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

摘要: Fumonisin toxicosis in swine was named porcine pulmonary edema (PPE) after outbreaks of a fatal disease pigs fed Fusarium verticillioides (F. moniliforme)-contaminated corn screenings from the 1989 crop Iowa, Illinois, and Georgia. Pigs that died had severe edema, which has not been identified other species exposure to fumonisins. The reproduced experimentally by feeding naturally contaminated corn, F. culture material, intravenous administration fumonisin B1 (FB1). Hepatic lesions consisting apoptosis, necrosis, hepatocyte proliferation also are observed. As species, alterations clinical pathology reflect hepatic injury as well elevated serum cholesterol concentration. In chronic studies, esophageal plaques, hyperplastic nodules, right ventricular hypertrophy were found. pigs, alters sphingolipid biosynthesis, with greatest sphingosine sphinganine concentrations kidney, liver, lung, heart. Our recent studies on have focused immune effects pathogenesis edema. specific system affected; however, FB1 inhibited phagocytosis biosynthesis macrophages. induced an accumulation membranous material capillary endothelial cells; this change appears cell type swine. short-term cardiovascular decreased left dP/dt(max) (an index cardiac contractility), mean systemic arterial pressure, heart rate, output, increased artery pressure wedge pressure. These changes compatible inhibition L-type calcium channels and/or Therefore, fumonisin-induced result acute left-sided failure mediated altered biosynthesis.