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An epizootic occurred among white-tailed deer (Odocoileus virginianus) from July through October 1988 in Missouri (USA). From late July through September, nine necropsied deer had lesions of the peracute or acute forms of hemorrhagic disease (HD) or no apparent lesions, whereas two deer necropsied in October had lesions of the chronic form of HD. Epizootic hemorrhagic disease virus was isolated from two necropsied deer. Based on changes in population indices, there is evidence that deer populations declined in seven of Missouri's 57 deer management units from 1987 to 1990. Based on a deterministic model designed to simulate deer populations in management units, it appeared that summer and fall 1988 mortality ranging from 6% to 16% accounted for the population decreases in deer management units with population declines. Heavily hunted areas where high deer mortality was not reported in the summer and fall of 1988 did not have population declines. Based on these results, we believe that HD mortality was high and resulted in deer population declines in parts of Missouri when combined with hunting harvest.

Amaranthus retroflexus (redroot pigweed)-induced nephrotoxicity was diagnosed in 6 herds of cattle from 3 counties in southwest Missouri. Forty-eight cows and calves died and another 35 were clinically affected. Serum urea nitrogen concentration, determined in 4 affected calves, was between 55 and 284 mg/dl, and serum creatinine concentration was between 6.7 and 29.9 mg/dl. Postmortem examination of affected cows and calves revealed amber-colored fluid in peritoneal cavities and retroperitoneal perirenal edema. Histologic examination of kidney sections revealed widespread degeneration and necrosis of proximal and distal tubules. Compared with archived kidney sections from cattle with Quercus (oak) poisoning, distal renal tubules were more severely affected. Oak poisoning also was associated with a higher prevalence of interstitial fibrosis and renal tubular oxalosis. We concluded that ingestion of the aerial and leafy portions of pigweed by cattle in drought situations does not necessarily lead to nitrate-induced sudden death associated with consumption of the nitrate-containing stems.

A sudden onset of bizarre neurologic dysfunction was found in 8 of 90 mixed-breed feeder calves. Seven other calves were dead, and 3 more died during the next week. A diagnosis of organochlorine toxicosis was made when rumen and abomasal contents from 1 of the calves revealed 22.4 and 20.6 micrograms of aldrin/g of ingesta, respectively. Complete feeds retrieved from self-feeders contained 54 and 528 micrograms of aldrin/g of feed. The initial concentration range in fat from 40 live calves was 6.01 to 42.44 micrograms of dieldrin/g of fat. Additional fat samples were analyzed to verify residue compliance until the entire herd was clear of residue 18 months after removal of the contaminated ration. The range of apparent half-lives for dieldrin in body fat of heifers and steers was 69 to 231 and 53 to 116 days, respectively. These findings demonstrate the considerable variability in apparent half-life of dieldrin in field cases. In cases of dieldrin-contaminated livestock, veterinarians and regulatory personnel must accurately determine the necessary slaughter withholding times so that informed economic decisions are made in the best interest of the producer while enhancing the probability of a safe food supply. Excretion rates of dieldrin from field-contaminated cattle may not be consistent with results obtained under experimental conditions.

A total of 340 cases of cutaneous neoplasia were diagnosed in 340 of 3,564 cats that were examined by biopsy or necropsy during a 41-month period from January 1, 1986 through May 31, 1989. Eighteen types of tumor occurred, but four types comprised 77% of the cases. These were basal cell tumor, 89 cases (26%, mean age 10.3); mast cell tumor, 72 cases (21%, mean age 8.6); squamous cell carcinoma, 52 cases (15%, mean age 11.6); and fibrosarcoma, 50 cases (15%, mean age 10.2). For each of these four types of tumors, peak number of cases occurred in cats older than 10 years. Mast cell tumor was the only tumor diagnosed in cats younger than 1 year. The head was the most common site for basal cell tumors, mast cell tumors, and squamous cell carcinomas. The legs were the most common location of fibrosarcomas. Siamese cats had approximately three times as many mast cell tumors as statistically expected, but only one-fourth as many squamous cell carcinomas. Breed predilection for other skin tumors was not apparent. Sex predilection was not detected for any skin tumor.

Chlamydia psittaci is a major cause of ovine abortion in the fourth to fifth months of gestation. During the lambing seasons of 1986, 1987, and 1988, fetuses from 52 cases of ovine abortion, stillbirth, or perinatal death were submitted to the laboratory for necropsy examination. Placenta or fetal tissues from 34 cases were cultured on mouse L cells for C. psittaci. Chlamydia psittaci was identified by immunofluorescence on cultures in 20 of these cases. The major gross lesion consistently associated with chlamydial abortion was placentitis with multifocal cotyledonary necrosis and accumulation of red-brown exudate in the intercotyledonary placenta. Chlamydiae appeared as spherical organisms, less than 1 micron in diameter, in the cytoplasm of trophoblasts in impression smears of cotyledons. Histologically, placentitis was sometimes accompanied by pneumonia or encephalitis in the fetus. Chlamydia psittaci was considered the cause for fetal death when chlamydial isolation was associated with placentitis or inflammation of other fetal tissues and when other abortifacient agents were not detected.

Seven of 365 dogs from Georgia and other southeastern states were seropositive for antibody to Trypanosoma cruzi by the complement-fixation (CF) test. Sera from 24 dogs, including the 7 dogs seropositive by CF test, were reactive at dilutions of 1:128 or 1:256 by the direct-agglutination (DA) test. Dogs with positive CF titers were significantly (P less than 0.05) younger than were the dogs in the total population surveyed. The occurrence of antibody to T cruzi was similar, regardless of the dogs' origin, sex, or length of hair. Dogs with specific antibody to T cruzi did not have clinical signs of disease related to the cardiovascular or gastrointestinal systems, the systems most frequently affected in American trypanosomiasis (Chagas' disease). Sera from an additional 20 dogs from Minnesota were examined by the DA test. One of these sera had a reaction at a dilution of 1:2, and 19 sera had no reaction in the DA test for antibody to T cruzi.

Cyclopiazonic acid (CPA) was purified from cultures of Aspergillus flavus, and ca. 14 g of the toxin was collected for use in feeding studies. Chicken rations were artificially contaminated with purified CPA at concentrations of 10, 50, and 100 ppm (microgram/g) and fed ad libitum to eight groups of chickens for 7 weeks. Chickens receiving feed with 100 ppm of CPA had high mortality, decreased weight gain, and poor feed conversion when compared with birds receiving other doses. Postmortem examination showed that chickens fed the two greatest doses of CPA had proventricular lesions characterized by mucosal erosion and hyperemia (100 ppm) and by thick mucosa and dilated proventricular lumens (50 ppm). Birds given 100 ppm of CPA in feed also had numerous yellow foci in their livers and spleens. Microscopic examination of tissues of birds that received 100 ppm of CPA revealed ulcerative proventriculitis, mucosal necrosis in the gizzard, and hepatic and splenic necrosis and inflammation. Birds given 50 ppm of CPA had hyperplasia of the proventricular mucosal epithelium. Birds given 10 ppm of CPA and control birds had no significant treatment-related lesions.

Approximately 70 feeder pigs developed ataxia and other signs of neuromuscular dysfunction. The ration fed the pigs was found to be contaminated with Cassia occidentalis seeds. Experimentally, other feeder pigs were fed this ration, and they developed ataxia and other signs of neuromuscular dysfunction within 6 to 8 weeks. In further experiments, feeder pigs fed diets containing 1%, 2%, or 4% ground cassia seeds also became intoxicated. Microscopically, diaphragmatic myopathy and pancreatic tissue necrosis were the principal pathologic findings.

Aflatoxicosis was diagnosed as the cause of deaths in a group of crossbred feeder steers. Corn used in the ration being fed the steers was found to be contaminated with 1,500 ng of aflatoxin/g. Residues of the mycotoxin were detected in kidney tissue, and microscopic examination of liver sections revealed lesions typical of aflatoxicosis.

A species of porcine coccidia, Isospora suis, when inoculated into piglets, produced diarrhea, dehydration, weight loss and death. Gross lesions were characterized by a fibrino-necrotic membrane within the jejunum and ileum. Villous atrophy and variable erosion, often with an adhered necrotic membrane, were seen microscopically. Asexual and sexual stages of I. suis were seen within the intestinal epithelium and oocysts were recovered from the feces. The severity of clinical disease and lesions were dose-related.

Coccidiosis is a disease of the young piglet due to infection with Isospora suis and is characterized by diarrhea which is nonresponsive to antibacterial therapy. There is variable morbidity and mortality. Piglets develop a more severe clinical illness and enteritis when infected with I. suis at one to three days of age than when infected at two weeks of age. Microscopic lesions range from villous atrophy and mild erosion to severe fibrinonecrotic enteritis.

Cocklebur (Xanthium strumarium) fed to feeder pigs was associated with acute to subacute hepatotoxicosis. Cotyledonary seedings fed at 0.75% to 3% of body weight or ground bur fed at 20% to 30% of the ration caused acute depression, convulsions, and death. Principle gross lesions were marked serofibrinous ascites, edema of the gallbladder wall, and lobular accentuation of the liver. Acute to subacute centrilobular hepatic necrosis was present microscopically. The previously reported toxic principle, hydroquinone, was not recovered from the plant or bur of X. strumarium. Authentic hydroquinone administered orally failed to produce lesions typical of cocklebur intoxication but did produce marked hyperglycemia. Carboxyatractyloside recovered from the aqueous extract of X. strumarium and authentic carboxyatractyloside, when fed to pigs, caused signs and lesions typical of cocklebur intoxication. Marked hypoglycemia and elevated serum glutamic oxaloacetic transaminase and serum isocitric dehydrogenase concentrations occurred in pigs with acute hepatic necrosis that had received either cocklebur seedlings, ground bur or carboxyatractyloside.

A paralytic disease in swine was observed on three farms located in the same geographical area of Georgia. Postmortem examinations revealed the paralysis to be related to spinal poliomalacia. Feed collected from two of the affected farms was used in a feeding study, and the paralytic condition was reproduced. In pigs from both the feeding trial and field cases, the poliomyelomalacia was characterized by focal, symmetrical lesions located in the cervical and lumbar intumescences. Selenium was detected in the feed at levels ranging from 19 to 24 ppm.

A group of 14 pregnant mares was exposed via contact to 4 mares bred to stallions infected with equine viral arteritis virus. There was a demonstrable febrile response in each donor mare and in 12 of the pregnant mares. All 18 mares became seropositive after exposure. Equine viral arteritis virus was isolated from the nasopharynx of 5 pregnant mares, but not from the donor mares. Ten of the pregnant mares aborted, and virus was isolated from fetal specimens or placenta of 8.

Piglets naturally exposed or experimentally infected with Isospora suis oocysts were given challenge doses of oocysts to determine the extent of development of immune resistance. Piglets in both studies shed low numbers of, or no detectable oocysts, following challenge. Administration of methylprednisolone acetate failed to induce oocyst shedding in previously infected piglets. Piglets rechallenged with I. suis following steroid injections also failed to shed significant numbers of oocysts suggesting development of immunity to reinfection.