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Toxicon : official journal of the International Society on Toxinology2013; 73; 88-95; doi: 10.1016/j.toxicon.2013.06.018

Experimental rayless goldenrod (Isocoma pluriflora) toxicosis in horses.

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 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 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 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 produce 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.
Publication Date: 2013-07-04 PubMed ID: 23831837DOI: 10.1016/j.toxicon.2013.06.018Google Scholar: Lookup
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  • Journal Article
  • Research Support
  • U.S. Gov't
  • Non-P.H.S.

Summary

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This research aims to understand the harmful effects of rayless goldenrod (Isocoma pluriflora) toxicity in horses. Initial findings reveal that extended exposure to various doses of benzofuran ketones (BFK) present in rayless goldenrod can lead to significant health complications in horses, such as myocardial disease, implying the need for further investigation to identify the specific toxic elements and their long-term effects.

Introduction to the Study

  • The experiment was designed to explore the impact of the rayless goldenrod plant (Isocoma pluriflora) on horses. This plant, commonly found in the southwestern United States, has been known to sporadically poison horses and other livestock. The toxic properties of the plant are believed to be attributed to benzofuran ketones (BFK).
  • Although theorized, the direct cause-and-effect relationship between rayless goldenrod consumption and its specific health impact has previously remained undocumented. Thus, the study attempted to reproduce the toxicity scenario under controlled conditions, detailing its effect on horses with known BFK concentrations.

Experiment and Findings

  • Four horses were fed increasing amounts of rayless goldenrod over a period of 14 days, with dosages corresponding to approximately 0, 10, 30, and 60 mg BFK/kg body weight (BW).
  • The horse that received the highest dosage (60 mg BFK/kg BW) began showing signs of illness after seven days. Symptoms included depression, reduced appetite, dehydration, trembling, and muscle fatigue. The horse also exhibited increased enzyme activity in the serum, evidenced by elevated levels of CK, AST, ALT, and LDH, along with a rise in cardiac troponin I concentration, indicating heart damage.
  • The affected horse also showed decreased endurance, reluctance to exercise on a treadmill, and prolonged heart rate recovery following exercise. This horse had to be euthanized on day 10 due to its deteriorating condition. The post-mortem examination revealed extensive myocardial degeneration and necrosis, fibrosis, mineralization, and muscle damage.
  • The horse that received the 30mg BFK/kg BW dosage also showed myocardial changes, but these were less severe and occurred over a longer duration, suggesting that the toxicity might be cumulative and long-term exposure to lower doses could also lead to harmful effects.
  • No adverse symptoms were observed in the horses subjected to the control dose (0 mg BFK/Kg BW) and the 10 mg BFK/kg BW dose.

Implications and Future Work

  • The research indicates that horses are particularly susceptible to myocardial disease caused by rayless goldenrod poisoning, and elevated cardiac troponin I levels may serve as a useful diagnostic marker for such poisoning.
  • However, the specific BFK responsible for inducing myocardial toxicity and the precise influence of dosage and duration on the poisoning need to be further investigated.

Cite This Article

APA
Davis TZ, Stegelmeier BL, Lee ST, Green BT, Hall JO. (2013). Experimental rayless goldenrod (Isocoma pluriflora) toxicosis in horses. Toxicon, 73, 88-95. https://doi.org/10.1016/j.toxicon.2013.06.018

Publication

ISSN: 1879-3150
NlmUniqueID: 1307333
Country: England
Language: English
Volume: 73
Pages: 88-95
PII: S0041-0101(13)00238-9

Researcher Affiliations

Davis, T Z
  • Poisonous Plant Research Laboratory, Agriculture Research Service, United States Department of Agriculture, 1150 E. 1400 N., Logan, UT 84341, USA. Zane.Davis@ars.usda.gov
Stegelmeier, B L
    Lee, S T
      Green, B T
        Hall, J O

          MeSH Terms

          • Alanine Transaminase / blood
          • Animals
          • Aspartate Aminotransferases / blood
          • Asteraceae / chemistry
          • Benzofurans / analysis
          • Benzofurans / blood
          • Benzofurans / toxicity
          • Cardiomyopathies / etiology
          • Dose-Response Relationship, Drug
          • Electrocardiography
          • Heart Rate / drug effects
          • Histological Techniques
          • Horses
          • Ketones / blood
          • Plant Poisoning / complications
          • Southwestern United States
          • Troponin I

          Citations

          This article has been cited 1 times.
          1. Davis TZ, Green BT, Stegelmeier BL, Lee ST. The comparative toxicity of Isocoma species in calves.. Toxicon X 2020 Mar;5:100022.
            doi: 10.1016/j.toxcx.2019.100022pubmed: 32550578google scholar: lookup