key: cord-022237-qxya4cs3
authors: Bryant, Everett
title: Biology and Diseases of Birds
date: 2013-11-17
journal: Laboratory Animal Medicine
DOI: 10.1016/b978-0-12-263620-2.50019-7
sha: 
doc_id: 22237
cord_uid: qxya4cs3

nan

The domestic fowl has been the most useful in experimental axonomy trials. The fast maturing and highly inbred chicken can be used with great statistical confidence. Diseases can be prevented Most avian species used for research purposes fall within ? a n d i s o l a t i o n r e a r j n g j s n e j t h e r d i f f i c u , t n Q r ^, three orders: Galliformes, which includes domestic fowl, quail, pheasants, turkeys, partridges, grouse, guinea fowl and brush turkeys; Anseriformes, which includes ducks, geese, swans, and screamers; and the Columbiformes, which includes c · Availability of Chickens for Research pigeons, doves, and sand grouse.

The bird fits into the overall taxonomic scheme as follows: Specific pathogen-free (SPF) fertile eggs, day-old chicks, or Kingdom, Animal; Phylum, Chordata; Class, Aves; Order, 27 started pullets are available for use in research. Specific pathoorders with approximately 8600 species. A clear outline of the gen-free chickens or eggs come from breeding stock negative avian orders listing the common names of birds in each may be to diseases caused by mycoplasmas, Newcastle disease, infecfound in Steiner and Davis (1981) .

tious bronchitis, avian encephalomyelitis, infectious bursal disease, quail bronchitis, salmonellosis, pasteurellosis, and in fectious coryza. Somes (1981) lists the sources of specialized lines, strains, mutations, breeds, and varieties of chickens, turkeys, and Ja panese quail. Chromosome linkage maps for the three species and modes of inheritance are also given for most genetic traits.

Bickford, 1979; Woodard et al., 1973; Schwartz, 1977) Quality animal welfare and optimal comfort for birds is nec essary to insure reliable research data. The ability periodically to observe birds on experimental test through a glass window is ideal; however, if an observation point is not available, the animal technician should check the birds at least twice a day for paleness, dehydration, and other signs indicative of diseases.

Death before 2 weeks of age may be due to chilling, over heating, crowding, and omphalitis. Mortality at 2-6 weeks in research chickens may be due to coccidiosis or one of the enteritides.

Brooding temperature for 1-day-old chicks should be be tween 90°-95°F and gradually reduced to 75°-80°F by the third week. Chicks will constantly peep if too hot or too cold. Lowered humidity will cause poor feathering, and if the en vironment is too moist, disease problems will be more pro nounced. A relative humidity of 30-40% is ideal. Therefore, frequent monitoring to control temperature and humidity should be practiced. Fresh air, without drafts, helps to mini mize moisture accumulation. Stale air retards growth of birds and enhances respiratory diseases.

The density of broilers and layer replacements may vary with the experimental procedure, but Table I will serve as a guideline.

There are many kinds of feeders, waterers, and brooders available. The simplest and least expensive may be the best for experimental work. While adjusting to the feeders newly hatched chicks and poults should be fed on papers from day 1 to day 7. Trough feeders work well for birds raised on the floor. It is important to have an adjustable feeder. The level of the feed in the trough should be equal to the level of the back of a standing chicken. This allows the bird access to the feed and prevents waste of feed.

Tube feeders that hang from the ceiling have the advantage of holding more feed without waste. They are adjustable, and the feed should be at the same level, as described for trough feeding. Too many feeders of either type impede available floor space for the chickens. Two 4-ft trough feeders or two tube feeders are adequate for 100 birds at any age.

Waterers should provide clean, fresh water ad libidum. Birds should never be without water. There are many types, but a simple gallon jug with a plastic bottom containing a groove circling the jug is ideal for birds from 1 to 10 days of age. An automatic trough waterer, one 4-ft long per hundred birds, is adequate. Automatic waterers can stop working, run over, and make it difficult to measure water consumption. Therefore, large can-type waterers or open pan-type waterers may be bet ter for some types of trials. They are more easily cleaned and control water intake better. Incidence of candidiasis in a flock of birds is directly related to the level of water sanitation, and proper attention to water quality greatly reduces this disease in research birds.

Commercially available cage equipment will also have feeders and waterers and sometimes a heat source. Daily clean ing of fecal material from cages enhances the level of sanita tion. External and internal parasitism is increased in birds reared in dirty cages.

For heat and ventilation, brooder stoves fueled by gas, oil, coal, and electricity are available. For small groups of birds, heat lamps are adequate. Supplementary room heat is neces sary for small groups in colder climates. Air conditioning may be necessary during extremely hot weather. An exhaust fan is necessary to ensure removal of stale air. For young chicks, è ft 3 /min will exchange air quite well and for older birds, 1 ft 3 / min is adequate. Modern animal facilities meeting the criteria for the NIH ' 'Guide for the Care and Use of Laboratory Ani mals" will provide acceptable heat, ventilation, and air condi tioning needs (see Chapter 17).

Nests are needed for laying birds. Adequate nests should be provided to ensure one nest for every four birds. Nests should be constructed of metal for ease of cleaning and should be well ventilated. Lack of sharp corners minimizes trauma, and dry materials, such as shavings, sawdust, or peanut hulls, make excellent nest material.

A completely sanitized and disinfected room with sterilized equipment is necessary for research purposes. Birds are coprophagic, and many diseases of the digestive tract are trans mitted in this manner. Physical cleaning of room surfaces with high pressure of hot water will remove fecal material, mucus, and other debris from walls and floors. Cages should be sani tized in appropriate cage washers. While the pen is still warm and wet, fumigation with formaldehyde gas is quite effective. The temperature should be 80°F and the humidity 70% or high er to be most efficient. Formaldehyde vapors have a potential health risk to humans, and the reader should refer to the discus sion of disinfectants by Hofstad et al. (1978) before using this product.

Once the area and equipment are cleaned, iodines, quatern ary ammonium compounds, chlorines, or other agents can be used to disinfect the premises.

No one should be admitted to isolation areas without a show er, clean clothing, and clean boots. Doors should be locked at all times, and animal technicians should not be assigned to care for any other birds.

Birds have pneumatic bones, with air spaces and channels, which add buoyancy in flight. This system of pneumatic bones provides direct channels from the air sacs through the bones so that air carrying infecting organisms may travel throughout the bird rather rapidly. Certain respiratory infections and parasites use these channels for distribution of the microorganisms. Small birds lack teeth; the organ of mastication is the gizzard which contains grit or gravel, thereby enabling grinding of hard grains. If the feed is an all-mash or all-pellet diet, no grit is needed in the diet.

Most birds possess a crop, a dilatation in the midesophageal region. Pigeons and pet birds regurgitate and feed their young on crop milk. This process allows transmission of parasites to the young from healthy adult carriers.

Only the left ovary and oviduct are functional in the hen. Frequently a cyst, the remnant of the right oviduct, is found; however, this causes no pathological disturbance.

B. Applied Physiology (see Sturkie, 1976) Birds can stand extreme variations of environmental tem perature for short periods of time. As the relative humidity increases, the temperature tolerance of the chicken decreases. Normal heart rate for the chicken is about 300 beats/min and will increase substantially during excitement and periods of stress. The normal respiration for the chicken is approximately 100/min, and will also increase rapidly as the temperature goes up. Artificial light is important. Fourteen to 16 hr of light per day is needed for optimum egg production. The optimum tem perature for egg production is between 50°-70°F. Any varia tion thereof may cause a decrease in egg production.

Growth rate has improved so rapidly that textbooks cannot keep up-to-date. Feed conversions of less than 2.0 are being reported on a 4 lb average weight broiler at 49 days of age. These are under excellent field management with optimum nu trition, genetics, and freedom from disease.

Egg production flocks have also improved their efficiency. The average flock today will peak above 90% by the time they reach 30 weeks of age.

For a complete treatment of avian hematology, the reader is referred to Sturkie (1976) . Blood volume in the bird is about 10% of total body weight. This will vary according to age, sex, and species. An atlas on avian hematology is also available (Lucas and Jamroz, 1961) .

Data shown in Table II were taken from Olson (1937) .

Chickens, turkeys, and other birds require the six major nu trients: carbohydrates for energy, fats for energy and essential fatty acids, protein for meat and egg production, minerals for bones and shells, vitamins for chemical catalysts, and water.

Birds should have a complete and balanced ration with very little supplementation. Unnecessary supplementation may create other deficiencies.

Age and functional status of the flock will determine the for mula needed. Table III lists approximate types of formulas needed for various ages and classes of birds. High quality protein is necessary for growth and mainte nance of birds. All the essential amino acids must be present in the diet as the bird cannot convert them from raw protein. Min erals and vitamins must be provided in balance. Calcium and phosphorus should be in a ratio of 2: 1 for young growing chickens.

Antioxidants should always be used to prevent oxidation of fats and fat-soluble vitamins. Feed additives, especially arsenicals and certain drugs, should be fed according to the manufac turer's directions. Consumption of eggs from these birds dur ing this time should be avoided. For a more detailed account of nutrition in birds, the reader is referred to the specific texts by Scott et al. (1976) , by the National Research Council of the National Academy of Sciences (1977) , and to the chapter in Hofstad ei a/. (1978) . Specific nutritional deficiencies will be discussed in Section VIII.

Poultry and other birds are easily startled. Flashing lights, loud noises, and shadows will cause birds to pile up on each other causing the pen mates underneath to suffocate.

Hysteria, caused by sudden fright, will result in birds flying against the wall for no apparent reason. Many experts argue that a sudden change in air pressure will cause hysteria. When the author has encountered this disease, the birds have usually been raised in a filtered-air, positive-pressure facility. b. Clinical Signs and Lesions. Escherichia coli may be a primary infectious agent; clinical onset is rapid and daily mor tality can approach 0.5-1.0%. The usual lesions noted are air sacculitis, fibrinous pericarditis, and fibrinous perihepatitis. Rarely is the trachea involved. Colîgranuloma (Hjarre's dis ease) may be caused by a pathogenic E. coli serotype. Avian tuberculosis may be confused with colibacillosis. Granulomas of the intestine are differentiated from tuberculosis by the use of the acid-fast stain. Escherichia coli, of course, is not acid fast. Other lesions caused by E. coli include arthritis leading to lameness and death, navel infection leading to high mortality, and foot pad infections.

c. Epizootiology. Hens with E. coli infection, especially of the oviduct, contaminate the egg shell. Bacteria may then penetrate the egg shell and the chick is hatched with a yolk sac infected with E. coli. d. Diagnosis. Escherichia coli should always be consid ered a potential pathogen in birds. If an air sacculitis syndrome develops, with no isolation of Pasteur ella sp., Mycoplasma sp., or Hemophilus sp., it is essential to consider E. coli as the potential pathogen. Isolations of E. coli from yolk sacs, joints, or bone marrow should always be considered a primary cause of disease. e. Prevention. Good management of the chicks must in clude proper ventilation and the proper care of hatching eggs. This is the most important means of preventing navel ill. Dirty, contaminated eggs should never be used for hatching. /. Treatment. As with all bacterial infections in poultry, antimicrobial susceptibility testing should be used to determine the treatment of choice for any generalized E. coli infection.

g. Research implications. Escherichia coli infection will damage experimental flocks, causing uneven growth.

a. Etiology. The cause of coryza is Hemophilus paragallinarum. It is a gram-negative, bipolar staining rod and can easily be demonstrated in sinus exudate.

b. Clinical Signs. Signs include a sudden onset with high morbidity, reduction in feed intake and growth, and depressed egg production. Uncomplicated coryza is a disease of the up per respiratory tract causing ocular and nasal discharge, facial edema, and swollen infraorbital sinuses.

c. Epizootiology and Transmission. Transmission is ac complished mainly by ill or recovered carrier birds. Inhalation of infectious material and ingestion of contaminated feed and water provide the best means of transmission.

d. Necropsy Findings. At necropsy, there is conjuncti vitis, cheesey exudate in the conjunctival sac, nasal discharge, and a catarrhal inflammation of the nasal passages and sinuses. The infraorbital sinuses may be filled with exudate. e. Diagnosis. History, signs, and lesions will suggest coryza. A gram-stained smear of sinus exudate showing gramnegative bipolar rods warrant a strong presumptive diagnosis of coryza. Incubation in a C0 2 atmosphere of a culture of the exudate on blood agar with a Staphylococcus nurse colony will confirm the presence of//, paragallinarum. f. Prevention. Depopulation of all birds before introducing chicks is essential, and a complete sanitizing and disinfecting of the brooder facilities is also necessary. A bacterin is avail able and can be used in birds 14 weeks of age or older with a booster every 3 weeks. Several injections are necessary to con fer protective immunity.

g. Treatment. Continuous medication appears to suppress clinical infection, but when removed relapses occur. Medica tions used with success include streptomycin, erythromycin, spectinomycin, tylosin tartrate, and sulfadimethoxine.

h. Research Complications. A diagnosis of H. paragallinarum infection in a research unit would warrant termina tion of the experiment. Salvage of an experiment with this dis ease would provide questionable research data at best. The chronicity of the disease and the recovered carrier bird would further jeopardize a research colony.

a. Etiology. The important etiological agents appear to be Clostridium septicum and Staphylococcus aureus (Frazier et al., 1964) . The host is likely to be immunosuppressed, and probably undergoing a simultaneous outbreak of infectious bursal disease. (See Section IV,B.) b. Clinical Signs. Signs in 4-to 16-week old chickens and turkeys include a sudden increase in morbidity and mortality. Wet, gangrenous areas can be seen in the skin of the wings and legs.

c. Epizootiology and Transmission. Skin wounds of chickens are a common occurrence, and secondary infections are expected. However, gangrenous dermatitis appears to be a specific disease complicated by the presence of heavily con taminated environment containing Clostridium spp. and Staphylococcus spp. The syndrome was rare until immunosuppression caused by bursal damage from infectious bursal disease virus, mycotoxins, and possibly other factors became more common.

d. Necropsy Findings. Usual findings include necrosis of the skin and underlying areas of the thigh, breast, wing tips, hip, and back. Hemorrhagic, necrotizing myositis has also been described.

e. Pathogenesis. It would appear that the toxin of the Staphylococcus species causes necrosis and anerobiosis; the Clostridium then multiplies and contributes to the gangrene.

/. Differential Diagnosis. Signs and bacterial cultures from the lesions will give a presumptive diagnosis. Selenium deficiency that causes an exudative diathesis may mimic gang renous dermatitits.

Eliminating all causes of skin trauma and improving the sanitation plus instituting an immunization pro-gram for infectious bursal disease will help prevent the disease.

h. Treatment. A susceptibility test for the Staphylococcus isolated will suggest the antibiotic of choice. Most broad-spec trum drugs will aid the recovery of affected birds.

i. Research Complications. Widespread gangrenous der matitis in birds may compromise the study. Because this dis ease is often a complication of infectious bursal disease im mune competence may have been altered; therefore research data collected on affected bird may be unreliable.

a. Etiology. The cause of necrotic enteritis is thought to be Clostridium perfringens. Other inciting factors may be neces sary, but have eluded investigators studying this disease. The disease is seen mostly when high energy, broiler-type rations are used.

b. Clinical Signs. Necrotic enteritis is usually seen in broilers; many times only the males, at about 2-8 weeks of age, are affected. Birds show profound depression, and mor tality may start at 1% per day and last about 1 week (Helmboldt and Bryant, 1971 ).

c. Epizootiology and Transmission. It appears that trans mission is direct and via the feces.

d. Necropsy Findings. A fibrinonecrotic enteritis is noted, and the entire small intestine becomes dilated with fluid debris and becomes very friable. e. Pathogenesis. There is evidence that a toxin damages the villus tips, and eventually the integrity of the rest of the intestinal wall is lost.

/. Differential Diagnosis. This disease can be differenti ated from ulcerative enteritis (quail disease) by isolation and identification of the Clostridium perfringens. Eimeria brunetti may be present as a secondary problem.

g. Prevention. Sanitation, disinfection, and isolation will provide the best protection against necrotic enteritis. Low level feeding of antibiotics at 100 gm per ton (50 mg/lb) of feed from 0 to 10 weeks of age will totally prevent the disease.

h. Treatment. The organism is very easily treated with high levels of tetracyclines, furazolidone, streptomycin, or bacitracin.

i. Research Complications. Diagnosis of disease in a pen warrants instituting a low level antibiotic therapy for succeed ing flocks.

a. Etiology. Clostridium colinum, a gram-positive, sporeforming bacillus, is the cause of ulcerative enteritis. This bac terium is best recovered from fresh liver cultured on tryptose agar or the yolk sac of 5-7 day embryos.

b. Clinical Signs. Affected quail exhibit high morbidity with mortality sometimes approaching 100%. Chickens and turkey poults, on the other hand, may experience low mor talities of only 2-10%. Listlessness, drooping wings, ruffled feathers, and diarrhea are typical signs of this disease.

c. Epizootiology and Transmission. The disease is highly contagious among quail. It spreads mainly through feces from ill or recovered carrier birds. f. Differential Diagnosis. Coccidiosis caused by Eimeria brunetti may produce a necrotizing enteritis of the large intes tine, which resembles ulcerative enteritis. Scrapings of the in testinal mucosa will usually reveal oocysts of E. brunetti. Nec rotic enteritis caused by Clostridium perfringens can also mimic quail disease. Histologically, necrotic enteritis produces no ulcers, and the intestinal lesion is villus tip loss and cystic dilatation of the deeper glands.

g. Prevention. Birds should be reared in a clean, disin fected and isolated environment. Low level of antibiotics, 50-100 gm per ton of feed, will prevent the disease. Strep tomycin, bacitracin, terramycin, aureomycin, and furazoli done are therapeutically effective.

h. Treatment. All of the above antibiotics at 200 gm per ton of feed (100 mg/lb) will curtail and in some cases termi nate the mortality.

/. Research Complications. Substantial morbidity and mortality would terminate most experiments. Preventive levels of antibiotics are indicated from 0 to 10 weeks in birds housed in a building where the disease was previously encountered.

a. Etiology. The ingestion of the toxin produced by Clostridium botulinum is the cause of botulism. The lethal tox in, which must be produced under anaerobic conditions, is found in decaying feed, dead birds, and maggots. Clostridium botulinum organisms per se are not considered pathogenic.

b. Clinical Signs. Drowsiness, weakness, and a progres sive paralysis of the legs, wings, and neck are all suggestive of botulism.

c. Epizootiology and Transmission. The ingestion of pre formed toxin is necessary to produce the disease. Poultry or wild birds should not be allowed to ingest wet, moldy feed. Accidental water spillage in a research unit could result in con ditions necessary for the development of the toxin.

d. Necropsy Findings. The absence of lesions may be the best indication that the birds are dying from botulism. The of fending decayed matter containing the toxin may be found in the crop, proventriculus, or intestine.

e. Differential Diagnosis. History, signs, and the presence of decaying feed may help identify the disease. Gizzard or in testinal contents may be washed and some of the fluid inocu lated into mice, half of which have been previously protected with C. botulinum antiserum, for a definitive diagnosis. Tran sient paralysis, a mild form of Marek's disease, can produce signs similar to botulism. In pheasants, paralysis caused by eastern encephalomyelitis virus could be confused with botulism.

/. Prevention. If birds are raised under clean conditions, botulism is rare.

g. Treatment. Type A and C antitoxin may be indicated when valuable animals are affected. Laxatives may also be used with some success. It is important to provide fresh, clean water in a botulism outbreak.

h. Research Complications. It would be a rare to encoun ter this disease under research condition.

a. Etiology. The cause of erysipelas is Erysipelothrix rhusiopathiae, a gram-positive, pleomorphic rod. It primarily affects turkeys, though chickens can be infected.

b. Clinical Signs. Usually the disease starts with sudden onset followed by depression, diarrhea, lameness, and a rapidly increasing morbidity and mortality. The snood of the male turkey often becomes swollen.

c. Epizootiology and Transmission. Fecal shedding of E. rhusiopathiae occurs in recovered turkeys and continues for about 6 weeks. The oral-fecal route is a significant source of transmission. Cutaneous injuries of the snood and head also may allow entry of the bacterium, and fighting among males is a common method of transmitting this disease.

d. Necropsy Findings. The lesions are those of a septicemia and vasculitis. There is a degeneration and hemorrhage in pericardial fat. The heart muscle, kidney, spleen, and liver may also show hemorrhage. Fibrinopurulent exudate in the joints, vegetative endocarditis, and dark, crusty skin lesions are also common.

e. Differential Diagnosis. History, signs, lesions, and cul ture of E. rhusiopathiae will aid in a diagnosis of erysipelas. It should be differentiated from colibacillosis, fowl cholera, salmonellosis, and possibly a velogenic strain of Newcastle disease.

/. Prevention. Turkey poults should be raised away from older turkeys, sheep, and swine. Poults should be vaccinated with a bacterin at 16-20 weeks of age. Raw fish meal may harbor E. rhusiopathiae organisms and should be avoided.

g. Treatment. Penicillin and erysipelas bacterin may be in jected simultaneously in an outbreak. Tetracyclines in the feed or water will also help reduce losses.

h. Research Complications. Erysipelas is a septicémie dis ease; therefore, it will significantly retard growth and weight gain in animals recovering from the disease.

a. Etiology. Predisposing causes of omphalitis may in clude excessive humidity and excessive fecal contamination of the incubator. Fecal contamination of eggs used for hatching purposes will also contribute to omphalitis. As the navel fails to close at hatching, a route of entry for bacteria, such as E. coli, Pseudomonas, and Proteus, as well as staphylococci is available. Chilling or overheating baby chicks may also pre cipitate or exacerbate this condition.

b. Clinical Signs. Depression, drooping of the head, and huddling near a heat source are usual signs. A scab over the unhealed navel is often present, and mortality usually is high-est on the third and fourth days posthatching, sometimes reach ing 1-10% during the first week.

c. Epizootiology and Transmission. The disease is trans mitted through infection of the yolk sac prior to hatching. It is not contagious from chick to chick.

d. Necropsy Findings. Infected navels, large unabsorbed yolks, and extensive peritonitis are the common lesions com monly noted.

e. Differential Diagnosis. Isolation and identification of the bacteria from infected yolk will pinpoint omphalitis and its cause.

/. Prevention. Proper hatching egg management, empha sizing care and sanitation of the incubators will reduce the inci dence of omphalitis.

There is no treatment for omphalitis except removing affected chicks. Effective drug levels cannot eradi cate the infection in the yolk sac.

h. Research Complications. Affected chicks usually die during the outbreak. Those that do survive, appear to grow well.

a. Etiology. Fowl cholera, an acute septicémie disease of poultry, turkeys, waterfowl, and wild birds, is caused by Pasteurella multocida, a gram-negative, bipolar rod (Panigraphy and Glass, 1982) . Thirteen serotypes of this bacterium have been identified.

b. Clinical Signs. Fowl cholera usually affects young adults. Birds affected with the acute form of fowl cholera may show no signs other than sudden deaths. Hens may die while laying an egg and will be found dead on the nest. In less acute cases, birds will show depression, anorexia, and cyanosis. A white-green diarrhea is usually present. In the chronic form, localized infections of the joints, wattles, foot pads, sinuses, and middle ear is clinically manifested by lameness and torticollis.

c. Epizootiology and Transmission. Ingestion of decaying carcasses, contaminated feed and water, and feces from re covered carriers are sources off*, multocida. Wild birds, and rodents are also potential transmitters. Transovarian transmis sion does not play a role in transmission.

d. Necropsy Findings. Peracute deaths may preclude the presence of gross lesions. Pinpoint hemorrhages are common in the coronary fat suggesting an acute septicemia. In birds that die less acutely, pericarditis and perihepatitis are usually found. Cheesy exudate may also be seen around the oviduct. Chronic lesions consist of inflammation of the wattles, joints, conjunctival sac, infraorbital sinus, middle ear, and sometimes the bones of the skull. Fibrinous pneumonia is common in turkeys.

e. Pathogenesis. Fowl cholera is a septicemia with the agent spreading via the bloodstream to many organs.

/. Differential Diagnosis. Isolation and identification of the organism is necessary to differentiate this disease from erysipelas in turkeys and colibacillosis in hens.

Birds reared in clean, isolated premises usually are free of Pastuerella infections. Addition of birds with unknown health status to a clean flock should be avoided. Healthy-appearing birds can carry P. multocida and are a com mon source of introduction of the organism to a premise. Bacterins are protective in hens. The key to successful production of immunity is to use the correct serotype for immunization. Two doses, about 1 month apart, are necessary for adequate protection. Live oral cultures of the Pasteurella are available for use in endemic areas; however, use of this product may cause disease in unvaccinated birds.

h. Treatment. Drugs will arrest mortality, but will not cure the disease. Sulfaquinoxaline will work well but will depress egg production. Therapeutic results are obtained with tetracycline at 200 gm per ton (100 mg/lb) of feed for about 2 weeks. However, it is important to note that not all Pasteurella isolates are susceptible to the tetracyclines. Improved sanita tion, immediate removal of sick and dead birds, and preven tion of cannibalism are necessary to control the disease.

/. Research Complications. Research birds affected with Pasteurella sp. do not yield reliable research data; termination of the experiment, therefore, is recommended.

a. Etiology. The cause of fowl typhoid is Salmonella gallinarum; it also cross-agglutinates with Salmonella pullorum. Salmonella gallinarum is a gram-negative rod with no spores or capsule.

b. Clinical Signs. Affected chickens have ruffled feathers, pale heads, and shrunken combs. In turkeys, listlessness and a greenish diarrhea are often recognized clinically.

c. Epizootiology and Transmission. Egg transmission via the yolk or shell surface often perpetuates the disease from dam to offspring. d. Necropsy Findings. A bile-stained liver, bronzed in ap pearance and greatly swollen, is the most distinguishing lesion of fowl typhoid. All other lesions are similar to pullorum disease.

e. Differential Diagnosis. This disease is now rare in the United States and must be differentiated from pullorum disease and paratyphoid infections. Isolation and identification of Salmonella is necessary for a diagnosis.

/. Prevention. The purchase of pullorum-typhoid-clean chicks from the National Poultry Improvement Program hatch eries is necessary for research.

No treatment is effective. It is a reportable disease to the state veterinarian, and depopulation will be recommended.

h. Research Complications. Salmonella-infected birds should not be used for research purposes.

a. Etiology. The cause of pullorum disease is Salmonella pullorum. It is a gram-negative bacillus and cross-reacts with S. gallinarum. b. Clinical Signs. Infected adults may show no signs but transmit the agent through their eggs. Young chicks and poults will show white pasting around the vents, and huddling near the heat source. Mortality may reach 90-100%.

c. Epizootiology and Transmission. Egg transmission through the yolk and hatchery transmission via the infected eggs and chicks in the incubators and hatchers are the usual methods of transmitting S. pullorum. d. Necropsy Findings. Myocarditis, pericarditis, and atro phied ovaries are classical lesions of pullorum disease in adults. In young birds, gray nodules may appear on the spleen, peritoneum, lung, liver, heart, and intestine. As with any Salmonella infection, cecal cores are commonly seen. An en larged spleen is present, but this is a nonspecific lesion since it is usually seen with many bacterial infections.

e. Differential Diagnosis. A positive serum agglutination plus isolation, identification, and typing of the agent from the yolk sac, gallbladder, spleen, or cecal tonsil will confirm the diagnosis of S. pullorum.

/. Prevention. The purchase of pullorum-typhoid-clean chicks and poults is essential for research.

No treatment is available. The disease is reportable to the state veterinarian, who when notified will prob ably insist on depopulation.

h. Research Complications. Salmonella-infected birds should not be used for research purposes.

a. Etiology. Any species of a large group of Salmonella sp. may infect birds and mammals and are not host specific. The most common one isolated from birds is Salmonella typhimurium. Other common serotypes include S. enteritis, S. oranienberg, S. montivideo, S. newport, S. anatum, S. derby, and S. bredeny. Many others exist and may cause mortality.

b. Clinical Signs. Dehydration, pasting of the vents, and huddling near the heat source are signs of a Salmonella out break. High morbidity and mortality are usually the first signs.

c. Epizootiology and Transmission. Diarrhea in the breeders will cause contamination of the Qgg shells, and Salmonella is often transmitted in this way. Contaminated feed ingredients such as meat scraps may also transmit infection. Transovarian transmission is possible, and human carriers may also be a factor in transmission (See Chapter 22 by Fox et al.).

d. Necropsy Findings. Dehydration, enteritis, and focal necrosis of the intestinal mucosa are common lesions. Pigeons usually have joint infections and conjunctivitis. Cheesy cores in the ceca, common in all Salmonella infections, will usually be found.

e. Differential Diagnosis. The isolation and identification of the offending bacterium is essential for diagnosis. All salmonella infections may have similar signs and lesions. In addi tion, coccidiosis and blackhead will produce cheesy cores in the cecae.

/. Prevention. Use clean birds free of Salmonella. Isolate the new brood and feed only pelleted feed or crumbles to pre vent introduction of Salmonella via the feed.

g. Treatment. Attempts to treat the infection usually have been discouraging. Most cases do not respond to therapy and carrier birds are produced. Furazolidone in pigeons is partially effective. Sulfa drugs will suppress mortality but will not cure the disease.

h. Research Complications. Salmonella-infected birds should not be used for research purposes.

a. Etiology. Avian tuberculosis is caused by Mycobacterium avium, an acid-fast, very resistant bacterium. It is sepa rate and distinct from human and cattle types, but will infect swine and sensitize cattle to the bovine tuberculin test.

b. Clinical Signs. Emaciation in the presence of good feed intake may suggest tuberculosis. Diarrhea and lameness is common. Birds appear very pale, especially the comb and wattles.

c. Epizootiology and Transmission. Transmission is by in gestion of M. avium. Association of young chicks with their dams during the growing period in backyard flocks ensures transmission of the bacteria to susceptible birds.

d. Necropsy Findings. Extreme emaciation, nodules along the intestinal tract, and discrete granulomas in liver and spleen are typical of tuberculosis. Granulomas may also be found in the bone marrow and more rarely in the lung.

e. Differential Diagnosis. Coligranuloma can mimic avian tuberculosis. The presence of acid-fast bacilli in liver or spleen impression smears will confirm the presence of M. avium.

f. Prevention. An all-in, all-out system of poultry rearing will prevent avian tuberculosis.

g. Treatment. Because of drug resistance and the possible public health significance of this disease, treatment is dis couraged. Depopulation is recommended by the state's veteri nary authorities.

No tuberculosis-affected birds should be used for research purposes.

Turkeys] (see Jordan, 1979) a. Etiology. The primary cause of CRD is Mycoplasma gallisepticum, but the following agents will enhance effects of M. gallisepticum and cause a complicated respiratory syn drome with high mortality: infectious bronchitis virus, infec tious laryngotracheitis virus, Newcastle disease virus, Escherichia coli, Pasteur ella multocida, Hemophilus gallinarum, and others.

b. Clinical Signs. Hens reaching the age of full egg pro duction (35 weeks) will not reach peak egg production referred to as genetic potential for that specific strain. Coughing and sneezing may be noticed, particularly at night. The disease is more pronounced in broilers. Chronic respiratory disease plus secondary bacterial infection, will produce high mortality, high morbidity and high condemnations due to air sacculitis, pericarditis, and perihepatitis. Turkeys may have sinusitis, with exudate in the infraorbital sinuses.

c. Epizootiology and Transmission. Transovarian trans mission is the most important method of transmitting M. gallisepticum. Lateral spread through aerosols from infected off spring occurs in the hatchers or brooders. Wild birds and fomites can also be a source of agent transmission.

d. Necropsy Findings. Thickened air sacs, mucus in the trachea, sinusitis, and air sacculitis are the common lesions in uncomplicated chronic respiratory disease. In chronic respira tory disease with secondary bacterial infection, the classic le sions include air sacculitis with fibrinous hepatitis and perciarditis.

e. Differential Diagnosis. Many of the respiratory dis eases of poultry appear similar and are differentiated with diffi culty. A positive M. gallisepticum agglutination test in at least ten birds from a previously known M. gallisepticum negative flock would strongly suggest a diagnosis of chronic respiratory disease. Histology of the trachea, lungs, and air sacs will show hyperplastic lymphoid follicles if M. gallisepticum is present; however, this lesion is not pathognomonic. Isolation of the Mycoplasma is the best means of establishing a diagnosis of chronic respiratory disease.

/. Prevention. Mycoplasma gallisepticum-ïrzt chicks are easy to obtain; therefore use of positive chicks in experimental work is not warranted. Controlled exposure using the live cul ture of the "Chick F " strain is not recommended except in multi-age, egg-producing flocks. It is not recommended in breeders or experimental trials.

g. Treatment. Improved management and broad-spectrum antibiotics may help control the losses due to secondary bac teria. Tylosin is the most effective drug against M. gallisepticum.

h. Research Complications. Positive Mycoplasma birds should not be used in research trials.

a. Etiology. The cause is Mycoplasma meleagridis, an egg-transmitted mycoplasmal agent of turkeys. The usual man ifestation is air sacculitis in young poults, but since organisms are shed in semen as well as yolk it can also be considered a venerai disease of this species.

b. Clinical Signs. The signs are usually found only in young growing turkeys. Mild respiratory signs, poor growth, crooked necks, and leg weaknesses are considered signs of this infection.

c. Epizootiology and Transmission. Transovarian trans mission is of primary importance. Semen contains the Mycoplasma organism, so toms as well as hens serve to transmit M. meleagridis. Lateral spread is similar to other mycoplasmas in that stresses and/or other infections seem to enhance the severity of this disease. h. Research Complications. Turkeys infected with M. meleagridis should not be used for research since birds free of the disease can be purchased.

a. Etiology. The cause of infectious synovitis is Mycoplasma synoviae. It can be isolated in broth media or in 5-to 7-day-old embryonating chicken eggs. Isolates of M. synoviae vary in their pathogenicity and also in their susceptibility to drugs.

b. Clinical Signs. Lameness and crouching are the most common signs. Usually morbidity and mortality are low, but retarded growth is a common finding.

c. Epizootiology and Transmission. The transovarian route is the most important means of transmitting the agent from dam to progeny. It is thought that a small number of infected eggs are laid and positive offspring spread infection to pen mates during the growing period.

d. Necropsy Findings. Lesions include yellow exudate in the leg and wing joints but may also be found in the tempormandibular joint, shoulder, and keel bursa. Foot pads are usu ally swollen and hot. The liver will be greenish due to bile retention. Air sacculitis may also be present. b. Clinical Signs. In mild cases, slight respiratory signs and diarrhea will be seen. In severe turkey cases, depression, weakness, anorexia, and reduced weight are noted. Mortality may reach 25%. In pigeons, conjunctivitis is a feature of the disease, while in the psittacine caged birds, depression, anorexia, diarrhea, rales, and death may be seen.

c. Epizootiology and Transmission. Transmission appears to be by direct contact with infected carriers. Inhalation and ingestion of feces are the two most important means of trans mission of Chlamydia psittaci. d. Necropsy Findings. An enlarged congested spleen is al most always found in chlamydiosis in all avian species. Le sions of air sacculitis, pericarditis, and perihepatitis are com monly noted. Unfortunately, these are the same lesions noted in turkeys suffering from mycoplasmosis.

e. Differential Diagnosis. History, clinical signs, and gross lesions aid in the diagnosis. The findings of intracytoplasmic inclusion (LCL bodies) in impression smears of the air sacs or cut surface of the spleen stained by the Macchiavello or Giemsa method will suggest a diagnosis of chlamydiosis. Isolation and identification of the agent should not be attempted by an inexperienced person or without proper hoods and facilities to protect laboratory personnel. This agent, in laboratory culture, is easily transmitted to research technicians.

/. Prevention. Avoid any cross-exposure of research birds to caged pet birds or wild birds. An all-in, all-out system will successfully prevent chlamydiosis. All new arrivals of psit tacine birds should be treated for 60 days at 2 gm per gallon of drinking water with tetracycline or with pellets containing an equivalent level of antibiotic.

g. Treatment. Chlamydiosis is a reportable disease and all infected flocks and their treatments should be reported to the proper authorities.

Chlamydia psittaci should be used for research purposes.

a. Etiology. Infectious bronchitis affects only chickens and is caused by a coronavirus. It does not hemagglutinate erythrocytes. Many serotypes exist, but the two most common are Massachusetts and Connecticut.

b. Clinical Signs. In young chicks, a sudden onset of coughing, sneezing, and rales occurs. The birds are weak and crowd toward the source of heat. Feed intake may drop by 50% in broiler-type birds. In adults, severe respiratory signs accom panied by a severe drop in egg production are evident. Egg quality, as evidenced by watery albumen and soft shells with sandpaperlike ends, renders the flock economically useless for egg production.

c. Epizootiology and Transmission. Aerosol transmission over long distances is common. Recovered carriers and con taminated premises may serve as a source of the virus for 30 days or more.

d. Necropsy Findings. Air sacculitis and excessive tra chéal mucus are the most common findings. In very young chicks, bronchi can be filled with yellow exudate (Fig. 1 ).

e. Differential Diagnosis. Isolation of the virus in 9-to 12day-old chick embryos will confirm the diagnosis. Determina tion of infectious bronchitis immunity with a serum neutraliza tion test using acute and convalescent serum will also help de termine the presence of infectious bronchitis virus. /. Prevention. Isolation of research birds may prevent in troduction of infectious bronchitis. However, it is one of the most widespread and contagious diseases of chickens. Vac cines are very effective. They are given at 10 days to 2 weeks of age in the drinking water. Correct serotypes must be se lected for the strain of agent present in the area.

g. Treatment. Antibiotics will usually stimulate feed con sumption. Increased pen temperature and improved ventilation are helpful in aiding recovery of young birds.

h. Research Complications. Adult laying flocks should be terminated because they will not return to normal egg production.

a. Etiology. Infectious bursal disease is caused by a virus loosely placed in the orbi virus category. It damages primarily B lymphocytes in the bursa of Fabricius, thymus, spleen, and cecal tonsil. Infection with this agent reduces and sometimes totally eliminates humoral immunity.

b. Clinical Signs. The age incidence is usually 3-6 weeks, but it may occur at a later age. Birds are depressed and droopy, with ruffled feathers. Morbidity is high, and mortality also may be high. Vent picking and a bloody diarrhea are some times noted.

c. Epizootiology and Transmission. Transmission by di rect contact is rapid. The agent is resistant and lives in the environment for long periods of time.

d. Necropsy Findings. The bursa of Fabricius will first en large and later atrophy (Fig. 2) . Serum-colored edema may be present on the surface of the bursa. The bursa may also contain yellow exudate and hemorrhages. Hemorrhages also may be present in the skeletal muscles, and the kidneys can contain urate crystals.

e. Differential Diagnosis. Signs and lesions provide a pro visional diagnosis. A serum neutralization test and histopathology will usually confirm a diagnosis of the infectious bursal disease.

/. Prevention. Drinking water vaccines are available and give adequate protection. A program for highly susceptible, antibody-free, 1-day-old research chicks require vaccination or possibly none at all depending on exposure risk and degree of isolation. Under field conditions, maternal antibodies interfere with vaccines administered early in life. To overcome this, some of the vaccines are quite pathogenic and should not be used in highly susceptible chicks.

Complications. An outbreak would dictate termination of most experiments, especially when immu nologie data is important. 

a. Etiology. Epidemic tremor is caused by a picornavirus. It will grow in the embryos from a susceptible flock, but will not cause lesions unless it becomes egg "adapted."

b. Clinical Signs. Signs of ataxia, paralysis, and fine tremors of the head and neck will usually be seen between 1 and 3 weeks of age. Turkeys, quail, and pheasants, as well as chickens, may be affected. Growing birds, past 3 weeks of age, show no clinical signs, although recovered birds may sometimes have cataracts.

c. Epizootiology and Transmission. The virus is usually spread through fecal shedding. Adult hens may shed virus in a small percentage of their eggs during infection. Chicks hatch infected with the agent or become infected by fecal contact.

d. Necropsy Findings. There are no gross lesions, but histologically a nonpurulent encephalomyelitis is present. Sec tions of the brain, proventriculus, and pancreas should be ex amined microscopically. Central chromatolysis and lymphoid aggregates are seen in the cerebellum and proventriculus, re spectively (Butterfield et ai, 1969) .

e. Differential Diagnosis. Signs, especially head tremors, will suggest avian encephalomyelitis. Histopathology will usu ally confirm the diagnosis. Direct fluorescent antibody tests, serum neutralization tests, and isolation of the virus are used to diagnose the disease. Avian encephalomyelitis signs are simi lar to those of Newcastle disease and encephalomalacia. In pheasants, Avian encephalomyelitis must be differentiated from eastern equine encephalomyelitis.

/. Prevention. To protect baby chicks, the dams must be immunized. Both live and inactivated virus vaccines are available.

g. Research Complications. Chicks from immune dams will be satisfactory research birds. However, chicks encounter ing an outbreak of avian encephalomyelitis are not reliable for research purposes.

a. Etiology. Eastern equine encephalomyelitis is caused by a togavirus, originally classified as an arbovirus. Wild birds appear to be the natural host of this agent, and serve as a reser voir of infection for man, horses, and swine, in addition to pheasants. 413 b. Clinical Signs. Pheasants and horses are the primary animals affected, but in epizootics, chickens, wild turkeys, sparrows, domestic turkeys, quail, and doves may be infected. Incoordination, paresis, and progressive paralysis are seen in about 5-20% of a flock. If the flock is debeaked, mortality and morbidity will be markedly reduced. If the flock is not de beaked, feather picking and cannibalism are common.

c. Epizootiology and Transmission. Clinical cases are usu ally found near swamps and lowland areas, especially during a season with a high mosquito population. Birds are bitten by the mosquito Culiseta melanura, whereas the disease in mammals is usually transmitted by Aedes and Mansonia spp. Horses are a monitor of the impending danger of eastern equine encepha lomyelitis to humans, since horses have equal susceptibility but a much greater risk of exposure.

d. Necropsy Findings. No gross lesions are seen; micro scopically, there is a nonsuppurative encephalitis characterized by perivascular infiltrates, diffuse gliosis, and vasculitis with vascular infiltrates.

e. Differential Diagnosis. Signs, histopathology, and virus isolation are required for a diagnosis as other viruses may produce encephalitis in domestic fowl. Newcastle disease, avi an encephalomyelitis in poults, and Marek's disease in poults and pheasants must also be considered in the differential diagnoses.

/. Prevention. It is important to protect against mosquitoes with screens and sprays and to discourage cannibalism with debeaking and spectacles. Vaccination at 5-6 weeks may re duce mortality, but this method has not been as successful in birds as it has in horses.

should be terminated if an outreak of EEE develops.

a. Etiology. Infectious laryngotracheitis (ILT) is caused by a herpesvirus producing type A intranuclear inclusion bodies in epithelium lining the trachea. Similar inclusions are produced in epithelium of the chorioallantoic membrane of ex perimentally infected fertile eggs. Domestic fowl, pheasants, and pea fowl may be naturally infected (Crawshaw et al., 1982) .

b. Clinical Signs. Marked dyspnea with "pump handle" breathing followed by coughing and moist rales are the promi-nent signs. Shaking of the head and expectoration of blood also are common. Mortality in adults rarely exceeds 10%. related or identical to the virus of hemorrhagic enteritis of turkeys.

c. Epizootiology and Transmission. Recovered carriers are a common source of infection for susceptible birds. It ap pears that fomites are more important in ILT transmission than most of the other respiratory diseases.

d. Necropsy Findings. The larynx and trachea are acutely inflamed and sometimes filled with blood clots, or later, case ous cores (Fig. 3) . There is usually sinusitis and conjunctivitis. Histopathology of the trachea will reveal intranuclear inclusion bodies in the epithelial tags pulled from the necrotic lining.

e. Differential Diagnosis. Signs, lesions, and virus isola tion are the main methods of arriving at a diagnosis. The pres ence of inclusion bodies in trachéal epithelium are pathognomonic.

/. Prevention. A modified live ILT vaccine is available and is relatively safe. It will spread to susceptible birds in the same pen but usually not to other pens. All birds should be vaccinated at the same time and quarantined for 2-4 weeks (Bryant, 1973 e. Differential Diagnosis. Clinical signs and gross lesions suggest the diagnosis. Intranuclear inclusions in the spleen will further support MSD as a diagnosis (Wyand et al., 1972) . Agar gel precipitin tests may be used to identify antibodies as an indication of prior infection.

No commercial vaccine is available, but avirulent strains of hemorrhagic enteritis virus are being uti lized in experimental vaccines.

h. Research Complications. This disease is usually found on range flocks. Infected birds would not contribute valid ex perimental data.

a. Etiology. The cause of marble spleen disease of pheas ants is an avian adenovirus (Iltis et al., 1977) . It is closely '£^< ;:^^# a. Etiology. The causative agent is an avian adenovirus, the type strain referred to as CELO (chick embryo lethal or phan) virus. It causes very high mortality in young bobwhite quail. 

b. Clinical Signs. In quail under 4 weeks, coughing, sneezing, rales, and huddling are common. Mortality may range from 10 to 100%, but usually ranges between 50 and 60%.

c. Epizootiology and Transmission. Chickens, turkeys, and other birds may be inapparent carriers. Airborne and me chanical transmission are thought to be important means of spread.

d. Necropsy Findings. Trachéal and bronchial mucus is present. Cloudy air sacs, conjunctivitis, and infraorbital si nusitis are quite characteristic lesions of this disease.

e. Differential Diagnosis. Isolation of virus is necessary for a definitive diagnosis. Pulmonary aspergillosis may present similar signs but the microscopic lesion would be a fungal granuloma and easy to differentiate from that produced by quail bronchitis virus.

/. Prevention. Isolation, sanitation, and good husbandry should prevent quail bronchitis.

g. Research Complications. The mortality in quail would cause termination of any research trial.

a. Etiology. Newcastle disease is the result of a paramyxovirus infection. There are three major strains as distinguished by their pathogenicity: (a) lentogenic, mild disease, used as vaccine, an example is serotype B-1; (b) mesogenic, moderate disease, domestic Newcastle disease usually seen in the United States; (c) velogenic, very pathogenic, exotic Newcastle dis ease. Newcastle disease virus hemagglutinates chicken erythrocytes and forms the basis for the hemagglutination inhi bition test for anti-NDV antibodies.

b. Clinical Signs. A sudden onset of anorexia and respira tory signs will develop in adults. The eggshells of brown-egglaying hens will often turn white. Egg production and egg quality will be diminished. In young chicks with no parental immunity, central nervous system signs are seen. Mortality will be high. Torticollis ("star-gazers") is very common. Se vere dypsnea, diarrhea, paralysis, and acute death are the signs of velogenic strains. Mortality may reach 100%. Caution must be advised regarding velogenic Newcastle disease since spe cies of pet birds may be inapparent carriers of velogenic strains.

c. Epizootiology and Transmission. Newcastle disease has a wide host range. Many wild birds can transmit Newcastle 415 virus to domestic birds. It affects many wild birds, pet birds, and most game birds. Aerosol transmission is the important means of spread. Contaminated feed, water, and equipment are almost as important. Egg transmission occurs but only for the first few hours during the acute onset of infection in breeders. Velogenic Newcastle disease may be brought into the country with pet birds and fighting cocks. The latter are often smuggled into the country.

d. Necropsy Findings. The mesogenic strains produce le sions characteristic of a tracheitis and a "frothy type" air sacculitis. Velogenic strains, on the other hand, produce massive hemorrhages in all the visceral organs especially the GI tract.

e. Differential Diagnosis. Signs, lesions, and HI tests are usually adequate for diagnosing Newcastle disease. Immunofluorescence tests may be done very quickly to detect the presence of the virus at the time of disease onset. All avian respiratory diseases must be differentiated from Newcastle dis ease. Histopathology will serve to differentiate the CNS form of Newcastle disease from those produced in avian encephalomyelitis and encephalomalacia.

/. Prevention. Excellent Newcastle disease vaccines are available for immunization of laying hens, breeders, and broilers. One-day-old chicks are given water vaccines and are given boosters several times before sexual maturity.

g. Control. Eradication has been practiced by the United States Department of Agriculture for the velogenic viscerotropic type of Newcastle disease. All Newcastle disease outbreaks should be reported if high mortality is a feature. Pet birds should be kept separate from poultry, turkey, or game bird flocks.

h. Research Complications. A researcher may immunize the flock or raise birds in strict isolation. The latter is ideal but not always successful as Newcastle disease can be transmitted through aerosols. If an outbreak occurs, the trial should be terminated.

a. Etiology. Pox is caused by a large DNA virus. The fol lowing commonly encounted strains infect their respective spe cies: fowl pox, turkey pox, pigeon pox, and canary pox. Pox virus is very resistant in the environment and spreads slowly through a flock.

b. Clinical Signs. Two forms exist. Skin pox affects the comb, head, and vent regions; wet pox affects mucous mem-branes of the larynx and can cause choking. Viremia exists in both forms, and decreased ^gg production is present for ex tended periods.

c. Epizootiology and Transmission. Scabs and skin debris that contaminate the litter feed and water are the usual source of virus. Mosquitoes and cannibalism are secondary means of spread.

d. Necropsy Findings. Scabs on the comb and other unfeathered areas of the body are suspect pox lesions. Diphtheri tic lesions of the pharynx, larynx, and trachea are common in wet pox. The laryngeal opening is usually plugged with a tight ly adhered plaque. If cannibalism is a simultaneous problem, the vents may show severe skin necrosis.

e. Differential Diagnosis. Demonstration of intracytoplasmic inclusion ibodies in cutaneous and oral lesions are pathognomonic for pox. Virus inoculation onto the chorioallantoic membrane of embryonating eggs will also produce pocks and cytoplasmic inclusions. Pox must be differentiated from can nibalism, infectious laryngotracheitis and mycoplasmosis. Trachéal plugs are seen in the latter if the strain is highly pathogenic.

/. Prevention. Vaccination by the wing-web stick method is recommended for pigeons and chickens. Turkeys should be vaccinated by the thigh-stick method. An experimental vaccine is available for canaries. The pigeon pox strain of vaccine is preferred in areas of low incidence, thus preventing spread of the fully virulent fowl pox vaccine to susceptible birds.

g. Research Complications. It would be unwise to collect data from pox-infected birds.

A. Coccidiosis a. Etiology. Coccidiosis is caused by a protozoan parasite. There are nine species of coccidia affecting chickens, six affect turkeys, but only three are pathogenic. In geese, three species affect the gastrointestinal tract, and one affects the kidney. The duck and pheasant, each have at least one species that is patho genic for the gastrointestinal tract. All species in the genus Rimeria appear to be host specific with no cross-transfer. Each species has a characteristic size and shape and specific life cy cle. Immunity is usually specific for one species only and af fords no cross-protection against other species of coccidia. b. Clinical Signs. Signs may include pale legs and beaks, ruffled feathers, and listlessness. Birds infected with certain species of coccidia may have bloody fecal droppings. Poor growth and high mortality are the effects of coccidia multiply ing in intestinal epithelial cells.

c. Epizootiology and Transmission. Ingestion of the sporulated oocysts from feces and litter is necessary for transmis sion. Each gram of feces may contain about 500,000 oocysts. Each sporulated oocyst will produce eight sporozooites, 150 first generation merozoites, 300 second generation merozoites, and will damage about 1,000,000 intestinal host cells.

d. Necropsy Findings. Table IV illustrates the complexity of diagnosing coccidiosis by gross lesions (see also Fig. 4 ).

e. Pathogenesis. Disease is based on the interrelation of age of host, species of coccidia, and dose of organism (degree of exposure). An unsporulated oocyst in the presence of oxy gen, 30% moisture, and room temperature will become an in fective oocyst in 24-72 hr. The infective oocyst is ingested by a susceptible host, and the life cycle begins. The prepatent period varies by species from 4 to 7 days. /. Differential Diagnosis. A differential diagnosis in the chicken and turkey must include various species of coccidia in addition to salmonellosis and histomoniasis. The signs and le- From Bryant and Helmboldt (1973) . sions of ulcerative and necrotic enteritis are similar to coc cidiosis. Direct scrapings of the gut accompanied by histopathology will aid in the diagnosis.

Prevention of coccidiosis must include re ducing the number of infective oocysts. Dry pens and good sanitation practices and/or wire floors will prevent coccidiosis. Immunity is species specific. Vaccines will protect birds but require skillful maintenance of litter at 30% moisture postvac cination to ensure cycling of coccidia for immunization. Coccidiostats are efficacious. Amprolium, coban, and others are available. They are administered continuously at a dose of 0.0125% to allow low level infection but protect against severe disease.

h. Treatment. Amprolium, sulfa drugs, and the nitrofurans have all been used with good success.

/. Research Complications. used for research purposes coccidiostat.

All birds from 0 to 12 weeks should be fed a low level

a. Etiology. The cause of histomoniasis is Histomonas meleagridis, a protozoan flagellate that inhabits the cecal lumen.

b. Clinical Signs. Turkeys, chickens, and pea fowl with this disease exhibit anorexia, droopiness, listlessness, yellow diarrhea, and cyanosis of the head and face. Morbidity and mortality may be high in young poults.

c. Epizootiology and Transmission. Fresh feces contain the histomonad and may be ingested. More often, the histomonad is contained within the cecal worm (Heterakis gallinarum) and the worm is ingested. A third possiblity is Heterakis larvae contained within earthworms which in turn may also be ingested.

d. Necropsy Findings. The liver will show discrete, irreg ular, depressed areas of focal necrosis. The thickened walls of the cecal lumen surround laminated, yellow, caseous cores (Fig. 5 ).

e. Differential Diagnosis. Hematoxylin and eosin sections of the liver and cecal wall are best for demonstrating the histomonads. Direct smears and scrapings may also reveal the organism.

/. Prevention. The continuous use of antihistomonal drugs is the most effective way to prevent blackhead. Hepzide, histostat and emtryl will all prevent the disease.

g. Treatment. The above drugs serve as effective thera peutic agents at the recommended treatment level.

h. Research Complications. Poults and game birds, es pecially pea fowl, should be administered anithistomonal drug until 12-15 weeks of age. 

a. Etiology. Ascaridia species are found in most birds. The following species have been reported: Ascardia galli, chicken; Ascaridia numidae, guinea fowl; Ascaridia columbae, pigeon; Ascaridia dissimilis, domestic and wild turkeys; Ascaridia compar, bob white quail.

b. Clinical Signs. Decreased egg production, poor growth and vigor, diarrhea, and visible presence of worms in the feces are often noted.

c. Epizootiology and Transmission. The life cycle is di rect. Infective eggs are swallowed and hatch in the proventriculus or anterior portion of the intestinal tract. Larvae live for 9-10 days in the lumen and then enter the mucosal wall and produce damage. On the seventeenth to eighteenth day, young worms again enter the lumen and remain there until maturity, usually 50 days postingestion.

d. Necropsy Findings. Evidence of anemia and retarded growth is seen. The presence of Ascardia sp. is the most out standing feature. A complete intestinal blockage is sometimes present (Fig. 6 ).

e. Differential Diagnosis. The presence of intestinal roundworms may not be the primary cause of clinical disease, especially when mortality is a common feature. Further exam ination may reveal capillariasis, coccidiosis, or bacterial infec tions in combination with ascaridia infestation. /. Prevention. A complete depopulation and disinfection will usually prevent recurrence of the disease in the next flock. Dirt floors or ranges are impossible to clean and should be rotated annually. 

a. Etiology. Capillaria obsignata infests the chicken, tur key, and probably other bird hosts. Capillaria columbae is as sociated with pigeons. In game birds, C. contorta is found in the crop and esophagus.

b. Clinical Signs. A sudden drop in egg production and an unthrifty appearance of the flock may often be the result of Capillaria infestation.

c. Epizootiology and Transmission. The life cycle is di rect. Eight-day embryonated capillaria eggs are ingested by the host, and larvae penetrate the duodenal mucosa. Adult worms are found within 18-20 days postingestion of embryonated eggs (Fig. 7) .

Slight enteritis may be present. Nematodes washed from mucosal scrapings will confirm the diagnosis. e. Prevention. Clean facilities will prevent Capillaria infestations. e. Prevention and Treatment. The continuous feeding of thiabendazole has been very effective. More recently, levamizole hydrochloride in the water has been used with success as a treatment. Rotating ranges for pheasants will also help mini mize infection. c. Epizootiology and Transmission. Spores of A. fumigatus are found in great numbers in old litter. When the spores are inhaled, they produce typical respiratory signs and lesions. d. Necropsy Findings. Yellow plaques are found in the lungs, air sacs, tracheas, and peritoneal surfaces (Fig. 8) . The brain also may contain foci of fungal growth. Histopathology will reveal the presence of hyphae in granulomas stained with periodic acid-Schiff or Gridley stain.

e. Differential Diagnosis. Signs and typical histologie le sions of lung and air sacs will confirm the presence of the Aspergillus spp.

/. Prevention. Use clean, dry litter. Wet sawdust may con tain numerous spores of Aspergillus fumigatus, and its use is contraindicated.

g. Treatment. Commercial poultry and turkey flocks are not usually treated. Individual, valuable birds may be treated with nystatin or amphotericin B.

h. Research Complications. Flocks infected with as pergillosis should be depopulated.

a. Etiology. Candida albicans, a yeastlike fungus, is the causative agent of crop mycosis. It grows well on Sabouraud's agar at room temperature. It is cautioned, however, that C. albicans can be a normal floral inhabitant of the crop and lower digestive tract.

b. Clinical Signs. Depressed egg production and diarrhea are the two most commonly observed signs.

c. Epizootiology and Transmission. Unsanitary waterers and warm humid weather will often combine to produce the necessary environmental conditions for the development of disease. Indiscriminate use of antibiotics may alter normal bac terial flora allowing the yeast to multiply and ellicit disease.

d. Necropsy Findings. The crop and esophagus are cov ered with a diffuse, white exudate. Often the pharnygeal mucosa is involved. Enteritis with a white, pseudomembrane covering duodenal and jejunal mucosa may sometimes be found.

e. Differential Diagnosis. Culture of the yeast and histo pathology will confirm the diagnosis.

/. Prevention. Optimum sanitation of waterers and feeders especially during hot, humid weather is necessary. Disinfec tants such as chlorine, iodine, and quaternary ammonium com pounds are needed to keep the yeasts and fungi from multiply ing in the drinking water. 

Depression and emaciation characterize visceral involvement. Palpable muscle tumors may also be noted.

c. Epizootiology and Transmission. The virus is released in association with dander from feather follicles, which then contaminates the environment.

d. Necropsy Findings. Tumors of various visceral organs, skin, or muscle may be seen. Swollen sciatic and brachial nerves are common. Microscopic lesions feature pleomorphic cellular infiltrates of plasma cells, macrophages, lymphocytes, and lymphoblastic cells. Nerves may have inflammatory or proliferati ve lesions or a combination of both types.

e. Differential Diagnosis.

Marek's disease must be differ entiated from lymphoid leukosis (LL). For many years, both these diseases were thought to be caused by a common agent.

Marek's disease occurs prior to sexual maturity, but both may occur after sexual maturity. Only Marek's disease affects the nerves and thus causes paralysis. Both produce tumors and en larged visceral organs. Gray eyes, feather follicle inflamma tion, and muscle tumors are found only in Marek's disease. Tumors of the bursa of Fabricius are rare in MD, but are an invariable finding in LL.

/. Prevention. Depopulation and thorough disinfection be fore introducing a new flock is recommended. Baby chicks should be vaccinated at 1 day of age with the nononcogenic turkey herpesvirus if it is not possible to provide strict isola tion. Genetic resistance varies among strains of chickens, and is effective in reducing losses in Marek's disease virus-ex posed birds.

h. Research Complications. Herpesvirus of turkeys (HVT) Marek's vaccine should be administered to all birds at 1 day of age to prevent the disease.

a. Etiology. Lymphoid leukosis is caused by an oncogenic retrovirus. It is a member of the leukosis-sarcoma group. Sub groups A and B occur in commençai chickens. Various virus strains may cause a variety of neoplasms of mesodermal tissues in addition to typical LL.

b. Clinical Signs. Sudden death of adult chickens may be the only sign. An enlarged abdomen due to a swollen liver is also a common finding. Thickening of the leg bones as a result of osteopetrosis is another possible consequence of infection with some strains of leukosis virus. Other lesions may include erythroid or myeloid leukemias, hemangiomas, or nephroblastomas.

c. Epizootiology and Transmission. Egg transmission is the most important means of introducing the virus into a flock. Lateral spread from infected saliva and feces then ensues. Ear ly infection is generally required for tumors to develop.

Findings. An enlarged liver, sometimes sig nificantly displacing other abdominal organs, is a common finding. Tumors in the spleen and kidney are also seen. The bursa of Fabricius will usually reveal a discrete, nodular tumor that constitutes the primary lesion. Other sites are thought to become involved as the result of métastases from the bursa.

e. Differential Diagnosis. Lymphoid leukosis does not de velop until 4-5 months of age. In contrast, Marek's disease may be seen as early as 3-4 weeks of age. Both diseases can simultaneously occur in the same bird. The presence of a bursal tumor frequently indicates LL, whereas nerve, skin, or muscle involvement indicates MD.

/. Prevention. Lymphoid leukosis-free chicks are avail able. A rigid isolation rearing system should be followed.

h. Research Complications. If birds are not kept until the age of sexual maturity, little or no LL should be encountered.

a. Etiology. Vitamin A is necessary for growth, normal vision, and integrity of epithelium lining the respiratory, diges tive, urinary, and genital tracts. Severity of deficiency signs and age of incidence will vary with the vitamin A levels in the feed and the maternal reserve of vitamin A passed onto the chick. Breeders on adequate vitamin A diets store this vitamin in the egg yolk, which provides the chick with sufficient vi tamin A to last for several weeks. Chicks hatched with margin al reserves of vitamin A and placed on a deficient diet will have clinical signs by 7-10 days of age. However, if chicks are hatched from hens receiving adequate vitamin A, they have no signs or lesions until about 6 weeks.

b. Signs. Signs of vitamin A deficiency include pale head, muscles of the thigh, and skin. Weakness, lethargy sometimes associated with ataxia, and lacrimation with conjunctivitis are other signs noted. Decreased sperm counts and reduced sperm motility are reported to be a common finding in vitamin Adeficient roosters. Cartilage and bone development may be de pressed. The incidence and severity of blood spots in eggs are increased as dietary vitamin A is reduced. Recovery from in testinal diseases is improved when the level of vitamin A in the feed is increased.

c. Gross Lesions. Lesions of vitamin A deficiency consist of small white pustules in the nasal passages, mouth, esopha gus, pharynx, and crop. In addition, there may be marked ac cumulation of urates in the renal tubules.

d. Histopathology. Histopathology reveals cytoplasmic atrophy and loss of cilia of the respiratory tract epithelium. There is marked karyorrhexis of nuclei. Chronic vitamin A deficiency results in squamous metaplasia in epithelial lining of the nasal cavities, trachea, bronchi, and submucous glands (Bryant and Helmboldt, 1974) .

e. Prevention. The normal requirement for vitamin A in chicks from 1 day old to 8 weeks of age is 5000 IU/lb of feed. For growing chickens and turkeys (8-22 weeks of age), 3000 IU/lb of feed is recommended. For laying hens, 4000 IU/lb of feed, and for breeding hens and turkeys, 5000 IU/lb of feed is needed. Five thousand IU/lb feed is also recommended for pheasants, pigeons, and quail. /. Treatment. Treatment levels for vitamin A deficiency is 5000 IU/lb of feed.

a. Etiology. Vitamin D is needed for metabolism of cal cium and phosphorus in the formation of bones, egg shells, beaks, and claws. Vitamin D stimulates the gastrointestinal ab sorption of calcium. Serum alkaline phosphatase is elevated when vitamin D-deficient diets are fed even in the presence of sufficient calcium and phosphorus.

b. Signs. Retarded growth, poor feathering, and soft bones (rickets) are features of vitamin D deficiency in young chicks 2-3 weeks of age. The chicks are unsteady and walk only a short distance before falling, or affected chicks may sit on their hocks and rest for several minutes (Bryant, 1972) . Adults will lay a large percentage of thin-shelled and softshelled eggs leading eventually to a decrease in total egg pro duction. Signs from a deficiency of vitamin D usually occur about 2 months after vitamin D is withheld. Hatchability is also reduced. c. Lesions. Characteristic lesions in young birds include soft pliable bones, beaded ribs, and S-shaped keel bone. The beak and long bones can be bent without breaking. An in dented rib cage is evident and causes pressure on the lungs and the heart. In adults, the lesions seen in young birds are present but usually to a lesser degree. Pathological fractures of the ribs and vertebrae may be a feature. The histological features of vitamin D deficiency include an enlarged parathyroid gland with a diffuse hyperplasia. A decrease of normal calcified bone with an excess of osteoid tissue in the long bones is also seen. Poor calcification is best identified at the epiphysis of the tibia or femur.

Turkeys of all ages should receive vitamin D in the amount of 600 IU/lb of feed. Hens and young chicks require 500 IU/lb, while growing chickens, 8-22 weeks of age, should have 300 IU/lb of feed. Pheasants, quail, and pigeons will grow well on 600 IU/lb of feed. e. Treatment. The feeding of a one-time, very high dose of Vitamin D 3 , approximately 15,000 IU/lb of feed, will pro vide the most effective therapy. This should be given in a sin gle dose, as hypervitaminosis D can result. Dystrophie cal cification of the aorta and certain arteries, in addition to kidney tubules, is one complication of hypervitaminosis D. Vitamin D 2 (irradiated ergosterol) is a poor form of vitamin D for birds and can even be toxic at high levels.

a. Etiology. Vitamin E is necessary for normal egg pro duction, fertility, and hatchability. Multiple problems result if a deficiency of vitamin E occurs in birds.

i. Encephalomalacia ("crazy chick disease"). This con dition is a vitamin E deficiency characterized by ataxia, back ward retraction of the head, increased incoordination, and death. It is usually seen between 2 and 4 weeks of age. If the breeder flock is deficient in vitamin E, signs may be seen dur ing the first week posthatching. Grossly, the cerebellum ap pears wet with petechial hemorrhages. Histologically, ische mie necrosis as a result of capillary thrombosis is the main feature. This disease must be differentiated from avian encephalomyelitis (AE) in which the neurons show central chromatolysis. This condition is characterized by cells appearing pale in the center due to loss of the Nissl substance (Helmboldt), 1972).

ii. Exudative diathesis. This condition is characterized by subcutaneous blood-tinged edema of young birds caused by an abnormal permeability of capillary walls. It appears that tissue peroxides increase causing damage to capillary membranes. Vitamin E and glutathione peroxidase, a selenium-containing enzyme, protect the capillary endothelium against damage by peroxides, thus explaining the dual role of vitamin E and se lenium in preventing exudative diathesis.

Hi. Nutritional muscular dystrophy. Dystrophie muscles in chickens, ducklings, and turkeys at approximately 4 weeks of age is caused by vitamin E deficiency, as well as by a defi ciency of sulfur-containing amino acids. It is primarily seen in breast muscle but may be found in any of the skeletal muscles. Grossly, there are separated muscle fiber bundles that appear light in color. The microscopic lesions consist of typical Zenker's necrosis, which include hyaline degeneration, pro liferation of muscle nuclei and fibroblasts, disruption of mus cle fibers, and edema containing heterophiles. Vitamin E defi ciency and selenium deficiency in the turkey may show heart and gizzard myopathy.

iv. Enlarged hocks. Turkeys on a vitamin E-deficient diet have enlarged hocks and bowed legs at 2-3 weeks of age. The same condition is produced by a deficiency of phosphorus, choline, glycine, nicotinic acid, zinc, and biotin.

b. Prevention. The recommended level of vitamin E for chickens and laying hens is 5 IU/lb of feed; for breeding hens 7.5 IU/lb is recommended. Poults from 0 to 16 weeks require 7 IU/lb, and breeder turkeys need 15 IU/lb of feed.

c. Treatment. Therapeutic levels of vitamin E and se lenium, 10 IU/lb and 0.1 ppm, respectively, will prevent en cephalomalacia, exudative diathesis, and gizzard myopathy.

a. Etiology. Vitamin K is needed to synthesize prothrombin, an important component of the blood clotting mechanism. If vitamin K is deficient, prolonged blood clotting time is noted.

b. Signs and Lesions. Diets deficient in vitamin K can cause cutaneous hemorrhage of the legs, wings, and breast in addition to hemorrhage into body cavities. Anemia is often seen due to blood volume loss and a hypoplastic nonregenerative bone marrow. Embryos will die during egg incubation from hemorrhages. c. Prevention. Vitamin K deficiency is rare and hard to reproduce. The dietary requirement for all birds at any age is 1 mg/lb of feed. d. Treatment. A normal clotting time returns within 5 hr after treatment with menadione sodium bisulfite. Cutaneous hemorrhages and anemia usually take several days to resolve once adequate vitamin K levels are fed.

E. Thiamin Deficiency (Vitamin B,) a. Etiology. Thiamin is important in carbohydrate metabo lism. Signs of thiamin deficiency include polyneuritis, extreme anorexia, and death.

b. Signs and Lesions. Vitamin B, deficiency can be seen in chicks and adults. Usual signs are weight loss, ruffled feath ers, leg weakness, and unsteady gait followed by muscle paral ysis. Due to anterior neck muscle paralysis, retraction of the head results in a typical posture referred to as "star gazing." c. Treatment. The requirement of thiamin is 1 mg/lb of feed for birds of all ages. Oral therapy with thiamin results in a rapid clinical recovery if the birds are eating; however if anorexia is present, force feeding or injection of thiamin may be necessary.

a. Etiology. Riboflavin is an important component of many enzymes associated with oxidation-reduction reactions and cell respiration.

b. Signs and Lesions. Signs in chicks may include poor growth, weakness and emaciation, diarrhea, and refusal to walk. Appetite is not affected. Toes will curl medially (Bryant, 1972) . In laying hens decreased egg production and hatchability occurs. Increased fat content of the liver is also noted. Embryos are dwarfed and edematous. In turkeys, riboflavin deficiency results in a dermatitis with defective down feathers similar to pantothenic acid deficiency in chickens. Micro scopic nerve lesions in chicks show degenerative changes in the myelin nerve sheath.

c. Prevention. The normal requirement for riboflavin in all birds is 2 to 2.5 mg/lb of feed.

d. Treatment. The administration of adequate riboflavin will usually cure the deficiency rapidly.

a. Etiology. Pantothenic acid is part of coenzyme A, which is involved in the metabolism of carbohydrates, pro-EVERETT BRYANT teins, and fats. It is required for hatchability and will prevent edema and subcutaneous hemorrhages in the embryos.

b. Signs and Lesions. Changes noted in pantothenic acid deficiency include a severe dermatitis, perosis, broken feath ers, poor growth, and death. Poor hatchability with the em bryos dying during the last 3 days of incubation is typically noted.

c. Prevention and Treatment. Six to 7 mg/lb of feed is needed for a normal diet. For therapeutic effect, 10-12 mg/lb of feed administered for a few days either orally or by injection is needed.

Biotin deficiency causes a dermatitis around the beak, eye lids, and feet. Biotin deficiency also can cause perosis. Ap proximately 0.1 mg/lb of feed will prevent the dermatitis and perosis caused by biotin deficiency.

a. Etiology. Vitamin B 12 is involved in nucleic acid syn thesis, methyl synthesis, and metabolism of carbohydrates and fats.

b. Signs and Lesions. Signs include retarded growth, poor feed efficiency, mortality, small egg size, and reduced hatchability. Vitamin B x 2 -deficient embryos may have hemor rhages, edema, perosis, and fatty livers.

c. Prevention and Treatment. The inclusion of 0.005 mg/lb of feed will prevent deficiency of Vitamin B I 2 . Therapy includes the addition of 4 mg/ton of feed into the breeding ration.

a. Etiology. Calcium is essential for bone formation, egg shell production, normal blood clotting, normal striated mus cle, and maintenance of acid-base balance. Phosphorus is required for carbohydrate and fat metabolism, calcium trans port, bone formation, and eggshell production.

b. Signs and Lesions. Calcium and/or phosphorus defi ciency will cause signs and lesions of rickets, decreased egg production, and increased numbers of soft shelled and shellless eggs (also see Section VII,B on vitamin D deficiency).

c. Prevention and Treatment. The recommended levels are as follows: for nonlaying chickens, 1% calcium and 0.5% available phosphorus; for laying and breeding hens, 3.5% cal cium and 0.5% available phosphorus; for nonlaying turkeys, 1.5% calcium and 0.7% phosphorus; and for laying turkeys, 2.0% calcium and 0.6% phosphorus. The above levels used therapeutically will correct any deficiency.

a. Etiology. Sodium is found in the blood and body fluids and is associated with regulation of the hydrogen ion con centration of blood. It is also necessary for normal physiologi cal activity of the heart. b. Signs. Poor growth, softening of the bones, corneal keratinization, gonadal inactivity, decrease in cardiac output, hypotension, hemoconcentration, and uremia are signs of so dium deficiency. In adults, a sodium deficiency results in de creased egg production and egg size in addition to loss of weight and cannibalism.

c. Prevention and Treatment. Levels of 0.15% sodium and 0.15% chlorine are recommended for optimum growth and egg production. Salt toxicity develops at a level of 4 gm/kg of body weight. Intense thirst, weakness, convulsions, and death are the signs associated with salt toxicity.

a. Etiology. Manganese is essential for growth, egg pro duction, and prevention of perosis.

b. Signs. Results of a manganese-deficient diet include poor quality eggshells, thickened and shortened leg bones, lowered hatchability, and chondrodystrophy in embryos.

c. Prevention and Treatment. The normal requirement of manganese is 50-60 ppm. This level is also used therapeu tically to treat manganese-deficient birds.

a. Etiology. Iodine is necessary for the normal function of the thyroid gland. Thyroxine is 65% iodine and regulates body metabolism. With iodine deficiency, the thyroid gland en larges and is referred to as "goiter."

b. Prevention and Treatment. The recommended level of

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International Registry of Poultry Genetic Stocks

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