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ARS Home » Pacific West Area » Logan, Utah » Poisonous Plant Research » Research » Publications at this Location » Publication #247229

Title: Buffalo calves intoxicated with Ageratum houstonianum mill

Author
item PAL, B - Tribhuvan University
item SINGH, D - Tribhuvan University
item Stegelmeier, Bryan

Submitted to: Poisoning by Plants, Mycotoxins, and Related Toxins
Publication Type: Book / Chapter
Publication Acceptance Date: 1/10/2010
Publication Date: 5/1/2011
Citation: Pal, B.B., Singh, D.K., Stegelmeier, B.L. 2011. Buffalo calves intoxicated with Ageratum houstonianum mill. In: Riet-Correa, F., Pfister, J., Schild, A.L., Wierenga, T., editors. Poisoning by Plants, Mycotoxins, and Related Toxins. Cambridge, MA. CAB International. 27:186-9.

Interpretive Summary: Ageratum houstonianum Mill, a noxious weed that can invade pastures and rangelands. The objectives of this work were to verify the toxicity of A. houstonianum and to determine and describe the symptoms of poisoning. Six buffalo calves were fed fresh A. houstonianum Mill ad lib for between 1 and 52 days. Blood and serum was collected and tested weekly. When the calves developed clinical disease they were euthanized, necropsied and samples were collected for histologic evaluation. After 1 to 5 days of feeding three calves developed acute liver failure characterized by loss of appetite, vomiting, recumbency and hypothermia. Later after 15-52 days of exposure the remaining 3 calves developed chronic liver failure with secondary photosensitization, alopecia and severe jaundice. Post-mortem lesions of the animals with acute liver failure included edema and hemorrhage in liver, gall bladder, abomasum, kidney, heart and intestine. The lesions of chronic liver failure included relatively rare hemorrhages in the abomasum and intestine. The livers from these calves were small and firm liver with fibrotic scars. Microscopically, the liver sections from animals with acute liver failure had severe panlobular necrosis with hemorrhage. There is lobular collapse and mild periportal fibrosis. The calves with chronic liver failure had bridging lobular fibrosis with multifocal hepatocellular degeneration and necrosis. Small numbers of megalocytes were also present. These findings indicated that A. houstonianum produced clinical, gross and histologic lesions consistent with those produced by pyrrolizidine alkaloid poisoning.

Technical Abstract: Ageratum houstonianum Mill, a noxious weed has been reported to contain pyrrolizidine alkaloids, saponins, triterpens and coumarin. It is an invasive weed that is commonly found in the pasturelands of tropical and subtropical regions. The objectives of this work were to verify the toxicity of A. houstonianum and to determine and describe the clinicopathologic alterations of poisoning. Six buffalo calves were fed fresh A. houstonianum Mill ad lib for between 1 and 52 days. Blood and serum was collected weekly for hematologic and biochemical analysis. When the calves developed clinical disease they were euthanized, necropsied and samples were collected for histologic evaluation. After 1 to 5 days of feeding three calves developed acute liver failure characterized by anorexia, vomiting, recumbency and hypothermia. Later after 15-52 days of exposure the remaining 3 calves developed chronic liver failure with secondary photosensitization, alopecia and severe icterus. Affected calves developed significant (p<0.05) anemia, hypoproteinemia, hypoalbuminemia, hypoglycemia, bilirubinemia and increased ALT and AST activities. Post-mortem lesions of the animals with acute liver failure included edema and hemorrhage in liver, gall bladder, abomasum, kidney, heart and intestine. The lesions of chronic liver failure included relatively rare hemorrhages in the abomasum and intestine. The livers from these calves were small and firm liver with fibrotic scars. Microscopically, the liver sections from animals with acute liver failure had severe panlobular necrosis with hemorrhage. There is lobular collapse and mild periportal fibrosis. The calves with chronic liver failure had bridging lobular fibrosis with multifocal hepatocellular degeneration and necrosis. Small numbers of megalocytes were also present. These findings indicated that A. houstonianum produced clinical, gross and histologic lesions consistent with those produced by pyrrolizidine alkaloid poisoning. It also suggests that hematology, biochemical evaluations of liver function and hepatic biopsy are optimal tests for the diagnosis of A. houstonianum intoxication in buffalo calves.