Equis ISSN 2398-2977

Neurology: mycotoxic leukoencephalomalacia

Synonym(s): Moldy corn disease, LEM

Contributor(s): Karen McCormick, Carla Sommardahl

Introduction

  • Cause: this condition occurs when horses ingest feed that is contaminated with the fungusFusarium moniliforme. This fungus produces many mycotoxins, including fumonisins, trichothecenes and zearalenone. Fumonisin B1 is the causative agent of leukoencephalomalacia.
  • Signs: depression, aimless circling, head pressing, paresis, ataxia, blindness, and death.
  • Diagnosis: history, clinical signs, neurological examination, cerebrospinal fluid analysis, necropsy.
  • Treatment: supportive care.
  • Prognosis: length of exposure, level of contaminant, individual animal differences, and previous exposure all impact the appearance and severity of clinical disease.

Pathogenesis

Etiology

  • Occurs when horses ingest corn contaminated with the fungusFusarium moniliforme.
  • Fumonisin B1 is the causative agent of leukoencephalomalacia.

Predisposing factors

General
  • A diet containing corn; fungus is more likely to be present in broken or small poorly formed kernels.
  • Feed purchased from a mill that may use damaged or low quality feedstuffs.
  • Corn has been grown or stored in an environment that is warm and moist enough to become contaminated with a fungus.
  • Dry growing period followed by a wet period.
  • Seasonal most cases occur from late fall through early spring.

Pathophysiology

  • Horses develop liquefactive cerebral necrosis, especially in the subcortical white matter.
  • Fumonisin B1 inhibits ceramide synthase, leading to an accumulation of bioactive intermediates of sphingolipid metabolism and depletion of complex sphingolipids.
  • This leads to a dysfunction of certain membrane proteins, resulting in disruption of cell signaling.
  • These changes are thought to play a part in the development of leukoencephalomalacia and hepatotoxicity in horses that ingest fumonisin B1.

Timecourse

  • Ingestion has likely occurred over the course of approximately 1 month.
  • Clinical signs often present very acutely.
  • After initial onset of clinical signs, horses usually become recumbent and comatose in 1-10 days and may show convulsions before dying.

Epidemiology

  • Outbreaks can occur if many horses consume feed containing contaminated corn.

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.
  • Caloni F & Cortinovis C (2009)Effects of fusariotoxins in the equine species.Vet JIn press 10.1016/j.tvjl.2009.09.020 PubMed.
  • He Q, Suzuki H, Sharma Net al(2006)Ceramide synthase inhibition by Fumonisin B1 treatment activates sphingolipid-metabolizing systems in mouse liver. Toxicological Sciences94(2), 388-397 PubMed.
  • Ross P F, Ledet A E, Owens D Let al(1993)Experimental equine leukoencephalomalacia, toxic hepatosis, and encephalopathy caused by corn naturally contaminated with fumonisins.J Vet Diagn Invest5, 69-74 PubMed.
  • McCue P M (1989)Equine leukoencephalomalacia.Comp Cont Educ Pract Vet11(5), 646-650 VetMedResource.

Other sources of information

  • Mayhew I G J (2009)Large Animal Neurology. 2nd edn. Oxford, UK: Wiley-Blackwell. 346-348.
  • Schmitz D G (2004)Toxicologic Problems.In:Equine Internal Medicine. Eds: Reed S & Sellon D C. 2nd edn. St. Louis: Elsevier. pp 1475-1477.


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