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Biomedical subjects

R A Mansmann

Publications and source records attributed to R A Mansmann.

15 recordsLinked to original sources
PubMed1992

Coccidioidomycosis in horses: 15 cases (1975-1984).

Fifteen confirmed cases of equine coccidioidomycosis that originated in California and Arizona were studied retrospectively. Age, breed, and sex varied among affected horses. The most common historical problems were chronic weight loss (53% of cases) and persistent cough (33% of cases). The most frequent physical examination abnormalities were related to the respiratory tract (60% of cases). In 27% of cases, horses had signs of musculoskeletal pain. Horses consistently had hyperproteinemia, hyperfibrinogenemia, leukocytosis, and neutrophilia. An antemortem etiologic diagnosis was made for 11 (73%) horses, all of which had positive serologic tests for coccidioidomycosis. Of the seropositive horses, 5 (46%) also had positive cultures for Coccidioides immitis. One horse died naturally. The other 14 were euthanatized. Prolonged treatment with specific antifungal agents was attempted in 4 horses without apparent benefit. Postmortem abnormalities included pulmonary parenchymal lesions (64% of cases), thoracic lymphadenopathy (57% of cases), hepatic parenchymal involvement (43% of cases), and osteomyelitis (29% of cases). The lesions were granulomatous or pyogranulomatous and C immitis was observed microscopically in 83% of cases.

Amphotericin B↗
PubMed1984

Midsagittal intraarticular fracture of the third phalanx in a colt.

A 6-month-old Quarter Horse colt, with severe left foreleg lameness of 6 weeks' duration, had swelling of the distal interphalangeal joint and a smaller-than-normal left front foot. Radiographs revealed a nondisplaced, midsagittal, intraarticular fracture of P3, which was treated with an eggbar shoe with 2 quarter clips, and stall rest for 10 weeks. The colt was sound after 10 weeks.

Animals↗
PubMed1983

Toxic hepatic failure in newborn foals.

Eight foals, 2 to 5 days of age, with similar clinical signs and laboratory and pathologic findings, died from hepatic failure. The predominant clinical signs were depression and icterus. Abnormally high values were found for plasma ammonia content, aromatic-to-branch-chain amino acid ratio, total serum bilirubin content, gamma glutamyl transferase activity, alkaline phosphatase activity, and PCV; partial thromboplastin time and prothrombin time were prolonged. Some foals had high sorbitol dehydrogenase activity. These laboratory findings were suggestive of subacute hepatic disease and failure. Predominant pathologic findings were limited to the liver and brain. The livers were less than half the expected size for 2- to 5-day-old foals, had prominent bile ductule proliferation, hepatic cell necrosis, and mild periportal fibrosis. These findings suggested both prenatal and postnatal diseases caused by exposure to a hepatoxin. The predominant lesion in the brain was the presence of Alzheimer type II astrocytes, which are characteristic of hepatoencephalopathy. Although the periportal fibrosis was suggestive of in utero exposure to a toxin, epidemiologic information suggested that the hepatic failure more likely resulted from oral inoculation of a microorganism culture product at birth. The same disease was reproduced in 2 newborn foals by feeding this product.

Animals↗