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 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
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 1–3 ppm fumonisins, but occasionally some years as much
as 20–100 ppm. The toxins are concentrated primarily in molded, damaged, or light
test weight corn. Major health effects are seen 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 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 seen 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.
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 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, and fatalities result from disturbances in
cardiopulmonary dynamics leading to acute pulmonary edema.
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
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 FDA have recommended total dietary concentrations (ppm) as
follows: horse <1, swine <10, ruminants <30, poultry <50, breeding
ruminants and poultry <15 ppm.
Last full review/revision December 2014 by Gary D. Osweiler, DVM, MS, PhD