WRAIR SEMINAR
22 OCT 86
MICHAEL S. RAND, CPT, VC
AFLATOXICOSIS
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.
COCCIDIOSIS
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.
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