Neurology: mycotoxic leukoencephalomalacia in Horses (Equis) | Vetlexicon
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Neurology: mycotoxic leukoencephalomalacia

ISSN 2398-2977

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Synonym(s): Moldy corn disease, LEM


  • 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.

Presenting signs

  • Early clinical signs:
    • Anorexia.
    • Lethargy.
    • Depression.
  • Neurotoxicity:
    • Somnolence.
    • Weakness of face and pharyngeal muscles.
    • Ataxia.
    • Conscious proprioception deficits.
    • Facial desensitization.
    • Leaning.
  • Hepatotoxicity:
    • Swelling of lips and nose.
    • Mucus membrane petechiae.
    • Icterus.
    • Abdominal breathing.
    • Cyanosis.
  • Neurotoxicity and hepatotoxicity can occur independently or simultaneously. Higher doses of toxin favor hepatotoxicity and chronic ingestion of lower concentrations is associated with neurotoxicity.

Acute presentation

  • Dementia.
  • Blindness.
  • Convulsions.
  • Sudden death.

Geographic incidence

  • Worldwide.

Cost considerations

  • Euthanasia and necropsy of severely affected animals in order to confirm the diagnosis may be the most economical strategy.

Special risks

  • Caution should be taken when examining and treating a severely neurologic animal.



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

Predisposing factors

  • 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.


  • 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.


  • 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.


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


Presenting problems

  • Sudden death.
  • Severe neurological signs.
  • Signs attributable to liver disease.

Client history

  • Feeding a diet containing corn.
  • Non-commercial feed, although disease has occurred in horses receiving commercial pelleted diets.
  • Sudden onset neurological signs or sudden death in one or multiple horses.

Clinical signs

  • Dementia.
  • Lethargy.
  • Blindness.
  • Circling.
  • Ataxia.
  • Weakness.
  • Excitability.
  • Pharyngeal paralysis.
  • Facial paralysis.
  • Seizures.
  • Evidence of liver disease.
  • Signs may be asymmetric.

Diagnostic investigation

  • History.
  • Neurological examination   Neurology: examination - adult  .
  • Cerebrospinal fluid analysis may be normal or reveal a neutrophilic pleocytosis and elevated protein concentration   CSF: collection  and interpretation.
  • Feed analysis concentrations of fumonisin B1 over 10 parts/million (ppm).

Definitive diagnostic features

  • Necropsy.
  • Feed analysis concentrations of fumonisin B1 >10 ppm.

Gross autopsy findings

  • Liquefactive cerebral necrosis, especially in the subcortical white matter.
  • Lesions are usually large and can be hemorrhagic.
  • Gray matter can occasionally also be affected in the forebrain and brainstem.
  • Cerebellum can also be involved.
  • Lobar herniations can occur from cerebral edema.

Histopathology findings

  • Liquefactive cerebral necrosis, especially in the subcortical white matter.
  • Necrosis with influx of macrophages, edema, and hemorrhage.
  • An associated inflammation may also include plasma cells and eosinophils.

Differential diagnosis


Initial symptomatic treatment

  • Removal of moldy feed.
  • Cathartics and activated charcoal.
  • Analgesics.
  • Reduction of cerebral edema glucocorticoids, DMSO.
  • Supportive care.


  • Horses usually die shortly after onset of clinical signs.
  • Some may survive if only mildly affected.
  • May have residual neurological deficits.



  • Advise owners to buy feed only from reputable sources.
  • Store feed in air and water tight containers to prevent mold from accumulating.



  • Horses usually die shortly after onset of clinical signs.
  • Some may survive if only mildly affected.
  • May have residual neurological deficits.

Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Caloni F & Cortinovis C (2009) Effects of fusariotoxins in the equine species. Vet J PubMed.
  • He Q, Suzuki H, Sharma N et al (2006) Ceramide synthase inhibition by Fumonisin B1 treatment activates sphingolipid-metabolizing systems in mouse liver. Toxicological Sciences 94 (2), 388-397 PubMed.
  • Ross P F, Ledet A E, Owens D L et al (1993) Experimental equine leukoencephalomalacia, toxic hepatosis, and encephalopathy caused by corn naturally contaminated with fumonisins. J Vet Diagn Invest 5, 69-74 PubMed.
  • McCue P M (1989) Equine leukoencephalomalacia. Comp Cont Educ Pract Vet 11 (5), 646-650 VetMedResource.

Other sources of information

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