Fumonisin Toxicosis in Animals

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 verticillioides (previously F 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. Corn grain may commonly contain 1 to3 ppm fumonisins, but occasionally some years as much as 20 to 100+ ppm. The toxins are concentrated primarily in molded, damaged, or light test weight corn. Major health effects occur in Equidae and swine. Some hepatic toxicosis can be observed in all species with increases in serum hepatic enzymes.

Signs in equids 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 up to several weeks. Icterus may be present when 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 which occurs in aflatoxicosis. Horses may develop leukoencephalomalacia from prolonged exposure to as little as 8–10 ppm fumonisins in the diet, and onset of neurologic signs almost invariably leads to death.

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 is 50%–100%. Signs include acute onset of dyspnea, cyanosis of mucous membranes, weakness, recumbency, and death, often within 24 hours 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 cholesterol concentration, bilirubin concentration, AST activity, lactate dehydrogenase activity, and gamma-glutamyltransferase activity.

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, and fatalities result from disturbances in cardiopulmonary dynamics leading to acute pulmonary edema. When fumonisin toxicosis is evident, complex sphingolipids and free sphingosine and sphinganine can be elevated in the serum of affected ponies. The ratio of serum sphinganine to sphingosine can increase to >1 during toxicosis, and may occur before elevations in liver enzymes, providing a marker of fumonisin exposure. These changes have been observed experimentally, but analysis for serum sphingolipids is not readily available diagnostically.

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 150–200 ppm cause inappetence, weight loss, and mild liver damage. Poultry are affected by concentrations of >200–400 ppm and may develop inappetence, weight loss, and skeletal abnormalities.

No effective treatment is available. Avoidance of moldy corn is the only prevention, although this is difficult because the corn may not be grossly moldy or may be contained in a mixed feed. However, most of the toxin is present in broken or small, poorly formed kernels. 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 US FDA have recommended total dietary concentrations as follows: horses < 1 ppm, swine < 10 ppm, ruminants for slaughter and mink for pelt production < 30 ppm, poultry for slaughter < 50 ppm, breeding ruminant, mink, and breeding poultry < 15 ppm, and all other species and pets < 5 ppm. Regulatory guidelines for fumonisins are provided in most countries and the EU.

• Smith GW, Constable PD. Fumonisin. In: Plumlee KH, ed. Clinical Veterinary Toxicology. St. Louis: Mosby, 2004;250-254.

• Wang E, Ross PF, Wilson TM, et al. Increases in serum sphingosine and sphinganine and decreases in complex sphingolipids in ponies given feed containing fumonisins, mycotoxins produced by Fusariummoniliforme. J Nutr 1992;122:1706-1716.

• US FDA. Guidance for industry fumonisin levels in human foods and animal feeds. November 2001. https://www.fda.gov/regulatory-information/search-fda-guidance-documents/guidance-industry-fumonisin-levels-human-foods-and-animal-feeds. Accessed 2021.

• Also see pet health content regarding fungal poisoning in animals.