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Equine Leukoencephalomalacia

Leukoencephalomalacia is an uncommon disease that can have grave consequences for the horses that it affects.   It is important that veterinarians be able to recognize cases early to limit the number of animals affected in an area or on a farm. This condition occurs when horses eat corn that is contaminated with the fungus Fusariummoniliforme.Monilifonnin is a toxin produced by this fungus that actually causes the clinical syndromes. The exact pathogenesis is still unknown.

Two syndromes can occur following ingestion of the toxin; neurotoxicity and hepatotoxicity. In many cases, the onset of the disease is sudden and few if any clinical signs are seen prior to death. Early clinical signs may include anorexia, lethargy and depression. If the animal survives the initial event,neurologic abnormalities related to the sensorimotor cortex will be seen. These include somnolence, weakness of the face and pharyngeal muscles, ataxia, conscious proprioception deficits, facial desensitization, and a tendency to lean to one side.  Horses showing these signs will usually become recumbent and comatose in 1 to 10 days and may show clonic-tonic convulsions before dying. In some cases, frantic behavior such as head pressing, agitation, hyperexcitability, profuse sweating and delirium may be observed as well as blindness.

Horses with the hepatotoxic syndrome will show clinical signs of swelling of the lips and nose, mucus membrane petechiae,icterus, abdominal breathing and cyanosis. Similar to the neurologic form, signs will often appear very acutely with death occurring in hours to days.

Antemortem diagnosis is difficult because there is no diagnostic ancillary test. CSF taps may be normal or indicative of a severe, acute inflammatory response. Early diagnosis will often rely on signs of cerebral cortical disease along with a history of exposure to moldy corn. Liver enzyme and ammonia levels may be elevated but other causes of hepatic failure must also be considered.

The only way to make a definitive diagnosis of leukoencephalomalacia is at necropsy. Horses with the neurologic syndrome will consistently have liquefactive necrosis of the subcortical white matter of one or both cerebral hemispheres.   These necrotic areas can vary in size from pinpoint to greater than 4 cm in diameter and will be yellow-orange with a creamy mucoid consistency. Areas surrounding the necrosis will usually be edematous and flattened. Histologically, a center of necrosis with no recognizable structure will be observed. The transition between normal and necrotic tissue will often show hemorrhage, edema, congested blood vessels and neuronophagia. In animals with the hepatotoxic syndrome, livers will be swollen and a diffuse yellow-brown color.   Irregular nodules and pale foci can be seen in hepatic parenchyma. Histologic examination will show centrilobular necrosis and fibrosis. It is important that gross lesions are recognized early, to limit exposure of other horses.

Cases of leukoencephalomalacia are most often seen in late fall through early spring. Outbreaks usually occur when a dry growing season is followed by a wet fall. Some studies have shown that 80-100% of corn is infected with Fusarium. Infected kernels of corn can sometimes be recognized by a pink to reddish brown color. Corn screenings and damaged corn are more likely to be affected. The presence of mold does not mean that disease will result; moniliformin must be secreted. Likewise, absence of visible mold is not a guarantee that corn will be toxin free.

Presently, there  is  no way to treat leukoencephalomalacia. Some horses survive, but will usually have severe deficits in cognitive and proprioceptivefunction.   Early recognition is critical.   Euthanasia and necropsy of severely affected animals in order to confirm the diagnosis may be the most prudent and expedient management tactic. On farms where there is a history of possible exposure to moldy corn, questionable feed should not be fed to horses.

Obviously, the best way to treat this disease is to prevent it.   Since at present, there is no screening test for the toxin and most corn is infected with the mold, testing each batch of feed is not a viable option. This mold has also been found in commercially prepared pelleted feed. At this time, the best recommendation for preventing leukoencephalomalacia and its devastating effects, is to advise horse owners to buy their feed from reputable mills that use quality, undamaged corn to make their horse feed.

-by JeffLogue, Class of 1997

• edited by Lydia Andrews-Jones, DVM


McCue, Patrick M. Equine Leukoencephalo­malacia, Compendium of Continuing Education for the Practicing Veterinary 1989; 11(5): 646-650.

Robinson, Edward N.   Current Veterinary Therapy in Equine Medicine, 3rd edition, Philadelphia, 1992, W.B.Saunders Company, 377-379.

Smith, Bradford P. Large Animal Internal Medicine, 2nd Edition, St. Louis, 1996, Mosby-Year Book, Inc., 1077-1078.

Uhlinger, Christine: Clinical and epidemio-logic features of an epizootic of equine leuko­encephalomalacia, Journal of the American Veteri­nary Medical Association 1991; 198(1): 126-128.




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