Equine leukoencephalomalacia

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Equine Leukoencephalomalacia

Moldy Corn Poisoning, Fumonisin Toxicosis, Equine Mycotoxic Encephalomalacia

Equine leukoencephalomalacia (ELEM), also known as equine mycotoxic encephalomalacia or moldy corn poisoning, is a devastating neurologic disease of horses caused by eating feed or hay contaminated with fumonisin mycotoxins. Fumonisins are produced by 3 species of Fusarium: F. proliferatum, F.verticillioides (formerly F. moniliforme), and F. subglutinans. There are many different types of fumonisins, however the two of most significance include fumonisins B1 and B2. Although many animals and humans are also affected by fumonisin contamination in food, horses are the most sensitive species to fumonisin intoxication, and only have to ingest a small amount to begin showing clinical signs of neurological damage.

ELEM can present in horses in two different forms, which can be neurotoxic and/or hepatotoxic. Usually the neurotoxic form is associated with chronic ingestion of low FB1s and the hepatotoxic form with acute, high-dose exposure. The neurotoxic form is more commonly seen in horses.

The Food and Drug Administration (FDA) in the United States and the European Union Commission have established regulatory limits for the amount of fumonisins that can be present in feeds, corn, and corn byproducts intended for horses; with a maximum of 5 ppm, with the stipulation that the contaminated feed will not constitute more than 20 percent of the horse's diet. Onset of ELEM can occur as early as 7 days after a change in a horse's diet, but usually it takes 14-21 days until clinical signs appear.

Clinical signs

ELEM is difficult to diagnose in horses, which delays treatment and leads to increased fatalities. Usually multiple horses are affected---those consuming the same batch of feed. Horses affected by ELEM die suddenly, with or without the occurrence of clinical signs. When clinical signs do occur, the most common are lost of appetite, lethargy, hypersensitivity and agitation, sweating, muscle fasciculation and weakness, hypermetria, staggering, circling, inability to swallow, blindness, dilated pupils, absence of a pupillary light reflex, head pressing, and tonic-clonic seizures.


Poor appetite
Head pressing
Altered behavior
Aimlessly walking
Muscle spasms over neck and withers


  • History
  • Clinical signs
  • Physical exam
  • Laboratory testing
  • Testing of grain
  • Histopathology - hemorrhage, malacia, and perivascular congestion involving the white matter of the brain. If the liver is used for analysis, lobular necrosis, periportal fibrosis, periportal vacuolation, and a proliferation of bile ducts can be found.



Removal of the feed source from the horse's diet
Supportive care
Activated charcoal to decrease absorption of the toxin


  • Proper feed and hay storage
  • Purchasing grain from a quality vendor
  • Evaluate feed and hay quality prior to feeding to horses
  • Feed and hay analysis test for mycotoxins


Once neurologic signs have developed the prognosis is poor.

Scientific Research

General Overviews

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Risk Factors

  • Corn fed to horses was harvested during wet weather, following a humid climate and dry summer.