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
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;
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):