Feline pyothorax caused by a Borrelia-like organism and Corynebacterium pyogenes.

A 2-year-old, neutered, male cat was euthanatized because of difficult repiration and inability to rise. Necropsy revealed pyothorax. Corynebacterium pyogenes was grown from the purulent thoracic exudate. A Borrelia-like microorganism was demonstrated in the exudate, using phase-contrast microscopy.

Kochia scoparia poisoning in cattle.

Cattle consuming only high-sulfate water (2.3 g/L) and Kochia scoparia in a marginal pasture in southeastern Colorado were periodically monitored by serum chemical profiles. Serum glutamic oxaloacetic transaminase, serum sorbitol dehydrogenase, and serum bilirubin values were abnormally high over extended periods, suggesting chronic toxicosis, but the toxicosis seemed accentuated after substantial rains, when plant growth was accelerated, and flowering, pollination, and early seed development were occurring. Clinical disease was manifested primarily as photosensitization. Polioencephalomalacia was also produced. Evidence of a thiamin-destructive principle in K scoparia was obtained.

Polioencephalomalacia and photosensitization associated with Kochia scoparia consumption in range cattle.

Cattle consuming only Kochia scoparia in a pasture southeastern Colorado became ill. Clinical signs were lacrimation, depression, anorexia, nystagmus, head pressing, and recumbency. Some cattle died acutely, with the only clinical signs being recumbency, nystagmus, and occasionally opisthotonos. Pathologic findings were pulmonary edema and congestion, hepatic necrosis and fibrosis, necrosis of proximal convoluted tubular epithelium in the kidneys, epidermal necrosis of lightly pigmented areas, and laminar cerebrocortical necrosis. When the cattle were removed from the pasture, the problem ceased.

Equine myositis and septicemia caused by Acinetobacter calcoaceticus infection.

Myositis and septicemia caused by Acinetobacter calcoaceticus were diagnosed in a mare. The infection was characterized clinically by ventral swelling and edema, diarrhea, listlessness, and rectal temperature of 39.4 C. The mare was treated symptomatically for 2 days but died on the 3rd day. Conditions seen at necropsy were myositis, enteritis, typhlitis, colitis, and hepatitis. Lymph nodes were moderately enlarged throughout the body. Gross lesions in musculature were edema, scarring, petechiae, and an occasional exxhymosis. The enteritis was catarrhal, with excessive mucus and moderate hyperemia. The typhlitis and colitis were hemorrhagic. The swollen liver had a diffuse mottled pale and red pattern. Microscopic lesions in skeletal muscle consisted of petechiation, necrosis, scarring, and edema. Cardiac muscle was also scarred and necrotic, but edema was not prominent. Periacinal necrosis was found in the liver. Acinetobacter calcoaceticus was isolated from myocardium and liver.

Enterotoxemia in two foals.

Two Quarter Horse foals from different premises died from enterotoxemia. Clostridium perfringens toxins alpha and beta were demonstrated in the foal's intestines by mouse protection tests. Clostridium perfringens type C was isolated from the intestines of each foal. Histologic examination revealed hemorrhage, necrosis, and massive numbers of C perfringens.

Polioencephalomalacia in range cattle.

Polioencephalomalacia developed in 27 of 225 cattle grazing on 486 hectares of dry, short, grama grass pasture. Chemicals in drinking water, toxin from nitrate-utilizing ruminal bacteria, and documented poisonous plants were considered as etiologic agents. Attempts to reproduce the disease by injecting mice and dosing sheep with broth filtrate from nitrate-utilizing ruminal bacteria were not successful. Mushrooms collected from the pasture and fed to a cow did not reproduce the disease.

Oxalate (Rumex venosus) poisoning in cattle.

Fifteen range cows died of oxalate poisoning caused by ingestion of Rumex venosus. Ecchymotic and petechial hemorrhages were prominent on the abdominal serosal surfaces. Approximately 2 L of thin, yellowish fluid was in the abdominal cavity, and mesenteric lymph nodes were enlarged and edematous. Other findings included catarrhal abomasitis; enteritis; pale, edematous kidneys; congested lungs; fatty infiltration of the liver; and nephrosis. In the kidneys, birefringent crystals resembling oxalate crystals were demonstrable only when frozen sections were examined.

Blue-green algae toxicosis in cattle.

Twenty-four of 175 heifers died after ingesting water from a stock pond containing blue-green algae (genus Microcystis) in southern Colorado. Affected cattle were found dead or had signs of nervousness, and were recumbent, weak, anorectic, and hypersensitive to noise when first examined. All cattle died within 3 days after the onset of signs. At necropsy, the rumen contained blue-green algae, and the liver was larger than normal, friable, and dark red. The most important histologic lesion was hepatocyte degeneration and necrosis. Intraperitoneal administration of lyophilized cell material from the bloom caused hepatic necrosis and death in mice, and water from the pond had clumps of cells surrounded by a clear calyx, consistent with the appearance of organisms of the genus Microcystis. Samples of pond water were examined by means of high-pressure liquid chromatography; microcystin-LR, one of the hepatotoxins produced by Microcystis spp, was found. Chromatography may be useful in the diagnosis of blue-green algae toxicosis.

Kochia scoparia oxalate content.

Kochia scoparia was collected periodically during the growing seasons of 1984, 1985 and 1986. The 10, 16 and 16 samples, respectively, from these years were air dried, hammer milled and analyzed at a later date for soluble and total oxalates. An additional 6 samples from New Mexico were analyzed from the 1987 growing season. A maximum of 4.7% soluble oxalates and 11.4% total oxalates were present in 1986 Colorado kochia following heavy rainfall. This concentration of soluble oxalate could cause chronic oxalate poisoning (alkalosis) in cattle.