- Definition
- Pathophysiology
- Systems Affected
- Genetics
- Incidence/Prevalence
- Signalment
- Signs
- Causes
- Risk Factors
BASICS
A generally fatal, rapidly progressing neurologic disease caused by ingestion of fumonisin mycotoxin and characterized by liquefactive necrosis of subcortical white matter of the cerebral hemispheres. FB1 is the most abundant in corn naturally infected with Fusarium verticillioides; and has also been recently identified in contaminated rolls of hay.
Fumonisin mycotoxins interfere with sphingolipid metabolism, resulting in damage to the vascular endothelium of the brain and, in some animals, hepatocellular necrosis and vacuolization.
- Nervous—damage to vascular endothelium of the central nervous system
- Hepatobiliary—pathogenesis not definitively known
- Cardiovascular—an association has been detected between experimentally induced fumonisin neurologic disease and decreased cardiovascular function in horses
- Sporadic but important equine toxicosis
- Worldwide, most often in humid climates after a dry summer and wet harvest season
- Outbreaks are seasonal, most occurring from fall through early spring
- Although variable, 15–25% or more of horses in a group can be affected
- There appears to be marked variation in the amount of toxin required to cause clinical disease, and individual susceptibility should be considered
- Anorexia
- Depression, with little response to stimuli
- Frantic behavior such as head pressing, agitation, and hyperexcitability
- Progressive ataxia and proprioceptive defects
- Delirium
- Blindness, 1 or both eyes
- Aimless wandering, often in circles; tendency to lean to 1 side
- Eventual recumbency
- Seizures
- Coma
- Body temperature generally normal
- Death from 12 h to as long as 1 week after onset of signs
- Often occurs subclinically concurrent with leukoencephalomalacia
- Signs of liver failure are uncommon but may occur with or without signs of leukoencephalomalacia
- Icterus
- Swelling of the lips and nose
- Petechiae in mucous membranes
- Lowered head
- Reluctance to move
- Abdominal breathing
- Hemoglobinuria
- Death within hours to a few days
Ingestion of corn products contaminated (>5 ppm) with fumonisin mycotoxins, especially FB1, which are produced by F. verticillioides (synonym Fusarium moniliforme) and Fusarium proliferatum molds growing on corn. Intoxication following ingestion of contaminated baled hay reported, however this is rare.
- Fumonisins are produced in corn during hot, dry weather at pollination, and increase when temperature and moisture remain high into harvest, resulting in contaminated corn products used for horse feed
- Corn screenings contain small, shrunken, and broken kernels—often heavily contaminated with fumonisin
- Development of disease depends on fumonisin concentration in feed and duration of exposure
- Death may result from the ingestion of 10 ppm for 30 days
- Onset of clinical disease generally occurs 2–9 weeks after start of continuous consumption of fumonisin-containing feeds
- Reported intoxication following ingestion of contaminated hay associated with rainy and cold weather. An additional contributing factor may be consumption of hay from hay rolls (versus square bales)
DIAGNOSIS
TREATMENT
MEDICATIONS
FOLLOW-UP
MISCELLANEOUS