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ARS Home » Pacific West Area » Logan, Utah » Poisonous Plant Research » Research » Publications at this Location » Publication #267725

Title: The resolution of rayless goldenrod (Isocoma pluriflora) poisoning in goats

Author
item Stegelmeier, Bryan
item Davis, Thomas - Zane
item Green, Benedict - Ben
item Lee, Stephen
item HALL, JEFFERY - Utah Veterinary Diagnostics Laboratory

Submitted to: International Journal of Poisonous Plant Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/31/2012
Publication Date: 4/1/2013
Citation: Stegelmeier, B.L., Davis, T.Z., Green, B.T., Lee, S.T., Hall, J.O. 2013. The resolution of rayless goldenrod (Isocoma pluriflora) poisoning in goats. International Journal of Poisonous Plant Research. 2:27-33.

Interpretive Summary: Rayless goldenrod (Isocoma pluriflora) occasionally poisons livestock causing muscle and heart disease. The objectives of this study were to describe the resolution of these changes in rayless goldenrod poisoned goats. Eight goats were treated for 7 days with ground rayless goldenrod. After treatment three goats were euthanized and the other goats were allowed to recover for 10 days, 2, 4, 8 and 16 weeks. All treated animals became poisoned. The clinical signs of poisoning quickly recovered and were near normal 2 weeks post treatment. Poisoned animals also had microscopic muscle lesions. These lesions were different as they had increased inflammation at 10 days and 2 weeks post treatment. In animals that were allowed to recover for 4 and 8 weeks the lesions were smaller and there was increased muscle regeneration and fibrosis. After 16 weeks there remained only edema and mild fibrosis. These findings indicate that rayless goldenrod poisoning causes skeletal muscle necrosis that continues to resolve 3 months after exposure. Though the remaining lesions are minimal, completely resolve could take many additional months or years.

Technical Abstract: Rayless goldenrod (Isocoma pluriflora) occasionally poisons livestock causing myocardial and skeletal muscle degeneration and necrosis. The objectives of this study were to describe the resolution of the clinical and pathologic changes of rayless goldenrod poisoning in goats. Eight goats were gavaged for 7 days with ground rayless goldenrod to obtain benzofuran ketone dosages of 40 mg/kg BW/day. After treatment three goats were euthanized and the other goats were allowed to recover for 10 days, 2, 4, 8 and 16 weeks. After 6 days of treatment, all the treated animals were reluctant to move, stood with an erect stance and became exercise intolerant. They also increased serum AST, ALT, LDH, and CK activities that are indicative of muscle damage. These clinical signs quickly recovered and were near normal 2 weeks post treatment. Histologically poisoned goats developed severe skeletal myodegeneration and necrosis characterized by myocyte swelling and hypereosinophilia, clumping and aggregation of myofibers, myocyte disruption with extensive perimysial edema and inflammation. This degeneration and necrosis persisted with increased inflammation in the goats that were euthanized at 10 days and 2 weeks post treatment. In animals that were allowed to recover for 4 and 8 weeks there was progressively less degeneration, necrosis and inflammation with more edema, regeneration and fibrosis. After 16 weeks there was edema and mild fibrosis. These findings indicate that rayless goldenrod poisoning causes skeletal muscle necrosis that continues to resolve 3 months after exposure. Though the remaining lesions are minimal, complete resolution could take many additional months or years.