Page Banner

United States Department of Agriculture

Agricultural Research Service

Research Project: THE TOXICITY OF PYRROLIZIDINE ALKALOID-CONTAINING PLANTS AND OTHER HEPATOTOXIC AND NEUROTOXIC PLANTS Title: Colic Caused by Panicum maximum Toxicosis in Equidae in Northern Brazil

Authors
item Cerqueira, V -
item Riet-Correa, G -
item Barbosa, J -
item Duarte, M -
item Oliveira, C -
item DE Oliverira, C -
item Tokarnia, C -
item Lee, Stephen
item Riet-Correa, F -

Submitted to: Journal of Veterinary Diagnostic Investigation
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: August 7, 2009
Publication Date: November 1, 2009
Citation: Cerqueira, V.D., Riet-Correa, G., Barbosa, J.D., Duarte, M.D., Oliveira, C.M., De Oliverira, C.A., Tokarnia, C., Lee, S.T., Riet-Correa, F. 2009. Colic Caused by Panicum maximum Toxicosis in Equidae in Northern Brazil. Journal of Veterinary Diagnostic Investigation, 21:882-888

Interpretive Summary: In the Amazon region of northern Brazil, Panicum maximum cultivars Mombaça, Tanzânia, and Massai cause colic and death in horses and mules. In the 8 separate disease outbreaks studied, a total of 52 out of 153 equidae were affected, including 19 that died. Clinical signs such as colic and abdominal dilatation occurred from 12 hr to 4 days. The primary gross and histologic lesions were observed in the digestive system. 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.

Technical Abstract: 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.

Last Modified: 12/18/2014
Footer Content Back to Top of Page