Toxicity: ionophore antibiotics in Horses (Equis) | Vetlexicon
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Toxicity: ionophore antibiotics

ISSN 2398-2977


Introduction

  • Cause: ionophores, used as antibiotics, coccidiostats, and growth promotants in ruminants.
  • Signs: usually within 24 h of exposure, include feed refusal, weakness, ataxia, tremors, tachycardia, recumbence, dyspnea, and unexpected death.
  • Diagnosis: clinical signs, clinical pathology, post-mortem findings, and analysis of feed or stomach contents.
  • Treatment: clean feed, early decontamination, stall rest, and supportive care.
  • Prognosis: guarded to poor.

Presenting signs

  • Feed refusal.
  • Weakness, ataxia, incoordination, tremors, hesitance to move or turn, recumbence.
  • Tachycardia.
  • Hypotension.
  • Dyspnea, hyperpnea.
  • Sweating.

Acute presentation

  • Usually within 24 h of exposure.

Public health considerations

  • Likelihood of decreased performance should be considered when determining how aggressively to treat.

Special risks

Pathogenesis

Etiology

  • Ionophore antibiotics:
    • Monensin.
    • Lasalocid.
    • Naracin.
    • Salinomycin.
    • Laidlomycin.
    • Maduramycin.

Predisposing factors

General

  • Access to ruminant feeds.
  • Cross-contamination of ruminant and equine feeds.

Specific

  • Clinical signs associated with a new batch of feed: multiple animals affected.

Pathophysiology

  • Ionophores form complexes with cations that are transported across lipid membranes following the gradient:
    • Cell membranes.
    • Mitochondrial membranes.
  • Ion concentration gradients are critical for muscle and neuron function.
  • Ion concentration gradients are critical for mitochondrial ATP production.
  • Loss of ion gradient leads to cellular necrosis.

Timecourse

  • Clinical signs usually occur within 24 h of exposure:
    • Sometimes delayed.
    • Continuous or intermittent.
  • Death can occur within 24 h:
    • Before clinical signs become apparent. 
    • Can be delayed over long periods, due to cardiac damage.

Epidemiology

  • Feed contamination has been associated with multiple-farm outbreaks.
  • Clinical course can be variable within a group of horses.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Bautista A C, Tahara J, Mete A et al (2014) Diagnostic value of tissue monensin concentrations in horses following toxicosis. J Vet Diagn Invest 26 (3), 423-427 PubMed.
  • Decloedt A et al (2012) Acute and long-term cardiomyopathy and delayed neurotoxicity after accidental lasalocid poisoning in horses. J Vet Intern Med 26 (4), 1005-1011 PubMed.
  • Peek S F, Marquis F D, Morgan J et al (2004) Atypical acute monensin toxicosis and delayed cardiomyopathy in Belgian draft horses. J Vet Intern Med 18 (5), 761-764 PubMed
  • Hall J O (2001) Toxic feed constituents in the horse. Vet Clin North Am Equine Pract 17 (3), 480-485 PubMed.

Other sources of information

  • Novilla M N (2015) Ionophores. In: Veterinary Toxicology Basic and Clinical Principals. Ed: Gupta R C. Elsivier Academic Press, USA. pp 1281-1299.