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Page 1 from 82 results
Pulmonary edema and hydrothorax in swine produced by fumonisin B1, a toxic metabolite of Fusarium moniliforme.
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Pulmonary edema and hydrothorax were observed in mature swine that died approximately 5 days after consuming corn screenings. These postmortem observations were reproduced in younger swine (16-24 kg) that died within 1 week when fed the corn screenings under experimental conditions. Additionally,
Sequence of cardiovascular changes leading to pulmonary edema in swine fed culture material containing fumonisin.
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OBJECTIVE
To determine the sequence of cardiovascular and blood gas changes induced by ingestion of fumonisin-containing culture material in swine and to examine the temporal relationship of these changes to plasma sphinganine and sphingosine concentrations.
METHODS
12 healthy castrated pigs (38 to
Species and organ specificity of fumonisin-induced endothelial alterations: potential role in porcine pulmonary edema.
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Fumonisins, mycotoxins that commonly contaminate corn, induce cardiovascular toxicity and pulmonary edema in pigs, leukoencephalomalacia in horses, and nephropathy in rats, rabbits, and lambs. The mechanisms of these species-specific target organ toxicoses are poorly understood. We have previously
Development of fumonisin-induced hepatotoxicity and pulmonary edema in orally dosed swine: morphological and biochemical alterations.
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The fumonisin (FB) mycotoxins induce liver injury in all species but induce fatal pulmonary edema (PE) only in pigs. They inhibit ceramide synthase in the sphingolipid biosynthetic pathway. To study the pathogenesis of PE, we examined the early events in the development of FB-induced PE and
Characterization of an epizootic of pulmonary edema in swine associated with fumonisin in corn screenings.
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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 micrograms
Fumonisin-induced pulmonary edema and hydrothorax in swine.
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Pulmonary edema and hydrothorax were observed in mature swine that died approximately 5 days after consuming corn screenings. These postmortem observations were reproduced in younger pigs that died within 1 week when fed the corn screenings under experimental conditions. Additionally, pulmonary
Fumonisin toxicosis in swine: an overview of porcine pulmonary edema and current perspectives.
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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
Production of fumonisins by Fusarium moniliforme and Fusarium proliferatum isolates associated with equine leukoencephalomalacia and a pulmonary edema syndrome in swine.
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Fumonisin B1 (FB1) and FB2 were isolated from corn cultures of both Fusarium moniliforme and Fusarium proliferatum. Respective concentrations in culture materials of FB1 and FB2 ranged from 960 to 2,350 and 120 to 320 micrograms/g for F. moniliforme and from 1,670 to 2,790 and 150 to 320
Preliminary communication: examination of the harmful effect to fetuses of fumonisin B(1) in pregnant sows.
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Three sows were fed a diet mixed with Fusarium moniliforme fungal culture from the 107th day of pregnancy until parturition. Fumonisin B(1) toxin was administered to two sows (sows 1 and 2) in a daily dose of 300 mg for an additional 7 days subsequent to parturition, i.e., for a total of 14-16 days.
Discovery and occurrence of the fumonisins: a historical perspective.
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This article describes the events leading to the discovery of the fumonisins in South Africa in 1988 and highlights the first 10 years (1988-1998) of fumonisin research. The predominant fungus isolated from moldy corn implicated in a field outbreak of equine leukoencephalomalacia (ELEM) in South
Fumonisin toxicosis in swine: clinical and pathologic findings.
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From a series of experimental studies with pigs (12-16 kg), either pulmonary edema or liver failure emerged as a distinct pathogenetic expression of fumonisin B1 (FB1) toxicosis. The primary determinant as to which pathogenetic consequence developed was the quantity (dose) of the mycotoxin fed or
Mechanism of Fumonisin Toxicity and Carcinogenesis.
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What are the molecular events that fumonisin-induced porcine pulmonary edema syndrome and equine leucoencephalomalacia have in common? Do these animal diseases relate mechanistically to fumonisin toxicity in laboratory rats? There is considerable data indicating that disruption of sphingolipid
Mechanism of Fumonisin Toxicity and Carcinogenesis.
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What are the molecular events that fumonisin-induced porcine pulmonary edema syndrome and equine leucoencephalomalacia have in common? Do these animal diseases relate mechanistically to fumonisin toxicity in laboratory rats? There is considerable data indicating that disruption of sphingolipid
Fumonisin exposure to Kansans through consumption of corn-based market foods.
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Fumonisins are secondary metabolites of the fungus Fusarium moniliforme Sheldon, a common corn contaminant world wide. Presently 6 different fumonisins (FB1, FB2, FB3, FB4, FA1 and FA2) have been identified and characterized. In veterinary medicine fumonisins cause equine leucoencephalomalacia and
Use of formalin-fixed tissues to determine fumonisin B1-induced sphingolipid alterations in swine.
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Fumonisin B1 is a mycotoxin that causes lethal pulmonary edema in swine. Sphinganine, sphingosine, and the sphinganine to sphingosine ratio are important biomarkers for fumonisin B1 exposure. Currently, tissues selected for sphinganine and sphingosine analyses are frozen at -80 degrees C until
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