Fall panicum ( Panicum dichotomiflorum) toxicosis in three juvenile goats.

Consumption of certain grasses belonging to the genus Panicum has been found to cause hepatogenous photosensitization and crystal-associated cholangiohepatopathy in small ruminants, and liver disease in horses, in many areas of the world. We describe herein the clinical findings, microscopic lesions, and steroidal saponin analysis of Panicum dichotomiflorum associated with fatal toxicosis in 3 juvenile goats in Nebraska. The disease presentation in our case was fulminant, with anorexia, marked icterus, and death for all affected animals in less than a week. Photosensitization was not observed. The microscopic lesions consisted of severe crystal-associated cholangiohepatopathy and nephropathy, with aggregates of clear or refractile and birefringent, acicular crystals present within bile ducts, macrophages, hepatocytes, and renal tubules. High-performance liquid chromatography-mass spectrometry of the grass samples demonstrated that dichotomin was the major steroidal saponin present (0.89 µg/mg); protodioscin was also present (0.059 µg/mg). The findings were consistent with ingestion of steroidal saponins, and P. dichotomiflorum was identified as the predominant forage available.

Colic caused by Panicum maximum toxicosis in equidae in northern Brazil.

In the Amazon region of northern Brazil, Panicum maximum cultivars Mombaça, Tanzânia, and Massai cause severe colic and death in horses and mules. The disease occurs in the rainy season, when sprouting pastures are grazed by equidae. In the 8 separate disease outbreaks studied, a total of 52 out of 153 equidae were affected, including 19 that died (10 mules and 9 horses). Clinical signs were colic and abdominal dilatation, with a clinical manifestation period of 12 hr to 4 days. Serum activities of gamma-glutamyl transferase and aspartate aminotransferase were within reference intervals; however, serum urea nitrogen and creatinine concentrations were occasionally elevated. The primary gross and histologic lesions were observed in the digestive system. The stomach, small intestine, and large intestine had severe hemorrhages and occasional mucosal erosions and ulcerations. Ulceration and hemorrhage of the urinary bladder were rarely observed. Histologic examination revealed diffuse lymphoplasmacytic gastritis and enteritis with severe congestion, hemorrhage, and occasional epithelial necrosis and ulceration. Lymphocellular necrosis was occasionally observed within gut-associated lymphoid tissue. Tubular nephrosis occurred in some animals. Degeneration and occasional necrosis of bile duct epithelial cells and degeneration of hepatocytes were observed in the liver. Toxic pastures were negative for diosgenin- and yamogenin-based saponins, and oxalate concentrations were within reference intervals for the species. The toxin or toxins causing disease and the reason for the toxicity of the plant in the northern region are unknown.

Fall panicum (Panicum dichotomiflorum) hepatotoxicosis in horses and sheep.

BACKGROUND: Fourteen horses at a boarding stable in Virginia were diagnosed with hepatic disease and locally grown hay was implicated as the cause. HYPOTHESIS: Panicum dichotomiflorum, the predominant grass species in the hay, is hepatotoxic to horses. ANIMALS: Naturally occurring cases were adult horses of various breeds. Two healthy adult horses and 2 healthy adult sheep were used in feeding trials. METHODS: Blood and liver specimens collected from affected animals during the outbreak were analyzed. Some of the affected animals were treated supportively; the main intervention was hay withdrawal. Feeding trials were not blinded and no treatments were provided. Blood and liver specimens were collected and analyzed throughout the trials. RESULTS: Five affected animals were euthanized, whereas the others recovered. One research horse was euthanized for postmortem examination, and the other research animals recovered after hay withdrawal. All affected animals had evidence of hepatic disease with abnormally high aspartate aminotransferase (AST), sorbitol dehydrogenase (SDH), gamma glutamyl transferase (GGT), and alkaline phosphatase (ALP) activity. Evaluation of liver biopsy specimens disclosed mild lymphocytic and histiocytic inflammation, mild vacuolar change (hydropic degeneration), prominently clumped chromatin, and necrosis of individual hepatocytes. CONCLUSIONS AND CLINICAL IMPORTANCE: Severe hepatotoxicosis developed rapidly after Panicum hay exposure. Patchy hepatocyte necrosis was observed, implicating apoptosis as the mechanism of hepatotoxicosis. Absence of fibrosis in the research animals indicates that immediate withdrawal of Panicum hay should allow all but severely affected animals to recover from acute exposure.

Ovine metabolism of diosgenin coated on cellulose in relation to hepatogenous photosensitization of ruminants.

Diosgenin (2.25 g) was coated onto cellulose and dosed daily to a lamb for 12 d by intraruminal intubation. Upon completion of dosing, samples of gut contents and internal organs were subjected to chemical analysis and histological examination. No clinical signs, changes in serum chemistry, or microscopic organ changes were observed. GC-MS analyses showed that in the rumen diosgenin was metabolised to free and, to a lesser extent, conjugated derivatives of tigogenin, smilagenin and epismilagenin. Reduction of diosgenin to smilagenin and tigogenin, and epimerization of smilagenin to epismilagenin, appeared to continue in the duodenum, ileum and jejunum. Deconjugation and the epimerization of smilagenin to epismilagenin appeared to continue in the cecum and colon. Epismilagenin was the dominant conjugated sapogenin constituent identified in a bile sample.

The effect of zinc supplementation on antioxidant and lipid peroxidation status during Brachiaria decumbens intoxication in sheep.

An attempt was made to clarify the association between zinc (Zn) and antioxidants due to Zn supplementation on lipid peroxidation occurring during Brachiaria decumbens intoxication. The concentration of Zn, copper, malondialdehyde (MDA), superoxide dismutase (SOD), and gluthathione peroxidase (GSH-Px) were determined in tissues. There was a gradual increment in the concentration of Zn and MDA in serum and hepatocytic SOD in groups given Zn + B decumbens. A decline in erythrocytic GSH-Px and SOD, and lower concentration of reduced glutathione in hepatocyte cytosols were also detected in these sheep. It is highly suggestive that Zn supplementation may depress antioxidant status and enhance lipid peroxidation during B decumbens intoxication.

Kleingrass (Panicum coloratum L.) poisoning in sheep.

Twenty-four lambs grazing pastures of Panicum coloratum developed photosensitization secondary to hepatic dysfunction. Lesions were necrosis of scattered hepatocytes, obstruction of small bile ducts and bile canaliculi by small aggregates of birefringent crystals, and accumulation of birefringent crystals in phagocytes within sinusoids. The number of crystals in livers of affected sheep varied, depending on the amount of time of exposure to toxic plants and severity of hepatic abnormalities. Crystals in the liver were soluble in acidified ethyl alcohol, acetic acid, pyridine, chloral hydrate, and methanol, but not in xylene, petroleum ether, diethyl ether, acetone, water, or cold ethyl alcohol. Crystals were not stained by oil red O. There was necrosis of epithelial cells in renal distal convoluted tubules, papillary muscles of the heart, and the adrenal cortex. Lesions of Panicum coloratum-associated disease are similar to those associated with photosensitization induced by Tribulus terrestris, Agave lecheguilla, and Nolina texana.

Presence of cyclopiazonic acid in kodo millet (Paspalum scrobiculatum) causing 'kodua poisoning' in man and its production by associated fungi.

Cyclopiazonic acid was isolated and identified from a sample of kodo millet seed that caused symptoms of 'kodua poisoning' in man. The extract of the toxic grain when injected intraperitoneally into mice produced symptoms of depression and complete loss of mobility. The seed was infected by Aspergillus flavus and A. tamarii and both fungi produced cyclopiazonic acid. This is the first report of the association of a mycotoxin with kodua poisoning and of A. tamarii with mycotoxicoses.