FINAL DIAGNOSIS -
Moldy Corn Poisoning (Equine Leucoencephalomalacia,
Fumonisin Toxicity) in Horses History: A 9-year-old quarterhorse gelding, from
a herd of 6, became increasingly ataxic and weak over a period
of 2 days. On the third day, it was found down, recumbent
and “colicky”. The referring veterinarian was
called to the farm. After obtaining a thorough history and
completing a physical examination, it was discovered that
the horses were being fed cracked and moldy corn that was
being scooped up from around a corn bin. The veterinarian
treated the horse with banamine. The horse was euthanized
after failing to respond to treatment.
Gross Findings: No disease-related gross lesions
were present. The cut surface of the brain was normal in
appearance.
Histologic Findings: There was multifocal liquefactive
necrosis of the white matter with infiltration of large numbers
of macrophages in the areas of necrosis.
Toxicology: HPLC analysis of the sample of moldy
cracked corn revealed fumonisin B1 at 57.1 ppm and fumonisin
B2 at 18.9 ppm for a total of (B1+B2) of 76 ppm.
Discussion: Equine leucoencephalomalacia is a generally
fatal, rapidly progressing neurologic disease of horses (and
other equids) caused by ingestion of fumonisin. It is characterized
by liquefactive necrosis of the cerebral white matter. Liver
lesions can also occur. Fumonisins are environmental toxins
produced by the molds Fusarium moniliforme (F. verticilloides),
F. proliferatum, and other Fusarium species that
grow on agricultural commodities in the field or during storage.
These mycotoxins have been found as common contaminants worldwide,
mainly in corn. More than ten types of fumonisins have been
isolated and characterized. Of these, fumonisin B1
(FB2) and fumonisin B3 (FB3)
are the major fumonisins produced in nature. The most prevalent
of these mycotoxins in contaminated corn is FB1
which is believed to be the most toxic.
The extent of contamination of raw corn with fumonisins
varies with geographic location, agronomic and storage practices,
and the vulnerability of the plants to fungal invasion during
all phases of growth, storage, and processing. The levels
of fumonisins in raw corn are also influenced by environmental
factors such as temperature, humidity, and rainfall during
pre-harvest and harvest periods. High levels of fumonisins
are associated with hot and dry weather, followed by periods
of high humidity. High levels of fumonisins may also occur
in raw corn that has been damaged by insects. Further, fumonisin
levels in raw corn can increase under improper storage conditions.
For example, optimal growth of fumonisin-producing molds that
lead to increased levels of fumonisins in raw corn can occur
when the moisture content of harvested raw corn during storage
is 18-23%.
Horses, along with rabbits, are the species most sensitive
to the toxic effects of fumonisin. Corn and corn by-products
used in rations of horses and rabbits should contain less
than 5 ppm (FB1 + FB2 + FB3)
and comprise no more than 20% of the dry weight of the total
ration. The total ration should contain less than 1 ppm
(FB1+FB2+ FB3). Horses should
never be fed corn screenings or moldy, damaged corn. Catfish
and swine are together as intermediate in sensitivity. Ruminants,
mink and poultry are more resistant than horses, rabbits,
catfish and swine to fumonisin.
Onset of clinical signs can occur from 1-21 weeks after
beginning eating feeds containing fumonisin, but generally
occur within 2-9 weeks. Time of onset depends on the concentration
of fumonisins in the feed. Clinical signs of fumonisin poisoning
in horses are usually related to liquefactive necrosis of
the white matter of the brain and include progressive ataxia,
depression, anorexia, delirium, aimless wandering, recumbency,
coma and death. Death can occur from 12 hours – 1 week
after onset of clinical signs. If leucoencephalomalacia is
suspected, gunshot should not be used for euthanasia as this
may render tissues unsuitable for postmortem examination.
At necropsy, lesions in the cerebral cortex can range from
none to multifocal areas of hemorrhage and necrosis, to the
presence of large cavitations of liquefactive necrosis. Histologically,
there are multifocal areas of liquefactive necrosis within
the cerebral cortex with infiltration of macrophages. Differential
diagnoses should include rabies, equine encephalomyelitis,
equine herpesvirus, botulism, head trauma, hepatoencephalopathy,
and bacterial meningoencephalitis.
Summary: Several cases of equine leucoencephalomalacia
have been presented to the ADDL since the beginning of the
year. Horse owners should be aware of the dangers of feeding
horses mold-dmaaged corn, waste corn and corn screenings.
If fumonisin contamination of corn and/or feed is suspected,
please send a minimum of ¼ pound (100 g) of a representative
sample to the Toxicology Section, ADDL. Horses suspected
of having died of leucoencephalomalacia should undergo a complete
necropsy to establish a definitive diagnosis taking appropriate
precautions remembering that rabies would be among the differential
diagnoses.
-by Dr. Steve Hooser, ADDL Toxicologist
Dr. Duane Murphy, ADDL Pathologist
Reference: Carson TL and Poppenga RH: 2002. Equine leucoencephalomalacia.
The 5-Minute Veterinary Consult (Brown CM and Bertone J, eds.)
624-625. |