Fumonisin toxicosis in swine was named porcine
pulmonary edema (PPE) after outbreaks of a fatal disease in pigs fed Fusarium verticillioides (F. moniliforme)-contaminated corn screenings from the 1989 corn crop in Iowa, Illinois, 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 corn, F. verticillioides culture material, and by
intravenous administration of
fumonisin B1 (FB1). Hepatic lesions consisting of apoptosis,
necrosis, and hepatocyte proliferation also are observed. As in other species, alterations in clinical pathology reflect hepatic injury as well as elevated serum
cholesterol concentration. In chronic studies, esophageal plaques, hyperplastic hepatic nodules, and
right ventricular hypertrophy were found. In pigs, as in other species,
fumonisin alters
sphingolipid biosynthesis, with the greatest alterations in
sphingosine and
sphinganine concentrations in kidney, liver, lung, and heart. Our recent studies on
fumonisin toxicosis in pigs have focused on immune effects and the pathogenesis of
pulmonary edema. The specific immune system was not affected; however, FB1 inhibited phagocytosis and
sphingolipid biosynthesis in pulmonary macrophages.
Fumonisin induced an accumulation of membranous material in pulmonary capillary endothelial 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 pressure, heart rate, and cardiac output, and increased mean pulmonary artery pressure and pulmonary artery wedge pressure. These changes are compatible with 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 altered
sphingolipid biosynthesis.