Characterization of an Epizootic of Pulmonary Edema in Swine Associated with Fumonisin in Corn Screenings

Abstract

Abstract. In 1989, corn screenings were associated with acute interstitial pulmonary edema, hydrothorax, and death in swine. Attack rate was 5-50%, case fatality rate was 50-90%, and clinical course was 1-2 days. Screenings from farms with pigs affected with pulmonary edema contained 20-330 µg fumonisin B 1 per gram. Screenings containing 92 µg fumonisin B 1 per gram fed to weanling pigs caused pulmonary edema and death. Sterilized corn inoculated with Fusarium moniliforme and diluted 1:1 with clean corn contained fumonisin B, (17 µg/g) and caused acute pulmonary edema when fed for 5 days. Survivors developed subacute hepatotoxicosis with individual hepatocellular necrosis, hepatomegalocytosis, and increased numbers of mitotic figures. Similar liver lesions occurred in pigs given fumonisin B 1 intravenously at 0.8 mg/kg body weight for 14 days.Previous experimental work established the chemical structure, toxic potential, and probable carcinogenic nature of Fusarium moniliforme and the associated toxin fumonisin B 1 (FB 1 ) in several animal speciesl-4,6,7,11 Previous experimental feeding of F. moniliforme culture material to swine resulted in pulmonary edema, 5 and pulmonary edema in swine was recently reported from natural exposure to the fungus and the associated toxin fumonisin B 1 via corn screenings.3 However, except for equine leukoencephalomalacia (ELEM), large outbreaks of toxicosis associated with F. moniliforme in other species have not been reported. This report describes fumonisin associated toxicosis in swine herds in Iowa and Illinois.During October and November 1989, the Iowa State University Veterinary Diagnostic Laboratory received numerous reports of an acute fatal porcine pulmonary edema (PPE) syndrome. Each instance was associated with feeding corn screenings from the 1989 harvest, and most deaths occurred in mature animals. Reports were primarily from the southeast quadrant of Iowa and the northwest corner of Illinois. Clinical course described by referring veterinarians included acute onset of dyspnea, weakness, cyanosis, and death. Abortions were observed from 1 to 4 days after the onset of acute signs. Pathologic findings included concurrent pulmonary edema and hydrothorax but no lesions of cardiac hemorrhage or necrosis. Deaths occurred with- Received for publication May 20, 1991. in 4-10 days after the first feeding of corn screenings. The epizootiologic, clinical, and pathologic features of 16 PPE cases in Iowa and Illinois are described. In addition, the experimental confirmation of PPE and the association of FB 1 with hepatotoxicosis is reported. Materials and methodsField investigation. Clinical and epizootiologic information for 16 PPE cases was associated with the 1989 corn crop. Clinical signs and gross lesions were observed and described, and where available, corn or feed samples were collected for fumonisin analysis and fungal culture. Nine herds were visited by veterinarians from the Iowa State University Diagnostic Laboratory, and attending veterinarians and owners provid...

Determination of Various Mycotoxin Concentrations in the Feedstuffs and Feed Produced by A Feed Manufacturer in Turkey

“…ZEN causes hyperoestrogenism, severe reproductive and infertility problems 7 . Fumonisins are known to be the cause of equine leucoencephalomalacia and porcine pulmonary oedema syndrome, which are both associated with the consumption of corn-based feed 8 .…”

Glucose Reaction with Fumonisin B1Partially Reduces Its Toxicity in Swine

“…Horses are the most sensitive species, known to develop leukoencephalomalacia (ELEM) after consuming corn contaminated with FB 1 at levels >0.001 µmol/g (6,7). In pigs, subacute dietary levels, in the range of 0.1 µmol of FB 1 /g, can cause liver disease in ∼15 days, whereas acute dietary levels, >0.14 µmol of FB 1 /g, may produce fatal porcine pulmonary edema (PPE) in <1 week (8,9). In the United States, widespread large-scale outbreaks of ELEM and PPE occurred during the fall of 1989 and the winter of 1990.…”

“…Serum markers of liver injury, such as aspartate aminotransferase (AST), γ-glutamyltransferase (GGT), total bilirubin (BIL), and total cholesterol (CHOL), increase after exposure to either acute or subacute levels of FB 1 . Hepatic lesions consist of apoptosis, necrosis, and hepatocyte proliferation (8,9). The toxicological effects of feeding 0.04 µmol of FB 1 /g of feed to weaned piglets for 28 days were recently evaluated.…”

Mycotoxin Fumonisin B 1 Increases Intestinal Colonization by Pathogenic Escherichia coli in Pigs

“…It induces leukoencephalomalacia in horses, pulmonary edema in pigs, and nephrotoxicity in rats, rabbits, lambs, and calves (3,14,21,22,32,54). In all species studied, both acute and chronic exposure to FB 1 are associated with alteration of sphingolipid metabolism and hepatotoxicity (9,20,21,26,44,46,48). FB 1 also has been implicated as a contributing factor in human esophageal cancers (45) and is a renal and hepatic carcinogen in male and female rats, respectively (22).…”