. 221, should be borne in mind. Treatment. Dodd reports that /'s grain of soamin dissolved in one c.c. of sterile water and injected intramuscularly, modified and shortened the attacks with rapid and complete recovery, lllilen- huth gave atoxyl in an average dose of 5 centigrams at the time of infection or two days later. It prevented infection or cured but the blood remained infective. Hauer concludes that salvarsan is capable of destroying spirochetes in the body. The curative action of this substance is established in all cases on the day of treatment and acts in a remarkable manner even after the use of a limited amount of salvarsan. Even in cases where the treatment was first given on the fourth day after infection, when the bird was somnolent and when the blood was swarming with spirochetes, one injection of the agent in not too small a dose led to striking improvement and recovery. The immunity which salvarsan confers upon birds protected with it, is of high degree and of long duration. Hauer experimented on fowls with a wide variety of doses of the drug. The lowest lethal dose was found to be .3 gram and .15 SPIROCHETOSIS AND RAEE INFECTIOUS DISEASES 141 gram was the maximum dose tolerated. The curative dose on the second day of infection when spirochetes were observed in the blood, varied from .02 to .003 gram per kilo of body weight. Even the lowest dose caused the disappearance of spirochetes from the circu- lation and the birds recovered. Birds treated on the third day of infection received doses varying from .03 gram to .0025 gram per kilo of body weight. The lowest dose that uniformly caused the dis- appearance of the spirochetes was .005 gram per kilo. A dose of .05 gram per kilo was effective when administered to birds on the fifth day of infection. Aragao recommends atoxyl in a dose of .03 gram, salvarsan .0035 gram and neosalvarsan in .0015 gram per kilo of body weight. Immunization. An attack of spirochetosis confers a certain amount of immunity. The blood serum of such a bird possesses strong immunizing properties and shows marked agglutinative action in vitro. Aragao induces immunity by injecting a vaccine prepared from the blood of infected fowls. On the fifth day of the infection the blood is drawn aseptically into flasks holding 300 c.c. each and de- fibrinated by shaking with shot. Blood drawings from the various fowls are mixed to secure a uniform distribution. The defibrinated blood is distributed in quantities of 50 c.c. each in flasks of a ca- pacity of 125 c.c. The flasks are plugged with cotton which has been dipped in formalin. The fluid is left thus exposed to the vapor of formalin for eight days and is shaken occasionally during that period. After carrying out suitable tests for sterility, it is in- jected subcutaneously in one c.c. doses for immunizing birds be- fore introduction into infected flocks. A similar product is pre- pared by Aragao by mixing defibrinated blood and glycerine in equal parts, omitting the formalin vapor treatment. It is used in two c.c. doses and is preferred to the one prepared by using formalin. A single injection is employed, for subsequent attacks by ticks in an infected flock are relied upon to strengthen the immunity. In unin- fected flocks where the vaccination is employed as a protection against imported infection only, revaccination is recommended once a year. Marchoux and Salimbini have observed that the virulence of the spirillum in blood is greatly diminished or lost after a period of about 48 hours. They produce successful vaccination by using virulent blood held for two to four days, or after heating at 55° C. for five to ten minutes. 142 DISEASES OF DOMESTICATED BIEDS Control of spirochetosis. The relation of fowl ticks to the spread of the disease is so direct, that the destruction of ticks is of necessity the first measure to be employed in combating the disease. See p. 223. Fowls not infested with ticks, but liable to become so, might be immunized with Aragao's vaccine. Susceptible birds before introduction into tick infected localities might be so im- munized. EARE INFECTIOUS DISEASES KABIES Several writers report the occurrence of rabies among fowls. Af- fected birds show restlessness and great fright. The feathers are ruffled and the bird attacks its fellows, other domestic animals and even man. Autopsy findings reveal no marked lesions. Injuries of the skin, foreign bodies in the gizzard together with congestion of the kidneys and intestines are conditions most frequently found. The prophylactic measures indicated are isolation of birds during outbreaks of rabies with slaughter of infected birds. Intracranial inoculation of fowls with rabies virus causes paraly- sis of the feet and neck, associated with uncertain gait. FOOT AND MOUTH DISEASE The occurrence of foot and mouth disease has been observed in fowls, waterfowl and pigeons but a few times. The lesions have been reported as occurring on the skin of the head, on the buccal mucous membrane and about the feet. Ehrhardt states that this disease is very rarely transmitted to fowls from cloven hoofed animals, for birds show a very high re- sistance to both natural and artificial infection. The disease is man- ifested by the occurrence of vesicles on the appendages of the head, on the mucous membrane of the mouth and throat as well as on the feet. In waterfowl the lesions appear mostly on the webs of the toes, and on the mucosa of the mouth and throat. In most cases the course of the disease is favorable and the lesions heal spontaneously in from eight to fourteen days without treatment. As a result of the cessation of eating, the affected birds appear weak and cease laying. In severe cases lameness and fever are observed followed by decline and death. SPIROCHETOSIS AND RARE INFECTIOUS DISEASES 143 MALTA FEVER IN FOWLS Dubois reports the occurrence of this disease in fowls. The out- break histed three months, with a mortality of 70 per cent. Symptoms. Birds of all ages are affected. The disease pre- sents two clinical forms: an acute or subacute form in which the duration is 8 to 10 days at the most, and a fulminating form lasting only a few hours. In the acute form the affected birds appear feeble, walk with dif- ficulty and display inappetence. After three or four hours the birds stop moving and appear depressed. The wings drop, the birds allow themselves to be caught easily, and sometimes show diarrhea with gi-een discharges. There is extreme emaciation at the last. In the fvilminating type few characteristic signs are observed. There is only weakness and depression. Some birds die suddenly without having shown symptoms. Morbid anatomy. In the fulminating type the lesions consist of ecchymoses on the lungs, a marked hypertrophy of the spleen and a certain degree of congestion of the liver. Inoculations made with the liver, the spleen, and heart blood of sick birds have given negative results. Likewise, inoculation of rabbit, guinea pig and pigeon with the pulp of the spleen and heart blood of sick birds has always failed to affect these animals. The writer determined the agglutinative properties against M. melitensis possessed by the blood of the affected birds. Of 8 fowls 2-5 years old, 3 presented a positive reaction; of 9 birds 2-4 months old, 5 gave positive reaction. ANTHRAX Dawson points out that chickens may contract anthrax by eating the carcass of an animal dead of that disease. The disease runs a rapid and fatal course within 24 hours. The affected bird shows fever, high temperature, weakness, tremors and convulsions, together with bloody fecal discharges. Swellings may occur on the comb, wat- tles, sides of the head, in the mouth or on the feet. Mollhoff concludes that birds are more or less susceptible to in- oculation with anthrax. Exception is made in the case of hens, which in his experiments showed high resistance. Out of sixteen hens exposed by subcutaneous, intramuscular and intraocular in- jection, with doses as high as 2 c.c. or by feeding, only one sue- 144 DISEASES OF DOMESTICATED BIRDS cumbed. This bird before inoculation was observed to be highly emaciated and anemic. Two geese receiving subcutaneous injections of 4 c.c. resisted infection. Of 16 pigeons inoculated, 7 contracted anthrax. Other birds such as ducks, sparrows, canaries, jays, hawks and crows, were very susceptible to inoculation. That writer makes a distinction between susceptibility to anthrax by inoculation, and susceptibility to the natural spontaneous infection. He knows of no instance of the latter. Mollhoff concludes that the resistance of the hen to anthrax con- sists of action of the body fluids or Ijanph by virtue of strongly bactericidal materials contained in them. The anthrax bacilli in the subcutaneous tissues are killed in a short time by the bacteri- cidal action of the lymph, so that no local development nor general infection can occur. The origin of this bactericidal material of the lymph, especially with reference to whether or not it originated in the leucocytes, could not be determined. Phagocytosis is not of decisive importance in connection with the destruction of anthrax infection in the hen. The resistance of hens against anthrax does not depend upon their high body temperature. Anthrax occurs in the ostrich as a common natural infection and is discussed in Chapter XVIII. REFERENCES 1. Aragao. Espirochetose (treponemose) das Gallinhas. Bev. de Vet. e Zootech. (Eio de Janeiro), Vol. 7, 1917, p. 3. 2. Bevan. Spirochetosis of fowls in Southern Rhodesia. /. Comp. Path, and Ther., Vol. 21, 1908, p. 43. 3. Dawson. Anthrax with special reference to the production of im- munity. TJ. 8. Dep. Agr. Bureau Animal Indust. Bull. 13. A. Dubois. La fievre de Malto chez les poules. Bev. Vet., Vol. 67, 1910, p. 490. 5. Ehrhardt. Die Krankheiten des hansgefliigels. 3. aufl. Aarau : E. Wirz. 1914. 6. Hauer. UntersuehiTngen liber die Wirkung des Mittels 606 auf die Hiihnerspirillose. CentralU. f. BaUeriol. {Etc.), 1 Aht. Orig., Bd. 62, 1912, p. 477. 7. Hindle. On the life-cycle of spirochseta gallinarum. Parasitology, Vol. 4, 1911, p. 463. 8. Jowett. Fowl spirochetosis at Cape Town. Vet. Jour., Vol. 18, 1911, p. 240. 9. Mhrchoux et Salimbini. La spirillose des poules. Ann. de I'Inst. Pasteur, T. 17, 1903, p. 570. 10. Mollhoff. Untersuchungen liber die Empfanglichkeit des Gefliigels SPIROCHETOSIS AND RARE INFECTIOUS DISEASES 145 fiir Mikbrand und iiber die Grunde der Eesistenz des Huhner gegen diese Krankheit. Inaug. Diss. Bern. 11. Noguchi. Cultivation of spirocliaeta gallmarum. J. hxpei. M., Vol. 16, 1912, p. 620. ^ T T7 ^ V ^ 7 12. Pereira. A Espirochetose das Gallinhas. Rev. de Vet. e Zootech., Vol. VI, 1916, p. 327. CHAPTEK XIV LEUKEMIA AND PSEUDO LEUKEMIA Characterization. Leukemia in fowls is a disease of the blood, and blood forming organs. It is marked by changes in the com- p®sition of the blood manifested principally by an enormous in- crease in the number of leucocytes and an accompanying decrease in the number of erythrocytes. Besides these changes, lymphoid en- largement of the liver, spleen and kidneys is usually to be observed. Pseudo leukemia is a term desigiiating a condition in which lymph- oid tissue is present in the various organs, without changes in the circulating blood. The two conditions are very closely related, if in- deed they are not different stages of the same process. History. The disease in fowls was first recognized by Warthin in 1907 and soon after by Ellerman and Bang. Butterfield in 1905 and Yutaka Kon in 1907 very likely observed cases of leukemia, but did not examine the blood. Pickens presents a thorough survey of the literature of the disease accompanied by original observations on a series of cases. The disease has been reported in Denmark, Germany and the United States. Etiology. Ellerman and Bang and also Yutaka Kon found pro- tozoa-like bodies in the organs and bone marrow of affected fowls. The significance of these bodies has not been definitely determined. In typical cases of leukemia encountered by the present writers, at- tempts to isolate an organism from the blood and parenchymatous organs have given negative results. The fact that Ellerman and Bang succeeded in transmitting leukemia to fowls by intravenous and intraperitoneal injection of a cell free filtrate of infected exu- dates, points to an ultra-microscopic virus as the causative agent. The disease is readily transmitted by non-filtered organ suspen- sion. The virus is present in all affected organs, but the infective properties of these organs are lost in a few days after death. There are three principal theories as to the etiology of the dis- ease in man which are reflected by various writers in the interpre- tation of lesions in the fowl: 1. The lesions of leukemia are a simple hyperplasia. 2. Leukemia is a neoplasm. (See lymphoma). 3. Leukemia is a result of the multiplication of an infective agent. 146 LEUKEMIA AND PSEUDO LEUKEMIA 147 Pathogenicity. Leukemia lias not been reported as occurring in pigeons, turkeys or guinea-fowls and experimental efforts have failed to produce the disease in these birds. Fowls appear insusceptible to subcutaneous inoculation but are infected in about 50 per cent of cases through intravenous or intraperitoneal injection of a suspension of the organs or of the blood of affected fowls. Ellerman and Bang observed that inoculation may produce either leukemia or pseudo leukemia. Course. The duration of the disease is variable. The period of incubation ranges from about 2 to 8 weeks. Death may result within several days after the appearance of symptoms or may be delayed for one to three months. Recovery is only rarely observed. Symptoms. While birds may die suddenly from an acute at- tack, the manifestations of leukemia are usually of a chronic char- acter. There is observed a progressive emaciation with dull, de- pressed appearance and noticeable weakness. In some cases the abdomen droops. The appetite generally remains good in the chronic cases but may fail in acute cases. The comb, w^attles and skin are pale as a result of the diminution of the red blood cells and increase of the white cells. Blood when drawn presents a pale red color and fails to clot readily, while normal fowl blood clots very rapidly. Morbid anatomy. The carcass has an anemic appearance. Us- ually the liver and spleen show the most marked changes. The kid- neys are at times also severely involved. The liver may be slightly enlarged, congested and sprinkled with minute whitish points, or it may be markedly enlarged and congested. iSTot infrequently rupture of the liver resulting in internal hemorrhage is observed. The en- larged liver may appear much darkened, soft and pulpy in more acute cases. In cases of longer duration, this organ is gTcatly en- larged and pale in appearance or else mottled and sprinkled with grayish white spots. It has a firm consistency and rigid contour. On cut section the tissue appears bloodless. The spleen generally shows changes in conformity with those of the liver. It may be only slightly congested or may be gTeatly enlarged and congested. As in the case of the liver, the consistency varies from soft and pulpy to a firm, compact mass. The color is bright mahogany in the case of severe congestion and sometimes grayish and brownish in spots. The kidneys may be several times the normal size, con- gested in the early stage or firm and pale at a later period. The intestine appears pale on the serous surface but areas of congestion 148 DISEASES OF DOMESTICATED BIRDS may be present on the mucous membrane, especially in the duo- denum. Microscopically, the blood is found to contain a greatly increased proportion of leucocytes to red blood cells. The normal number of leucocytes per cubic millimeter is approximately 30,000. This is increased in leukemia to from 100,000 to 500,000 per cubic milli- meter, while the normal number of red blood corpuscles, approxi- mately 3,000,000 per cubic millimeter is reduced to nearly 1,000,000 per cubic millimeter. The normal proportion of about 1 white cell to 100 red cells is thus changed to 1 to 2 or 1 to 3. The mononu- clear leucocytes increase more rapidly than the polynuclear leuco- cytes, or the smaller lymphocytes. Round nucleated red blood cells representing normoblasts and megaloblasts are to be seen in stained preparations. The hemoglobin content decreases from a normal of 50-65° to 15-20°. The blood is pale red in color and clots with difficulty. The liver, spleen and kidneys are found engorged with leucocytes. These fill the smaller capillaries and occupy a peri- vascular position in the parenchyma. There is a hyperplasia of the cells of the bone marrow and spleen, the latter being an important source of the leucocytes which infiltrate the liver and kidneys. De- generative changes are observed in the affected organs. Diagnosis. The presence of the disease is indicated by the an- emic condition of the fowl, the enlarged liver and spleen, and the absence of a demonstrable microorganism in these tissues. This lat- ter feature distinguishes it from bacterial septicemias in which the liver and spleen may be swollen and congested. Microscopical ex- amination of the blood is of the gTcatest value in differentiating from other affections. In simple leucocytosis accompanying infectious diseases, the proportion of white to red blood cells while at times ap- proaching 1—25 is not as striking as in infectious leukemia. Also the absence of myelocytes is noted in the former disease. In leu- kemia the white cells in the blood have approximately the following percentage relation : Mononuclear 70 per cent, small lymphocytes 20 per cent and eosinophiles 6 per cent. The diagnosis of pseudo leukemia during life presents great difficulties. Treatment. As in the case of other deep seated diseases of a maligiiant type, treatment of individuals is unfortunately of question- able value. There is no definite method of treatment known which alters the course of the disease so as to bring about recovery. Potas- sium iodide in doses of 3 to 7 grams daily, and careful nursing to- gether with the administration of tonics, such as gentian, nux vomica LEUKEMIA AND PSEUDO LEUKEMIA 149 and iron, may be of benefit in mild forms of the disease. Arsenic might also prove beneficial. Prevention. In sporadic cases of leukemia, no special precau- tions against the spread of the disease can be recommended other than the usual precaution of isolating or destroying the sick bird. Where several cases develop in the course of a few days, all birds showing the slightest abnormal appearance should be immediately separated from the flock. The droppings, litter, etc., should be re- moved and the quarters thoroughly disinfected. The drinking water may be medicated with permanganate of potash up to a 1-1000 so- lution. Pseudo leukemia. Ellerman and Bang regard this affection as being indicated by the same lesions as the true leukemia. The en- largement of the spleen and of the liver is often very noticeable. The blood is not leukemic. They consider it very probable that this disease has the same cause as true leukemia for cases of pseudo leukemia are encountered in outbreaks of the true disease. Inocu- lation of a hen with organs from a case of pseudo leukemia caused alteration of organs, typical of leukemia, with a blood picture sug~ gesting the beginning stage of leukemia. REFERENCES 1. Pickens. Leukemia and pseudo leukemia. Rept. N. Y. State Vet. Co/. 1915-1916, p. 226. 2. Ellerman u Bang. Experimentelle leukamie bei Huhnern. Ccn. train f. BaMeriol. (Etc.), 1 Alt. Orig., Bd. 46, 1908, S. 595. -3. Warthin. Leukemia of the common fowl. J. Inf. Dis., Vol. 4, 1907, p. 309. CHAPTEE XV GENERAL DISEASES GOUT Characterization. Gout is a disease characterized by the in- crease of uric acid content of the blood and the deposition of uric acid salts in the joints as well as in various organs, especially on the serous membranes. The disease apj)arently does not occur in birds living free but is frequent in cage birds of zoological gardens and in all sorts of domestic birds. Among these, hens are affected most fre- quently, waterfowl less frequently, and pigeons least. Etiology. Gout appears to depend for its causation, upon the use of feeds rich in protein in the absence of which many breeders believe that it will not occur. Furthermore, a one sided diet, close confinement, lack of exercise and heredity appear to be predisposing factors. Two types of gout are recognized, a rare gouty arthritis and a more common visceral gout. Visceral gout. In visceral gout the serous membranes of the chest and abdominal cavities are covered with a layer of uric acid crystals of greater or less thickness. In the pericardium which is affected with gout with greatest frequency, there is often a deposition of a layer of uric acid salts 1 to 2 mm. in thickness. Articular gout. This type preponderates in the joints of the feet as well as in those of the wings. The joints are thickened and inflamed, while the joint capsule shows a doughy swelling. Knotty swellings varying in size up to that of a cherry, occur in the vicinity and break outwards, discharging white or grayish yellow masses which consist of uric acid salts. Hebrant and Antoine describe a case showing unusually marked articular lesions. The subject from which the legs were taken was a cock two years old. The bird otherwise appeared in good health. The feed had been corn and wheat. The subject could not walk for it was unable to stand upon the feet. The lesions consist of a number of tumors, some of which are as large as a pea. They are particularly numerous on the inferior 150 GENERAL DISEASES 151 Fig. 16. Legs of cock showing lesions of articular gout. (Drawn from plioto- graph by Hebrant and Antoine) surface of the digital region in the vicinity of the articulations. Because of interference with circulation the tumors have a grayish yellow color. Some of the tumors fluctuate and their appearance is suggestive of peri-articular abscesses. On incision the tumors are found to contain a whitish, creamy, pasty mass consisting of crystals of uric acid. The majority of the tumors are located in the peri- articular connective tissue and a small number communicate with the articulation. Gout produced experimentally. In order to determine what influence is exerted by protein on nutrition and the occurrence of gout, Kionka fed hens exclusively on horse meat that had been minced, and freed completely from fat. They were allowed to drink water as desired and soon became accustomed to the compulsory diet. Within a period varying from three to fifteen months they all became affected with gout appearing in three forms. In every case at first the gait became uncertain and difiicult and the affected birds fell often while walking. In the first type of 152 DISEASES OF DOMESTICATED BIRDS the disease the pain seemed to appear suddenly and on account of it the bird crouched and stopped eating. This coincided with the appearance of isolated gouty nodules. Gradually the periods of pain became more frequent, the appetite was entirely lost and death followed. The deposits of uric acid crystals in the joints were not especially marked. In the second form the attacks of pain did not appear in so typical a manner, but the nodules were larger and oc- curred j3rincipally on the joint capsules and tendon sheaths of the wings. The third type was visceral and the deposits were limited principally to the serous membranes and the kidneys. The experi- ment proves the dietetic origin of gout. Diagnosis. The symptoms of the joint inflammation are dis- tinct: occasional loss of appetite, swelling of the joints, disinclina- tion to move. At other intervals, the appetite is good and the swell- ings decrease. At last there is no eating, inability to move, ema- ciation, rapid loss of strength and death. Visceral gout cannot be recognized in the living bird. Treatment. Operative treatment is of little use but may be re- sorted to in valuable birds. The joint tubercles should be opened to evacuate the contents and an antiseptic dressing applied. As soon as the cause of death is revealed by autopsy an appropriate diet should be provided for the other birds kept under similar conditions. The feeding of a rich proteid diet should be restricted, with a fast of one day a week. Grain feed, abundant gTcen feed or roots should be provided. RACHITIS Characterization. The disease consists of disturbance of normal bone formation of which the most prominent evidence is the deficient deposition of calcium salts. While the course of the disease is not well understood, it seems clear that it is caused by a general inter- ference with nutrition. Deficiency of intake of lime is concerned. Rachitis is a disease of young birds and seldom occurs in birds over half a year old. It is limited almost exclusively to fowls and occurs seldom in the turkey, waterfowl and pigeons. Symptoms. The birds show exhaustion, difficulty in locomo- tion, inappetence, diarrhea, paleness of the mucosae and emacia- tion. Morbid anatomy. Autopsy reveals intestinal catarrh and lesions of the bones. The large bones of the extremities are bent as GENEKAL DISEASES 153 is also the breast bone which becomes S shaped. The present writers conducted an autopsy on a young turkey in which the skeleton was apparently wholly lacking in mineral constituents. The larger bones could be bent with the fingers and sliced with a knife. The bird was reported as being one of a number affected in a similar manner. Treatment. ]S[ormal feeding should be the first matter con- sidered. Birds should be supplied with dry, warm quarters, with access to grass if possible. Feed coarsely cracked grain, cracklings, or meat meal and burned oyster shells. Calcium phosphate may be administered in doses of .5 to 2.0 grams per bird, according to size. Small amounts of sulphate of iron may be given by putting this ma- terial in the drinking water in the proportion of one or two parts per 1000 parts of water. 'No treatment should be attempted on those birds liable to become cripples. Such should be killed. LEG WEAKNESS Leg weakness is a term designating unsteadiness of gait, which may be followed by total inability to stand on the legs. At first the bird otherwise appears healthy, but soon shows the effect of in- ability to compete with its fellows for food. If the condition con- stitutes paralysis, " limbemeck " may also be observed. Leg w^eakness also is observed in rachitis. It occurs in well fed young growing birds under conditions not well understood. Under such circumstances the ration should be reduced and green feed should be supplied. At other times it occurs in closely confined birds kept on a monotonous diet. In such cases trouble disappears when birds have access to the soil with consequent variety of diet. Polyneuritis of fowls, a condition induced by feeding polished rice or similar products, is the one form of leg weakness, the etiology of which is understood. The affection may be produced experi- mentally in from fifteen to twenty-five days by feeding a diet limited exclusively to polished rice, while a diet of natural unpolished rice does not produce this result. The condition of the fowl designated polyneuritis is generally regarded as identical with the disease of man called beri beri, which latter is common among people living almost exclusively on polished rice. It is evident that the rice hull contains substances, the absence of which induces neuritis. These have been designated vitamines. Vitamines of this character are not restricted to rice. It has 154 DISEASES OF DOMESTICATED BIRDS been demonstrated that they are found in a large number of natural foodstuffs. They are very common in the seeds of plants such as cereals. In these, the vitamines are mainly deposited in the germ or embryo and to a less extent in the bran. "White wheat flour is deficient in vitamines and is capable of producing polyneuritis. The facts observed during experimentation on fowls in connection with the study of the etiology of beri beri of man, suggest the possi- bility that in isolated instances, leg weakness of chickens may be induced by a similar cause. LIMBERNECK Limberneck is a symptom resulting from partial or complete loss of control of the muscles of the neck. Probably various causes such as digestive disturbances, intestinal parasites and the eating of spoiled meat may cause this symptom. Feeding on maggots from decaying meat will cause limberneck. According to Dickson, chickens when fed botulinus toxin, become dull and inactive, refuse to eat, remain quiet in one place with the feathers ruffled. They gradually develop weakness of the legs, wings and neck so that they are unable to stand. The wings droop and the beak or the side of the head rests upon the floor of the cage. Death occurs within 24 hours after feeding. Treatment consists of administering castor oil. Preventive meas- ures should include precautions against allowing birds access to de- caying meat. DISEASES OF THE ALIMENTARY TRACT PIP The condition commonly termed " pip " does not represent a spe- cific disease, but is usually found associated with avian diphtheria. When the nasal passages become closed by the presence of mucous secretion or exudate, the fowl is compelled to breathe through the mouth. The constant passage of air over the tongue tends to dry and harden it at the tip. The dry, horny covering contracts and presses upon the soft tissues beneath, causing the fowl much annoy- ance. The hardened layer may partially separate from the soft tissues and expose a raw, inflamed surface. The practice among some poultrymen of removing the horny tip should be discouraged since it only increases the discomfort of the fowl by leaving a raw, sensitive surface exposed to foreign irritants and microorganisms. GENEKAL DISEASES 155 To alleviate this condition tlie primary cause should be removed. An effort should be made to keep the nostrils open by removing exu- dates and syringing the parts with an antiseptic solution such as 3 per cent boracic acid or 2 per cent permanganate of potash. If the disease which is responsible for ^' pip " is successfully treated the condition will disappear. When the symptom is noticed it is advisable to rub the tongue with some substance such as vaseline, cottonseed oil or glycerine. THKUSH Thrush or soor has been observed to affect the mouth and crop of fowls, pigeons and turkeys. The affection is characterized by the for- ^^^ /jl mation of grayish white or yellowish ^ ^nX^ Jy. // colored patches adhering to the mu- "^^^^ ?• °.^^^^^^c. ecus membrane without inflammatory ^^^^^^^^^^^^ changes in the latter. Severe involve- <^^^^^^ l^ ^yM\i, ment causes death. The organism '^^^^^^B^»^- iW^^^' causing the infection is designated Old- ' M^^M^^^^^^^i^l^'?/] iutn ( Saccliaromyces) albicans. Treat- ^^^^^^^f^lu^M ment of oral lesions may consist of the '^^If'^^^^^^II''^'// application of bichloride of mercury in // ' '^'^^^q ^ /^ a solution of 1 :1000. The crop may ^^^ ^^ q^^^^^^ albicans, a, cyl- be irrigated with boric acid solution as indrical mycelium; b, spore; c, in catarrh of the crop. Authoritative ^^^ ^^ '^ reports of the occurrence of the disease in fowls are rare. CATAKRH OF THE CROP This is a mild inflammation of the lining membrane of the crop due to excessive irritation by ingestion of material of an irritating nature, or by the products of fermentation when food for one reason or another, stays in the crop for an unusual length of time. It occurs in cases of impaction and may also be associated with certain infectious diseases. Parasites at times may cause the condition. Symptoms. The crop is usually distended with food or gas. The fowl appears sluggish and the appetite is diminished or lost. Occasionally the beak is opened wide as if to catch the breath or as if attempting to voinit. The head and neck also describe tossing movements. Later a gray, sour, ill-smelling fluid is discharged from 156 DISEASES OF DOMESTICATED BIKDS the beak or from the nostrils. Without treatment the strength of the subject fails rapidly. When the disease has existed for some time in a chronic mild form it may assume the condition designated hanging crop. In such cases the musculature of the crop has been overstretched, so that after recovery from the catarrh, the organ does not return to its normal position. Treatment. This consists of the removal of the contents of the crop as soon as symptoms are noticed. If the contents are soft the fowl may be held head downward and the crop manipulated in such a manner that the material will be passed back through the esophagus to the mouth. This is relatively easy owing to the large diameter of the esophagus of fowls. Should the crop contents be hard or dry they may be softened by giving the bird several teaspoonfuls of water before attempting to remove the material. When the crop is empty, administer 1 teaspoonful of castor oil. Feed should be withheld for about 24: hours, but buttermilk, or sour milk may be freely given together with water. A small amount of bicarbonate of soda may be administered and the bird should have access to charcoal in case fermentation is noticeable. Fowls showing frequent attacks or chronic catarrh of the crop should not be retained. IMPACTION OF THE CROP Feeding with dry grains such as corn, peas, oats, or with bran may cause a distention of the crop. Various foreign bodies may cause the same condition. The enlargement of the organ will first attract attention. If not remedied, the condition will cause death of fowls in a few days, and in waterfowl in a few hours, because of pressure on the trachea. Massage may permit the removal of ma- terial through the beak, but usually incision of the crop is indicated. INFLAMMATION OF THE CROP IN PIGEONS The crop of the pigeon secretes a milk-like fluid for the nourish- ment of the young. If the parent birds lose their young while the crop is secreting this fluid, an inflammation of the crop glands frequently results and the organ feels hard and solid. The disease may be quickly remedied by substituting another squab. Only one should be substituted for often pigeons will not adopt two young ones, but kill them and throw them out of the nest. Besides, if two GENEEAL DISEASES 157 were taken, the parents thus robbed of their young, would develop the same trouble. If such a procedure is not possible, the sick ones should be isolated without food. They may be allowed water slightly acidulated with vinegar. If abscess-like lesions occur on the breast they should be opened. GASTRITIS Gastritis is an inflammation of the mucous membrane of the pro- ventriculus or first stomach. It may result from digestive disturb- ances but is generally associated with the presence of strong irritants such as certain mineral poisons, or with infectious diseases of a septicemic type. Inflammation of the crop may extend to the pro- ventriculus. In itself, it is not of gTcat importance. Symptoms. The diagnosis of gastritis is difficult. If no symp- toms of disease are noticed other than a loss, of appetite and a slug- gish appearance, simple gastritis may be suspected. When associated with other diseases the s^nnptoms which accompany these will be observed. Treatment. The affected fowl should be given 2 teaspoonfuls of castor oil to which 10 drops of oil of turpentine have been added. Feed lightly for a time. Buttermilk or sour milk may be freely given. Give 30 drops of tincture of gentian twice daily. INDIGESTION Megnin distinguishes four sorts of indigestion in birds. It may result from lack of quality or appropriate volume of food or by ingestion of foreign bodies. Thus pigeons which naturally are granivorous will suffer if circumstances necessitate theiv consum- ing herbage. Birds in zoological gardens are liable to suffer from lack of appropriate food. Storks, herons, swans, geese and ducks in the winter and spring failing to obtain their natural food such as molluscs, slugs, etc., attempt to cheat the appetite with plants or aquatic mosses. These materials are to them true foreign bodies which cause fatal indigestion. It is the same in the case of the small insectivorous or semi-insectivorous birds. T\lien it is at- tempted to feed them exclusively on grains or vegetable mashes they succumb to the diet. Grains too large for the digestive organs of a bird act like a for- eign body and cause fatal indigestion. Parroquets and young pheas- ants may be killed in this way by grains of maize. 158 DISEASES OF DOMESTICATED BIEDS Overloading the digestive organs is a second general cause of indi- gestion. Dry grain whicli is inviting to certain birds like the gallinacese is less suitable to others such as palmipeds which are ac- customed to soaking their food in water. Thus such birds may readily overload their stomachs with dry grain which may swell and cause death. Indigestion may be caused by lack of silicious gravel in the giz- zard. This material is indispensable to granivorous birds to tritu- rate the grain in that organ. Omnivorous birds likewise need grit. In the absence of such material, trituration is not accomplished and grain accumulates in the gizzard. Thus death may be caused by indigestion occasioned by repletion, or whole grains may pass into the intestine and cause a fatal inflammation. This may occur among a large number of birds. The present writers have observed severe enteritis in a wild goose occasioned by heavy snowfall and prolonged freezing of a pond, which circumstances prevented access to grit. In the absence of grit of suitable size, birds will attempt to swallow articles entirely too large, with fatal results. There is in the opinion of Megnin, an indigestion resulting from lack of food, or disease of hunger. Domesticated birds may acci- dentally be deprived of food or may be prevented from eating by stronger companions. Indigestion in birds is rarely recognized during life and is only encountered at autopsy. That caused by overloading may be recog- nized and treated with a little olive oil. Prevention along the line of providing suitable food and grit must be relied upon chiefly. INDIGESTION IN PAKKOTS The affection may result from a variety of causes such as improper feeding and failure to provide grit which impairs the natural function of the gizzard. The affected bird yawns, displays loss of appetite and occasionally manifests nervous symptoms. Correction of feeding is of first importance. Castor oil in a dose of from 5 to 10 minims may be administered. Bicarbonate of soda in 5 grain doses may be given in the drinking water for several days, l^ux vomica is indicated. ENTERITIS Enteritis is an inflammation of the mucous membrane of the in- testine. It is perhaps the most common symptom observed in con- nection with poultry diseases. GENERAL DISEASES 159 Etiology. Enteritis is associated with a large number of impor- tant diseases. It varies in the intensity of the inflammation with different affections. In fowl cholera, fowl plagiie and several other septicemias the inflammation is very severe, while in fowl typhoid and infectious leukemia the mucous membrane may show little or no congestion. Enteritis is associated with such protozoal diseases as coccidiosis and infectious entero-hepatitis, and with intestinal worm infestation. Mineral poisons may set up an inflammatory condition, as may also moldy or putrid food. In birds deprived of grit, the food passes from the gizzard with- out being triturated and causes severe enteritis with hemorrhage into the lumen of the intestine. Symptoms. The most prominent symptom of enteritis is diar- rhea. The droppings may be watery or semi-solid. The color varies according to the particular disease which is present. It may be white, brownish, gTeenish, yellowish or mixed in color. The fowl displays a loss of appetite in the more severe forms of enteritis, be- comes droopy, weak and somnolent. Paralysis of the legs frequently occurs in connection with inflammations of the intestine. Unusual thirst is often in evidence. Treatment. As enteritis is usually associated with some more important disease, the disease should be properly diagnosed and treated. Simple enteritis due to minor causes may be treated by re- moving the irritating substances from the intestinal tract by means of a purgative such as castor oil in 2 teaspoonful doses or Epsom salts in Ys to ^2 teaspoonful doses, A tonic consisting of powdered gentian 1 dram, powdered ginger 1 dram and powdered sulphate of iron 15 grains may be given. Mix /4 teaspoonful in the feed twice daily. The water for the entire flock may be made antiseptic by the addition of % oz. of carbolic acid to the gallon of water. This will tend to prevent the spread of infection to others of the flock in the event that the affected bird or birds are harboring an infectious disease. The carbolic acid treatment may be discontinued after a few days in the event that no more fowls are attacked. SIMPLE DIARRHEA Fowls are sometimes affected by a diarrhea which is not appar- ently associated with one of the more important diseases. A watery or semi-fluid discharge may result from an irritation or derangement 160 DISEASES OF DOMESTICATED BIRDS of the intestine independent of the action of infectious organisms. Among the causes which may produce a catarrhal condition of the intestinal mucous membrane and result in simple diarrhea are diges- tive disturbances of an obscure nature, sudden changes in the feed or an unusually large supply of green feed, too much meat scrap, especially irritating substances in the feed, moldy grains or decom- posed flesh. Mineral or other irritants which are not taken in suf- ficient quantity to cause poisoning or enteritis may produce a simple diarrhea. Fermentation of the contents of the intestine may result in diarrhea. Treatment. The cause of simple diarrhea being direct intestinal irritation, the obvious remedy is to remove the cause. Where only a few birds are affected they should be given 2 teaspoonfuls of castor oil each. The entire flock may be given Epsom salts if necessary, in the proportion of Vs to Y2. teaspoonful to each grown fowl. The salts may be dissolved in water and mixed in a mash to be fed early in the morning. If suspicion points to the feed as the cause of diar- rhea it should be changed or fed in smaller amounts combined with other feeds. CONSTIPATION This is apparently not a common ailment of fowls. It does, how- ever, occur to some extent in fowls confined in small quarters for long periods with insufficient exercise. Lack of green or succulent feed also tends toward constipation. Following diarrhea there may be a temporary or slight constipation. The condition in young chicks suffering from white diarrhea known as " pasting up behind " can- not be considered a true constipation since the droppings are merely held back by the drying of the discharges in the do^vn surrounding the vent. Fowls allowed free range, or large runs and properly fed are practically free of constipation. Treatment. The condition may be relieved by administering substances which will cause an increased secretion of fluid from the intestinal mucosa, or increased peristalsis. Two teaspoonfuls of castor oil or Ys to Y teaspoonful of Epsom salts to each affected bird would be indicated. Gage and Opperman have determined the dosage of Epsom salts for birds of various ages as follows : GENERAL DISEASES 161 Age Dose 1 to 5 weeks 10 grains 5 to 10 weeks 15 grains 10 to 15 weeks 20 grains 15 weeks to 6 months 30 grains 1 year and over 40 to 45 grains To facilitate figuring quickly the number of ounces required for treating a number of birds they furnish the following information concerning equivalent weights: 1 pound avoirdupois equals 7000 grains. 1 ounce avoirdupois equals 437.5 grains. 1 pound Troy or apothecary equals 5,760 grains. 1 ounce Troy or apothecary equals 480 grains. The constipation may be due to obstruction by foreign bodies, to worms in the intestines, or to matting of feathers over the cloaca. In the latter condition, softening of the mass and removal of the obstruc- tion is first in order. After removal of the material in the cloaca, rectal injections of soapy water or olive oil may be made. In very small birds a probe wet with glycerine or castor oil may be in- serted in the rectum. DISTENTION OF THE BURSA OF FABRICUS Occasionally the bursa of Fabricus may become enormously dis- tended into a cyst-like structure containing a clear, colorless fluid. Schantyr has observed two cases in which the fluid amounted to over 700 c.c. He observes that when an exploratory puncture is made in case of distention of the abdomen with fluid, a yellowish fluid in- dicates ascites, while a colorless fluid indicates hydrops of the bursa of Fabricus. DISORDERS OF THE LIVER Disorders of the liver such as enlargement, fatty degeneration, jaundice and the occurrence of various sorts of diseased areas in the organ cannot be classified as separate entities. In most cases, livei' lesions merely consist of a portion of the lesions characteristic of the common infectious diseases. Various septicemias, tuber- culosis, ontero-hepatitis, leukemia and tumors may display more or loss characteristic lesions in the liver. Perhaps under some condi- tions hypertrophy or enlargement of the organ may be due to heavy 162 DISEASES OF DOMESTICATED BIEDS feeding undej in the winter. feeding under close confinement as occurs among fowls fed on com DISEASES OF THE RESPIRATORY TRACT BRONCHITIS Fowls are quite frequently affected by a catarrhal inflammation of the mucous membrane lining the air passages of the throat and lungs. This condition usually results from the extension of inflammation from the mouth and nasal chambers. Often birds which have recov- ered from avian diphtheria are observed to be affected with bron- chitis. This may persist for a short time or become chronic. Symptoms. In severe cases the fowl displays a marked difficulty in breathing. The neck is more or less straightened out to facilitate the passage of air. The breathing is noisy and the fowl may gasp in a manner similar to that shown by a chicken affected with gapes. The beak may be kept open, and a mucous discharge is given off through the mouth. The bird is observed to make efforts to dislodge this discharge by shaking the head. In less severe or chronic bronchitis the symptoms are not so notice- able. There may be only slight difficulty in breathing, accompanied by a wheezing sound. The mucous membrane of the bronchi and trachea becomes thickened and may show patches of yellowish exu- date especially in the two large bronchi. Treatment. Since bronchitis is often attributed to exposure to cold draughts and dampness these conditions should be corrected. Affected birds should be placed in warm quarters, free from air cur- rents. Under good hygienic surroundings the attack may pass off in a short time. In acute cases the administration of 5 drops of wine of ipecac is beneficial. In chronic bronchitis treatment is not satisfactory. CONGESTION OF THE LUNGS The lungs may become congested as a result of the extension of an inflammation from the larger bronchi into the minute air tubes and air sacs. The congestion is generally of an acute type. It may be induced by the fowl becoming wet and severely chilled. In the early stages of pneumonia congestion of the lungs is the most marked symptom. Symptoms. Simple congestion is differentiated from pneumonia on post mortem examination by the bright red appearance of the GENEEAL DISEASES 163 lungs in the former and by the fact that pneumonic lungs are hepa- tized and will sink when placed in water. Affected birds show a distressed appearance and breathe with difficulty. The respirations are short and panting. The discharge and wheezing observed in bronchitis are absent. The normal temperature of 107° to 108° F. is raised 2 or 3 degrees. The birds have an increased thirst. Evi- dence of pain is produced by pressure on the ribs over the lung area. Wher-e both lungs are affected death may follow shortly after the onset through pressure on the air cells resulting in a shutting off of the air supply and suffocation. In less severe cases the congestion may subside or the condition may develop into pneumonia. Treatment. The bird should be placed in warm quarters and given a diet consisting largely of green food. One third to one half teaspoonful of Epsom salts dissolved in water should be administered once a day for two or three days. Also give 10 drops of spirits of nitre twice daily. PNEUMONIA Characterization. Pneumonia of fowls is of relatively rare oc- currence in the classic form distinctive of this disease in other ani- mals. The disease is sporadic in character and frequently only one bird in a large flock may be infected. Etiology. Pure pneumonia cases which have come under the observation of Gallagher have been due to the presence of the pneumococcus. It has the characteristic diplococous form on micro- scopic examination and is similar in its cultural characteristics to the pneumococcus of Frankel. Its infrequent sporadic invasion sug- gests that the fowl is normally resistant, and that predisposing causes of an obscure nature are responsible for its pathogenicity in certain individuals. Symptoms. The most characteristic symptoms are more rapid breathing with physical signs of distress and general malaise. There may be a mucous discharge from the nostrils, and the tempera- ture is elevated. As the disease progresses, the comb assumes a darker color at the tips, or rear, or in hanging combs at the more dependent portions. This darkened appearance progresses with the disease and practically the entire comb may assume a purplish color due to lack of oxygen in the circulating blood and weakened heart action. In fatal attacks, the strength fails rapidly and the bird reaches a comatose condition in which it may linger for several hours before death. 164 DISEASES OF DOMESTICATED BIRDS Morbid anatomy. In the normal fowl, on post-mortem examina- tion, the lungs are found deflated, fairly compact and closely applied to the ribs. They occupy less volume relatively, than is the case in other animals. This is, no doubt, due to the peculiar respiratory system of birds which has, in addition to the lungs, a number of air sacs in the pleural and abdominal cavities, and also air canals in the larger bones. In a pneumonic condition the lungs are distended, darkened and solidified to a greater or less degree, approaching the condition known as red hepatization or liver consistency. They will sink in water, while normal or simply congested lungs will float. The pneumonic lung stands out in a firm position surrounding the heart and may be found adhering to the pericardial sac. There are usually no visible areas of necrosis, but the bronchioles and larger air tubes are filled with an emphysematous mucous discharge. Treatment. Owing to the fact that pneumonia is induced by the presence of organisms in the lung tissues, and that these cannot be reached by disinfectants which would not destroy the sensitive mem- branes of the air cells, treatment has been found futile in most cases. During the early stages, or in milder cases, stimulants such as strych- nine in doses of %o to Vso gr., or 50 per cent alcohol in quantities of H dram may be given by way of the mouth. Because of the dense breast muscles, local external applications are not indicated. The patient should be placed in quarters where the temperature ap- proximates 70° F. and soft mashes, or sweet or buttermilk given as a food. Since the disease is sporadic in a flock, no special prevent- ive measures are necessary to guard against its spread. DISEASES OF THE OVIDUCT INFLAMMATION OF THE OVIDUCT The oviduct may be highly congested or inflamed as a result of the condition known as " egg bound," prolapse, or the presence of ac- cumulated egg material which has been arrested by a tumor forma- tion in the wall of the oviduct. Organisms which gain access to the oviduct find a favorable medium for development in such ma- terial. They give rise to decomposition products which irritate the mucosa of the organ and set up an inflammatory condition. Broken eggs in the oviduct or excessive effort in laying may lead to inflam- mation. The oviduct may become affected through the spread of inflammation from the ovary or other adjacent organ or it may be involved with other organs in certain generalized diseases. GENEKAL DISEASES 165 Symptoms. Where the inflammation is confined to the oviduct no general change in the appearance may be apparent except in severe cases. A tendency of the fowl to make efforts to lay at fre- quent intervals is often noticed. Eggs w^hich are abnormal either in their structure or form may be passed. These may be blood stained. Most frequently the eggs are small and contain only al- bumin. Shell-less eggs are also laid. In fatal cases the fowl ex- hibits symptoms of general debility, with loss of appetite, pale comb and leg paralysis. Treatment. When symptoms are apparent an effort should be made to locate the cause of the trouble. Manipulation with the finger through the cloaca or over the abdominal wall may disclose the presence of an obstructed egg, broken egg or egg concretion which may be removed after the manner described for the treatment of " egg bound." The fowl should be isolated, given green food, soft mashes and /4 teaspoonful of Epsom salts. RUPTURE OF THE OVIDUCT In severe inflammation of the oviduct when a large mass of egg concretion is present, or an attempt to pass an egg of large size is made, the wall of the oviduct may be split allowing the mass or egg to pass into the peritoneal cavity. Other eggs or egg material may follow through the opening and accumulate in the cavity. These later induce peritonitis, or the rupture may heal and the ovi- duct continue its normal activities. The condition would be suspected by the sudden suspension of laying accompanied in many cases by a rapid increase in the size of the abdomen. Manipulation would disclose the presence of abdomi- nal egg concretions or accumulated eggs. Rupture of the oviduct is of comparatively rare occurrence. Treatment if advisable would be by surgical means. EGG BOUND This condition is of frequent occurrence in fowls, especially in young pullets. It represents an inability on the part of the bird to pass the egg in the normal manner from the oviduct, or cloaca. This failure may be due to an inflammatory condition, stricture, or tumor formation in the posterior portion of the oviduct, or cloaca, or to prolapse of the oviduct. In pullets which are beginning to lay, however, the usual cause is the undeveloped state of the egg 166 DISEASES OF DOMESTICATED BIRDS passage which has not jet become sufficiently dilated to accommodate eggs of large size. Mature hens may become egg bound through at- tempts to pass malformed, or double yolked eggs. It is generally noted that the first eggs of the pullet are elongated and of smaller diameter than those delivered after laying has become well estab- lished. Also the first eggs frequently show streaks of blood indicating the difiieult passage through the last portion of the oviduct or through the vent. Cross breeding which unites a breed of large egg type with one of a smaller egg; type would be conducive to the formation of a large egg for which the egg passage might not be developed in proportion. Symptoms. The affected hen is observed to be restless, leaving the others and going frequently to the nest to make attempts to lay. The effort after a time results in an inflamed condition of the oviduct and cloaca. The condition often results in an eversion or prolapse of these organs. The distress of the fowl and the extruded, inflamed parts may attract other fowls. These begin to pick at the mem- branes and if the victim is not rescued in time a large portion of the intestine may be torn away and dragged through the vent causing the death of the bird. Where prolapse has not occurred the affected fowl may continue to make an effort to lay the egg until successful or overcome by weakness. Diagnosis. The presence of an egg in the oviduct may be de- termined by palpation of the posterior abdomen or exploration through the vent. Treatment. Several methods of treatment are practiced. The fowl may be held vent downward over steaming water for a time and then placed upon the nest. The steam has a tendency to relax the parts and make easier the voiding of the egg. Lubricating the vent and cloaca with sweet or linseed oil may also aid the fowl in mild cases of egg bound. However, the quickest and surest method is the removal of the egg by the following procedure. The hen is held by an assistant with her back downward, while the operator passes the forefinger through the vent and pushes aside the mem- branes until the egg shell is felt. With the fingers of the other hand pressing on the external wall of the abdomen the egg is forced toward the vent, being guided along the inflamed membranes of the egg passage by the inserted finger. When the shell is visible through the vent it is punctured by means of a sharp pointed instrument such as a knife or awl. It is broken into small pieces with a pair of forceps or with the finger and is removed with its contents. The GENEEAL DISEASES 167 patient should be isolated and the inflammation reduced by fre- quent injections of cold or ice water into the cloaca. Fowls which have sutiered from egg bound due to the presence of a large egg or to tardy development of the egg passage are not perma- nently alfected. Egg bound due to pathologic alterations in the oviduct is not open to practical treatment. PROLAPSE OF THE OVIDUCT Eversion of the oviduct is usually associated with difficulty in lay- ing as in the condition known as '' egg bound." The mucosa of the extruded cloaca and oviduct becomes highly congested. The pro- lapsed organs are observed as a dark red or purplish mass projecting through the vent. The affected fowl is soon noticed by the others of the flock and if it is not rescued in time it will be attacked and de- stroyed as a result of the pi-otruding tissue being torn away and devoured. As soon as the bird is discovered it should be placed by itself and carefully treated. The oviduct should be explored with the finger, which should be greased or oiled, to locate an egg or other cause. If an egg is present it may be removed as described for " egg bound." The prolapsed tissue is carefully returned through the vent, after which cold water is injected to reduce the congestion and promote the contraction of the oviduct wall. This may be continued for some time or repeated at frequent intervals until a cure has been effected. VENT GLEET Characterization. Vent gleet or cloacitis is an inflammatory disease of the vent and cloaca of fowls. It appears to be spread en- tirely by coitus and may be considered an infectious venereal disease. Its causative agent has not been determined. Symptoms. In the early stages of the disease there is a conges- tion of the membrane of the posterior portion of the cloaca and mar- gin of the vent. This may extend to the lower portion of the oviduct and rectum. The fowl exhibits signs of severe irritation, frequently voiding small droppings. A watery discharge which later becomes purulent and foul smelling is passed out through the vent. The skin around the vent becomes swollen and reddened and an offensive odor is usually present. The irritation causes the fowl to peck at the part. Other fowls may be attracted by the discharge, and the red- dened appearance of the affected region and may peck at the skin 168 DISEASES OF DOMESTICATED BIKDS causing an ulceration of the surface. Frequently the diseased fowl dies as a result of the tearing of the cloaca and rectum by its canni- balistic mates. The presence of the disease in a flock causes a marked falling off in the egg yield and a decrease in the fertility of the eggs. Treatment. Vent gleet is very resistant to treatment. It is usually better to destroy the diseased bird than to attempt treatment. This is especially so in the case of the first birds attacked as by this means its spread may be prevented. Where treatment is desired the affected birds should be isolated. The discharge may be removed from the skin and feathers by washing with warm water. Anti- septics such as 5 per cent carbolic acid, or 1-1000 corrosive sublimate are to be applied to the external affected area, or a 2 per cent car- bolic ointment may be rubbed over the part. Argyrol in 15 per cent solution or cresol in 2 per cent solution may be injected into the cloaca twice daily. Roosters should be removed from the flock Mdiile the disease is present and if any are found diseased it would be advisable to destroy them. STRUCTURE OF THE FECUNDATED EGG OF THE FOWL The ovum or yolk on its release from the ovary and entrance to the oviduct appears as a yellowish ellipsoid body about one inch in diame- Fio. 18. 1, air sac; 2, shell; 3, white yolk; 4, blastoderm; 5, yellow yolk; 6, dense albumin; 7, chalaziferous layer of albumin; 8, fluid albumin; 9, chalaza; 10, shell membrane. (Original) ter. It is somewhat flattened on one surface, which presents an opaque whitish circular spot, the germinal disc (Fig. 18). Cell GENEKAL DISEASES 169 multiplication is already taking place in this disc, from whicli the embryo develops. The yolk is composed of a central light colored portion (Fig. 18) and an outer mass colored a deeper yellow. The latter is formed of concentric layers showing different stages of yolk deposit (Fig. 18). The germinal disc and yolk are surrounded by a thin strong vitelline membrane (Fig. 18). The ovarian ovum on entering the oviduct is passed along by peristaltic movement in a rotary course to its completion in the uterus or shell secreting por- tion. In the anterior portion of the oviduct the membrane chal- azifera is applied over the vitelline membrane. It consists of a dense layer of albumin and gives rise to the two chalazse which ex- tend from each pole of the ovum. These strands become twisted in opposite direction during the further passage of the ovum through the oviduct. Over the chalaziferous membrane are several albumi- nous layers secreted by the glands of the oviduct. When the ovum enters the isthmus or narrow portion two egg membranes are secreted. These become separated at the large end of the egg as air is absorbed. The shell is acquired in the uterus. FOREIGN BODIES IN EGGS Eggs may contain a variety of foreign bodies such as pebbles, frag- ments of plants, feathers, roundworms, etc. Such bodies after gain- ing access to the cloaca penetrate the oviduct far enough to encounter an egg and thus be included within the shell. Otherwise normal eggs have been found to contain such parasites as the fluke Prosthogonimus ovatus and the roundworm Ascaridia perspi^cillum. The latter worm may be present surrounded by al- bumin in an abnormal egg lacking a yolk. It is apparent that under such circumstances the presence of the worm has stimulated the secre- tion of the albumin. Tapeworms and segments of the same have been found in eggs. The parasites found in eggs evidently have migi-ated into the oviduct for a sufficient distance to meet a developing egg and to become enclosed in shell. Parasites of microscopic size such as coccidia, amebse, aspergillus fungi and bacteria have been demon- strated in eggs. BLOOD SPOTS IN EGGS. (lIVER SPOTs) It frequently happens that streaks of blood, or clots of varying size are found in eggs. This abnormality is especially noticed during the heavy laying period. At such time the ovary is plentifully supplied 170 DISEASES OF DOMESTICATED BIRDS with blood to promote the rapid formation of ova. As an ovarian follicle ruptures to release an ovum some blood may escape from a congested blood vessel of the follicle. The blood passes into the oviduct along with the ovum where it becomes surrounded by al- bumin and is incorporated in the egg. The size of the spot or clot depends upon the amount of blood which has escaped. These clots are often taken for pieces of flesh and are commonly referred to as liver or meat spots. The wholesomeness of such an egg is not im- paired. There is no practicable means known for preventing the occurrence of blood spots in eggs. However by candling the entire product of a flock, it is possible to prevent such eggs from going on the market. DISCOLORED YOLKS N^ewly laid eggs in some instances exhibit a darkened appearance of the yolk which is not due to developmental changes in the ovum or to decomposition as a result of bacterial action. The entire yolk may appear dark in color or the discoloration may be confined to spots or streaks on the surface or in the depths of the yolk material. In testing for freshness by candling or on opening the egg, such a discoloration may be mistaken for an evidence of addling. The con- dition results apparently from the action of sulphur, normally pres- ent in the yolk, on small globules of cottonseed oil which are absorbed into the yolk. This occurs when the fowls are being fed cottonseed meal or material containing cottonseed oil. This oil may be present in table scraps since it is often an ingredient of butter, oleomar- garin or cooking oils. Cattle or hog fats or their products may contain cotton seed oil where the animals have been fed cotton seed meal shortly before slaughter. Yolk is composed of albumin 17.50 per cent, oil and salts 28.75 per cent, and water 53.75 per cent. The yolk granules are ar- ranged in thin concentric layers as they are received through the surrounding vitelline membrane from the blood vessels in the ovarian capsule or follicle. This arrangement would explain the disposi- tion of the discoloration, depending on whether the fowl was re- ceiving cottonseed oil constantly or only at intervals. The color reaction between sulphur and cottonseed oil is utilized in the Halphen test for the presence of the latter as an adulterant in certain food products. In a positive test a pink color is produced but this is changed in the yolk to a brownish or dark yellowish color. It is not improbable that discolored yolks may result also from the GENEKAL DISEASES 171 action of the contained sulphur on certain metallic salts which the fowl may ingest and which through metabolism may be incorporated into a yolk. There is no apparent reason why eggs so affected should be un- wholesome. They may be detected by candling. DOUBLE YOLKED EGGS The inclusion of two yolks within one shell is due to rapid ovulation or delay of one yolk in its progress to the isthmus or egg membrane-secreting part of the oviduct, thus allowing the following yolk to reach it and be surrounded by a common membrane. When the two yolks do not meet until arrival at the isthmus, each is sur- rounded by a separate layer of albumin. When two yolks are ovu- lated within a short interval or meet in the anterior portion of the oviduct they may have a common layer of albumin and common membranes. SOFT SHELLED EGGS When the egg reaches the uterine portion of the oviduct under normal conditions the double membrane secreted by the isthmus is covered by a felty fibrous layer into which is deposited the ma- terial which forms the calcareous shell. Absence of the hard shell may be due to several causes. If the bird does not have feed con- taining lime salts in sufficient quantity, or access to substances rich in these salts it is apparent that a normal shell cannot be produced. Providing the fowls with crushed oyster shells or mortar will remedy this defect. Irritation of the oviduct as a result of inflammation may cause an abortion of the egg before it is properly formed. Sudden fright may also lead to a premature laying of the egg before it has acquired its hard shell. Excessive attention by the male is said to cause the laying of soft-shelled eggs. Where this is con- sidered as the cause the removal of the cock is indicated. Except when eggs are desired for incubation the presence of a male bird in the flock is not necessary since fowls lay equally well or better in his absence. Unfertilized eggs keep better than fertilized ones, a fact which causes many poultry men to place cock birds in the flock during the breeding season ©nly. 172 DISEASES OF DOMESTICATED BIEDS DISEASES OF THE PERITONEAL CAVITY ABDOMINAL YOLK CONCKETIONS The presence of masses of yolk material lying free in the peri- toneal cavity of hens is frequently observed on post-mortem ex- amination. The cause of this condition is not always apparent. Injuries to the membrane of the fallopian tube, or tumor forma- tions in the oviduct which interfere with the entrance of the yolk or its passage through the oviduct are usually responsible. Yolks or partly formed eggs may be returned through the oviduct and aborted into the peritoneal cavity by reverse peristalsis induced by inflammatory changes in the wall of the oviduct. At times the contents of only one yolk or ovum may be present while in other cases the concentric layers of yolk substance indicate that the process has been going on for a considerable period of time. In the latter instance the mass may be as large as a tennis or base ball and of firm consistency. The layers are easily separated when newly formed or before organization or decomposition changes have pro- gressed. Some accumulations reveal a center of albumin, or par- tially formed shell membrane, while others exhibit a yolk formation throughout. Occasionally a normal yolk is found surrounded by a small amount of albumin and inclosed in a soft or partially cal- cified membrane. In this case there is evidence that the ovum has passed into the oviduct and owing to an abnormal state of this organ, reverse peristalsis has caused its return through the fallo- pian membrane into the abdominal cavity. Quite frequently as many as five to seven perfectly formed yolks in a good state of preservation are found between the intestinal convolutions. These apparently represent a recent discharge from the ovary in contrast to the solidified yolk substance constituting the typical yolk con- cretion. Symptoms. The presence of yolk deposits is not disclosed by external appearances where putrefactive changes are absent. The tendency is for the material to become partially absorbed. The un- absorbed portion is formed into a rounded body which increases in size according to the number of ova aborted into the cavity. In the event that organisms find their way into the peritoneal cavity, pre- sumably by way of the oviduct, a favorable culture medium is at hand and decomposition changes may be inaugurated which lead to a septic condition and result in peritonitis, or septicemia. GENEEAL DISEASES 173 Treatment. The removal of the yolk masses is easily accom- plished by an incision through the abdominal wall once the nature of the affection has been determined by digital exploration. As a rule the presence of aborted egg material is not suspected during the life of the fowl and treatment is therefore not practiced. It is also apparent that treatment to be effective would require the correction of the factors which lead to the misplacement of the ova. The ob- scure nature of these renders attempts at their control impractical. DROOPING ABDOMEN In the heavy breeds, especially, the abdomen may show a tend- ency to assume a pendant position, frequently coming into contact with the ground when the bird is in a standing position. The skin of the abdomen may be devoid of feathers, and usually shows a reddened appearance. This is often due to a marked accumulation of fat in the abdominal wall and visceral organs. More often it results from a displacement of the gizzard. This organ, owing to an elongation of the proventriculus or true stomach, is carried back- ward and instead of resting in its normal position on the posterior floor of the sternum, takes up a position on the much less resistant membranous wall of the abdomen. As a result of its weight and muscular activity in a cavity already overfilled with distended in- testines and accumulated fat it forces the inferior abdominal wall into a drooping or dragging position. The abnormal position of the gizzard may be detected by palpation of the parts immediately behind the sternum where the outline of the dense muscular organ can easily be followed. Treatment consists of the restriction of fat forming foods in the diet. It is inadvisable to use birds showing this condition for breeding purposes, since the evident tendency to lack of tone and resistance in the parts concerned would be perpetuated to a greater or less extent in the progeny. ASCITES (dEOPSY) Characterization. This condition consists of an accumulation of fluid in the peritoneal cavity or abdomen. Etiology. 'No one specific causative agent is responsible. The accumulation of fluid results from a filtration of blood serum through the serous membranes of the intestine, or the peritoneal covering of the abdominal cavity or paryenchymatous organs. It 174 DISEASES OF DOMESTICATED BIRDS may be present in severe, or chronic cases of enteritis, sarcomatosis, tuberculosis, peritonitis or other debilitating diseases affecting the abdominal organs. Symptoms. Except in a marked dropsical condition, no external manifestations of ascites are readily noticeable. On palpation of the abdominal region the presence of fluid may be detected. Its presence has no great diagnostic importance since it is merely as- sociated with a more serious affection which may be difficult of ac- curate determination during the life of the bird and which in the large percentage of cases is not open to practical treatment. Differential diagnosis. Ascites is often confused with an ex- cessive formation of fat in the abdominal wall or with a drooping abdomen. Palpation of the abdomen and the absence of emaciation or other signs of disease would eliminate ascites. When the latter is present a distinct fluctuation of liquid is felt, much the same as in the palpation of a water bag. Treatment. When detected, the fluid may be evacuated by punc- ture of the abdominal wall with a hypodermic needle. Except in cases of septic ascites this method of procedure would be of little permanent value since the fluid would be readily absorbed in the event that the primary cause of its presence were corrected. PEEITONITIS Characterization. Peritonitis occurs frequently in domesticated birds. It is manifested by an inflammatory condition of the serous coverings of the visceral organs accompanied by a serous, or coagu- lated exudate in the peritoneal cavity. Etiology. Various causes may be responsible for this affection. There are numerous specific diseases of a septicemic nature in which the involvement of the peritoneum is of secondary consideration. Besides these the most important direct causes of peritonitis are infected yolk concretions or deposits, ovarian infections, extension of inflammation of the oviduct, or rectum, as a result of rupture, perforation of the digestive tract by foreign bodies or as a result of ulcerative changes in the intestinal wall such as sometimes occur in coccidiosis of fowls, or entero-hepatitis of turkeys. Symptoms. These are nonspecific since the general attitude of an affected bird is similar to that displayed in several other in- fectious diseases. Diagnosis is difficult except through post-mortem examination. The disease is usually of an acute nature, death GENERAL DISEASES 175 resulting- sliortly after the appearance of symptoms. The affected fowl shows loss of appetite, ruffled feathers, elevation of temperature, weakness and extreme dc])ressi(m. Diarrhea is frequently observed especially when the intestinal serosa is extensively involved. In cases of peritonitis due to rupture of the rectum, the droppings are scanty owing to the passage of a portion of the intestinal contents into the peritoneal cavity. The presence of yolk concretions, or fluid in the abdominal cavity may assist in a diagnosis. In either case the abdomen may show a pendant position. On palpation, the fluctuation of liquid may be felt, while the presence of concretions is determined by their dense consistency, free disposition and rounded contour. Morbid anatomy. The pathologic picture in peritonitis in birds is not usually marked by extensive congestion of the serous lining of the abdominal cavity and visceral organs. There may be localized areas of congestion, or hemorrhagic spots on the visceral peritoneum, especially that covering the ovary. In the majority of cases no macroscopic evidence of congestion is apparent. The disease is more often marked by exudates either of a serous, or semi-solid form. Evidently the morbid condition results principally from the absorp- tion of toxins generated by the action of microorganisms on foreign matter which has gained entrance to the cavity. The serous exudate is at times clear and straw colored, at other times cloudy and putrid. The septic condition is generally associated with a cheesy exudate which covers the viscera in small masses and is non-adherent to the membrane. Yolk concretions, or individual aborted yolks, display putrefactive changes. Where rupture of the oviduct or intestine has occurred, egg material or intestinal contents respectively will be found and the rupture may be easily located. Treatment. The difficulty in diagnosing peritonitis during the life of the bird and the advanced stage reached when symptoms be- come apparent renders attempts at treatment impractical. Should a physical examination reveal the presence of yolk masses free in the abdominal cavity, or a dropsical condition of the abdomen, surgical methods could be employed to remove the accumulations. The cavity could then be washed with sterile water or a mild antiseptic to remove septic exudates. VICIOUS HABITS Toe pecking. The conditions surrounding incubator chicks kept together in large numbers in brooders, are very different from those 176 DISEASES OF DOMESTICATED BIRDS afforded a brood of chicks under the care of a hen. One of the most troublesome results is the habit of pecking toes. Anything unusual about the foot of a chick attracts the attention of another member of the flock which pecks at the foot. The attention of others is drawn to the action and they repeat the pecking. As soon as blood is drawn, the deep seated instinct of chickens to attack the injured or the weakling, is aroused and the victim is soon killed or seriously maimed. The habit is likewise manifested by pecking at the vent. In this way a chicken is disembowled in a surprisingly short length of time. Once the taste for blood is aroused, the chicks attack one another indiscriminately and cause heavy losses. The immediate remedy is to remove instantly all wounded birds, which must be kept in isolation until entirely recovered. General precautionary measures will include those designed to keep the chicks occupied with harmless pursuits. Various kinds of food hung so as to be somewhat inaccessible, furnish diversion. Dried meat has been so employed. Egg eating. The habit of eating eggs is often established by the accidental breaking of an egg. The practice spreads rapidly by imitation. Careful observation will reveal yolk stains on the beaks of offenders, who should be isolated or killed. ISTests well supplied with straw will minimize the possibility of the accidental breaking of eggs, and darkened nests will prevent a broken egg from being seen. Craving for lime in the egg shells may be forestalled by supplying an abundance of oyster shells and bone. Feather eating and feather pulling. These habits constitute very troublesome vices not only among fowls but also in cage birds. A bird may pull out its own feathers or those of its companions. The sensation of having the feathers plucked apparently is not dis- agreeable, for a bird will stand quietly while another pulls out its feathers. Finally the birds taste blood on the emerging feather and as a result, never allow a feather to develop. The vice is often observed in cage birds such as parrots, among hens that are closely confined, and occasionally among hens lacking certain elements in the feed. Parasites of the skin are important causes of the itching leading to feather pulling. In some instances the eruption of nor- mal feathers during molting, occasions an itching sensation and starts the habit. Perhaps the most common cause is a monotonous diet of a restricted number of elements. Hens at large in warm weather can satisfy individual food requirements from among the GENEKAL DISEASES 177 various materials available, siicli as grass, insects and mineral sub- stances. Klee finds it very useful to supply blood in a cooked form, mixed with bran and curd. Under these conditions the birds do not acquire a taste for blood. Burned shells and green feed are also desirable elements in the ration. Green feed is best surrounded by a wire netting in such a way that the birds are compelled to reach through the meshes to obtain the feed. In winter time cooked beets or sprouted oats may be used. Breaking up the habit in parrots often causes difficulty. Daily sprinkling with water and providing variety of feed are useful. Klee also has observed many cases benefited by smearing the feathers with sepia, or unsweetened chocolate and by keeping the bird in the dark. It is possible to fit a broad aluminum collar on the neck of a parrot in such a way as to prevent the bird from reaching the feathers. According to Klee, lack of feathers is observed in pigeons from time to time without being due to feather pulling. In some in- stances the pin feathers are present in the skin but do not break through. Persistence of the feather sheath also occurs in pigeons, in which case the feathers develop while rolled up in a horny cover- ing. Under normal conditions this sheath is shed early in the de- velopment of the feather. Sometimes if the bird is kept until the molting period the new feathers will develop normally. In chickens and in any growing birds, interference with nutrition such as intestinal catarrh will cause retardation of the feather de- velopment in the molting period. Molting exerts such a drain upon the strength of birds that only a well nourished bird is able to molt normally. As a result, birds are more inclined to become diseased during molting than afterwards. REFERENCES 1. Dickson. Botulism. A cause of liinberneck in chickens. /. Am. Vet Med. Ass., Vol. 3, 1917, p. 612. 2. Hebrant et Antoine. A propos de la goutte ou diathese urique. Ann. de Med. Vet., T. 58, 1909, p. 321. 3. Klee. Die hauptsachlichsten Geflugel-Krankheiten. Leipsig. 1905. CHAPTER XVI INTERNAL PARASITES PAKASITES OF THE ESOPHAGUS, CROP, PKOVEXTEICULUS AND GIZZARD FOWLS Dispharagus nasutus, a filarial worm 7 to 9 mm. long, is one of the most important parasites occurring in the portion of the ali- mentary tract of fowls anterior to the gizzard. The worms are found in great numbers in the mucosa of the proventriculus and of the gizzard. The aftected birds become emaciated and depressed without losing appetite. The mucosa of the gizzard has been ob- served to be bristling with the parasites, some in the mucosa and others attached to the mucosa by one end and floating free in the lumen. The proventriculus when infested may be increased to double the usual size, becoming spherical in form. The mucosa is greatly thickened in places where the parasites are most numerous. Cases have been observed in which the worms were so numerous as Fig. 10. Spiroptera pectinifera. Male. Caudal extremity. X l"-"^- Neumann) to give the glands a villous appearance. Colucci obtained good re- sults by the administration of capsules of .5 gram of oil of turpentine morning and evening. D. liamuloms has been reported from fowls in Brazil as occurring in little fleshy excrescences on the surface of the gizzard. D. laticeps has been found in the fowl and certain rapacious birds. Physa- loptera truncata has been observed in the gizzard of a fowl in Brazil. Spiroptera pectinifera is a hair worm which infests the gizzard of 178 INTERNAL PARASITES 179 fowls. Individuals vary from 4 to 9.5 mm. in Icng-th and are 2 mm. broad. The worms are attached to the mucosa of the gizzard by their anterior extremities. The mucosa is covered by a brownish deposit 2 to 3 mm. thick, consisting of a mixture of blood and debris of the parasites. The affected mucosa shows irregiilar depressions which are granulated, reddened and hemorrhagic. The affected birds show anemia, progTessive cachexia and good appetite to the last. One to three months may elapse between appearance of symptoms and death, depending upon the age and vigor of the subject. This parasite has been reported as causing heavy mortality among chickens in France. Its presence in the gaiinea-fowl has been re- ported. Eansom has described a nematode worm Gonglyonema ingluvicola parasitic in the crop of fowls. The presence of the females may be detected by noting the occurrence of small coiled ridges on the sur- face of the mucosa, discernible with the naked eye. The males are only discovered by the use of a hand lens. Specimens may be ob- tained for detailed study by teasing the tissue. The females vary from 32 to 45 mm. in length, while the males are from 17 to 19 mm. long. The infestation does not so far as known, result in serious disturbance of health. The same parasite has been recognized in Europe by Oiurea. Trichosoma annulatum is a worm 15 to 80 mm. in length which has been reported as occurring under the epithelium of the mucosa cf the esophagus of the fowl. Another member of this genus, T. no- dularis causes serious trouble in waterfowl, Displiaragus spiralis, a worm 7 to 9 mm. long has been reported in the same location as well as in the gizzard. Prosthogonimus pellu- cidus, a trematode, has been found in the esophagus of fowls. PHEASANTS Trichosoma. sfnimosum, causes serious loss among young pheasants. It lives in the large folds of the epithelium of the esophagus and sometimes penetrates the mucosa. It forms passages in which the female de- _,t|^^^^^^^^^^^^^^^^ posits eggs. This destruction of epi- W'T''''^u''^^X^ ^^^^^^ ^^^^ ^i thelium occurs in the esophagus, buccal ^""^^ • , J J.1 i 1 T"! J • Fio. 20. Trichosoma stnimosuni. cavity and the trachea. The disease p,,^^,, interior extremity. causes great weakness at the beginning, ( Reibisch ) followed by rapid emaciation. Death 180 DISEASES OF DOMESTICATED BIRDS occurs four to six days after the appearance of the first symptoms. Treatment consists of administering a 2.5 per cent solution of car- bolic acid in the drinking water or in the mash. WATERFOWL Strongylus nodularis has been reported as occurring in water- fowls, most frequently in the mucosa of the gizzard. The female worms vary in length from 12 to 22 mm. while the males vary from 10 to 16 mm. The parasites are about 5 mm. in diameter, and are threadlike in form. They are more narrow at the ends, especially at the head end. Freese reports a loss of 200 out of 700 geese, due to the parasite. Symptoms. Single individuals occur very frequently in healthy geese without causing symptoms or noteworthy lesions. Extensive invasion of young geese is attended with serious results. At the beginning of sickness the young geese appear weak, sit most of the time and move with reluctance. They make characteristic choking movements and soon show more or less diarrhea. The birds have a very good appetite and consume their feed ravenously. In spite of the large amount of food consumed, the birds gradually become ema- ciated almost to skeletons. Finally they fall from weakness and are unable to rise again. In this stage the birds stop eating and die in a day or so. The whole course of sickness occupies three to eight days. The younger the geese, the more they are affected. The young, as a rule, die. Morbid anatomy. The carcass is excessively emaciated and only traces of the breast muscles remain. The mucosa of the small in- testine, especially near the gizzard, is reddened, thickened and cov- ered with a large amount of viscid mucus. The principal lesions are found in the gizzard. Except where the epithelium normally forms horny plates, it is covered with a thick, bark-like mass, dark brown or dark brownish red in color. The consistency of the mass is more or less tough and in some places, is more like mucus. In and under this material are innumerable parasites in coils. Kot infrequently the worms are attached to the bark-like mass by their heads, with the other ends free in the lumen. Sometimes a mucous layer, with worms, is located in the lower third of the esophagus. Occasionally a few worms may be found on the mucosa of the small intestine. The statement of some authors that the parasites occur under the mucosa is incorrect, for they occur only under the epithelium and less com- monly directly in the epithelium. INTERNAL PARASITES 181 Displiaragiis uiicinatus has been reported as occurring in the esoph- agus and proventriculus of geese, ducks and swans. They occupy cyst-like structures which are most frequently encountered in the wall of the proventriculus. When these are opened the worms are found surrounded by a bloody fluid or a yellowish caseous mass. The wall of the proventriculus is thickened and the mucosa is covered by a large amount of yellowish green viscid mucus. A stage of the life cycle of the parasite is passed in a certain aquatic form, Dapluiia juJex. The embryos, free in the stomach of the bird, gain access to the water where they are taken in by the DapJinia, which creature is in turn eaten by the waterfowl. Prophylaxis must depend chiefly upon killing of infected birds, and upon keeping birds away from stagnant water, colored brownish or yellowish by the presence of Daplima in large numbers. Sclerostomum anseris infests the gullet, proventriculus and gizzard of geese. It burrows under the mucous membrane and causes the formation of dark brown crust- like layers on the epithelium. In young ducks it causes gradual emaciation and debility. The location of the parasites discourages the use of antihelminthics. Hystricliis tricolor is a worm which infests the proventriculus of ducks, and causes extensive destruction of tissue. Very large ulcers are formed wdiich al- most perforate the walls of the organ. Cysts about the size of a bean, containing the parasite, are also found. A similar parasite Hystrichis elegans also occurs in the proventriculus of ducks and of a large number of palmipeds. H. ciffini occurs in similar location in the swan. Tropisurus fissipinus form cysts in the sub- mucous region of the esophagus of ducks, some- times causing a fatal inflammation. Trichosoma coniortum occurs in ducks and geese besides other birds. They infest the dilated portion of the giillet, which in ducks Fig. 21. Dispharagus uncinatus. Dorsal view of anterior ex- tremity. Enlarged 60 times. (Schneider) Fig. 22. Hystrichis tricolor Cephalic ex- tremity, (v. Ratz) 182 DISEASES OF DOMESTICATED BIRDS and geese, performs the func- tions of a crop. The pres- ence of the parasites causes a distention of the gullet and a condition quite similar to dis- tention of the crop in fowls. The infested birds display ar- rested development, emacia- tion, difficult locomotion, epi- leptic movements, somnolence and lack of appetite. Death is frequently due to asphyxia resulting from over disten- tion of the gullet. At autopsy it is observed that the galleries formed by the worms appear as whitish curved lines which stand out prominent relief against m the congested mucosa. Mi- croscopic examination of the tissue will reveal the presence in the galleries of the worms and their eggs. Positive diagnosis is diffi- cult during life unless micro- scopic examination is made of the feces or of water with which the crop has been rinsed. Fig. 23. Trichosoma contortum. A, caudal extremity of female; B, eggs from the uterus in various stages; C, caudal ex- tremity of the male. Enlarged 300 diam- eters. (Railliet) Treatment may consist of administering two tablespoonfuls of a mixture of turpentine with twice its volume of olive oil. Filaria cygni has been observed in the intestine and ceca of a swan which was exceedingly emaciated. TAPEWORMS General character. Tapeworms, also designated cestodes, con- stitute important parasites of the intestines of birds. When present in large numbers they occasion a disease designated tseniasis. The individual worm is composed of a head called the scolex and a INTERNAL PARASITES 183 variable segments designated Fig. 24. Segment of Davainea echino- bothrida showing the reproductive or- gans. Enlarged. (Ransom) number of proglottides. The scolex is armed with a series of hooks by which it becomes at- tached to the intestinal mucosa of the host. Each proglottid or segment of the worm is virtually an individual and is bisexual. The segments are not provided with an alimentary canal, but absorb nourishment directly from the intestinal contents of the host. As the terminal segments in turn mature, they are separated from the worm and are discharged in the droppings. Species of cestodes. A large number of species of tapeworms have been reported as occurring in the intestines of domesticated and wild birds. Kansom has examined nine species in American chickens and turkeys as follows : In chickens, Hymenolepis carioca, Choanotaenia infundihulum, Davainea tetragona, D. echinoboihrida, D. proglottina, Amoehotaenia sphenoides; in chickens and turkeys, D. cesticillus, Hymenolepis cantaniana; in turkeys, Metroliasthes lucida. He notes that the tapeworms of American ducks, geese, and pigeons have not yet been investigated. Neumann lists four more species as having been found in fowls. These are Cotugnia diagono- pora. Taenia fasciolaris, T. exilis and Bothriotaenia longicollis. Tapeworms found in the various birds are listed by Neumann as follows : Turkey: Choanotaenia infundihulum, Metroliasthes lucida, Davainea cantaniana, D. cesticillus, D. friedbergeri, Hymenolepis carioca, H. musculosa, H. meleagris. Not named. Pheasant: Choanotaenia infundihulum, Davainea echinohoth- rida, D. cantaniana, D. friedhergeri, Hymenolepis phasianina. Pigeon : Choanotaenia infundihulum, Davainea echinohothrida, D. crasmla, Bertiella delafondi. Duck : Hymenolepis anatina, H. gracilis, H. sinuosa, H. coronula, H. parvula, H. megalops, H. lanceolata, Choanotaenia infmidibulum, Davainea crassula, Flmhriaria fasciolaris. Goose : Hymenolepis lanceolata, H. setigera, H. gracilis, H. fasciata, H. sinuosa, H. teriuirostris, Fimhriaria fasciolaris. Neumann considers tapeworms as occurring infrequently in pig- eons and rarely present in sufficient number to cause trouble. In ducks they exert feeble pathogenic action. Hymenolepis setigera and 184 DISEASES OF DOMESTICATED BIEDS H. lanceolata, singly or together cause injury among geese in Europe. Davainea friedhergeri causes great losses among pheasants. Life history. From time to time the tapeworm in the intestine of the chicken discharges ripe segments filled with eggs, which are voided in the feces. To maintain the life cycle it is necessary tliat the tapeworm eggs be taken with the food into some creature known as a secondary host. In this host the embryos escape from the eggs and migrate to some organ where they form a cyst-like structure known as a cysticercoid. The life cycle is completed in case the intermediate host is eaten by a chicken in which event the cysticercoid develops into the adult form. Comparatively little is known about the secondary hosts of tape- worms of poultry. Of the five species of tapeworms that have been reported in chickens in the United States, tlie intermediate host of but one has been discovered. It has been determined that the inter- mediate host of Choanotcenia infundihulum is the common house fly, Musca domestica. The intermediate hosts of a number of tapeworms of birds re- ported as occurring in other countries have been discovered. Thus a slug is necessary for the life cycle of Davainea 'proglottina,. a chicken tapeworm. The intermediate hosts of certain tapeworms of the duck have been found to be various species of fresh water crustaceans. In general, the intermediate host is to be sought among the various insects and other forms of animal life to which the infested birds have access such as snails, insects, crustaceans or worms. Symptoms. These vary to some extent in different birds ac- cording to age and the degree of infestation. A few worms are not harmful to the bird and can hardly be noticed. Young birds are af- fected more seriously than old ones. In moderate infestation the bird is always hungry and experiences excessive thirst. Restless- ness is marked and doubtless accounts fur the lean condition of the bird. Heavily infested birds show such symptoms as drooping wings, emaciation, rutHed feathers and isolate themselves from the flock. The condition of the feces is more or loss altered in tapeworm in- festation. Heavy infestation causes inliammation of the intestine and diarrhea with mucous droppings. The secretion is at first clear, transparent, semi-liquid and slighily \>..,;su in coLr, Later the mucus becomes brownish yellow in col r xiio to hemorrhage caused "loy the worms, and this coloration cons itiues one of the most char- INTERNAL PARASITES 185 acteristic symptoms. When the bird is very heavily infested, gas bubbles are observed in the droppings, and remain visible for some time. Segments of tapeworms may be found in the feces by careful search, and microscopic examination may be utilized for detecting the presence of tapeworm eggs. Tapeworm infestation in geese has been reported in Germany as causing very marked nervous symptoms. The birds walk very lit- tle and assume an upright position like that of the penguin. Morbid anatomy. In excessive infestation the carcass is anemic and emaciated. On slitting the intestine, worms will be found in greater or less number throughout its whole ex- tent between the gizzard and the ceca. They are attached to the mucosa by their heads and may cause more or less inflanunation. The most serious patho- logical changes are caused b}'' infestation with Davav- Fic. 25. Gravid segment of Davainea echino- bothrida. Enlarged. (Ransom) 7iea echinohothrida which results in the formation of nodules in the intestine. This condition has been described by Moore under the name of nodular tsenia- sis. The nodules are most numerous in the lower third of the small intestine. Exceptionally they occur in the duode- num and colon. In severe infestation the presence of nodules causes numerous protuberances from the serosa, varying in size from those barely perceptible, to elevations 4 mm. high. The color varies from pale or dark yellowish in the larger ones, to the normal gray of the serosa shown by the smallest ones. Similar elevations are observed on the mucosa of the intestine. Small tapeworms occur attached to the mucosa over the nodules. Over some of the nodules there are areas in which the mucosa has sloughed, leaving ulcers. The contents of the larger nodules consist of greenish yellow, ne- crotic material which on section has a glistening, homogeneous ap- FiG. 26. Head of Davainea echinohothrida. Enlarged. (Ransom) 186 DISEASES OF DOMESTICATED BIRDS pearance. Surrounding this, there is a thin layer of infiltrated tis- sue. The smaller nodules contain a substance more resembling pus, and in these the microscopic study of sections most readily reveals the presence of tapeworm heads. The penetration of the intestinal wall by the heads induces infiltration and eventually results in the forma- tion of nodules. Diagnosis. The chief points to be relied upon in diagnosis are emaciation, excessive appetite and thirst together with the character- istic yellowish-brown color of the droppings. The detection of tape- worm segments in the feces is best done by immersing the suspected white mass in water. If it consists of urates alone, it will be dissi- pated in fine granules, while the worm segments will be recognized as firm masses. Some of the general symptoms of unthriftiness are also indicative of nematode infestation, but in this case the birds often pass blood. Ultimate decision will rest upon the information Fig. 27. Hymenolcpis lanceolata. Natural size, in a medium state of extension. (Railliet) yielded by an autopsy. The intestine should be opened while im- mersed in warm water, to facilitate recognition of the worms. They will be found attached to the mucosa, and vary in size from micro- scopic objects to worms four or five inches long. Treatment. Turpentine is held in high repute as a tseniafuge and has the additional advantage of expelling round worms also. The fowls are fasted for twenty-four hours during which time they should receive a dose of Epsom salts. One teaspoonful of salts is allowed for each bird, the whole being dissolved in warm water and mixed with mash. Greater accuracy of dosage will be assured if the dose is administered directly to each bird. The most convenient sys- tem of carrying out the vermifuge treatment is to withhold food in the morning and give the salts in the evening. The following morn- ing the turpentine should be given in a dose of from one to two teaspoonfuls per fowl. Owing to the offensive qvialities of turpen- tine it is not possible to give it in food, but it must be administered to each bird individually. The most expeditious method is to inject the dose directly into the crop with a hypodermic syringe. A slower INTERNAL PARASITES 187 method is to introduce the dose into the crop by means of an oiled rubber tube inserted through the oral cavity and esophagus. The turpentine, diluted with an equal amount of olive oil may be ad- ministered by the mouth. If the mixture is given slowly with a spoon or medicine dropper the bird will swallow it naturally and will cause very little trouble. Three or four hours after giving the tur- pentine, the birds should receive another laxative dose of salts ad- ministered in a mash as before. Owing to the habit of burying their heads in the intestinal wall, tapeworms are very resistant to treatment. Consequently it is ad- visable to repeat the vermifuge treatment in about three weeks. Gutberlet reports favorably upon the use of lye for expelling tape- worms. A tablespoonful of concentrated lye was added to one gal- lon of a mixture of wheat and oats which was cooked slowly for two hours. Fifteen birds, after fasting for about fifteen hours, were allowed to eat the mixture. A second dose is given twelve hours after the first one. A number of other substances are employed to e^^pel tapeworms, but some fail on account of having lost their active properties. Areca nut in doses of 30 to 45 grains may be administered to fowls in the form of a pill, but turkeys do not tol- erate this remedy well. Powdered pomegranate root bark may be fed to fowls in a dose of one teaspoonful to each 50 birds. It may be followed by a purgative dose of 2 or 3 teaspoonfuls of castor oil per bird. Male fern in a dose varying from 30 grains to 1 dram of the powder may be given morning and evening before feeding. Megnin recommends treating pheasants for tapeworm with kamala, mixed into a paste with hard boiled eggs and bread. Prophylaxis. An accurate knowledge of the secondary host for each species of tapeworm, might suggest very effective preventive measures but in the absence of much of this information, such measures must be of a general nature. It is desirable to collect the droppings and treat with lime. Lime or ashes may be scattered over the droppings under the roosts. General sanitary measures Fig. 28. Hymenolepis lanceolata. A, cephalic extremity, enlarged 100 times; B, egg enlarged 300 times. (Railliet) are of value, and particularly, the practice of moving birds to new 188 DISEASES OF DOMESTICATED BIKDS ground should be encouraged. The knowledge that the house fly is the intermediate host of a chicken tapeworm suggests the advisability of combating that insect. It breeds commonly in bird or horse ma- nure and any decaying vegetable matter. These breeding places should be eliminated as far as possible besides using fly traps. ROUND WORMS General nature. Eound worms or nematodes are common para- sites of the intestines and are capable of inflicting considerable damage. They are long, slender and thread-like in form. Mouth, alimentary canal and anus are present. The female worm is gener- ally larger than the male. Species of round worms. There are two principal species in fowls. Ascaridia (HeteraMs) perspicillum occurs in the small in- testine. The male is 3 to 8 cm. long, while the female is 6 to 12 cm. in length. The color of the body is yellowish white. They are often present in numbers sufficient to occlude the lumen of the intestine. The same species is found in the turkey and guinea-fowl. Heter- aMs papillosa, a much smaller worm with white body, is very com.- mon in the ceca. The male is from 7 to 13 mm. long while the fe- male varies from 10 to 15 mm. in length. This species is found also in the turkey, guinea-fowl, peafowl, and pheasant. Five other less important species, Heterakis lineata, H. brasiliensis, H. compar, H. cojyipressa and //. differens have been reported by J^eumann as occurring in fowls. This writer lists other nematodes of the intes- tine as follows : Pigeon : Heterakis columboe. Duck: Ascaris crassa, Heterakis dispar, H. vesicularis, H. lineata,. Strongylus tenuis. Goose: Heterakis dispar, H. vesicularis, Strongylus tenuis, Tri- chosoma anatis. Life history of Ascaridia perspicillum. Eggs are deposited by the worms within the intestine and are expelled in the feces. The length of time worm eggs will remain alive in the droppings is not fully determined, but there is evidence that they are viable up to a year. The life cycle of the worm is completed by eggs gaining access to a fowl through contaminated feed or water. Ordinarily, eggs do not hatch until they are taken into the alimentary canal of a fowl. The worms require three to four weeks to develop into sexually ma- ture forms. INTERNAL PARASITES 189 Symptoms of Ascaridia infestation. Affected birds appear un- thrifty and emaciated. Either diarrhea or constipation may occur. The affection is most severe in young birds. Treatment. Beach conducted experiments with a number of remedies to determine their vahie in causing the expulsion of the worms and came to the conclusion that tobacco stems are most ef- ficient. For one hundred fowls he takes one pound of finely chopped tobacco stems and steeps them for two hours in enough water to keep the mass covered. The liquid and the stems are mixed with half the amount of ground feed usually allowed the birds for one feed- ing. On the evening before the day of administering the remedy, the birds should be fed only half a ration and they should be kept without feed until afternoon of the following day. Then the mixture of tobacco and feed is given and under the circumstances is sometimes readily eaten. Occasionally, fowls refuse the mixture. Two hours later, the birds are given a quarter size ration of ground feed mixed with water containing eleven ounces of Epsom salts for each hundred birds. ISFo difference of dosage to correspond to birds of different ages is attempted, for the matter is adjusted by the amounts of the mixtures that the birds can eat. Reasonable care should be exercised to make certain that birds have equal opportunity to eat. The treat- ment is calculated to cost about ten cents per hundred fowls. The same procedure should be repeated in two weeks which has been found to be sufficient to free the birds entirely from parasites. Difficulty in administering the treatment is sometimes encountered because the birds will refuse to eat the mash containing the tobacco. Theobald recommends thymol as an agent against nematodes. The dose for the fowl is .06 gram given in the form of a pill. Two or three hours after giving the thymol, a teaspoonful of olive oil is administered. Megiiin recommends administering santonin in the food in a dose of 4 to 5 grams for every ten birds. Klee recommends 5 to 10 drops of anise oil in 1 to 2 teaspoonfuls of olive oil, also 4 to 6 drops of benzol with oil. Prophylaxis. Thorough disinfection of the yards and quarters is necessary in order to minimize the possibility of reinfection from worm eggs that have been deposited in the feces. Ilerms and Beach have determined that worm eggs are found only in the top two inches of the soil of infected yards. After sweeping the yard and removing rubbish the area was treated with a 1 : 1000 solution of bichloride of mercury. About one gallon of solution to each ten square feet of 190 DISEASES OF DOMESTICATED BIRDS soil was found necessary to secure penetration of the fluid to a depth of two inches. A trial of the effectiveness of the treatment in pre- venting the reinfection of birds that had been freed of worms yielded evidence of its value. Such birds increased in size rapidly and post mortem examination of the poorest specimens after three weeks yielded no evidence of worms. Other fowls on a control area, not disinfected, became seriously infested in a similar length of time. Bichloride treatment of roosting houses and other buildings to which birds have access, is indicated. Netting under the roosts is of value in keeping birds from contact with feces. Round worms in the pigeon. HeteraJcis coluniboe occurs in the intestines of pigeons in enormous numbers. As many as 400 to 500 worms have been observed in one individual. The infestation causes loss of appetite, periodic mucous diarrhea and emaciation which is particularly marked in the pectoral muscles. At autopsy the worms are observed packed closely to- gether. The mucosa is distended in patches which are engorged with blood and ulcerated. These areas are covered with thick mucus. Occasionally the parasites perforate the wall of the intestine and are found in various parts of the thoracic and ab- dominal cavities. Treatment advised by Ziirn con- sists of administering 6 centigrams of calomel in Fig. 29 Hetera- ^j^g form of pills with bread or with butter. More kis columbce. A, . ^ i • i male; B, female, serious cases may be treated with areca nut m 1 "'^^y.^^l. s i ^ ® • gTam doses, given in the same manner. Two hours after administering the pills, each bird is given a teaspoonful of castor oil. The affected birds may be given a weak decoction of garlic to which one-half per cent of sodium salicylate has been added. Strongylus quadriradiatus has been observed by Stevenson in the intestine of the pigeon. The presence of a few worms causes no harm, but large numbers cause harm attributed to injury of the wall of the intestine permitting subsequent invasion by bacteria. TKICHOSOME INFESTATION OF CHICKENS Several worms of the genus Trichosoma have been described as harmless inhabitants of the intestines of fowls. However, Freese has observed that Trichosoma retusum, is capable of causing great de- struction among chickens. The same parasite has been reported in the guinea-fowl. The worms vary from 13 to 19 mm. in length INTERNAL PARASITES 191 and from .06 to .07 mm. in breadth. Other species reported in the fowl are T. collar e, T. duhium, T. caudinflatum and T. gallinum. Symptoms. The chickens become less lively, allow the wings to droop and show diarrhea. The appetite is at first very good but later becomes poorer. There is increased thirst. The bird becomes more and more emaciated and finally can hardly move because of loss of strength. Without treatment the disease usually ends fatally. The duration of the disease varies from three to ten days according to the resistance of the victim. When old hens are affected, they show similar symptoms. At the beginning of sickness egg laying drops off and soon stops entirely. The disease in hens runs a course of 2 to 4 weeks. Morbid anatomy. The carcass is greatly emaciated and anemic. All organs with the exception of the intestinal canal, are free from lesions. The mucosa of the small intestine throughout its whole extent is covered with a grayish yellow exudate. The mu- cosa is thickened and reddened on the surface by short streaks and points. The contents of the ceca and rectum are thin and viscid. Innumerable trichosome worms are present on the mucosa of the small intestine throughout its whole extent, and a few also occur in the ceca. Diagnosis. The disease caused by the trichosomes can be recog- nized with certainty only by autopsy. On account of the hair-like fineness of the worms they can only be discovered after the closest scrutiny. The contents of the intestine are teased with a needle, or the needle is stroked over the mucosa. If the worms are present, it is likely that several will adhere to the needle. Another method is to remove a portion of the exudate from the mucosa and mix with water. The hair-like worms may be detected with the naked eye. In any event it is desirable that microscopic examination be made. Treatment. Freese recommends the administration of oil of anise in early stages of infestation. On each of two successive days each chicken is given a dose of 5 drops of etherial oil of anise in 1 teaspoonful of olive oil. Old hens require twice as much anise oil. Trichosomes in the pigeon. Trichosoma columbce is fre- quently found in the large intestine of the pigeon. It is capable of causing an intense intestinal catarrh. It may be present in colossal numbers in the intestine causing the mucosa to show tumefaction, in- filtration, petechiae and red streaks. 192 DISEASES OF DOMESTICATED BIRDS FLUKES General nature. Trematodes (flukes) are hermaphroditic worms possessing suckers by which they become attached to the mucosa of the intestine of the host. The intestinal tract ends blindly without an anus. In the temperate zone they are generally harmless and uncommon parasites. Species and hosts. ISTeumann states that Echinostomum echin- atum occurs in the fowl, duck, goose and swan ; E. conoideum in the fowl, duck and goose; E. recurvatum in the fowl and duck; Clino- stomum commutatum in the fowl, turkey and pigeon ; N otocotyle ver- lucosa in the fowl, duck and goose. Bunodera linearis has been re- ported in the fowl alone, Cyclocoelum mutabile in the turkey alone, while Holostomum gracile and H. splicer ocephalum occur in the duck alone. THOKN HEADED WORMS Three species of the genus Ecliinorhynchus occur in ducks but only one has been reported as causing injury. Echinorhynchus polymorphus is fusiform in shape and colored or- ange red. The anterior extremity of the worm is provided with an ovoid proboscis armed with eight rows of hooks. The male worm measures 4 to 6 mm. in length while the female varies from 15 to 25 mm. in length. The wonns usually are fixed firmly to the wall of the intestine. Before opening the intestine the serous surface of the same is seen to be covered with numerous nodules, the centers of which are orange colored. On opening the intestine the mucosa is found studded with worms of the sam-e color attached by their anterior ex- tremities. Their presence sets up a severe inflammation of the mu- cosa and causes the formation of the nodules on the serous surface. The condition described often causes diarrhea, emaciation and anemia. The same species occurs in the swan. E. filicollis and E. spwro- cephalus are found in the duck. FLAGELLATES Flagellated protozoan organisms constitute a small number of forms parasitic in the intestines of birds. These are nucleated bodies provided with one or more flagolla and sometimes possess an undulating membrane. Neumann lists the following species : Tri- chomonas eherthi has been observed in the glands of Liebcrkuhn of a duck and in a goose. It is little known and without pathogenic INTERNAL PARASITES 193 importance. T. columhce lias been reported as causing the forma- tion of caseous foci in the liver of the pigeon with fatal result. Moiias (Monocercomomis) anatis has been reported as occurring in the small intestine of the duck. Martin and Ivobertson have studied the flagellates of the ceca of fowls dividing them into the four species: Chilomastix gallinarum, Tricliomorias gallinarum, T. eherthi and I'richomastix gallinarum. Hadley observes that the intestinal fauna of any young turkey after it has been on the gTound for a few days will contain a variety of protozoan parasites. Among these, the most common are flagel- lates, certain sporozoa and amebas. At least three types of flagellates are usually present, Trichomonas, Chilomastix and Lamhlia. He considers that Trichomonas plays a pathogenic role in cecal and he- patic infection in birds comparable to intestinal and hepatic ame- biasis as observed in mammals. Hadley considers the flagellates de- scribed by him as identical with bodies described by Theobald Smith under the name Amoeba meleagridis and the cause of blackhead in turkeys. He regards Trichomonas as a facultative parasite in that under certain conditions it exists as a harmless, ever-present intes- tinal parasite. According to this view the Trichomonas under cer- tain unknown circumstances invades the tissues and causes disease. Trichomoniasis of chicks. Weinzirl has described a highly fa- tal disease of chicks attributed to a new species designated Tricho- monas pullorum. Symptoms. Chicks under a month old only are attacked. The disease most commonly appears about the tenth day after hatching. The affected birds droop, they huddle together, the wings drag, the eyes are closed and the skin of the head is pale. Acute cases suc- cumb in a day or two without showing diarrhea. Other cases be- come chronic, in which stage diarrhea is present. The temperature is subnormal and is usually about 102° F. The disease is not ob- served until late spring and summer. Morbid anatomy. Autopsy reveals no lesions except a gen- eral anemic condition. The ceca may be slightly enlarged and the contents thin and slimy. The parasites collect in the crypts of the mucosa frequently in pure culture. When diarrhea exists, the pro- tozoan may be found in the intestine and in the voided mucus. Etiology. The flagellate Trichomonas pullorum regarded by Weinzirl as the cause of the chick disease occurs in two forms. One, the pear shaped type moves about actively by means of flagella and also exhibits active ameboid movements. This type varies from 3.5 194 DISEASES OF DOMESTICATED BIRDS by 7 microns to 5.5 by 9 microns, and is the only form occurring in the cecal crypts. The globular form occurs in the lumen of the ceca. Control of disease. Feeding of sour milk is favorably regarded as a means of saving life. PAKASITES OF THE LIVER The liver of birds is rarely subject to parasitism, if entero-hepatitis of the turkey be excepted. A flagellate Cercomonas hepatica has been reported in the liver of squabs, causing yellowish nodules. Echinococcus polymorplius, the cystic phase of the tapeworm of the dog, occurs sometimes in birds, and exhibits a preference for the liver. Echinococci have been reported in the goura, the peafowl and the turkey. The liver becomes enlarged by the presence of the cysts until it occupies a large part of the abdominal cavity. The hepatic tissue is reduced to thin pieces between the cysts. Three species of flukes, Opisthorchis simulans, Metorchis xantho- somiis and Billiarziella polonica have been found in the hepatic canals or biliary vesicles of the domestic duck. The latter species occurs in the blood of a large number of species of wild ducks. Heterahis columhcc, normally a parasite of the intestines of pigeons, has been reported as occurring in nodules in the liver. Blastomycosis. Martin and Daille have described lesions in the liver of the goose, due to Blastomyces (Cryptococcus) anseris. The parasites are contained in small sacs about the size of a pea, attached to Glisson's capsule. These sacs are yellowish white in color, fluctu- ate on pressure and are connected with one another by narrow chan- nels. The contents of the sacs consist of a yellowish white gelatinous material enclosing the blastomyces. These latter consist of round or oval nucleated refractile bodies surrounded by a distinct membrane. PARASITES OF THE BURSA OF FABRICUS According to ISTeumann, the bursa of Fabricus harbors species of flukes of the genus Prostliogonimus. They are encountered there but rarely, for that pouch disappears in the adult. The parasites conse- quently are obliged to leave that diverticulum and enter some of the other canals connecting with the cloaca. Sometimes they enter the rectum, or they may penetrate the oviduct and become enclosed in an eg^g. Probably all the forms found in the oviduct and the egg also occur in the bursa of Fabricus. INTERNAL PARASITES 195 Prostliogonimus ovatus occurs in the bursa of Fabricus of a large number of birds. It has been found in the oviduct of the hen and many observers have found it in hen's eggs. Pr. pellucidus and Pr. japonicus have been found in eggs. Pr. cuneatus has been reported as occurring in the oviduct of a pea hen. COCCIDIA Coccidia occurring in the intestines are discussed under the head- ing coccidiosis, page 127. PARASITES OF THE NASAL CAVITY A species of mite of the genus Ehinonyssus infests the nasal cavity of fowls, causing a sort of coryza. The mites also occur in squabs which sometimes succumb to the parasite. Stemostomum rhinolethrum occurs in the nasal fossae of the duck. A leech Hemiclepsis tessellata occurs in the nasal and oral cavi- ties of geese and ducks, attached to the mucosa. The parasites also attach themselves in the eyes, esophagus, larynx and trachea. The affected birds are tormented by the presence of the parasites and rapidly become emaciated. Megnin recommends applying a two per cent salt solution to cause the detachment and death of the parasites. A fluke Cyclocoelum arcuatum is reported as a harmless parasite of the infraorbital sinus of the domestic goose. GAPE WORMS Gapes is caused by the roundworm designated Syngamus trachealis which attaches to the mucous membrane of the trachea and causes jsevere inflammatory changes. These lesions and the additional factor of mechanical blocking of the air passages may cause death. The air sacs are sometimes infested. Species affected. The fowl, pheasant, turkey, peafowl, pigeon, certain cage birds and a considerable number of wild birds have been reported as hosts of Syngamus trachealis. The adult turkey appears to be very much more frequently infested than the adult fowl. Ran- som found about 23 per cent of a number of turkeys infested when no parasites were found in 635 chickens examined. A related species 8. bronchialis occurs in the trachea, air sacs and bronchi of young geese. 196 DISEASES OF DOMESTICATED BIRDS General character. The female worais are about four-fifths of an inch in length and reddish in color. In most cases, the male, about a quarter of an inch long, is in copulation, attached to the female near the anterior extremity. Thus the appearance of a forked worm is induced. Symptoms. The presence of the worms is indicated by the peculiar wheezing cough, gasping and the expulsion of frothy saliva from the beak. The birds appear dull with ruffled feathers, lose appetite, breathe with difficulty and display cachexia. Spontaneous recovery is rare, and in the absence of treatment the parasites cause heavy mortality. Only young birds experience harm from their presence. Morbid anatomy. The presence of the parasites in the air passages enveloped in foamy mucus is the most important feature observed at autopsy. The point at which the parasites adhere ofteti consists of an abscess filled with yellow colored pus of caseous con- sistency. Such an abscess may cause asphyxia. Life history. The sexually ripe females are expelled by cough- ing, whereupon the eggs are disseminated by the disintegration of the female. Thus water and soil become contaminated with the larvae hatching from the eggs. It is not believed that an intermediate host is necessary in the life cycle of the parasite, even though it has been shown that the feeding of earthworms will induce the disease among chicks otherwise protected against infection. Undoubtedly earthworms may contain larvse in the intestinal tract, due to earth ingested by them, without however, playing the role of a host. It has been demonstrated repeatedly that chicks may be infected by drink- ing boiled water artificially infected with ova and young gape worms. The j^oung worms may live for some time in water, and the per- sistence cf the infection is favored by a wet soil. Infection undoubt- edly occurs through ingestion. The embryos probably make their way frcm the gullet or crop, to the trachea by perforating the walls of the organs in question. Treatment. The practice of dislodging the worms by the appli- cation of various remedies applied by inserting the tip of a feather into the trachea and twisting, is. widespread. The small size of the trachea in young chicks and the fact that some worms are located at i^s lower extremity out of reach, makes the operation painful and uncertain in its results. Among the remedies applied are oil of cloves, oil of turpentine thinned with double its volume of olive oil ;'nd kerosene oil. The feather also acts mechanically in dislodging INTERNAL PARASITES 197 the parasites, whereupon they are expelled by coughing. A coiled horse hair is frequently employed for the same purpose, but like the feather its use is dangerous to the chick. A few worms may be caught with tweezers if the larpix is raised high enough. It has been asserted that pounded garlic in the proportion of one bulb per day added to the food of ten birds would result in the ex- pulsion of the worms. Asafoetida has been administered in the food with the idea that the agent, eliminated through the air passages, would kill the parasites. Fumigation with various agents has been employed. Exposure to sulphur fumes has been used to induce coughing and expulsion of the worms but is dangerous. Affected birds may be exposed to tobacco smoke until they become almost insensible, after which they are allowed to recover in the open air. Fumes of heated carbolic acid have been employed. Klee has great confidence in intra-tracheal injection which re- quires no more time than other more dangerous kinds of individual treatment and is regarded as more effective. The affected bird is in- jected in the trachea with 1 c.c. of a 5 per cent aqueous solution of sodium salicylate, administered with a hypodermic syringe. This fluid simultaneously loosens all the parasites occurring there and a Fig. 30. Apparatus for making injections in trachea, a. Syringe; b, Straight canula; c. Curved canula. (Klee) 198 DISEASES OF DOMESTICATED BIRDS violent cough will expel them. The operation in question can be performed by one person, for a syringe with two rings on the barrel can be guided easily with one hand. The sick bird is held between the knees with the breast in front. The neck is bent up and back with the left hand and the trachea lies between the thumb and index finger. N^ext, the syringe lying conveniently, is grasped with the right hand. The needle is placed near the trachea, after which with necessary care it is inserted into the trachea slanting downwards and the injection made quickly. The introduction of a dull canula into the glottis through the beak is even more suitable than the foregoing method. After the injection the bird suffers a light attack of choking but soon recovers. A very safe but a somewhat less effective remedy is to cause the affected birds to breathe air containing finely powdered chalk and camphor. Theobald recommends a mixture of two parts by weight of powdered chalk and one part of powdered camphor. This is dusted into a closed box in which the chickens are confined. Prevention. Contaminated water and soil are to be regarded as the chief sources of infection. Infectious larvae have been kept alive for a year in moist soil. Chicks raised on board floors and thus iso- lated from the soil with separation from older birds until a month or six weeks old, will escape infection provided the water and food supply are not infected. Rotation in the use of land to which chicks are allowed access is a valuable practice in avoiding the use of con- taminated soil from year to year. Above all, chickens should not be kept on soil that has been occupied by turkeys within a year or so. Disinfection of drinking vessels and of soil, so far as possible, de- serves consideration. Salicylate of soda, 3 drams to the quart of drinking water is said to kill the embryo worms. Contaminated soil may be disinfected by drenching with a one per cent solution of sul- phuric acid. Wet areas should so far as possible be dried by drain- ing. The isolation of the sick and thorough disposal of the dead are obvious precautions. THE AIR SAC MITE Cytoleichus (Cytodites) nudus has a wide distribution in the United States and Europe affecting a large number of gallinaceous fowls and also pigeons. The mites are barely large enough to be de- tected by the unaided eye. They have been observed in the trachea, INTERNAL PARASITES 199 lungs, air sacs, hollow bones and the peritoneum. They have been reported as occurring exceptionally in the heart, liver and kidneys. Their presence within tissues is not readily explainable since their structure is not adapted to the penetration, of tissue. They are most commonly noted in the air sacs. Hens apparently in perfect health may be heavily in- fested, so that the economic im- portance of the parasite seems to be not very great. The method of transmission has not been thor- oughly explained. Their exit from the body could occur through the trachea by expulsion during coughing. Fig. 31. Cytodites nudus. Male, ven- A few writers have obsei-ved tral aspect. Enlarged 100 times, cases in which the parasites ap- pear to be of pathological impor- tance. Gerlach regarded them as the cause of enteritis as did also Zundel. Williams attributed high importance to them as a parasite Fig. 32. Cytodites nudus. Ovigerous female, ventral aspect. Enlarged 100 times. (Railliet) 200 DISEASES OF DOMESTICATED BIKDS of fowls in Montana, a view that Wilcox was not able to confinn. Among the later observers Walker has reported npon two autopsies of fowls in Grahamstown, Cape Province, in which lesions occurring in the lungs, were in his opinion, the cause of death. The owner reported that the comb turned purple, appetite was lost and the birds* seemed fretful and weak in the legs. Birds were noticed to be sick for a week, when sudden collapse occurred. Observations bv Walker follow. Morbid anatomy. Cytodites are frequently found in the thorax and peritoneal cavity, fairly frequently on the mesentery and in the trachea. The lungs are mottled in appearance by some purple patches .2 to .3 cm. in diameter. On section, hyperemia is observed and serous fluid exudes from the cut surfaces. Small miliary tubercles of a gelatinous consistency are scattered through the af- fected portion of the lung, and parasites are visible in the midst of each of these. The larger bronchi and some of the bronchioles con- tain an exudate in which the parasites are imbedded. Other organs and blood appear normal. The conditions observed warrant the pathological anatomical diagnosis of hyperemia and edema of the lungs, and bronchial pneumonia. Microscopic examination of sections of stained tissue, under 300 magiiification shows that the lung tissue surrounding the invaded air passages is infiltrated with leucocytes and red blood corpuscles. The blood vessels are congested. Some of the parasites have wandered from the air conduits into the surrounding parenchyma breaking down the regular network conformation of the latter. In some of the invaded air passages, the parasites have lodged themselves in the inner lining and have broken it down. In places cytodites are to be seen in the inter- lobular fibrous tissue. The larger bronchi contain an exudate. Pig. 33. DitJii/ridhim variabile. fi'om a fowl. Enlarged 10 to 12 CESTODE CYSTS IN TIIE LUNGS times. (Neumann) ^N^eumann has described a case in which the encysted parasite known as D ithyridium variabile occurred in great numbers in the lung of a fowl. These represent the cystic stage of a tapeworm, which has not been identified with the adult form. The cysts were observed in the inferior surface of the lungs in the an- INTERNAL PARASITES 201 terior and posterior diaphragmatic reservoirs. They were globular or ovoid bodies 3 to 4 mm. in diameter, somewhat transparent and filled with a colorless liquid containing a parasite. Some were free, and others adhered slightly to adjoining tissues. The dithyridium has a milk-white body, varying in length from 1.5 to 2.5 mm. It is sometimes as broad as long and sometimes much longer than broad. An invaginated cestode scolex is present. manson's eye worm At least 38 species of nematode worms have been reported as parasitic in the eyes of birds throughout the world. However, only one, Oxyspirura mansoni, is known to affect com- mon domesticated birds. This has been found in fowls and peafowls. Ransom has reported upon its ' • j-i, TT -4- J 04. J. J j-i, Fig. 34. Manson's presence m the United states, and upon the preva- gyg ■worm (Ox- lence of nematodes in wild birds. yspirura man- General description. The parasite known as ^^^oJq and female Oxyspii'ura mansoni or Filaria mansoni or Spi- below. Natural roptera emmerzii is a small white, thread-like ^^^^' ^ an^om) worm slightly over half an inch in length and about as thick as a fine sewing needle. It is thickest in the middle and tapers toward the ends. The number present in the eyes may vary from a few located beneath the nictitating membrane to as many as 200. Symptoms. In some cases the worms are present in the eyes without causing apparent inconvenience. In more severe infesta- tion, symptoms of irritation become evident. The affected bird ap- pears uneasy and scratches the eyes. The latter show acute inflam- mation with abundant lachrymation. Subsequently white cheesy exudate collects within the conjunctiva and upon the edges of the lids, causing them to adhere together. The inflammation extends to the tissues surrounding the eye and to the infra ocular sinuses. Eventually the whole eyeball becomes affected, with consequent de- struction of the organ. Catarrhal changes also involve the nasal cavities. In severe cases the subject dies. Treatment. The first requisite to successful treatment consists in removing the worms. This may be done by the use of forceps or by irrigating the eyes with some solution such as bicarbonate of soda or a two per cent solution of creolin. When the worms are partially dislodged by the fluid, they may be entirely removed with a soft cloth. The inflammation may be alleviated by instilling into 202 DISEASES OF DOMESTICATED BIRDS the eyes a few drops of saturated solution of boric acid. Ransom recommends anointing the eyes with a mixture of lard 9 parts and iodoform, 1 part or with carbolized vaseline. Life history of the worm. Very little is known of the life his- tory of the parasite. It seems probable that the embryos pass a portion of their existence either free or in a secondary host. The reports of the presence of the worm in chickens are, so far as known, limited to sea coast regions. This suggests the possibility that some conditions peculiar to the sea coast are necessary to the development of the parasite. LEECHES IN THE EYE One incomplete report exists of the occurrence of leeches in the eyes of geese in Ireland. Intense irritation of the eye occurred, with symptoms of severe pain. The birds had access to a pond teeming with leeches. Fig. 3.5. Lamin- osioptes cysti- cola. Male, ventral aspect. Enlarged 200 times. (Rail- liet) MITES PARASITIC IN CONNECTIVE TISSUE Laminosioptes cysticola, accord- ing to Neumann, is a mite occur- ring in gallinaceous birds such as fowls, pheasants and turkeys. The parasites live on the surface and in the thickness of the skin caus- ing the formation of scurf. They are encountered rarely except in the subcutaneous tissue especially in the places where it is very loose, such as the flanks, the vent, on the thighs, the breast and the neck. They are able to penetrate the deep connective tissue. Microscopic ex- amination of fragments of subcu- taneous connective tissue permits all phases of their development to be observed. When they die, the carcass acts as a foreign body and causes the formation of a miliary nodule about it. This promptly undergoes calcareous infiltration. On treating these nodules with Fig. 36. Laminosi- optes cysticola. Ovigerous female, ventral aspect. Enlarged 2 times. (Railliet) INTERNAL PARASITES 203 acidulated water, the remnants of the parasite may be recovered. The nodules are yellowish in color, oval in shape and may become as large as 1 mm. in diameter. They may be very numerous in an individual and are very common in old cachectic birds. These para- sites are not injurious to health except perhaps when they are present in excessive numbers. Two other connective tissue parasites occur in the pigeon. A feather mite, Falculifer rostratus, spends a portion of its life cycle in the subcutaneous connective tissue. Filaria clava is located in the subcutaneous connective tissue of the pigeon. Neither have any effect upon the health of the host. TRYPANOSOMIASIS OF BIRDS The blood of a very large number of wild birds is infested with trypanosomes which apparently do not exert much pathogenic effect. Gray lists nine species of these parasites occurring in birds. Among domesticated birds, they have been observed in the fowl and pigeon. FILARIA IN THE BLOOD Filaria anatis has been observed in the heart of a duck. Embryos of filaria have been observed in the blood of a pigeon. PARASITE OF AVIAN MALARIA Symptoms. The parasite of Danielewsky, n!"> J"^t Mow the ear, where the nington and Betts) hinged joint cau be felt. The skin which 316 DISEASES OF DOMESTICATED BIEDS makes the corner of the mouth and limits the length of the beak ends is indicated in the anatomical drawing marked "A." The skin and lower jaw have been cut awaj in order that the position of the veins which lie far back on the roof of the mouth and just below its surface may be seen. The groove which occurs in the roof of the chicken's mouth is a guide to the position of the blood vessel which it is desir- able to cut, this point being behind and to the left of the end of the groove when the chicken is held head down and with the lower side of the head uppermost. The direction and position of the cut which coffJi£CT ct/r GROO\/e /// EYE. eNO OF BEAK Fig. 66. Lower jaw removed, showing position of veins, anatomy of skull, and location of cut. (Pennington and Betts) is to sever the veins is shown in Fig. 66 to be on the left side of the chicken's head when in the position just described. Because the short blood vessel connecting the two long veins, which we have termed the " bridge," does not run straight but at an angle, the point just indicated is farthest front and the most easily reached by the knife. As stated before, these veins lie just below the skin of the roof of the mouth, hence a deep cut is not needed, neither is any amount of strength required for the operation. It will be observed that just in front of the line which indicates the point at which these veins are to be cut they divide into two small branches, the course of which is not further shown. This is because they very soon pass through small holes in the bone and go into the KILLING POULTKY 317 inside of the skull, and into the deep tissue, where they are quite safe from the killer's knife. If, then, these large veins are to be sev- ered, the cut must be made far enough back to reach them before they penetrate the bones of the skull. On the other hand, if the cut is made too far back and over the edge of the skull, as will be dis- cussed in connection with Fig. 6Q, B, much of the blood will settle in the loose tissue of the neck instead of running out of the mouth, thereby clogging the vessels and preventing complete bleeding, as well as making unsightly discolored areas on the neck near the head. It is better to make one cut as shown in this plate rather than to cut the " bridge " in the middle or to cut each side vein separately, since this sometimes results in the clotting of the blood at the ends of the veins before the bleeding is completed. ANATOMY OF THE SKULL From what has been said concerning the necessity of cutting far back in order to reach the point desired, it will be seen that it is necessary to know something of the position and shape of the bones of the chicken's skull and their relation to the external parts of the head. This information is given in Fig. 66, B. Dotted lines around the drawing of the skull show the position of wattles, comb, etc. In this sketch, too, is shown clearly the length of the chicken's jaw, as before mentioned. Its hinge will be found on the head of the live bird just below the ear. Still farther back there is a U-shaped depression in the skull into which fits the upper part of the spinal column. The spine is not shown in the sketch, but the bridge vein connecting the two large veins of the neck lies directly across the U-shaped depression. It can be seen by studying this drawing how far back the knife must go if the veins are to be cut at the angle, and it will also be ob- served that when they are cut in this position the knife will have a bony backing which will prevent it from going too deep, thereby obviating the spongy mass of blood in the neck tissues which was dis- cussed in connection with Fig. 66, A. This illustration also shows where the fingers can grasp the head of the chicken firmly and yet not press against the soft parts of the neck. Just above the angle of the jaw — that is, about at the chicken's ear — there is a smooth, strong area of bone large enough to support the thumb on one side and the forefinger on the other, and this is where the head should be held while killing. N 318 DISEASES OE DOMESTICATED BIKDS POSITION OF HAND AND KNIFE Figure 67 shows the position of a chicken ready for killing and held by the feet in a U-shaped shackle. Notice that the thumb of the killer is pressed finnly down on the head just below and behind Fig. 67. Correct grasp of head at angle of jaw and position of small knife when cutting vein. (Pennington and Betts) the ear in the space to which attention was called when discussing the bones of the skull. Here, too, is the hinge of the jaw. Pressure of the thumb on one side of this portion of the skull and on the other side at the same place with the forefinger, or with the forefinger and second finger, will result in opening the chicken's mouth and holding it open while the operator makes the cut to bleed. Held in such fashion, there is nothing to constrict the blood vessels, thereby pre- venting the blood from escaping even though these vessels be cut. The pressure against the jaw makes accurate cutting of the veins easier, since the bird can not close its mouth until the pressure is removed. Of course, care must be taken not to stretch the neck unduly, else the vessels will be pulled to such a narrow diameter that they are more difficult to find and also more difficult to empty. The position of the knife in the mouth, which is shown by the dotted line, needs no further explanation. The knife itself, how- ever, is very different from that ordinarily used in the bleeding of KILLING POULTRY 319 Fig. 68. Location of cuts in mouths of badly bled chickens (lower jaw removed). (Pennington and Betts) chickens. The knife in common use is much too large, both too long and too broad for the most successful work. Generally it is provided with a heavy handle, large enough to be grasped easily by a large, strong hand. As has already been observed in this dis- cussion, the heavy slashing inside the bird's mouth is not only fre- quently futile so far as cutting the veins goes, but is really harmful in that it makes a pathway for the entrance of bacteria and the con- sequent hastening of the bird's decomposition. The operation calls for accuracy rather than for strength, and therefore it is desirable that the knife should have a smaller handle, which can not be gripped so hard. The blade of the knife should be about 2 inches long and one-fourth of an inch wide and of a heavy piece of steel, so that it will not bend. It is advisable, therefore, to have the back of the blade about one-sixteenth of an inch thick. It should be made of good hard steel and ground to a sharp point with a straight cutting edge, the slope for the point being taken from the back rather than 320 DISEASES OF DOMESTICATED BIEDS from the edge. Tlie working space in the back part of the month of the chicken where the blood vessels lie is very small. Often the knife which is used by the killer is too broad to go into this space without cutting the sides of the mouth, and as for turning and guid- ing it, that is quite out of the question. EXAMPLES OF BAD CUTTING Ineffectual cutting, due to lack of knowledge of the structure of the chicken's neck and head, the use of force rather than skill on the part of the operator, and a knife ill adapted to the work which it has to do, is illustrated in Figs. 68 and 69 which show some of the most common types of cuts in badly bled chickens. A study of these illus- trations indicates very plainly why these chickens are badly bled. The lower jaws from these heads were removed so that the position of the cuts could be noted. Head A has had two cuts. One has run Fig. 69. Attempts at " cross cutting," showing veins untouched. and Betts) ( Pennington KILLING POULTKY 321 parallel with the connection between the two veins and very close to it but has not cut it, and another has run from the angle of the mouth to close to the point where the blood vessel on the left side of the head breaks into the two smaller vessels and penetrates the bones of the skull. The only vessels which were cut in this chicken were the small superficial veins supplying the roof of the mouth and from which the bleeding amounted to almost nothing. Head B shows a cut in the right direction but it did not go quite far enough back to reach the veins at their junction. Head A, in Fig. 69, shows the cross cut which is advocated by so many killers. In this case it was made too far front. Both of the large veins escaped and only the small vessels of the roof of the mouth were disturbed. " B " is a good illustration of indiscriminate cutting by a badly directed knife, which in all probability was far too large, since the upper cut extends all the way across the roof of the chicken's mouth and almost as far front as the beak. Another cut which partly follows the groove in the roof of the mouth would indicate that the killer had tried to make a cross cut. Such examples of bad cutting might be multiplied indefinitely. Yet the general principle is the same and the result is the same — namely, a fowl which is not completely bled, which is unsightly, even in the packing house, and which deteriorates as a food stuff more rapidly than does the well-bled chicken under similar conditions. SUMMARY The facts which have been stated in the foregoing pages may be summarized as follows: (1) Grasp the chicken when killing by the bony part of the skull. Do not let the fingers touch the neck. (2) Make a small cut inside the mouth on the left side of the throat just where the bones of the skull end, using a narrow-bladed sharp-pointed knife. The direction of the knife is upward and to- ward the left when the bird is held head downward with the throat toward the operator while killing. (3) Brain for dry picking by thmsting the knife through the groove which runs along the middle line of the roof of the mouth until it pierces the brain in the back part of the skull, causing a loosening of the feathers. (4) For chickens use a knife the blade of which is 2 inches long. 322 DISEASES OF DOMESTICATED BIEDS one-fourth incli wide, with a thin, flat handle, a sharp point, and a straight cutting edge. For turkeys the blade may be 2^ inches long. Keep knives very sharp. REFERENCE 1. Pennington and Betts. How to kill and bleed market poultry. TJ. 8. Dep. Agr. Bureau Chemistry Circ. 61, Revised. AUTPIOR INDEX Adam and Medler, 254, 259 Aragao, 141, 144, 203, 206 Archibald, 229, 240 B Balfour, 118 Beach, 109, 189 Beach and Halpin, 118 Beach, Lother and Halpin, 108, 109 Belfanti and Ascoli, 86 Bertegh, 97, 109 Bevan, 136, 144 Binder, 252, 254, 260 Bishopp, 221, 225 Bishopp and Wood, 208, 209, 210, 211, 212, 216, 218, 225 Bordet and Fally, 107, 109 Borrel, 97 Boyce and Warrington, 19 Bradley, 19 Bugge,"^ 250 Burnet, 19, 109 Burnett, 98 Bushnell and Maurer, 79 Butterfield, 146 C Cardamatis, 203, 206 Centanni, 86 Chauveau, 19 Ciurea,' 206 Claussen, 61, 65 Cobbold, 63 Cogny, 39 Colucci, 178 Cominotti. 82, 86 Cornil and Toupet, 250 Curtice, 50, 65, 121, 126, 242, 250 Curtis, 261, 274 Cushman, 126 Danielewski, 203 Dawson, 50, 64, 143, 144 Dickson, 154, 177 Dodd, 140 Douglas, 229 Dubois, 86, 143, 144 Dupuy, 65 E Eastwood and Griffith, 89 Edwards, 290, 294 Ehrenreich, 262, 274 Ehrenreich and Michaelis, 262, 274 Ehrhardt, 142, 144 Ellenberger, 19 Ellenberger and Baum, 19 Ellerman and Bang, 146, 149 Elley, 311, 313 Fantham, 127, 134, 204 Fiorentini, 46, 47, 48 Freese, 83, 86, 190, 246, 247, 250, 255 Friedberger and Frohner, 97 Frosch and Birnbaum, 243, 250 Fuller, 225 G Gage and Hyland, 79 Gage and Martin, 79 Gage and Opperman, 160, 206 Gage and Paige, 80 Gallagher, 16, 39, 48, 109, 163, 276, 294 Gerlach, 199 Gilruth, 254, 260 Gorig, 271, 274 Gray, 203, 233, 260 Greve, 31, 33 Gutberlet, 187, 206 H Dammann and Manegold, 30, 33 323 Hadley, 36, 48, 65, 120, 126, 193, 206 Hadley and Beach, 109 324 AUTHOR INDEX Haidub, 225 Halasi, 97, 109 Faring and Kofoid, 98, 103, 109 Harrison and Streit, 107, 109 Hasenkamp and Sachweh, 246, 251 Hassall, 225 Hastings and Halpin, 95 Hauer, 140, 144 Hausser, 107, 109 Hebrand and Antoine, 150, 177 Herms and Beach, 189, 206 Herrick, 211, 225 Hertel, 86 Higgins, 48 Hindle, 144 Hutcheon, 238 Iturbe and Gonzales, 204, 206 J Jackley, 108, 109 Joest, 86, 254, 260 Jones, 75, 77, 80, 274 Jowett, 43, 48, 134, 144, 240 K Kanpp, 19 Kern, 260 Kinyoun, 252, 260 Kionka, 151 Kitt, 39, 48 Klee, 177, 189, 197, 295, 298, 300, 301 Klein, 50, 62, 65 Kleine and Moellers, 87 Koch, 263, 265, 274 Koch and Rabinowitsch, 95 Kon, Yutaka, 146 Kraus and Schiffmann, 87 Lignieres and Petit, 119 Lignieres and Zabala, 59, 66 Lipschutz, 87 Lisi, 42, 249, 251 Lode and C ruber, 87 Loer, 18, 19 Loffler, 243, 246, 251 Lounsbury, 225 Lucet, 43," 48, 119, 246, 247, 251 Mc M'Fadyean, 43, 48, 243, 251 M Mack, 109 Mack and Records, 48, 109 Maggiora and Valenti, 87 Magnussen, 28, 33 Mane, 87 Manegold, 31 Manninger, 254, 260 Manteufel, 109 Marchoux and Salimbini, 141, 144 Martel, 61, 66 Martin and Daille, 194, 206 Martin and Robertson, 193, 206 Marx, 231, 232, 233, 240 Marx and Sticker, 97, 98 Matruchot and Dassonville, 119 Mazza, 44, 48 Megnin, 65, 157, 187, 189, 195, 301 Meyer and Crocker, 134 Miessner and Schern, 252, 260 Milks, 126 Mohler and Buckley, 119 Mollhoff, 143, 144 ' Moore, 50, 53, 56, 66, 95, 96, 107, 126, 185, 206 Morse, 63, 66 Murphy and Rous, 274 N" Lamson, 287, 294 Lamson and Manter, 211, 225 Landsteiner and Berliner, 87 Lange, 274 Laurie, 225 Leclainche, 45, 48, 87 Leiclitenstern, 54, 65 Lewin, 272, 274 Lignieres, 61, 66 Neumann, 119, 183, 188, 192, 194, 200, 202, 206, 209, 220, 240 Nocard and Leclainche, 42, 48 Noguchi, 135, 145 Norgaard and Mohler, 28, 33 Ostertag and Bugge, 87 AUTHOR INDEX 325 Ostertag and Wolfhiigel, 87 Ottolenghi, 81, 87 Owen, 19 Palamidessi, 66 Pasteur, 39, 48 Pearl and Surface, 295, 301 Pearl, Surface and Curtis, 27 Pennington and Botts, 314, 322 Pereira, 145 Petit and German, 274 Pfaff, 252, 260 Pfeiler, 254, 260 Pfeiler and Rehse, 66 Pfeiler and Roepke, 50, 66 Pick, 262, 274 Pickens, 146, 149, 263, 274 R Eabieaux, 42, 49 Ransom, 179, 183, 195, 202, 206 Regenbogen, 272, 274 Reinhardt, 278, 294 Reinholdt, 60, 66 Reischauer, 98 Repp, 216, 225 Rettger, 80 Rettger and Harvey, 68, 80 Rettger, Hull and Sturges, 80 Rettger, Kirkpatrick and Card, 80 Rettger, Kirkpatrick and Jones, 80 Rettger, Kirkpatrick and Stoneburn, 80 Rettger and Koser, 66 Rettger and Stoneburn, 80 Rieck, 252, 260 Riemer, 243, 251 Ritzier, 280 Robertson, 206, 225, 231, 232, 233, 238, 240, 241 Rous, 268, 269, 274, 275 Rous and Lange, 270, 275 Rous and Murphy, 269, 275 Rous, Murphy and Tjtler, 267 Russ, 87 Sabouraud, 119 Sabouraud. Suis and Suffran, 119 Salmon, 27, 220 Sanfelice, 62, 66 Schantyr, 161 Scherago and Benson, 79 Schlegel, 275 Schmid, 97 Schneider, 292, 294 Seddon, 41, 49 Sigwart, 97, 107 Slocum, 302, 313 Smith, 120, 126, 193, 242 Smith and Ten Broeck, 66 Steen, 19 Stevenson, 190 Stiles, 206 Suffran, 289, 294 Tartakowski, 259, 260 Taylor, 50, 66 Theiler, 226, 241 Theiler and Robertson, 236, 241 Theobald, 189, 198, 206, 207 Tretop, 45, 49 Tytler, 275 Tyzzer and Ordway, 265, 267, 273, 275 U Uhlenhuth, 140 Uhlenhuth and Manteufel, 97 Vages, 39 Van Es and Schalk, 92, 94, 95 W Walker, 200, 228, 229, 239, 241 Ward, 34, 36, 49, 95, 280 Ward and Gallagher, 80 Warthin, 146, 149, 226, 275 Wasielewski and Hoffmann, 252, 260 Watson, 275 Weil, 40 Weinzirl, 193, 207 Wickware, 205, 207 Wilcox, 200, 207 Willach, 250, 251 Williams, 199, 207 X Y Z Yutaka Kon, 146 Zeiss, 66, 252, 254, 260 s 326 AUTHOR INDEX Zeiss and Schlegel, 61 Ziirn, 252 Zingle, 57, 66 Ziirn and Pauly, 272 Zundel, 199 Zwick, 260 SUBJECT INDEX Abdomen, drooping, 173 Acanthia columbara, 2] 4 Acanthia lectularia, 213 Acetabulum, 4 Acorn poisoning in the ostrich, 240 Aggressin for fowl cholera, 40 Air sacs, 15 Air sac mite, 198 Alimentary system, 10 tract, diseases of, 154 Aloes, Barbadoes, 240 Ammonia, 237 Ammonium chloride, 277 Amoeba meleagridis, 120, 193 Amcebotfpnia sphenoides, 183 Analges bifidus, 220 Anesthetizing fowls, 295 Anatomy, 1 Anise oil, 191 Anthrax in the fowl, 143 in the ostrich, 226 vaccine, 227 Apoplectiform septicemia, 28 Areca nut, 187, 190 Argas americanus, 221 miniatus, 221 reflexus, 224 Arsenious acid, toxicity, 278 Arteries, 6 Arthritis in pigeons, 295 Ascaridia perspicillum, 169, 188 Ascaris crassa, 188 Ascites, 173 Aspergillosis in the fowl, 111 in the ostrich, 228 Aspergillus fumigatus. 111, 230 candidus, 112 glaucus, 112 nigressens, 112 Asthenia of fowls, 64 Atropine sulphate, 295 Autopsy directions, 25 Avian diphtheria. 96 salmonellosis, 59 tuberculosis, 88 B Bacillary white diarrhea, 68 327 Bacillus avicida, 34 avisepticus, 34 bipolaris septicus, 34 canariensis necrophorus, 253 cholerse gallinarum, 34 coscoroba, 45 enteritidis, 60 gallinarum, 50 loxiacida, 259 paratyphosus B, 57, 58, 60, 252, 254 septicemia anserum exudativae, 243 suipestifer, 56 Bacterium anthracis, 226 asthenise, 64 diphtheriae, 108 pullorum, 52, 68 pullorum infection in grown fowls, 74 sanguinarium, 50 tuberculosis, 88 typhi gallinarum alcalifaciens, 50 Balsam of Peru, 220 Bed bugs, 213 Bertiella delafondi, 183 Bichloride of mercury, disinfectant, 23, 40 toxicity of, 279 Bilharziella polonica, 194 Bird fever, 252 flea, 212 pest, 81 plague, 81 pox, 96 Bismuth subnitrate, toxicity, 280 Blackhead, 120, 193 Blastomyces anseris, 194 Blastomycosis, 194 Blood. 7 platelets, 8 spots in eggs, 169 Blue stone, toxicity, 282 Bones, broken, 298 Boracic acid, 105 Bothriotaenia longicollis, 183 Brisket, 3 Bronchitis, 162 Brooder pneumonia. 111 Bumblefoot, 296 Bunodera linearis, 192 Bursa of Fabricus, 13 distention of. 161 parasites of, 194 328 SUBJECT INDEX Calcium oxide, toxicity, 280 Calomel, toxicity, 281 Camphor, powdered, 198 Canary birds, infectious diseases of, 252 fever, 252 Canker, 96 Caponizing cockerels, 302 ostrich, 311 Caraway oil, 219 Carbolic acid, disinfectant, 23 toxicity, 281 vermifuge, 236 Carcinoma, 262 Carpal bones, 4 Caruncle, 18 Castor oil, toxicity, 282 Catarrh, 96 contagious, 96 of crop, 155 Catechu, 133, 282 Ceea, 13 Cercomonas hepatica, 194 Cerebellum, 9 Cestodes, 182 Chalk, powdered, 198 Chicken cholera, 34 Chiggers, 217 Chigoe. 213 Chilomastix gallinarum, 193 Chloride of lime, disinfectant, 23 toxicity, 282 Chlorinated lime, 23 Choanotrenia infundibulum. 183, 184 Cholera-like septicemias, 42 Cholera des poules, 34 Cimex columbara, 214 inodorus, 214 lectularia, 213 Circulatory system, 6 Clinostomum commutatum, 192 Cloaca, 13 Cloacitis, 167 Cnemiodocoptes mutans, 218, 219 Coal tar disinfectants, 23 Coccidiosis, 127 Coccidium avium, 127 Colds, 96 Colibacillosis tetraonidarum, 63 Collodion, styptic, 301 Colon bacilli," septicemias caused by, 61 Comb, 18 frozen, 300 Compound solution of cresol, 22 Congestion of lungs. 162 Connective tissue, mites in, 202 Constipation, 160 Contagious catarrh, 96 Copperas, toxicity, 283 Copper sulphate, toxicity, 282 Coracoid, 3 Corrosive sublimate, disinfectant, 23 toxicity, 279 Coryza, 96 Coscoroba swans, 45 Cotugnia diagonopora, 183 Creosote oil, 23 Cresol, compound solution, 22 Crop, anatomy, 10, 12 catarrh of, 155 impaction of, 156 incision of, 300 inflammation of. in pigeons, 156 parasites of, 178 Cropping wattles, 298 Crude carbolic acid, 23 petroleum, 216 Cryptococcus anseris. 194 Cutaneous emphysema, 297 horn, 298 Cvclocnplum arcuatum, 195 "mutabile, 192 Cysto-adenoma, 263 Cytodites nudus. ins Cytoleichus nudus, 198 D Daphnia pulex, 181 Davainea cantaniana. 183 cesticillus, 183 crassula. 183 echinobothrida, 183 friedbergeri, 183, 184 proglottina, 183, 184 tetragona, 183 Depluming scabies, 219 Dermaglyphus elongatus, 220 minor, 220 varians, 220 Dermanyssus gallinte, 214 Dermestes lardarius, 214 Diaphragm, 56 Diarrhea, simple, 159 Digits. 5 Diphtheria, avian, 96 Discolored yolks, 170 Diseases of the alimentary tract, 154 of the oviduct. 164 of the peritoneal cavity, 172 of the respiratorv tract, 162 Disinfectants. 22, 23, 24 Disinfecting buildings. 22 Dispharagvis hamulosus, 178 laticeps, 178 nasutus, 178 spiralis, 179 imcinatus, 181 SUBJECT INDEX 329 Distention of the bursa of Fabricus, 161 Dithyridium variabile, 200 Docophoriis icterodes, 29 Double-yolked eggs, 171 Drooping abdomen, 173 Dropsy, 173 Dubbing wattles, 298 Duck cholera, 250 Ducks, infectious diseases of, 242 septicemia of, 249 Duodenum, 12, 13 E Echinococcus polymorphus, 194 Echinorhynchus polymorphus, 193 Echinostomum conoideum, 192 echinatum, 192 filicollis, 192 recurvatum, 192 spserocephalus, 192 Edema of wattles, 41 Egg, blood spots in, 169 bound, 165 double yolked, 171 eating, 176 soft shelled. 171 structure of, 168 Eimeria avium, 127 Epsom salts, 160, 186 Emphysema, cutaneous, 297 Enteritis, 158 Entero-hepatitis of turkeys, 120 Eosinophiles, 8 Epidermoptes bifurcatus, 220 bilobatus, 220 Episternal process, 3 Epithelioma contagiosum, 96 Epizootic dysentery of fowls and tur- keys, 43 pneumo-pericarditis in the turkey, 43 Ergot, toxicity, 283 Esophagus, parasites of, 178 External parasites, 208 Exudative septicemia of geese, 243 F Falculifer anatina, 220 anserina, 220 cornutvis, 220 rostratus, 203, 220 Favus, 116 Feathers. 17 Feather cysts, 265 pulling, 176 Femur, 4 Ferrous sulphate, toxicity, 283 Filaria anatis, 203 clava, 203 cygni, 182 mansoni, 201 spicularia, 238 Fimbriaria fasciolaris, 183 Flagellates, 192 Flea, bird, 212 Flight, prevention of, 300 Flukes, 192 Foot and mouth disease, 142 Foot mange, 218 Formaldehyde gas, 22 Formalin, 22 Fowl cholera, 34 fever, 135 plague, 81 tick, 221 typhoid, 50 Fractures of bones, 298 Freyana chanayi, 220 Frozen comb, 300 Furculum, 3, 4 G Gangrene of ovary, 75 Gape worms, 195 Gasoline, 211, 238 Gastritis, 157 Geese, infectious diseases of, 242 Gefliigelpest, 81 General diseases, 150 Generative system, 16 Gizzard, 12 parasites of, 178 Gonglyonema ingluvicola, 179 Goniocotes abdominalis, 209 chrysocephalus, 209 compar, 209 hologaster, 209 rectangulatus, 209 Goniodes colchicus, 209 damicornis, 209 dissimilis, 209 falcicornis, 209 minor, 209 numidanus. 209 parviceps, 209 stvlifer, 209 truncatus, 209 Gout, 150 Grouse disease, 62 H Habits, vicious, 175 Hsemomoeba danielewskyi, 203 '« 330 SUBJECT INDEX Haemoproteus columbse, 203 danielewskyi, 203 Harvest mites, 217 Heart, 6 Hematozoa, 203 Hemiclepsis tessellata, 195 Hemorrhagic septicemia of fowls, 34 of geese, 242 of the ring dove, 45 of the swan, 46 Heterakis brasiliensis, 188 columb£e, 188, 190, 194 compar, 188 compressa, 188 differens, 188 dispar, 188 lineata, 188 papulosa, 188 perspicillum, 188 vesicularis, 188 Holostomum gracile, 192 sphaerocephalum, 192 Horn, cutaneous, 298 Hiihnercholera, 34 Hiihnerspirillose, 135 Hiihner typhus, 50 Humerus, 4 Hymenolepis anatina, 183 cantaniana, 183 carioca, 183 coronula, 183 fasciata, 183 gracilis, 183 lanceolata. 183, 184 megalops, 183 meleagris, 183 musculosa, 183 parvula, 183 setigera, 183 sinuosa, 183 tenuirostris, 183 Hvpiene, 20 Hystrichis cygni, 181 elesans, 181 tricolor, 181 Heum, 13 Ilium, 4 Impaction of crop, 156 Incision of crop, 300 Incubating periods, 18 Indigestion, 157 in parrots. 158 Infectious diseases of geese and duck 242 enteritis of pheasants, 47 Infectious entero-hepatitia of turkeys, 120 necrosis of canaries, 252 Inflammation of crop in pigeons, 156 of the oviduct, 164 Infraorbital sinuses, 14 Internal parasites, 178 Intestines, 12 Ipecac, toxicity, 283 Ischium, 4 Jejunum, 13 K Keel, 3 Kerosene emulsion, 215 oil, 213 Kidneys, 16 Killing poultry, 314 Laminosioptes cysticola, 202 Large mononuclear leucocytes, 8 Larynx, 14 Lead water, 295 Leg weakness, 153 Leiomyoma, 267 Leucocytes, 7 Leucocytozoa, 204 Leucocytozoon anatis, 205 infection in ducks. 205 infection in ostrich, 239 struthionis, 239 Leukemia, 146 Lice, 208 Limberneck, 154 Linseed oil, raw, 240 Liotheum longicaudum, 209 Lipeurus anatis, 209 anseris. 209 baculus, 209 crassicornis, 209 heterographus, 208 meleagridis, 209 numidae, 209 temporalis, 209 variabilis, 208, 209 Liver, 14 complaint, 88 parasites of, 194 Lophophvton gallinse, 116 Limgs. 15 cono-estion of, 162 Lymphatics. 7 Lymphocytes, 8 SUBJECT INDEX 331 Lymphoma, 265 Lympho sarcoma, 272 Lynchia maura, 204, 213 livicolor, 204 M Macroblasts, 8 Maladie du somneil, 30 Malaria, avian, 203 Male fern, toxicity, 285 Malta fever, 143 Manson's eye worm, 201 Mast cells, 8 Megninia cubitalis, 220 columbse, 220 ginglymura, 220 velata. 220 Megrims of pigeons, 57 Menopon biseriatiim, 208, 209 giganteum, 209 longicephalum, 209 niimidte, 209 obscurum, 209 pallidum, 208 phaeostomum, 209 productum, 209 Mercurial ointment, 212 Mercuric chloride, toxicity, 229 Metroliaathes lucida, 183 Metorchis xanthosomua, 194 Microblasts, 8 Micrococcus melitensis, 143 Microlynchia persilla, 204 Mites, 214 in connective tissue, 202 Monas anatis, 193 Monocercomonas anatis, 193 Mouth, 10 ]\Tuscular system, 5 Myelogenous leucocytes, 9 Myxo fibroma, 274 sarcoma, 273 N Nasal cavity, parasites of, 195 Nervous system, 9 Nest bugs, 214 Nodular tapniasis, 185 Nostrils, 14 Notocotyle verrucosa, 192 O Oidium albicans, 155 Opisthorchis simulans. 194 Ornithonomus cycni, 209 Ornithomyia avicularia, 213 Osteo arthritis in geese and ducks, 246 Osteochondrosarcoma, 267 Ostrich, caponizing, 311 diseases of, 226 Ovary, 16, 17 Oviduct, 16 diseases of, 164 Oxyspirura mansoni, 201 Palate, 1 Pancreas, 12, 13 Paralysis of the ostrich, 231 of bursa of Fabricus, 194 Parasites, external, 208 internal, 178 of nasal cavity, 195 Parrot septicemia, 54 Parrots, indigestion in, 158 Pasteurella avium, 34 Pasteurellosis avium, 34 Patella, 4 Pectoral muscles, 5 Pelvic bone, 4 Perchloride of iron, 297, 301 Peritoneal cavity, diseases of, 172 Peritonitis, 174 Permanganate of potash, 105 Peste aviaria, 81 Petrol, 238 Petroleum, crude, 216 Phalanges, 5 Pheasants, infectious enteritis in, 47 Phenol, 23 Philopterus cygni, 209 Phosphorus, toxicity, 285 Physaloptera truncata, 178 Pip, 101, 154 Plasmodium danielewskyi, 203 Pneumo-mycosis, 111 Pneumonia, 163 brooder, 111 Poisons, 276 Polymorphonuclear leucocytes, 8 Polyneuritis, 153 Pomegranate root bark, 187 Post-mortem examination, 25 Potassium permanganate, 24, 72 toxicity, 286 Poultrv houses, 21 Pox, bird. 96 Prevention of flight, 300 Prolapse of oviduct, 167 Prosthogonimus cuneatus, 195 japonicua. 195 ovatus, 195 in eggs. 169 pellucidus, 179, 195 s 332 SUBJECT INDEX Proven triculus, 12 parasites of, 178 Pseudo leukemia, 146 Psittacosis of parrots, 54 Pterolichus obtusus, 220 Pterophagus strictus, 220 uncinatus, 220 Pubis, 4 Pulex avium, 212 Pulse rate, 18 Pygostyle, 3 Quail disease, 63 Q R Rabies, 142 Rachitis, 152 Red blood corpuscles, 7 Respiration frequency, 19 Respiratory system, 14 tract, diseases of, 162 Rheumatism, 88 Ribs, 3 Ring dove, 45 Rose chafers, toxicity, 287 Roimd worms, 188 Roup, 96 Rump gland, 17 Rupture of the oviduct, 165 Saccharomyces albicans, 155 Salicylic acid, 288 Salmonellosis, avian, 59 Sanitation, 20 Santonin, toxicity, 288 Sarcopsylla gallinacea, 213 Sarcoptes Ispvis, 219 mutans, 218 Scaly leg, 218 Scapula, 3 Schlafkrankheit, 30 Schlafsucht, 30 Schleg's solution, 220 Sclerostomum anseris, 181 Septic enteritis of cross bills, 259 fever of the canary, 252 of the parrot, 54 Septicemia of ducks, 249 caused by colon bacilli, 61 Shadow cells, 8 Simple diarrhea, 159 Skeleton, 1 Skin, 17 Skull, 1 Sleeping disease, 30 Small mononuclear leucocytes, 8 Sodium chloride, toxicity, 289 fluorid, 210 nitrate, toxicity, 290 salicylate, 197 Soft-shelled eggs, 171 Soil, relation to health, 20 Soor, 155 Spinal cord, 9 Spindle cell sarcoma, 268 Spirochseta anserina, 135 gallinarum, 135 Spirochetosis, 135 Spiroptera emmerzii, 201 . pectinifera, 179 Spotted liver, 88 Spur, 5 Staphylococcus pyogenes aureus, 232, 246 Sternostomum rhinolethrum, 195 Sternum, 3 Stomoxysis calcitrans, 99 Streptococcus, 28 capsulatus gallinarum, 31 Strongylus douglasi, 233 nodularis, ISO quadriradiatus, 190 tenius, 188 Strychnine sulphate, toxicity, 291 Styptic collodion, 301 Suborbital sinuses, 14 Sulphur, flowers of, 211 ointment, 219 toxicity, 293 Swan, hemorrhagic septicemia in, 46 Syngamus bronchialis, 195 trachealis, 195 Svrinx, 15 Taenia exilis, 183 fasciolaris, 183 struthionis, 237 Taeniasis, 182 Tapeworm of the ostrich, 237 Tapeworms, 182 Tarso-metatarsal bone. 5 Tartar emetic, toxicity. 293 Temperature, normal, 19 Tenebrio molitor, 214 Thrush. 155 Thorn-headed worms, 192 Thymol, 237 Tibia, 4. 5 Ticks. 221 Tobacco, vermifuge, 189 Toe pecking, 175 SUBJECT INDEX 333 Toxicology, 276 Trachea, 15 Trematodes, 102 Treponema gallinarum, 135 Trichomastix eberthi, 193 gallinarum, 103 Trichomonas, 120 cohimbse, 192 eberthi, 192 gallinarum, 193 pullorum, 193 Trichomoniasis, 193 Trichosoma anatis, 188 annulatum, 179 candinflatum, 191 collare, 191 cohimbfe, 191 contortum, 181 dubium, 191 gallinum, 191 nodularis, 179 retiisum, 190 strumosum, 179 Trichostrongylus douglasi, 233 pergracilis, 63 Trinoton anseris, 209 litiiratum. 209 luridum, 209 Tropisurus fissipinus, 181 Trypanosomiasis, 203 Tuberculin, avian, 91 test. 91 Tuberculosis, avian, 88 Tvimors, 261 Turbinated bones, 14 Turpentine, 186, 294 U Ulna, 4 Ureters, 16 Urinary system, 16 Uropygium, 17 Veins, 7 Vent gleet, 167 Ventriculus bulbosus, 12 Vertebrae, 1 Vertebral column, 1 Vicious habits, 175 Visceral gout, 150 Vitamines, 153 W Wattles, 18 Weisser Kamm, 116 White blood corpuscles, 7 White comb. 116 White diarrhea, 68 Whitewash, 24 Wireworms in the ostrich, 233 Wishbone, 3 Wounds, 301 Yolks, discolored, 170 PRINTED IN THE UNITED STATES OF AMERICA 'XHE following pages contain advertisements of a few of the Macmillan books on kindred subjects. s The Clinical Pathology of the Blood of Domesticated Animals By SAMUEL HOWARD BURNETT, A.B., M.S., D.V.M. Professor in Comparative Pathology, New York State Veterinary College, Cornell University, Ithaca, N. Y. III., Cloth, 8°, $2.25 The purpose of this book is to furnish a text-book of hematology for the use of students and practitioners of veterinary medicine. It is also intended to render easily accessible for investigators data con- cerning the blood of the kinds of experimental animals commonly used. TABLE OF CONTENTS CHAPTER 1. Methods of Examination. 2. Morphology of the Formed Elements. 3. Normal Blood of the Several Domesticated Animals. 4. Variations in Red Corpuscles and Hemoglobin. 5. Influences Affecting the Leucocytes. 6. Special Diseases of the Blood. 7. General and Infectious Diseases. 8. Specific Infectious Diseases Due to Bacteria and Fungi. 9. Infectious Diseases Due to Protozoa. ID. Diseases Whose Cause Has Not Been Definitely Determined. II. Diseases Due to Animal Parasites. A Text-Book of Parasitology: For Veterinary Students By benjamin M. UNDERHILL, V.M.D. Instructor in Zoology, Parasitology and Histology, University of Penn- sylvania School of Veterinary Medicine Preparing. This work, while designed primarily as a text and reference for students and practitioners in veterinary medicine, will be found a concentrated and handy reference book by practitioners of human medicine, students in zoologJ^ and laboratory workers. Heretofore veterinary students in this country have had to rely upon circular matter of this character or upon special chapters scattered in works of other titles. The work contains little that is historical or critical. Parasitic species un- common in this country, or pathogenically unimportant, are omitted, though such as are now regarded as rare, but which in the future may become numerous and important, are given warranted consideration. A feature of the work which marks a distinct advance in the text-book treat- ment of parasitology is the attention given to the biological side of parasitism. This is essential to the student for his proper conception of the whole subject, and is certainly a prerequisite to intelligently applied measures of parasitic control. The work fills a long felt want in our veterinary schools, and altogether, it is a valuable and much needed addition to our American veterinary literature. THE MACMILLAN COMPANY Publishers 64-66 Fifth Avenue New York S Practical Veterinary Pharmacology and Therapeutics By HOWARD JAY MILKS Professor of Therapeutics and Small Animal Clinic, New York State Veterinary College, Cornell University 8vo. $4.25 This book is designed as a text-book for students and practitioners in veterinary medicine. In addition to the usual discussion on the action and uses of drugs there are chapters on the method of action of drugs, incompatibilities, solubilities, prescription writing and biologic prepa- rations. Drugs are grouped according to their therapeutic indications or uses and the general therapeutic considerations are taken up just before the members of the group are discussed in detail. Thus the general ac- tions and uses of the group and the detailed study of the drugs belong- ing to it are discussed in the same chapter. This plan differs from many texts in which the various therapeutic groups are discussed briefly in the first part of the book and to which no reference is made under the detailed discussion of the drugs. The Diseases of Animals By nelson S. MAYO Cloth, Illustrated, i2mo, $1.75 The author gives advice in a brief and popular manner on the dis- eases and ailments of farm animals. It is a book which will enable those who have the care of animals to detect indications of disease and to make timely application of the necessary remedies. " It includes about all that the practical keeper of live-stock has need of, and the method of presentation could hardly be better. The expo- sition has the charm of perfect clearness and simplicity, which makes the book agreeable even to the reader not in search of specific facts." — Country Gentleman. THE MACMILLAN COMPANY Publishers 64-66 Fifth Avenue New York The Pathology and Differential Diagnosis of Infectious Diseases of Animals By VERANUS ALVA MOORE, B.S., M.D., V.M.D. Professor of Comparative Pathology, Bacteriology and Meat Inspec- tion, and Director of the New York State Veterinary College, Cornell University, Ithaca, N. Y. Cloth, 8vo, III., $4.00 This edition has been carefully revised, much of it rewritten and numerous additions made. It has been kept, however, within the limits of a text-book. Two appendices have been added, one on the requirements for interstate ship- ment of live stock and the other on the Federal regulations for the veterinary inspection of meat. These may be of much assistance to veterinarians. The diseases not indigenous to, or imported into, this country have been accorded much less space than those existing here. The desire is to emphasize the nature of the diseases our veterinarians are liable to encounter and, at the same time, give the characteristics of the others. The same plan of presenting the subject and of grouping the diseases according to their etiology, that was followed in the previous editions, has been retained in this. Principles of Microbiology: A Treatise on Bacteria Fungi and Protozoa Pathogenic for Domesticated Animals By VERANUS ALVA MOORE, B.S., M.D., V.M.D. Cloth, 8°, III., $4.00 This volume has been prepared as a text-book for veterinary students begin- ning the study of microbiology. It is the outgrowth of a lecture course which has accompanied the laboratory work in bacteriology and protozoology. The author has endeavored to choose the material that will be of most help to the student of animal diseases and to avoid as much as possible matters of contro- versy. In its preparation, the purpose has been to point out the place and role of micro-organisms in nature; to give the methods for their study and identifi- cation; to indicate the relation of certain species to animal diseases; to give a description of the more important species pathogenic for animals; and a brief discussion of the reaction of the tissues to microbian invasion and the theories of immunity. In order that the volume be of further aid as a key to the entire subject, numerous references to the literature are given where the student can obtain at first hand the results of original research. THE MACMILLAN COMPANY Publishers 64-66 Fifth Avenue New York Medical and Veterinary Entomology By WILLIAM B. HERMS Associate Professor of Parasitology in the University of California; Consulting Parasitologist for the California State Board of Health, etc. Cloth, 8vo, illustrated, $4.00 A work of interest to physicians, veterinarians, health officers, and sanitarians as well as to students. Herein is contained a discussion of all the more important insects and arachnids relating to disease and irritations of man and beast. The author has placed special emphasis on control and prevention. He has aimed to familiarize the student with the specific parasite treated in a chapter, its identity, life history, habits, relation to disease transmission or causation, and to indicate methods for its control and prevention. There are 228 illustrations in the text, largely made from original photographs or drawings. General Surgery By dr. EUGEN FRoHNER Professor in the Royal Veterinary College in Berlin Third Revised Edition Authorized Translation by D. HAMMOND UDALL, B.S.A., V.M.D. Professor of Medicine and Hygiene, N. Y. State Veterinary College, Ithaca; Major, Veterinary Reserve Corps, U. S. Army Cloth, 8°, $3.00 The new third edition of general surgery is improved and enlarged in many respects. The chapter on etiology of tumors has been re- written, and many additions made. The chapter on botryomycosis has been newly written to harmonize with the most recent investigations on this subject. The chapter on tuberculosis has been retained and even enlarged. The important chapter on chronic deforming ar- thritis has been supplemented with the results of recent inve-^^-'^^ations made in D. Frohner's clinic upon ring-bones, chronic gonitis, and omar- thritis. Recent investigations on myositis, neuritis, healing of frac- tures, necrosis bacilli, pseudo-edema bacilli, and foal-lameness have also been considered. THE MACMILLAN COMPANY Publishers 64-66 Fifth Avenue New York LIBRARY OF CONGRESS -m-i^- .•■. ■ \f.v.'k^;;i.;,,-' m ;.;(::;, ^^^^i.:::^^ 't''^ ■vV '.', •>-' ■• : ;■■ ; -1 x-'-,;- ■ ■• -.V ,', '!-': ••V- ;M>,V;.',-::|-,v :;-^' :'i ':v-:,.:-^;;^ ■; .-:^l-^-.