Fumonisins are responsible for two well-described diseases of livestock, equine leukoencephalomalacia and porcine pulmonary edema.
Equine leukoencephalomalacia is a mycotoxic disease of the CNS that affects horses, mules, and donkeys. It occurs sporadically in North and South America, South Africa, Europe, and China. It is associated with the feeding of moldy corn (maize), usually over a period of several weeks. Fumonisins are produced worldwide primarily by Fusarium verticilloides (previously Fusarium moniliforme Sheldon) and F proliferatum. Conditions favoring fumonisin production appear to include a period of drought during the growing season with subsequent cool, moist conditions during pollination and kernel formation. Three toxins produced by the fungi have been classified as fumonisin B1 (FB1), B2 (FB2), and B3 (FB3). Current evidence suggests that FB1 and FB2 are of similar toxicity, whereas FB3 is relatively nontoxic. Major health effects are observed in Equidae and swine.
Signs in Equidae include apathy, drowsiness, pharyngeal paralysis, blindness, circling, staggering, and recumbency. The clinical course is usually 1–2 days but may be as short as several hours or as long as several weeks. Icterus may be present if the liver is involved. The characteristic lesion is liquefactive necrosis of the white matter of the cerebrum. The necrosis is usually unilateral but may be asymmetrically bilateral. Some horses may have hepatic necrosis similar to that seen in aflatoxicosis. Horses may develop leukoencephalomalacia from prolonged exposure to as little as 8–10 ppm fumonisins in the diet.
Fumonisins have also been reported to cause acute epidemics of disease in weanling or adult pigs, characterized by pulmonary edema and hydrothorax. Porcine pulmonary edema (PPE) is usually an acute, fatal disease and appears to be caused by pulmonary hypertension with transudation of fluids in the thorax resulting in interstitial pulmonary edema and hydrothorax. Acute PPE results after consumption of fumonisins for 3–6 days at dietary concentrations >100 ppm. Morbidity within a herd may be >50%, and mortality among affected pigs ranges from 50 to 100%. Signs include acute onset of dyspnea, cyanosis of mucous membranes, weakness, recumbency, and death, often within 24 hr after the first clinical signs. Affected sows in late gestation that survive acute PPE may abort within 2–3 days, presumably as a result of fetal anoxia. Prolonged exposure of pigs to sublethal concentrations of fumonisins results in hepatotoxicosis characterized by reduced growth; icterus; and increased serum levels of cholesterol, bilirubin, AST, lactate dehydrogenase, and γ-glutamyltransferase.
The biochemical mechanism of action for PPE or liver toxicosis is believed to be due to the ability of fumonisins to interrupt sphingolipid synthesis in many animal species.
Cattle, sheep, and poultry are considerably less susceptible to fumonisins than are horses or swine. Cattle and sheep tolerate fumonisin concentrations of 100 ppm with little effect. Dietary concentrations of 200 ppm cause inappetence, weight loss, and mild liver damage. Poultry are affected by concentrations >200–400 ppm and may develop inappetence, weight loss, and skeletal abnormalities.
No treatment is available. Avoidance of moldy corn is the only prevention, although this is difficult because it may not be grossly moldy or it may be contained in a mixed feed. However, most of the toxin is present in broken kernels or small, poorly formed kernels. Therefore, cleaning grain to remove the screenings markedly reduces fumonisin concentration. Corn suspected of containing fumonisins should not be given to horses. Binding of fumonisins with glucose has been demonstrated to alleviate or eliminate toxicosis in pigs, but development of the process on a commercial scale has not yet been accomplished. Advisory exposure guidelines by the FDA recommend total dietary concentrations (ppm) as follows: horse <1; swine <10; ruminants <30; poultry <50; breeding ruminants and poultry <15 ppm.
Last full review/revision March 2012 by Gary D. Osweiler, DVM, MS, PhD, DABVT