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Australian veterinary journal1977; 53(9); 446-447; doi: 10.1111/j.1751-0813.1977.tb05496.x

An outbreak of Swainsona poisoning in horses.

Abstract: On 6 properties in south-western Queensland an outbreak of nervous disease occurred horses due to ingestion of Swainsonia (Darling pea). Loss of condition, depression, hyperaesthesia and hyperexcitability were seen in affected horses. At autopsy of 2 horses generalised c ytoplasmic vacuolation was seen in the neurones of the central nervous system and in the liver, adrenal and thyroid. The clinical and pathological features were similar to those described in horses suffering from Swainsona poisoning in Australia and Astragalus and Oxytropis in North America.
Publication Date: 1977-09-01 PubMed ID: 588181DOI: 10.1111/j.1751-0813.1977.tb05496.xGoogle Scholar: Lookup
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Summary

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The research focuses on an outbreak of a nervous disease in horses on six properties in south-western Queensland, caused by the ingestion of Swainsona, also known as Darling pea.

Overview of the Research

The study investigates a sudden outbreak of a neurological disease among horses on six separate properties in the southwestern region of Queensland. The cause of the disease was identified as consumption of a plant known as Swainsona or Darling pea. The primary symptoms observed in the affected horses included weight loss, depression, hypersensitivity and hyperexcitability.

Clinical Presentation and Symptoms

  • The primary symptoms presented by the affected horses included weight loss, depression, hypersensitivity, and hyperexcitability. These clinical signs were indicative of a systemic issue, possibly neurological in nature.
  • Other clinical features associated with Swainsona poisoning were identical to those found in similar cases documented in both Australia and North America. In the North American instances, two other plants, namely Astragalus and Oxytropis, were identified as the cause.

Pathological Observations

  • Post-mortem examinations were performed on two of the affected horses. The primary pathological alteration observed was generalized cytoplasmic vacuolation.
  • This kind of cellular change was seen in the neurons of the central nervous system, as well as in the liver, adrenal, and thyroid tissues. Such vacuolation is a significant symptom of cellular damage or dysfunction, often related to toxin exposure, such as from Swainsona ingestion.

Similarities to Other Cases

  • The clinical symptoms and pathological changes seen in this Swainsona-related outbreak were very similar to prior findings related to poisoning from other toxic plants in horses.
  • Both the clinical and pathological signs observed were identical to those found in cases of Swainsona poisoning in other parts of Australia. Simultaneously, they were also similar to those listed for Astragalus and Oxytropis poisonings reported in North America.

In conclusion, the research highlights the hazards of toxic plant ingestion in horses and underscores the need for preventive measures to avoid such instances. The findings lay the groundwork for future studies to develop a better understanding of this form of poisoning and devise appropriate treatment strategies.

Cite This Article

APA
O'Sullivan BM, Goodwin JA. (1977). An outbreak of Swainsona poisoning in horses. Aust Vet J, 53(9), 446-447. https://doi.org/10.1111/j.1751-0813.1977.tb05496.x

Publication

ISSN: 0005-0423
NlmUniqueID: 0370616
Country: England
Language: English
Volume: 53
Issue: 9
Pages: 446-447

Researcher Affiliations

O'Sullivan, B M
    Goodwin, J A

      MeSH Terms

      • Animals
      • Australia
      • Disease Outbreaks / veterinary
      • Female
      • Horse Diseases / pathology
      • Horses
      • Plant Poisoning / pathology
      • Plant Poisoning / veterinary

      Citations

      This article has been cited 1 times.
      1. Zhang S, Zhang Y, Yin H, Liu Y, Tang L, Zhu Y, Sun P, Wu K, Zhao B, Lu H. Metabolomic analysis of swainsonine poisoning in renal tubular epithelial cells. Front Vet Sci 2024;11:1387853.
        doi: 10.3389/fvets.2024.1387853pubmed: 38835895google scholar: lookup