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Neurotoxic syndrome
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The clinical course is generally short with an acute onset of signs and deaths within 2 - 3 days. This syndrome is currently termed as equine leukoencephalomalacia (ELEM), although historical names include blind staggers, cerebritis, leukoencephalitis, encephalomyelitis, cornstalk disease, moldy corn poisoning, foraging disease, and cerebrospinal meningitis.
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Partial anorexia often occurs early in the course.
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Depression, ataxia, blindness, and hysteria are common. Head is often held low, especially when left alone.
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Reluctance to move and loss of equilibrium are noted in some horses when forced to walk.
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Anorexia progresses and coincides with glossopharyngeal paralysis, paralysis of the lips and tongue, and loss of the ability to grasp and chew food. Incoordination increases.
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Aimless walking, circling, and ataxia often occur. Head pressing, marked stupor, and hyperesthesia are common.
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Hyperexcitability, profuse sweating, delirium, mania, or convulsions are often present, especially terminally. Death-may occur even without previous signs being noted .
Hepatotoxic syndrome
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Icterus is usually prominent in horses with hepatic degeneration. There may also be edema of the face and submandibular space and oral petechia.
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Elevated bilirubin, liver enzymes are typically present. Terminal diaphoresis, coma, and sometimes clonic convulsions may be noted, presumably due to hepatoencephalopathy.
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Swine exhibit decline in feed consumption is usually the first sign. If toxin consumption is significant, acute pulmonary edema and, often, death follows. At low doses, slowly progressive liver disease may occur.
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Poultry-poor performance, feed refusal, diarrhoea, weakness, and high mortality may be noted.
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Rats exhibit hepatic neoplasia while rabbits show sudden renal failure.
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Human beings-oesophageal cancer is suspected to be related to consumption of fumonisin-contaminated corn.
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