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Spring 2003 Newsletter

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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 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.


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Fax: 765-494-9181

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Phone: (812) 678-3401
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