OCCURRENCE

Young birds appear to be more susceptible than adult birds.

ETIOLOGY

Most often caused by Aspergillus flavus growing in peanut meal, corn meal, cottonseed meal cake, many grains and in poultry litter.

CLINICAL SIGNS

Initially: lethargy, loss of appetite, impaired growth, ruffled feathers and drooping wings.

Later: ataxia, opisthotonos and convulsions.

In chickens, there is impaired and uneven growth in the flock with low mortality. It may be subclinical and unrecognized.

MORBIDITY & MORTALITY

Variable but often high.

LESIONS

Liver: Swollen and discolored initially but later becomes cirrhotic and nodular. May have necrotic foci.

Ascites and hydropericardium are frequently present and may have generalized edema. Petechial hemorrhages at various sites and renal swelling may be present. Marked catarrhal enteritis is usually a feature.

Histopath.: hyperplasia of biliary epithelium

Aflatoxin is carcinogenic. Tumors usually develop in the liver.

DIAGNOSIS

History, gross and micro. lesions.

Analysis of affected feed.

PREVENTION

Avoid storing feed for long periods. Store feed under cool & dry conditions.

Addition of antimycotics to the feed.

TREATMENT

Treatment isn't necessary if the aflatoxin is eliminated from the ration.

ASPERGILLOSIS

OCCURRENCE

All species of birds are susceptible.

ETIOLOGY

Aspergillus fumigatus

EPIZOOTIOLOGY

Infection usually occurs after inhalation of large numbers of spores from heavily contaminated feed or litter which overwhelms the resistance of the bird.

Aspergillus can penetrate egg shells under ideal conditions and infect the embryo. Such eggs may appear green when candled. Infected embryos may hatch with well developed lesions.

CLINICAL SIGNS

Dyspnea, gasping, accelerated breathing, diarrhea, anorexia, somnolence, progressive emaciation and increased thirst.

If metastasis to the brain has occurred, signs of CNS disturbance may be seen.

If metastasis to the globe has occurred, one or both may have a gray-white opacity.

LESIONS

Yellow or gray nodules and/or plaques in the lungs, air sacs, or trachea; less often in the peritoneal cavity, liver, or at other sites.

Mycelial growth with sporulation may be apparent as fuzzy green material in the air sacs.

Yellow or gray metastatic foci may be apparent in the brain, eye, or at other sites. Infection in the conjunctival sac may result in accumulation of cheesy exudate.

Histopath.: Hyphae within the nodules or plaques.

DIAGNOSIS

Signs & lesions.

Culture. Caution, Aspergillus is a common contaminant.

CANDIDIASIS

OCCURRENCE

Usually chickens or turkeys. Young birds are more susceptible.

ETIOLOGY

Candida albicans

EPIZOOTIOLOGY

Candida is present in the normal digestive tract of birds & mammals. Debilitation or alterations in the normal gut flora can cause the fungus to invade the mucosa and produce lesions.

CLINICAL SIGNS

Retarded growth, listlessness, ruffled feathers or diarrhea. The signs may be masked by the primary disease.

LESIONS

Diffuse and/or focal thickening of the affected mucosa with white or gray pseudomembranous or diphtheritic patches. Focal lesions may have sloughed into the lumen as soft cheesy material. Lesions are usually located in the mouth, pharynx, esophagus, and crop.

Lesions of the primary disease may be present.

DIAGNOSIS

Lesions & histopathic evidence of invasion of the fungus into tissue.

Culture. Caution, remember Candida is present normally.

PREVENTION

Good sanitation.

Prevention of primary disease and management practices that might debilitate the birds.

Avoid overtreatment with antibiotics, drugs, coccidiostats, growth stimulants.

TREATMENT

Gentian violet in feed.

Copper sulfate in drinking water.

Treat primary disease or management problem.

OCOCCIDIOSIS

OCCURRENCE

Common in chickens and less often in turkeys. Occasionally in geese, guineas, pigeons, pheasants, quail, chukars and many
other birds.

Usually seen in young birds under conditions of warmth and high humidity or conditions that lead to wet litter.

ETIOLOGY

Host specific species of Eimeria. A protozoa.

EPIZOOTIOLOGY (in chickens)

Oocysts are present in the litter having been deposited there by infected chickens. Oocysts are easily transported by blowing dust, boots, clothing, crates, vehicle wheels, other animals, and people.

Susceptible chickens ingest sporulated oocysts in feed, water, litter and become infected. If exposure is moderate, the chickens become immune to that species of coccidia.

Outbreaks occur when susceptible chickens ingest massive numbers of oocysts.

Coccidia produce lesions by destruction of epithelial cells in which they develop and multiply and by trauma to the intestinal mucosa and submucosa.

CLINICAL SIGNS

Varies with species of coccidia. Pathogenic species cause diarrhea which may be mucoid or bloody, dehydration, ruffled feathers, anemia, listlessness, weakness, retraction of the head and neck, somnolence, depigmentation of skin.

In turkeys, the signs are the same except the diarrhea isn't bloody.

LESIONS (in chickens)

Anterior 1/3 of the Gut

E. acervulina. Mild to severe enteritis that can lead to thickening of the mucosa. Transverse white to gray striations are often visible in the mucosa.

Middle 1/3

E. necatrix. Enteritis characterized be congestion, hemorrhage, necrosis, and bloody feces. Intestine is often markedly dilated, inflamed, and thickened. White to yellow foci and petechial hemorrhages may be seen thru the serosa.

E. maxima. Thickening of the intestinal wall and marked dilation. Intestinal content may be bloody.

Posterior 1/3

E. brunetti. A fibrinous or fibrinonecrotic mass of debris may cover the affected mucosa or produce caseous cores.

E. tenella. Blood often apparent in the ceca and feces in early cases. Later, cheesy cecal cores may be found.

MORBIDITY & MORTALITY

Varies greatly but may be very high.

DIAGNOSIS

Signs & lesions.

PREVENTION

Anticoccidials in the feed.

Purposeful small exposures to stimulate immunity.

Genetic resistant strains are being developed.

TREATMENT

Not very satisfactory. Can try Amprolium, Agribon, Sulfaquinoxaline, Sulfamethazine.

Increase Vit. A & K in feed or water.

HEXAMITIASIS

OCCURRENCE

Seen in 1-9 week old turkey poults. Also occurs in gamebirds, peafowl, ducks, and pigeons.

ETIOLOGY

Hexamita columbae in pigeons & Hexamita meleagridis in all other birds. A protozoa.

EPIZOOTIOLOGY

Recovered birds often are carriers and shed the parasite in their feces which contaminate feed, water and range. Susceptible birds get the organism by ingestion.

CLINICAL SIGNS

Initially: Birds are very nervous and active. They also chirp excessively, shiver, crowd around any heat source and have subnormal temps. There is watery or foamy diarrhea and the birds dehydrate rapidly.

Later: Birds are depressed, stand with their heads retracted, feathers ruffled and wings drooping.

Terminally: Birds go into coma, struggle, and die due to hypoglycemia.

MORBIDITY AND MORTALITY

Morbidity is high. Mortality may be 75-90% in young birds that are poorly housed and receive no treatment.

LESIONS

Cadaver is dehydrated. Intestines are flabby with areas of bulbous dilation and contains excessive mucus and gas. Proximal 1/2 of intestines is inflamed. Cecal tonsils may be congested.

DIAGNOSIS

Duodenal scrapings on a freshly killed bird using reduced light or phase contrast microscopy reveal the organism.

PREVENTION

Short periods of depopulation combined with thorough cleaning and disinfection.

TREATMENT

Nithiazide, Emtryl, Ipronidazole, Furazolidone, tetracycline.

Increase room temperature.

HISTOMONIASIS

OCCURRENCE

Occurs most frequently in exposed, unmedicated turkeys, esp. under 3 mths.. Also occurs in chickens and captive game birds. Young birds are more frequently and severely affected.

ETIOLOGY

Histomonas meleagidis, a protozoa.

EPIZOOTIOLOGY

Transmission is via 3 routes:

Ingestion of fresh feces. Ingestion of infected ova of Heterakis gallinarum. Ingestion of larva of Heterakis that are within earthworms.

CLINICAL SIGNS

Initially: Listlessness, anorexia, drooping wings and yellow feces. Headparts may be cyanotic. In chickens there may be bloody feces.

Later: Depression, drooping wings, eyes closed, head drawn close to the body, and emaciation.

MORBIDITY AND MORTALITY

Approaches 100% in young turkeys.

LESIONS

Bilateral enlargement of the ceca with thickening of the walls. Mucosa is usually ulcerated. The ceca often contain laminated yellow, gray, green, or red caseous cores.

Liver: Contains irregularly-round, depressed lesions that vary in color (yellow, gray, green or red).

Above lesions are considered pathognomonic.

DIAGNOSIS

Lesions. Isolation of organism from cecal or hepatic scrapings.

PREVENTION

Addition of antihistomonal drugs to the ration.

Good sanitation.

Do not mix turkeys with other species of birds.

Deworm for cecal worms frequently.

TREATMENT

None.

LEUCOCYTOZOONOSIS

OCCURRENCE

Acute outbreaks occur mostly in young birds and chronic in older birds. Maintained in wild bird populations.

Occurs most frequently in the SE U.S. and Minnesota & Wisconsin.

ETIOLOGY

Species specific Leucocytozoans, a protozoa.

EPIZOOTIOLOGY

Birds that survive the disease become carriers. Black flies and midges transmit the disease to susceptible birds.

CLINICAL SIGNS

Sudden & explosive onset. Depression, anorexia, thirst, loss of equilibrium, weakness, anemia, rapid labored breathing.

MORBIDITY AND MORTALITY

High.

LESIONS

Splenomegaly, hepatomegaly, anemia.

Histopath.: Megaloschizonts in the brain & schizonts in the liver.

DIAGNOSIS

Examination of Wright or Giemsa-stained blood or finding schizonts in the brain or liver.

PREVENTION

Dispose of old birds.

Control Black Fly & Midges population.

Clopidol in feed.

TREATMENT

None.

TRICHOMONIASIS

OCCURRENCE

Occurs in pigeons and doves and raptors that feed on them. Occasionally in turkeys, chickens, and game birds. Outbreaks usually occur in warm weather in warm climates.

ETIOLOGY

Trichomonas gallinae, a protozoa.

EPIZOOTIOLOGY

Pigeons are carriers and contaminate surface water or water containers. Pigeons can transmit trichomonads to their young during feeding.

Raptors expose themselves and their young by feeding them infected doves and pigeons.

CLINICAL SIGNS

Pigeons, doves, and raptors have trouble closing their mouth due to oral lesions. Drooling and repeated swallowing movements. Watery eyes in birds with lesions in the sinuses or periorbital area. In rare cases with penetrating cranial lesions may show CNS signs.

Turkeys have a gaunt appearance with a hollowed area over the crop. Swallowing movements. Bird may have an unpleasant odor.

MORBIDITY AND MORTALITY

Varies but can be high.

LESIONS

Pigeons, doves and raptors: yellow plaques or raised cheesy masses involving the upper digestive tract. Most extensive in mouth, pharynx, esophagus, crop, proventriculus, sinuses.

Raptors: Same as above, lesions may also occur in the liver and be accompanied by peritonitis.

Turkeys: Same as above but usually found  only in crop or esophagus.

DIAGNOSIS

Signs & lesions.

Finding trichomonads in the oral fluids.

PREVENTION

Good sanitation.

Provide clean water.

Avoid mixing species.

Add protozoacides to the ration or water.

TREATMENT

Dimetridazole, aminonitrothiazole, Enheptin.

DISSECTING ANEURYSM

OCCURRENCE

Turkeys & chickens.

ETIOLOGY

A high protein intake with lipemia.

Puberty in tom turkeys coincides with an increased incidence. Hormonal changes may increase lipidemia and increase blood pressure.

There may be genetic susceptibility.

CLINICAL SIGNS

Sudden death in a rapidly growing flock.

LESIONS

Large amount of blood in abdominal cavity.

Rupture in wall of aorta.

DIAGNOSIS

History & lesions.

PREVENTION

Avoid overfeeding protein and fats in 16-20 week old birds.

Add reserpine to the feed after 4 weeks of age.

TREATMENT

None.

PEROSIS

OCCURRENCE

Young birds. Correlates with crowded confinement, using slat or wire floors, feeding rations with high mineral content or unsupplemented.

ETIOLOGY

Mainly due to deficiency of manganese or choline.

CLINICAL SIGNS

Malposition of one or both legs from the hock distally. The hock is swollen and the obvious site of malposition.

LESIONS

Initially: Hock is flattened, widened, and enlarged.

Later: Leg from hock distally deviates laterally. Gastrocnemius tendon at the hock has slipped from its trochlea. The tibia and metatarsus may be bowed and twisted. Shortening and thickening of the long bones of the legs and wings or displacement of the articular cartilage of the distal end of the tibia may be apparent.

DIAGNOSIS

Lesions, age, and size of bird.

Feed analysis.

PREVENTION

Feeding balanced ration.

TREATMENT

None for the bird affected. Prompt supplementation of the feed with manganese, choline, and B vitamins may minimize the problem.

RICKETS

OCCURRENCE

Young chicks or poults mainly.

ETIOLOGY

Phosphorus or Vit. D3 deficiency.

CLINICAL SIGNS

Young Birds: Stiff-legged gait. Retardation of growth. Enlargement of the ends of long bones. Birds rest in squatting position.

Laying Birds: First lay fewer eggs with egg shells thin. In a few days birds cease laying. Later birds get down on their hocks, become paralyzed and die within a few days.

LESIONS

Young Birds: Bones are soft and rubbery. Epiphyses of long bones often are enlarged. There is beading of the ribs. Ribs are thickened and bent so that thorax is flattened. The beak becomes soft and rubbery. Parathyroids are enlarged.

Laying Birds: Bones are osteoporotic with history of fractures. May have beading of ribs and softening of the keel bone.

DIAGNOSIS

Signs & lesions.

Analysis of bone ash.

Analysis of feed.

PREVENTION

Feed a balanced diet.

Provide oyster shell or limestone as a supplement.

TREATMENT

Adjust ration to proper levels.

Give calcium carbonate.

VITAMIN A DEFICIENCY

OCCURRENCE

Usually chicks or poults 1-7 weeks old.

ETIOLOGY

If rations don't contain alfalfa meal and if stored corn is used, the ration may be low in vit. A.

CLINICAL SIGNS

Recently hatched birds: Cessation of growth, drowsiness, ataxia. Combs and wattles may be pale. In birds that survive over one week, the eyelids become inflamed and adhered. There is sticky exudate from the nostrils and eyes. Eyelids soon swell and cheesy exudate may accumulate under the lids.

Laying hens: Decreasing egg production and unthriftiness. Inflammation of the eyes or sinuses and the eyes and sinuses may be swollen. Mucoid or cheesy exudate accumulates in the conjunctival sac. Nasal or ocular discharge may be present.

LESIONS

Young birds: Eyelids inflamed with sticky exudate present. Excessive urates in the ureters, in collecting tubules of the kidneys and bursa of Fabricius.

Laying hens: 1-3 mm pustule-like lesions in the mucosa of the mouth, pharynx, esophagus and crop. Mucoid exudate in nasal passages. Conjunctival sacs or sinuses contain mucoid or caseous exudate and may be distended. There may be a delicate pseudomembrane lining the trachea.

Histopath.: Squamous metaplasia of the secretory and glandular epithelium of the upper respiratory and digestive tract.

DIAGNOSIS

Feed analysis.

Signs & lesions.

Analysis of vit. A levels in liver.

PREVENTION

Feeding balanced ration.

Avoid storing feed for long periods.

TREATMENT

Add Vit. A to water and feed.

VITAMIN E DEFICIENCY

OCCURRENCE

Young chicks, turkey poults or ducklings. Most outbreaks occur in birds fed rations that are high in polyunsaturated fats or contain rancid fats.

ETIOLOGY

Vit. E and the selenium containing enzyme glutathione peroxidase prevent cell membrane destruction caused by peroxides and other oxidants.

CLINICAL SIGNS

Encephalomalacia: CNS signs.

Exudative Diathesis: Edema along the ventrum of the thorax and abdomen and mandible. The edematous skin is red-black or blue-black. Edema causes difficulty in walking.

Muscular Dystrophy: May have locomotor problems.

LESIONS

Encephalomalacia: Swollen cerebellum with congested, hemorrhagic or necrotic areas visible. In turkeys poliomalacia of the lumbar spinal cord may occur.

Exudative Diathesis: Blood stained edema in the skin & subcutis.

Muscular Dystrophy: In chicks, white to yellow muscle fibers in skeletal muscles of the breast or legs. In poults, musculature of the gizzard may contain gray areas of muscle degeneration.

DIAGNOSIS

Signs & lesions.

Analysis of the feed.

PREVENTION

Avoid storage of feed for longer than 4 mths. & store under dry, cool conditions.

Use only stabilized fats in the feed.

TREATMENT

Add vit. E to feed.

Oral supplementation with vit. E.

RIBOFLAVIN DEFICIENCY

CLINICAL SIGNS

When chicks are fed a diet deficient in riboflavin, they grow very slowly and become weak and emaciated; their appetite is fairly good; diarrhea develops between the 1st and 2nd wk. Chicks do not walk except when forced to, and then frequently walk on their hocks with the aid of their wings. Toes are curled inward when both walking and resting. Chicks are usually found in a resting position. The wings often droop as though it were impossible to hold them in the normal position. Leg
muscles are atrophied and flabby, and the skin is dry and harsh. Young chicks in advanced stages of deficiency do not move around but lie with their legs sprawled out.

A deficiency of riboflavin in the diet of hens results in decreased egg production, increased embryonic mortality, and an increase in size and fat content of the liver. Hatchability of eggs decreases within 2 wk after hens are fed a riboflavin- deficient diet but improves to near normal levels within 7 days after adequate amounts of riboflavin are added to the diet. Embryos that fail to hatch from eggs of hens fed diets low in this vitamin are dwarfed and show a high incidence of edema,
degeneration of Wolffian bodies, and defective down. The down is referred to as "clubbed" and results from failure of the down feathers to rupture the sheaths, causing feathers to coil in a characteristic way.

Riboflavin deficiency in young turkeys is characterized by poor growth and incrustations in the corners of the mouth and on the eyelids. Severe dermatitis of the feet and shanks-marked by edematous swelling, desquamation, and deep fissures-appears in some deficient poults.

LESIONS

Necropsy of chicks shows no marked abnormalities of internal organs, and bacteriologic exams reveals no specific infection of the blood or internal organs. In some cases the thymus shows congestion and premature atrophy. In severe cases of deficiency chicks show marked swelling and softening of sciatic and brachial nerves. Sciatic nerves usually show the most pronounced effects, sometimes reaching a diameter four to five times normal size.

Histologic exam of affected nerves shows degenerative changes in myelin sheaths of the main peripheral nerve trunks. This may be accompanied by axis cylinder swelling and fragmentation. Schwann cell proliferation, myelin changes, gliosis, and chromatolysis occur in the spinal cord. In cases of curled-toe paralysis, degeneration of the neuromuscular end plate and muscle tissues is often found. This indicates that riboflavin is necessary for normal functioning of the nervous system of growing chicks. Riboflavin is probably also essential for myelin metabolism of the main peripheral nerve trunks. No gross dystrophy develops, although muscle fibers are in some cases completely degenerated. The sciatic nerve exhibits myelin degeneration in one or more branches. Similar changes are apparent in the brachial nerve trunks.

The nervous system of embryos that fail to hatch from eggs laid by hens fed riboflavin-deficient diets has degenerative changes very much like those described in riboflavin-deficient chicks.

Chicks fed riboflavin-deficient diets develop pancreatic and duodenal lesions as described for thiamin deficiency in addition to the more classic nervous signs.

TREATMENT

Chicks receiving rations only partially deficient in riboflavin may recover spontaneously, indicating that the requirement rapidly decreases with age. 100ug of riboflavin given SID for 2 days is sufficient for treatment of deficient chicks or poults, followed by incorporation of an adequate level in the ration. However, when the curled-toe deformity is of long standing, irreparable damage has occurred and administration of riboflavin no longer cures the condition.

FATTY LIVER SYNDROME

OCCURRENCE

Occurs in fat, high producing, caged hens in hot weather.

ETIOLOGY

Excessive caloric intake or decreased energy utilization.

Metabolites of mold in feed, litter or drinking water may produce toxic damage in the liver.

Deficiency of lipotrophic agents.

Stress.

CLINICAL SIGNS

Egg production drops.

Sudden deaths.

Obesity.

Pale combs & wattles.

LESIONS

Obese cadavers.

Pale head parts.

Liver: yellow, greasy, and soft with hemorrhages and hematocysts. Blood in abdominal cavity due to rupture of hematocyst.

DIAGNOSIS

History & lesions.

PREVENTION

Avoid obesity,. adequate lipotrophic agents in the feed.

Avoid moldy feed, litter, and water.

Minimize stress.

TREATMENT

None of proven value.

GOUT

OCCURRENCE

Gout has been observed in turkeys and chickens of all ages.

ETIOLOGY

The hyperuricemia that must precede deposition of urates in tissues may be the result of increased rate of synthesis of purine precursors of uric acid, decreased elimination of uric acid by kidneys, or a combined effect. Excess dietary protein would lead to an excess of purine precursors; certain chemicals, toxins, feed ingredients, infectious agents, and vitamin A deficiency may damage kidneys or cause kidney dysfunction. Genetics may play a role in susceptibility to gout.

LESIONS

The condition is characterized by deposition of chalklike uric acid crystals on the visceral surfaces, in tendon sheaths, and on articular cartilages.

TREATMENT

The sick bird should be kept at a fairly constant temperature and drafts must be avoided. The perches must be smooth, flat, broad, and of soft wood, and be placed at a low level because of the difficulty the bird has in climbing. The food and water containers should also be placed within easy reach. The protein content of the food is to be lowered as much as possible. Concentrates, esp. of animal origin, are taboo. Low-protein seed mixtures should be provided, along with a rich supply of
vegetables and fruit, supplemented by vit. A.

For general treatment, give sodium bicarbonate (0.5 to 2%) or lithium carbonate (1%). Atophan (2-phenylquinoline-4- carboxylic acid) or cinchophen is recommended for budgerigars, 120 mg SID, and for fowl, 250 mg BID. In birds suffering from articular gout presumably no more than arrest of the development can be expected at best. Aspirin is given solely for analgesic effect, since it has no curative properties. Dosage is 0.3g (5 gr) dissolved in 240 ml of water, given as drinking water or by dropper. Allopurinol ("Zyloprim") at 20 mg/p.o./SID will cause regression of tophi but recurrence occurs when medication is stopped.

TUMORS

ADENOCARCINOMA

OCCURRENCE

By far the most common type of ovarian tumor in the chicken. It has also been reported in turkeys. It has also been reported in Budgerigars and pigeons.

CLINICAL SIGNS

Abdominal distension, dyspnea, and difficulty in passing droppings. Affected hens are thin and assume a penquinlike position.

LESIONS

Early cases may only be detected microscopically or grossly as minute fleshy enlargement of atretic follicles. In advanced cases the ovary is enlarged, cauliflowerlike in shape, firm, and gray-white. Numerous transcelomic implants vary from small and pearllike to massive nodular growths on serosal surfaces of the pancreas, mesentery, oviduct, and intestines, with other abdominal organs less affected. Ascites usually develops, presumably because of hindered lymphatic circulation, and
intestines become thickened, knotted, and often blocked. Since the oviduct is so often involved, care must be taken to rule out a primary oviductal adenocarcinoma, which can grossly and histologically resemble ovarian adenocarcinoma. This can be done by looking for tumors in the mucosal lining of the oviduct, because primary oviductal carcinomas are always found there and their absence indicates an ovarian primary. Usually there are no maturing follicles in advanced carcinomas, and the
oviducts are atrophic. The tumor is probably multifocal in origin, grows fairly slowly, and does not produce hormones.

In ovarian adenocarcinomas the stroma is often very reactive; in some cases thick bands of smooth muscle predominate, giving an impression of thecal cell tumors in mammals. This appears to be a reactive, not a neoplastic, process since the connective tissue component does not metastasize. When the epithelial component of the ovarian tumor metastasizes, it also produces a reactive response in the smooth muscle of implanted tissues, accounting for thickening of the mesentery and
intestinal wall. Division of ovarian adenocarcinomas into medullary and scirrhous types no longer appears tenable, since tumor size appears to be such an important factor in determining morphology; generally, large tumors are scirrhous, composed of cuboidal epithelium forming small acini heavily interlaced with connective tissue. Occasionally, ovarian adenocarcinomas are found in ovaries covered with grapelike clusters of what look like follicles filled with yellow fluid. These cysts are
not neoplastic growths and thus are entirely unrelated to ovarian cystadenocarcinomas of mammals.

Histologically, the commonest structures in ovarian adenocarcinomas are acini composed of a single layer of low columnar or cuboidal epithelium. These nonciliated eosinophilic cells with a basal, round vesicular nucleus are oriented around a variably sized lumen sometimes containing an intensely eosinophilic homogeneous material that is PAS-positive and mucicarmine-negative. Some tumors are more densely cellular, and acinar structures are compressed, giving the impression of
sheets of tumor cells, while in others the lumen may be enlarged with epithelial infolding, forming papillary structures. The tumor develops in the theca externa of small follicles and within the stroma. The origins of neoplastic cells remains unknown, but possibly include thecal glands, interstitial cells of the stroma, remnants of embryonic sex cords, and the mesonephros.

LEIOMYOSARCOMA

OCCURRENCE

This tumor has been found in budgerigars.

CLINICAL SIGNS

Egg-bound, anorexia, and bulging abdomen.

LESIONS

A firm, white mass attached to the smooth muscle of the oviduct. The tumor is composed of smooth muscle and fibrous elements.

SQUAMOUS CELL CARCINOMA (SCC)

OCCURRENCE

A few cases of SCC have been reported in chickens, pigeons, and budgerigars.

LESIONS

In cases described, downward growth of rete pegs into the dermis was of normal appearing cells of the basal layer and stratum corneum. Normal transition of the deeply basophilic basal cells to the eosinophilic keratinized cells, with cellular bridges and epithelial pearls, was seen. In other SCC there may be a tendency toward anaplasia in more malignant tumors, with structural disorganization and atypical cells.

Large numbers of inflammatory cells may be seen as the result of superficial ulceration often associated with carcinomas of the skin. There are no sites of predilection for the round ulcerous lesions that are surrounded by a rim of thickened skin and dermis. Penetration of the dermis and occasionally of arrector muscle but not of skeletal muscle has occurred, and no distant metastases have been observed.

REFERENCES

Hofstad, M. 1984. Diseases of Poultry, 8th ed.. Iowa State University Press, Ames.

Ivens, R., Mark, D., &Levine, N. 1978. Principal Parasites of Domestic Animals in the U.S.. University of IL Press, Urbana.

Petrak, M. 1982. Diseases of Cage and Aviary Birds, 2nd ed.. Lea & Febiger, Philadelphia.

Randall, C. 1985. Color Atlas of Diseases of the Domestic Fowl & Turkey. Iowa State University Press, Ames.

Sloss, M., Kemp, R. 1978. Veterinary Clinical Parasitology, 5th ed.. Iowa State University Press, Ames.

Whiteman, C. & Bickford, A. 1983. Avian Disease Manual, 2nd ed.. University of PA Press, Kennett Square.

AVIAN DISEASES: FUNGAL, NUTRITIONAL, TUMORS, PARASITES

AFLATOXICOSIS Aspergillus flavus growing in peanut meal, corn meal, cottonseed meal cake, many grains and in poultry litter; Young birds more susceptible

CLINICAL SIGNS: Initially, lethargy, anorexia, impaired growth, ruffled feathers & drooping wings; Later, ataxia, opisthotonos & convulsions.

In chickens, there is impaired & uneven growth in the flock with low mortality. It may be subclinical & unrecognized.

MORBIDITY & MORTALITY:  Variable but often high.

LESIONS

Liver: Swollen & discolored initially but later becomes cirrhotic & nodular. May have necrotic foci.

Ascites & hydropericardium are frequently present & may have generalized edema. Petechial hemorrhages at various sites & renal swelling may be present. Marked catarrhal enteritis is usually a feature.

Histopath: hyperplasia of biliary epithelium

Aflatoxin is carcinogenic. Tumors usually develop in the liver.

DIAGNOSIS:  History, gross & micro. lesions; Analysis of affected feed;

PREVENTION:  Avoid storing feed for long periods. Store feed under cool & dry conditions; Addition of antimycotics to the feed.

TREATMENT:  Treatment isn't necessary if the aflatoxin is eliminated from the ration.

ASPERGILLOSIS Aspergillus fumigatus

OCCURRENCE:  All species of birds are susceptible.

EPIZOOTIOLOGY

Infection usually occurs after inhalation of large numbers of spores from heavily contaminated feed or litter which overwhelms the resistance of the bird.

Aspergillus can penetrate egg shells under ideal conditions & infect the embryo. Such eggs may appear green when candled. Infected embryos may hatch with well developed lesions.

CLINICAL SIGNS:  Dyspnea, gasping, accelerated breathing, diarrhea, anorexia, somnolence, progressive emaciation & increased thirst.

metastasis to the brain, signs of CNS disturbance metastasis to the globe, one or both may have a gray-white opacity.

LESIONS:  Yellow or gray nodules and/or plaques in the lungs, air sacs, or trachea; less often in the peritoneal cavity, liver, or at other sites.

Mycelial growth with sporulation may be apparent as fuzzy green material in the air sacs.

Yellow or gray metastatic foci may be apparent in the brain, eye, or at other sites. Infection in the conjunctival sac may result in accumulation of cheesy exudate.

Histopath.: Hyphae within the nodules or plaques.

DIAGNOSIS:  Signs & lesions; Culture. Caution, Aspergillus is a common contaminant.

CANDIDIASIS Candida albicans

OCCURRENCE:  Usually chickens or turkeys. Young birds are more susceptible.

EPIZOOTIOLOGY

Candida is present in the normal digestive tract of birds & mammals. Debilitation or alterations in the normal gut flora can cause the fungus to invade the mucosa & produce lesions.

CLINICAL SIGNS:  Retarded growth, listlessness, ruffled feathers or diarrhea. The signs may be masked by the primary disease.

LESIONS:  Diffuse and/or focal thickening of the affected mucosa with white or gray pseudomembranous or diphtheritic patches. Focal lesions may have sloughed into the lumen as soft cheesy material. Lesions are usually located in the mouth, pharynx, esophagus, & crop. Lesions of the primary disease may be present.

DIAGNOSIS

Lesions & histopathic evidence of invasion of the fungus into tissue.

Culture. Caution, remember Candida is present normally.

PREVENTION:  Good sanitation; Prevention of primary disease & management practices that might debilitate the birds; Avoid overtreatment with antibiotics, drugs, coccidiostats, growth stimulants.

TREATMENT:  Gentian violet in feed; Copper sulfate in drinking water; Treat primary disease or management problem.

COCCIDIOSIS Eimeria spp.

OCCURRENCE

Common in chickens & less often in turkeys. Occasionally in geese, guineas, pigeons, pheasants, quail, chukars & etc.

Usually seen in young birds under conditions of warmth & high humidity or conditions that lead to wet litter.

EPIZOOTIOLOGY (in chickens)

Oocysts, fecal-oral & transmitted by fomites.  moderate exposure- immunity to specific coccidia spp.; Massive exposure- outbreaks.

CLINICAL SIGNS:  Varies with species of coccidia. Pathogenic species cause diarrhea which may be mucoid or bloody, dehydration, ruffled feathers, anemia, listlessness, weakness, retraction of the head & neck, somnolence, depigmentation of skin. In turkeys, the signs are the same except the diarrhea isn't bloody.

LESIONS (in chickens) Anterior 1/3 of the Gut

E. acervulina. Mild to severe enteritis that can lead to thickening of the mucosa. Transverse white to gray striations are often visible in the mucosa.

Middle 1/3

E. necatrix. Enteritis characterized be congestion, hemorrhage, necrosis, & bloody feces. Intestine is often markedly dilated, inflamed, & thickened. White to yellow foci & petechial hemorrhages may be seen thru the serosa. E. maxima. Thickening of the intestinal wall & marked dilation. Intestinal content may be bloody.

Posterior 1/3

E. brunetti. A fibrinous or fibrinonecrotic mass of debris may cover the affected mucosa or produce caseous cores. E. tenella. Blood often apparent in the ceca & feces in early cases. Later, cheesy cecal cores may be found.

MORBIDITY & MORTALITY:  Variable

DIAGNOSIS:  Signs & lesions.

PREVENTION:  Anticoccidials in the feed; Purposeful small exposures to stimulate immunity; Genetic resistant strains are being developed.

TREATMENT:  Not very satisfactory. Can try Amprolium, Agribon, Sulfaquinoxaline, Sulfamethazine; Increase Vit. A & K in feed or water.

HEXAMITIASIS Hexamita columbae- pigeons Hexamita meleagridis- other birds

OCCURRENCE:  Seen in 1-9 week old turkey poults. Also occurs in gamebirds, peafowl, ducks, & pigeons.

EPIZOOTIOLOGYD:  Recovered birds often are carriers & shed the parasite in their feces which contaminate feed, water & range. Susceptible birds get the organism by ingestion.

CLINICAL SIGNS:

Initially, Birds are very nervous & active. They also chirp excessively, shiver, crowd around any heat source & have subnormal temps. There is watery or foamy diarrhea & the birds dehydrate rapidly. Later, Birds are depressed, stand with their heads retracted, feathers ruffled & wings drooping. Terminally, Birds go into coma, struggle, & die due to hypoglycemia.

MORBIDITY & MORTALITY:  Morbidity is high 75-90% in young birds, poorly housed w/o treatment.

LESIONS:  Cadaver is dehydrated. Intestines are flabby with areas of bulbous dilation & contains excessive mucus & gas. Proximal 1/2 of intestines is inflamed. Cecal tonsils may be congested.

DIAGNOSIS:  Duodenal scrapings on a freshly killed bird using reduced light or phase contrast microscopy reveal the organism.

PREVENTION:  Short periods of depopulation combined with thorough cleaning & disinfection.

TREATMENT:  Nithiazide, Emtryl, Ipronidazole, Furazolidone, tetracycline; Increase room temperature.

HISTOMONIASIS Histomonas meleagidis

OCCURRENCE:  protozoa, occurs most frequently in exposed, unmedicated turkeys, esp. under 3 mths.. Also occurs in chickens & captive game birds. Young birds are more frequently & severely affected.

EPIZOOTIOLOGY:

Transmission is via 3 routes:  Ingestion infected fresh feces, ova of Heterakis gallinarum or,  earthworms harboring larva of Heterakis. CLINICAL SIGNS

Initially, Listlessness, anorexia, drooping wings & yellow feces. Headparts may be cyanotic. In chickens there may be bloody feces. Later, Depression, drooping wings, eyes closed, head drawn close to the body, & emaciation.

MORBIDITY & MORTALITY:  Approaches 100% in young turkeys.

LESIONS

Bilateral enlargement of the ceca with thickening of the walls. Mucosa is usually ulcerated. The ceca often contain laminated yellow, gray, green, or red caseous cores.

Liver: irregularly-round, depressed lesions that vary in color (yellow, gray, green or red). pathognomonic.

DIAGNOSIS:  Lesions. Isolation of organism from cecal or hepatic scrapings.

PREVENTIOND:  Addition of antihistomonal drugs to the ration; Good sanitation; Do not mix turkeys with other species of birds; Deworm for cecal worms frequently.

TREATMENT: None.

LEUCOCYTOZOONOSIS Leucocytozoan spp.

OCCURRENCE:  Acute outbreaks occur mostly in young birds & chronic in older birds. Maintained in wild bird populations; Occurs most frequently in the SE U.S. & Minnesota & Wisconsin.

EPIZOOTIOLOGY:  Birds that survive the disease become carriers. Black flies & midges transmit the disease to susceptible birds.

CLINICAL SIGNS:  Sudden & explosive onset. Depression, anorexia, thirst, loss of equilibrium, weakness, anemia, rapid labored breathing.

MORBIDITY & MORTALITY:  High.

LESIONS:  Splenomegaly, hepatomegaly, anemia.

Histopath.: Megaloschizonts in the brain & schizonts in the liver.

DIAGNOSIS:  Examination of Wright or Giemsa-stained blood or finding schizonts in the brain or liver.

PREVENTION:  Dispose of old birds; Control Black Fly & Midges population; Clopidol in feed.

TREATMENT:  none.

TRICHOMONIASIS Trichomonas gallinae

OCCURRENCE:  Occurs in pigeons & doves & raptors that feed on them. Occasionally in turkeys, chickens, & game birds. Outbreaks usually occur in warm weather in warm climates.

EPIZOOTIOLOGY:  Pigeons are carriers & contaminate surface water or water containers. Pigeons can transmit trichomonads to their young during feeding. Raptors expose themselves & their young by feeding them infected doves & pigeons. CLINICAL SIGNS:  Pigeons, doves, & raptors have trouble closing their mouth due to oral lesions. Drooling & repeated swallowing movements. Watery eyes with sinus or periorbital lesions & rarly CNS signs.  Turkeys have a gaunt appearance with a hollowed area over the crop. Swallowing movements. Bird may have an unpleasant odor.

MORBIDITY & MORTALITY:  Varies but can be high.

LESIONS:

Pigeons, doves & raptors: yellow plaques or raised cheesy masses involving the upper digestive tract. Most extensive in mouth, pharynx, esophagus, crop, proventriculus, sinuses. Raptors may also have liver lesions & peritonitis. Turkeys: lesions found only in crop or esophagus.

DIAGNOSIS:  Signs & lesions; Finding trichomonads in the oral fluids.

PREVENTION:  Good sanitation; Provide clean water; Avoid mixing species; protozoacides

TREATMENT:  Dimetridazole, aminonitrothiazole, Enheptin.

DISSECTING ANEURYSM

OCCURRENCE:  Turkeys & chickens.

ETIOLOGY:  high protein intake with lipemia; Puberty in tom turkeys coincides with an increased incidence. Hormonal changes may increase lipidemia & increase blood pressure. There may be genetic susceptibility.

CLINICAL SIGNS:  Sudden death in a rapidly growing flock.

LESIONS:  Large amount of blood in abdominal cavity; Rupture in wall of aorta.

DIAGNOSIS:  History & lesions.

PREVENTION:  Avoid overfeeding protein & fats in 16-20 week old birds; Add reserpine to the feed after 4 weeks of age.

TREATMENT:  None.

PEROSIS

OCCURRENCE:  Young birds. Correlates with crowded confinement, using slat or wire floors, feeding rations with high mineral content or unsupplemented.

ETIOLOGY:  Mainly due to deficiency of manganese or choline.

CLINICAL SIGNS:  Malposition of one or both legs from the hock distally. The hock is swollen & the obvious site of malposition.

LESIONS:

Initially, Hock is flattened, widened, & enlarged. Later, Leg from hock distally deviates laterally. Gastrocnemius tendon at the hock has slipped from its trochlea. The tibia & metatarsus may be bowed & twisted. Shortening & thickening of the long bones of the legs & wings or displacement of the articular cartilage of the distal end of the tibia may be apparent.

DIAGNOSIS:  Lesions, age, & size of bird; Feed analysis.

PREVENTION:  Feeding balanced ration.

TREATMENT:  None for the bird affected. Prompt supplementation of the feed with manganese, choline, & B vitamins may minimize the problem.

RICKETS

OCCURRENCE:  Young chicks or poults mainly.

ETIOLOGY:  Phosphorus or Vit. D3 deficiency.

CLINICAL SIGNS:

Young Birds: Stiff-legged gait. Retardation of growth. Enlargement of the ends of long bones. Birds rest in squatting position. Laying Birds: First lay fewer eggs with egg shells thin. In a few days birds cease laying. Later birds get down on their hocks, become paralyzed & die within a few days.

LESIONS:

Young Birds: Bones are soft & rubbery. Epiphyses of long bones often are enlarged. There is beading of the ribs. Ribs are thickened & bent so that thorax is flattened. The beak becomes soft & rubbery. Parathyroids are enlarged. Laying Birds: Bones are osteoporotic with history of fractures. May have beading of ribs & softening of the keel bone.

DIAGNOSIS:  Signs & lesions; Analysis of bone ash; Analysis of feed.

PREVENTION:  Feed a balanced diet with supplemental oyster shell or limestone.

TREATMENT:   Adjust ration to proper levels & Give calcium carbonate.

VITAMIN A DEFICIENCY

OCCURRENCE:  Usually chicks or poults 1-7 weeks old.

ETIOLOGY:  If rations don't contain alfalfa meal & if stored corn is used, the ration may be low in vit. A.

CLINICAL SIGNS

Recently hatched birds: Cessation of growth, drowsiness, ataxia. Combs & wattles may be pale. In birds that survive over one week, the eyelids become inflamed & adhered. There is sticky exudate from the nostrils & eyes. Eyelids soon swell & cheesy exudate may accumulate under the lids. Laying hens: Decreasing egg production & unthriftiness. Inflammation of the eyes or sinuses & the eyes & sinuses may be swollen. Mucoid or cheesy exudate accumulates in the conjunctival sac. Nasal or ocular discharge may be present.

LESIONS:

Young birds: Eyelids inflamed with sticky exudate present. Excessive urates in the ureters, in collecting tubules of the kidneys & bursa of Fabricius. Laying hens: 1-3 mm pustule-like lesions in the mucosa of the mouth, pharynx, esophagus & crop. Mucoid exudate in nasal passages. Conjunctival sacs or sinuses contain mucoid or caseous exudate & may be distended. There may be a delicate pseudomembrane lining the trachea.

Histopath: Squamous metaplasia of the secretory & glandular epithelium of the upper respiratory & digestive tract.

DIAGNOSIS:  Feed analysis; Signs & lesions; Analysis of vit. A levels in liver.

PREVENTION:  Feeding balanced ration; Avoid storing feed for long periods.

TREATMENT:  Add Vit. A to water & feed.

VITAMIN E DEFICIENCY

OCCURRENCE:  Young chicks, turkey poults or ducklings. Most outbreaks occur in birds fed rations that are high in polyunsaturated fats or contain rancid fats.

ETIOLOGY:  Vit. E & the selenium containing enzyme glutathione peroxidase prevent cell membrane destruction caused by peroxides & other oxidants.

CLINICAL SIGNS:

Encephalomalacia: CNS signs; Exudative Diathesis: Edema along the ventrum of the thorax & abdomen & mandible. The edematous skin is red-black or blue-black. Edema causes difficulty in walking. Muscular Dystrophy:  May have locomotor problems.

LESIONS:

Encephalomalacia: Swollen cerebellum with congested, hemorrhagic or necrotic areas visible. In turkeys poliomalacia of the lumbar spinal cord may occur. Exudative Diathesis: Blood stained edema in the skin & subcutis.

Muscular Dystrophy: In chicks, white to yellow muscle fibers in skeletal muscles of the breast or legs. In poults, musculature of the gizzard may contain gray areas of muscle degeneration.

DIAGNOSIS:  Signs & lesions; Analysis of the feed.

PREVENTION:  Avoid storage of feed for longer than 4 mo. & store under dry, cool conditions; Use only stabilized fats in the feed.

TREATMENT:  Add vit. E to feed; Oral supplementation with vit. E.

RIBOFLAVIN DEFICIENCY

CLINICAL SIGNS:  chicks: slow growth; weak & emaciated; appetite is fairly good; diarrhea 1st & 2nd wk; object to walking & then frequently walk on hocks with the aid of their wings; Toes are curled inward; usually found in a resting position; wings often droop; Leg muscles atrophied & flabby; skin dry & harsh; advanced stages:   lie around with their legs sprawled out. hens:  decreased egg production; increased embryonic mortality;, increase in size & fat content of the liver;
Hatchability of eggs decreases within 2 wk after riboflavin-deficient diet but improves to near normal levels within 7 days after adequate amounts of riboflavin are added to the diet; Embryos that fail to hatch from eggs of hens fed diets low in this vitamin are dwarfed & show a high incidence of edema, degeneration of Wolffian bodies, & defective down. The down is referred to as "clubbed" & results from failure of the down feathers to rupture the sheaths, causing feathers to coil in a
characteristic way. young turkeys: poor growth & incrustations, mouth & eyelids; Severe dermatitis of feet & shanks-marked by edematous swelling, desquamation, & deep fissures-appears in some deficient poults.

LESIONS:  chicks:  no marked gross lesions except occassional thymic congestion & premature atrophy; severe cases marked swelling & softening of sciatic & brachial nerves;  Histologic:  degenerative changes in myelin sheaths of the main peripheral nerve trunks, brachial & sciatic; Schwann cell proliferation, myelin changes, gliosis, & chromatolysis spinal cord. In cases of curled-toe paralysis, degeneration of the neuromuscular end plate & muscle tissues is often found; No
gross muscular dystrophy develops, although muscle fibers are in some cases completely degenerated. pancreatic & duodenal lesions in addition.

TREATMENT:  100ug of riboflavin SID for 2 days followed by incorporation in the ration. However, when the curled-toe deformity is of long standing, irreparable damage has occurred.

FATTY LIVER SYNDROME

OCCURRENCE:  Occurs in fat, high producing, caged hens in hot weather.

ETIOLOGY:  Excessive caloric intake or decreased energy utilization; Mold Metabolites- feed, litter or drinking water; Deficiency of lipotrophic agents; Stress.

CLINICAL SIGNS:  Egg production drops; Sudden deaths; Obesity; Pale combs & wattles.

LESIONS:  Obese cadavers; Pale head parts; Liver: yellow, greasy, & soft with hemorrhages & hematocysts. Blood in abdominal cavity due to rupture of hematocyst

DIAGNOSIS:  History & lesions.

PREVENTION:  Avoid obesity; insure adequate lipotrophic agents in the feed; Avoid moldy feed, litter, & water; Minimize stress.

TREATMENT:  None of proven value.

GOUT

OCCURRENCE:  Gout has been observed in turkeys & chickens of all ages.

ETIOLOGY:  The hyperuricemia that must precede deposition of urates in tissues may be the result of increased rate of synthesis of purine precursors of uric acid, decreased elimination of uric acid by kidneys, or a combined effect. Excess dietary protein would lead to an excess of purine precursors; kidney dysfunction, 2o to  toxins, infectious agents, & vitamin A deficiency; Genetics may play a role in susceptibility to gout.

LESIONS:  The condition is characterized by deposition of chalklike uric acid crystals on the visceral surfaces, in tendon sheaths, & on articular cartilages.

TREATMENT:  Maintain optimum room temperature & avoid drafts; Keep perch, feed & water easily accessible;  feed protein content lowered as much as possible; Concentrates, esp. of animal origin, are taboo. Low-protein seed mixtures should be provided, along with a rich supply of vegetables & fruit, supplemented vit A. For general treatment, give sodium bicarbonate (0.5 to 2%) or lithium carbonate (1%). Atophan (2-phenylquinoline-4-carboxylic acid) or cinchophen is recommended for budgerigars, 120 mg SID, & for fowl, 250 mg BID. In birds suffering from articular gout presumably no more than arrest of the development can be expected at best. Aspirin is given solely for analgesic effect, since it has no curative properties. Dosage is 0.3g (5 gr) dissolved in 240 ml of water, given as drinking water or by dropper. Allopurinol ("Zyloprim") at 20 mg/p.o./SID will cause regression of tophi but recurrence occurs when medication is stopped.

TUMORS

ADENOCARCINOMA

OCCURRENCE:  Ovarian, By far the most common- chicken, turkeys, Budgerigars & pigeons.

CLINICAL SIGNS:  Abdominal distension, dyspnea, & difficulty in passing droppings. Affected hens are thin & assume a penquinlike position.

LESIONS:  Early cases may only be detected microscopically or grossly as minute fleshy enlargement of atretic follicles. advanced cases the ovary is enlarged, cauliflowerlike in shape, firm, & gray-white. Numerous transcelomic implants vary from small & pearllike to massive nodular growths on serosal surfaces of the pancreas, mesentery, oviduct, & intestines, with other abdominal organs less affected. Ascites usually develops, presumably because of hindered lymphatic circulation, & intestines become thickened, knotted, & often blocked. Since the oviduct is so often involved, care must be taken to rule out a primary oviductal adenocarcinoma, which can grossly & histologically resemble ovarian adenocarcinoma. This can be done by looking for tumors in the mucosal lining of the oviduct, because primary oviductal carcinomas are always found there & their absence indicates an ovarian primary. Usually there are no maturing follicles in advanced carcinomas, & the oviducts are atrophic. The tumor is probably multifocal in origin, grows fairly slowly, & does not produce hormones.

In ovarian adenocarcinomas the stroma is often very reactive; in some cases thick bands of smooth muscle predominate, giving an impression of thecal cell tumors in mammals. This appears to be a reactive, not a neoplastic, process since the connective tissue component does not metastasize. When the epithelial component of the ovarian tumor metastasizes, it also produces a reactive response in the smooth muscle of implanted tissues, accounting for thickening of the mesentery &
intestinal wall. Division of ovarian adenocarcinomas into medullary & scirrhous types no longer appears tenable, since tumor size appears to be such an important factor in determining morphology; generally, large tumors are scirrhous, composed of cuboidal epithelium forming small acini heavily interlaced with connective tissue. Occasionally, ovarian adenocarcinomas are found in ovaries covered with grapelike clusters of what look like follicles filled with yellow fluid. These cysts are not
neoplastic growths & thus are entirely unrelated to ovarian cystadenocarcinomas of mammals.

Histologically, the commonest structures in ovarian adenocarcinomas are acini composed of a single layer of low columnar or cuboidal epithelium. These nonciliated eosinophilic cells with a basal, round vesicular nucleus are oriented around a variably sized lumen sometimes containing an intensely eosinophilic homogeneous material that is PAS-positive & mucicarmine- negative. Some tumors are more densely cellular, & acinar structures are compressed, giving the impression of sheets of tumor cells, while in others the lumen may be enlarged with epithelial infolding, forming papillary structures. The tumor develops in the theca externa of small follicles & within the stroma. The origins of neoplastic cells remains unknown, but possibly include thecal glands, interstitial cells of the stroma, remnants of embryonic sex cords, & the mesonephros.

LEIOMYOSARCOMA

OCCURRENCE:  This tumor has been found in budgerigars.

CLINICAL SIGNS:  Egg-bound, anorexia, & bulging abdomen.

LESIONS:  A firm, white mass attached to the smooth muscle of the oviduct. The tumor is composed of smooth muscle & fibrous elements.

SQUAMOUS CELL CARCINOMA (SCC)

OCCURRENCE:  A few cases of SCC have been reported in chickens, pigeons, & budgerigars.

LESIONS:  In cases described, downward growth of rete pegs into the dermis was of normal appearing cells of the basal layer & stratum corneum. Normal transition of the deeply basophilic basal cells to the eosinophilic keratinized cells, with cellular bridges & epithelial pearls, was seen. In other SCC there may be a tendency toward anaplasia in more malignant tumors, with structural disorganization & atypical cells. Large numbers of inflammatory cells may be seen as the result of superficial ulceration often associated with carcinomas of the skin. There are no sites of predilection for the round ulcerous lesions that are surrounded by a rim of thickened skin & dermis. Penetration of the dermis & occasionally of arrector muscle but not of skeletal muscle has occurred, & no distant metastases have been observed.

REFERENCES

Hofstad, M. 1984. Diseases of Poultry, 8th ed.. Iowa State University Press, Ames.

Ivens, R., Mark, D., &Levine, N. 1978. Principal Parasites of Domestic Animals in the U.S.. University of IL Press, Urbana.

Petrak, M. 1982. Diseases of Cage & Aviary Birds, 2nd ed.. Lea & Febiger, Philadelphia.

Randall, C. 1985. Color Atlas of Diseases of the Domestic Fowl & Turkey. Iowa State University Press, Ames.

Sloss, M., Kemp, R. 1978. Veterinary Clinical Parasitology, 5th ed.. Iowa State University Press, Ames.

Whiteman, C. & Bickford, A. 1983. Avian Disease Manual, 2nd ed.. University of PA Press, Kennett Square.