Fumonisin toxicosis in swine was named porcine pulmonary edema (PPE) after
outbreaks of a fatal disease in pigs fed Fusarium verticillioides (F. monil
iforme)-contaminated corn screenings from the 1989 corn crop in lowa, Illin
ois, and Georgia. Pigs that died had severe pulmonary edema, which has not
been identified in other species after exposure to fumonisins. The disease
has been reproduced experimentally by feeding of naturally contaminated cor
n, F. verticillioides culture material, and by intravenous administration o
f fumonisin B-1 (FB1). Hepatic lesions consisting of apoptosis, necrosis, a
nd hepatocyte proliferation also are observed. As in other species, alterat
ions in clinical pathology reflect hepatic injury as well as elevated serum
cholesterol concentration. In chronic studies, esophageal plaques, hyperpl
astic hepatic nodules, and right ventricular hypertrophy were found. In pig
s, as in other species, fumonisin alters sphingolipid biosynthesis, with th
e greatest alterations in sphingosine and sphinganine concentrations in kid
ney, liver, lung, and heart. Our recent studies on fumonisin toxicosis in p
igs have focused on immune effects and the pathogenesis of pulmonary edema.
The specific immune system was not affected; however, FB1 inhibited phagoc
ytosis and sphingolipid biosynthesis in pulmonary macrophages. Fumonisin in
duced an accumulation of membranous material in pulmonary capillary endothe
lial cells; this change appears specific to this cell type and to swine. In
short-term cardiovascular studies, fumonisin decreased left ventricular dP
/dt(max) (an index of cardiac contractility), mean systemic arterial pressu
re, heart rate, and cardiac output, and increased mean pulmonary artery pre
ssure and pulmonary artery wedge pressure. These changes are compatible wit
h the inhibition of L-type calcium channels by increased sphingosine and/or
sphinganine concentration. Therefore, fumonisin-induced pulmonary edema in
swine appears to result from acute left-sided heart failure mediated by al
tered sphingolipid biosynthesis.