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United States Department of Agriculture

Agricultural Research Service

Research Project: Understanding and Mitigating the Adverse Effects of Poisonous Plants on Livestock Production Systems

Location: Poisonous Plant Research

Title: Experimental rayless goldenrod (Isocoma pluriflora) toxicosis in horses

Authors
item Davis, Thomas
item Stegelmeier, Bryan
item Lee, Stephen
item Green, Benedict
item Hall, Jeffery -

Submitted to: Toxicon
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: June 26, 2013
Publication Date: October 1, 2013
Citation: 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.

Interpretive Summary: Rayless goldenrod, or southern jimmyweed (Isocoma pluriflora) is a toxic range plant found on dry rangelands growing in alkaline and gypsic soils of river valleys and drainage areas, in the southwestern United States. Rayless goldenrod is a bushy, perennial shrub with narrow leaves that are sometimes sticky and yellow flowers at the top of the stem. Rayless goldenrod is reported to cause livestock losses in cattle, swine, sheep, goats, and horses when green plant is ingested daily at doses of 1 to 1.5% of an animal’s body weight over a 1 to 3 week period. In this study rayless goldenrod was fed to horses and found to be toxic at doses of 30 and 60 mg BFK/kg BW for 10 to 14 days can produce significant cardiotoxicity. Toxicity was first seen as decreased exercise tolerance and a prolonged recovery of heart rate following exercise. These changes were soon followed by biochemical changes indicative of myocardial degeneration and necrosis. Though there are some degenerative and necrotic skeletal myocytes, rayless goldenrod toxicity in horses seems to primarily affect cardiac myocytes which may be diagnosed by measuring serum cardiac troponin I concentrations. Additional equine studies are needed to determine which BFK compounds are toxic and to better determine the method and pathogenesis of poisoning. Additionally rayless goldenrod plant populations need to be analyzed to better predict when rayless goldenrod poisoning is likely to occur and provide diagnostic and prognostic information and formulate management protocols to avoid poisoning.

Technical 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-oxyangeloyltremetone) are responsible for the toxicity of rayless goldenrod. However, experimental reproduction of rayless goldenrod-induced disease and detailed descriptions of poisoning in horses in which the concentration of tremetone and other rayless goldenrod BFK are known 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 60 mg BFK/kg BW for 14 days. After seven days of dosing the horse dosed with 60 mg 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 she 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 30 mg 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 10 mg BFK/kg BW. These results suggest that doses of 60 mg BFK/kg BW for seven days produces extensive myocardial lesions in horses. The horse dosed with 30 mg 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.

Last Modified: 8/1/2014
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