Experimental rayless goldenrod (Isocoma pluriflora) toxicosis in horses

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Abstract

Rayless goldenrod (Isocoma pluriflora) sporadically poisons horses and other livestock in the southwestern United States. Similar to livestock poisoning by white snakeroot (Ageratina altissima) in the midwestern United States, previous research suggests that benzofuran ketones (BFK: tremetone, dehydrotremetone, 6-hydroxytremetone, and 3-oxyangeloyl-tremetone) are responsible for the toxicity of rayless goldenrod. However, experimental reproduction of rayless goldenrod-induced disease and detailed descriptions of poisoning in horses with known concentrations of tremetone and other BFK has not been documented. In this study four horses were fed increasing amounts of rayless goldenrod to obtain doses of approximately 0, 10, 30, and 60mg BFK/kg BW for 14 days. After seven days of dosing the horse dosed with 60mg BFK/kg BW horse developed depression, reluctance to eat, dehydration, trembling, and muscle fatigue. Biochemical alterations including increases in the serum enzyme activities of CK, AST, ALT, and LDH, and increased cardiac troponin I concentration, were also identified. Physiologically the clinically poisoned horse had decreased endurance seen as reluctance to perform on the treadmill with increased resting heart rate and a prolonged recovery of heart rate following treadmill exercise. The condition of the horse continued to decline and it was euthanized and necropsied on day 10. At necropsy the myocardium was pale and soft and many of the appendicular and large apical muscles were pale and moist. Histologically, the myocardium had extensive myocardial degeneration and necrosis with extensive fibrosis and multifocal mineralization. Several of the large appendicular muscles in this horse also had small foci of skeletal muscle degeneration and necrosis. Less severe myocardial changes were also identified in the horse dosed with 30mg BFK/kg BW after 14 days of dosing. No clinical, biochemical or histologic changes were identified in the control horse and the horse dosed with 10mg BFK/kg BW. These results suggest that doses of 60mg BFK/kg BW for seven days produceextensive myocardial lesions in horses. The horse dosed with 30mg BFK/kg BW developed less severe, but similar myocardial lesions over a longer duration, this suggests that poisoning may be cumulative and lower doses of longer duration are also toxic. Horses seem to be uniquely sensitive to rayless goldenrod-induced myocardial disease, therefore cardiac troponin I may be a useful marker of rayless goldenrod poisoning in horses. More work is needed to determine which BFK produce myocardial toxicity and better determine the effects of dose and duration on poisoning in horses. •The first report of the benzofuran concentrations in a toxic dose of rayless goldenrod fed to horses.•A complete report of the serum biochemical changes associated with rayless goldenrod poisoning in horses.•Cardiac troponin I is identified as a sensitive marker of rayless goldenrod poisoning in horses.•A complete description of the histopathological changes associated with rayless goldenrod poisoning in horses. © 2013.

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APA

Davis, T. Z., Stegelmeier, B. L., Lee, S. T., Green, B. T., & Hall, J. O. (2013). Experimental rayless goldenrod (Isocoma pluriflora) toxicosis in horses. Toxicon, 73, 88–95. https://doi.org/10.1016/j.toxicon.2013.06.018

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