The Resolution of Rayless Goldenrod (Isocoma pluriflora) Poisoning in Goats

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 pathological 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 and 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. Serum enzymes such as AST, ALT, LDH, and CK had elevated activities indicative of muscle damage. Animals quickly recovered and showed few clinical signs at 2 weeks post treatment. Histologically, poisoned goats developed severe skeletal myodegeneration and necrosis characterized by myocyte swelling and hypereosinophilia, clumping and aggregation of myofibers, and 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.