Fumonisins are mycotoxins produced by Fusarium moniliforme and F. proliferatum which are known to grow on grains and other agricultural products worldwide. An analysis of maize from 18 different countries demonstrated mycotoxin in 93% of the samples tested. In the horse fumonisins cause a neurotoxicity and in swine pulmonary oedema. The mycotoxins are known to be hepatotoxic, nephrotoxic, atherogenic, immunosuppressive and embryotoxic in laboratory animals. Fumonisins are potent inhibitors of sphingolipid biosynthesis. They are suspected to cause oesphageal cancer in humans and are known to be hepatocarcinogenic in rats.
Fusarium moniliformegrow on corn, sorghum, millet and other grains. High concentrations of fumonisins have been found in maize screenings (damaged maize kernels).
Fumonisin is an aliphatic hydrocarbon with a terminal amine group and two tricarboxylic acid side chains. These mycotoxins are classified as fumonisin B1, fumonisin B2 and fumonisin B3 according to the number and position of the hydroxyl groups. Fumonisins are water soluble, heat stable and resistant to alkali treatment.
In horses as little as 10 ppm in the diet when fed daily for 30 days results in a fatal leukoencephalomalacia.
Cattle and sheep are mildly affected by 100 ppm in the diet.
Pigs receiving less than 25 ppm of fumonisin B1 have no apparent clinical effects. Pigs fed a diet containing 50 ppm of fumonisin B1 develop mild liver lesions within 7-10 days. A diet of greater than 100 ppm of fumonisin B1 produces an acute pulmonary and hepatic toxicosis when fed for 5-10 days.
The mechanism of action is the inhibition of the conversion of sphinganine to sphingosine.
Clinical effects are species specific.
Horse
Fumonisins are neurotoxic in the horse. Horses become depressed, blind, ataxic, wander aimlessly, develop facial paralysis, comatose and die. The disease is known as equine leukoencephalomalacia (ELEM)and is fatal. Death may occur from 24 hours to a week after the onset of clinical signs.
Pigs
The clinical findings after the ingestion of high doses of fumonisins are characterised by pulmonary toxicity. Pigs become dyspnoeic, cyanotic and weak within 4 7 days of ingestion. Death may occur as soon as 4 hours after the onset of clinical signs.
Less toxic doses develop icterus, decreased feed intake, weight loss and may have diarrhoea.
Ruminants
Diets containing up to 200 ppm of fumonisins may cause anorexia and weight loss but fatalities are unusual.
Poultry
Diets containing 200 400 ppm of fumonisins may cause anorexia, diarrhoea, lameness and death. Laying hens ingesting feed contaminated with 8 mg/kg of fumonisin B1 had a 10% mortality rate and a 20% reduction in egg production. fed a diet containing 50 ppm of fumonisin B1 develop mild liver lesions within 7 10 days. A diet of greater than 100 ppm of fumonisin B1 produces an acute pulmonary and hepatic toxicosis when fed for 5 10 days.
Fumonisin is a known carcinogen.
In the horse and donkey massive softening and liquefaction of the cerebral white matter is characteristic of leukoencephalomalacia. Haemorrhages are present. Histological changes show liquefaction with a proliferation of macrophages.
In pigs acute pulmonary oedema with marked to massive intralobular pulmonary oedema and hydrothorax occurs. The lungs are distended and firm. Interstitial and interlobular oedema is seen histologically. Other lesions include focal pancreatic necrosis and a hepatopathy with increased mitotic figures, necrosis of hepatocytes and mild bile retention. Pigs with severe hepatic lesions are icteric.
In poultry pale yellow livers with peripheral congestion, mild haemorrhage in the proventriculus and watery contents in the intestine have been reported. In turkey poults hepatocellular hyperplasia a loss of cardiomyocyte cross striations were found at 200 mg/kg of fumonisin B1 in the diet.
In rats tubular nephrosis and necrosis of the liver have been observed at 25 mg/kg or greater doses.
Hepatic dysfunction is a consistent feature in animals measured by an increase in cholesterol, gamma glutamyl transpeptidase (GGT), aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactic dehydrogenase (LDH) and bilirubin. The ratio of serum sphinganine to sphingosine is increased but this analysis is not performed by all clinical laboratories.
Symptomatic care should be provided for animals with hepatic dysfunction. If a known exposure has occurred before clinical signs develop, activated charcoal or other means of decontamination may be useful. Do not feed corn screenings to horses. Corn or other grains suspected to be contaminated should be tested and cleaned if necessary.
Due to the carcinogenic nature of fumonisins contaminated feed should not be fed to food producing animals.
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