Equine Leukoencephalomalacia:

Clinical Features, Diagnosis, and Treatment 

Equine leukoencephalomalacia (ELEM), commonly called “Moldy Corn Poisoning”, is a disease of the central nervous system that affects horses, mules, and donkeys.  It is commonly associated with feeding of moldy corn over several days to weeks.  The fungus that is most commonly isolated is Fusarium moniliforme which produces three toxins, fumonison B_1, B_2,  and B _3.   Fumonisin B₁ and B₂  appear to have similar toxicity, while fumonisin B₃ is mostly nontoxic.  The toxin fumonisin has been associated with both central nervous system and liver damage.  Fusarium proliferatum has also been implicated as another possible agent in this disease.  The toxin has been described as causing damage to the vascular endothelium of the central nervous system and, in some cases, hepatocellular necrosis and vacuolization.  The incidence of finding corn infected with F. moniliforme increases after a long, dry summer, followed by a wet harvest.  Outbreaks of ELEM occur sporadically from late fall to early spring.

  The clinical signs associated with the neurologic form of ELEM in horses include apathy, drowsiness, pharyngeal paralysis, blindness, circling, difficulty backing, staggering, hyperexcitability, seizures and eventual recumbency.  However, in some cases, sudden death may be the only clinical sign observed.  Once animals show the neurological signs, death usually occurs within 48-72 hours.  If an animal survives the acute syndrome, neurological deficits are observed.  A recovered horse is sometimes referred to as a “dummy” because of its loss of intelligence.

  The signs associated with the hepatic form include petechial or ecchymotic hemorrhages of the mucous membranes, icterus, edema of the head and neck, decreased appetite, depression, lingual paralysis, clonic convulsions, and coma.

  On postmortem examination, the classic finding is gray to brown areas of malacia and cavitation of white matter of the cerebral hemisphere.  It is usually unilateral, but may be asymmetrically bilateral.  Histologically, there is marked, multifocal, liquefactive necrosis, multifocal vascular congestion, and perivascular hemorrhage throughout the white matter of the cerebrum.  A cellular inflammatory response is generally absent.

  In the hepatic form, the liver may appear normal or may appear small and firm.  Histologically, there may be diffuse vacuolization of hepatocytes, fatty degeneration, centrilobular necrosis with inflammatory cell infiltrate, bile duct proliferation, bile stasis, increased mitotic figures within the hepatocytes, or periportal fibrosis.

  There is no specific therapy for ELEM.  By the time clinical signs are noted, it is usually too late in the course of the disease.  Removal of the contaminated feed from susceptible animals is very important.  Avoidance of the mycotoxins is the only way to prevent the disease.  If the animal is acting delirious or agitated, sedation is necessary.  The majority of the therapy is symptomatic.  These include gastrointestinal protectants such as activated charcoal and laxatives to aid elimination of the toxin, fluids, and dextrose for hydration and energy.  If the clinical signs have progressed to recumbency, euthanasia may be needed for humane reasons.

 - by Ryan Rothenbuhler, Class of 2001

 - edited by Marlon Rebelatto, DVM,

   ADDL Graduate Student