Fumonisin toxicosis in swine: An overview of porcine pulmonary edema and current perspectives

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.