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PubMed1989

Acute aflatoxicosis in feeder pigs, resulting from improper storage of corn.

Aflatoxicosis was diagnosed in 600 feeder pigs, of which 400 died, 150 were destroyed, and 50 were marketed. The pigs were exposed to 2,500 to 3,500 micrograms of aflatoxins/kg of feed. Drought-stressed damaged corn infected with Aspergillus flavus was stored under ambient conditions in a glass-lined silo, and this storage environment provided conditions that favored rapid fungal growth and mycotoxin production.

Aflatoxins↗
PubMed1989

A field outbreak of chronic aflatoxicosis in dairy calves in the western Cape Province.

An outbreak of mortality in Friesland dairy calves in which 7 out of 25 calves died in the western Cape Province, Republic of South Africa is described. Clinical signs included a loss in body mass, staring hair coat, diarrhoea and rectal prolapse. Histopathological changes in the liver were characterised by severe portal fibrosis with bile duct proliferation and mild portal round cell infiltration. The calves were fed a ration containing locally-produced maize. The implicated maize was infested with Aspergillus flavus and contained aflatoxins B1, B2, G1 and G2 with total aflatoxin levels as high as 11,790 ng g-1. This is the first report of a field outbreak of bovine aflatoxicosis in South Africa.

Animals↗
PubMed1989

Ultrastructure of hepatic and renal lesions in chickens fed aflatoxin.

Male broiler chicks were given feed and water ad libitum from hatching through 3 weeks of age. The feed contained 0, 1.25, 2.5, and 5.0 micrograms of aflatoxin/g of feed. The chicks were killed by cervical dislocation and specimens of liver and kidney were obtained for electron microscopy on days 3, 6, 9, 17, and 21. In chicks fed 5.0 micrograms of aflatoxin, the primary lesions in liver were hepatocellular lipidosis, enlargement of bile canaliculi, reduction in mitochondrial size, mild lymphocytic infiltration, and hepatocellular degeneration and necrosis. Similar lesions were noticed in some chicks fed 2.5 micrograms of aflatoxin, but none was observed in chicks fed at 1.25 micrograms of aflatoxin. At 5 micrograms of aflatoxin, the most consistent lesion in the kidney was thickening of the glomerular basement membrane. Similar glomerular lesions were observed at 2.5 micrograms of aflatoxin, but not at 1.25 micrograms of aflatoxin. Some foot processes of the glomerular epithelial cells were poorly developed. Fusion of foot processes was not observed and fibrous material was not evident in the basement membrane. The pseudopodia of endothelial cells lining the thickened basement membrane were depleted in number or were absent. Degenerative changes also were observed in the cells of the proximal convoluted tubules, but these were less consistent than those of the glomerulus.

Animals↗
PubMed1986

Aflatoxin B1 toxicosis in dairy calves pretreated with selenium-vitamin E.

Effects of a single IM injection of selenium-vitamin E (Se-E; 5 mg of Se + 68 IU of alpha-tocopherol/60 kg of body weight) as a pretreatment 14 days before an oral dose of aflatoxin B1 (1.0 mg/kg) were studied in 24 dairy calves. Treatment groups were designated as follows: group 1 = no Se-E or aflatoxin B1 (control); group 2 = Se-E supplementation only; group 3 = aflatoxin B1 dose only; and group 4 = Se-E supplementation before aflatoxin B1 dose. Clinical signs of toxicosis in aflatoxin B1-treated calves included anorexia, ataxia, rough haircoats, increased respiration rates, dyspnea, dehydration, and nasal discharge. Packed-cell volume, RBC, WBC, and hemoglobin were increased in aflatoxin-treated calves. Significant increases in serum aspartate aminotransferase (P less than 0.05) and gamma-glutamyl-transferase (P less than 0.001) activities and prothrombin times (P less than 0.001) were observed in aflatoxin-treated calves, indicating that there was hepatic involvement. Although aflatoxin exposure caused a significant decrease in body weight (P less than 0.01) and feed intake (P less than 0.001) in treatment groups 3 and 4, Se was demonstrated to interact significantly (P less than 0.001) with aflatoxin B1 for feed intake, causing an improved feed intake in treatment group 4 calves.

Aflatoxin B1↗
PubMed1987

Fatty and hemorrhagic liver and kidney syndrome in breeding hens caused by aflatoxin B1 and heat stress in the Sudan.

Fatty liver in animals is commonly associated with toxic or nutritional disease. In tropical Africa, fatty liver in poultry is of considerable economic importance. However, it's occurrence and association with renal damage have not yet been reported. We now report the effects of hemorrhagic and fatty hepatorenal syndrome in Hybro breeding hens naturally exposed to heat stress and fed low level of aflatoxin B1.

Aflatoxin B1↗
PubMed1987

Pathological findings in a natural outbreak of aflatoxicosis in dogs.

The gross and histopathological lesions of 10 cases in a natural outbreak of aflatoxicosis amongst dogs in the Republic of South Africa are reported. The 10 cases were classified as acute (1 case), subacute (7 cases) and chronic (2 cases) on the basis of the nature, degree and extent of the following histopathological fractures: hepatocellular fatty degeneration, necrosis or regeneration; proliferation of bile ductules; accumulation of bile within the canaliculi; fibroplasia; and, mucoid degeneration, necrosis or segmental atrophy of the larger intrahepatic bile ducts. Fatty degeneration was noted grossly in the livers of all 10 cases and bile stasis in 4. Varying degrees of fibrosis were present depending on the stage of the disease. In the 2 chronic cases in which nodular regeneration was also observed fibrosis was pronounced. Other macroscopic findings included icterus, anaemia, ascites, hydrothorax, hydropericardium, anasarca, pulmonary oedema, gastro-enterorrhagia and nephrosis.

Animals↗
PubMed1987

Experimental aflatoxicosis in hybro-type chicks: sequential changes in growth and serum constituents and histopathological changes.

The effects of aflatoxin B1 on Hybro-type chicks were determined. Seven day-old chicks of both sexes were fed a diet containing aflatoxin at 0.5 ppm for 4 weeks. When compared to the controls, body weights and efficiency of feed utilization were depressed in the aflatoxin-fed group. The activities of serum sorbitol dehydrogenase (SDH) and glutamic dehydrogenase (GDH) and concentrations of potassium were significantly elevated, and total protein and calcium levels were decreased in aflatoxin-fed chicks. There were no consistent differences in the concentrations of other serum constituents between the controls and test birds. Histopathological examinations of liver and kidney sections revealed typical lesions of aflatoxicosis. In the kidney, recovery was slow as indicated by the presence of vacuolation and necrosis of the cells of many renal convoluted tubules 3 weeks after withdrawal of the experimental ration.

Animal Feed↗
PubMed1987

[Experimentally induced aflatoxicosis in broilers].

Aflatoxicosis was induced under experimental conditions in two groups of broiler birds fed in the course of the entire fattening period upon feed, containing 0,250 and 0,600 ppm aflatoxin. Dependable changes were established in the investigated haematological and biochemical indices. There was a drop of the body weight and an increase in the feed to gain ratio. Pathologic changes were recorded in the liver.

Animal Feed↗
PubMed1986

Bovine abortion and death associated with consumption of aflatoxin-contaminated peanuts.

Approximately 12% of a herd of 68 crossbred cows aborted third-trimester fetuses after consuming moldy peanuts for 4 days. Further investigation revealed that less than 20% of the herd had access to this supplemental feed. Results of serum biochemical analysis indicated liver damage in the affected cows. All of these cows died within 8 days of aborting. The peanuts contained 77 micrograms aflatoxin B1/g, as determined by liquid chromatography. Tissues were submitted from 1 cow, and liver contained 5 ng aflatoxin B1/g. Results of other laboratory tests were negative for common toxins and abortifacients.

Abortion, Veterinary↗
PubMed1986

Canine aflatoxicosis: a continuing problem.

Aflatoxins are hepatotoxic in many species including dogs. In two separate outbreaks, the primary signalment was high morbidity and mortality in hunting dogs presenting with clinical signs of icterus, anorexia and listlessness. Preliminary laboratory examinations revealed toxic hepatitis, bilirubinuria and anemia. In the first case, a feed sample was not available and the diagnosis was established by confirming the presence of significant levels of aflatoxin B1 in tissues. In the second case, cornmeal utilized in formulating the ration contained 511 ng aflatoxin B1 and B2/g. These cases illustrate that aflatoxicosis is a continuing problem despite widespread awareness and testing for aflatoxin.

Aflatoxins↗
PubMed1985

Reye syndrome.

Reye syndrome has emerged as the quintessential example of an acute metabolic encephalopathy. The clinical presentation is quite stereotyped in most instances permitting rapid, accurate diagnosis and early therapeutic intervention. Intoxications and certain inborn metabolic errors may mimic Reye syndrome. All patients with a recurrent episode should be investigated thoroughly for evidence of a metabolic disorder associated with an enzyme deficiency. Notable in this regard are inborn errors affecting organic acid, ammonia, and carbohydrate metabolism. The mitochondrial disturbance in Reye syndrome is well documented but the pathophysiologic sequence linking the antecedent viral illness to the mitochondrial injury remains obscure. Recent identification of a spontaneous Reye-like illness in mice that is associated with a coronavirus infection may provide an opportunity to investigate this initial phase of the pathophysiologic sequence. The primary cerebral insult presumably derives from insufficient substrate availability and results in massive cytotoxic cerebral edema. Treatment revolves around the continuous infusion of hypertonic glucose and intermittent infusion of hypertonic mannitol. Management is designed to attenuate or avoid the various compounding metabolic insults during this critical period when the child is metabolically crippled. In 1963, the disorder was considered to be rare and almost irreversibly fatal. Today, the disorder is recognized to be more common, and the outcome is very satisfactory in 85 to 90 per cent of the cases. The role of aspirin remains very controversial. A number of studies suggest an association between this potential mitochondrial toxin and Reye syndrome, but a causal relationship has not been established. Until better understood, it seems advisable to avoid use of aspirin in children exhibiting symptoms suggestive of Reye syndrome.

Anesthesia, General↗
PubMed1985

Aflatoxicosis in feedlot cattle.

Aflatoxicosis was diagnosed in lightweight feedlot cattle fed aflatoxin-contaminated cottonseed or gin trash. Clinical signs of hepatic damage and death were recorded for more than 200 of the 14,000 animals in a feedlot. Aflatoxin concentration in feedlot products fed to these cattle ranged from 96 to 1,700 ng/g. Diagnosis was based on the correlation of characteristic microscopic liver lesions, high concentration of aflatoxin in cottonseed feed products, and isolation and detection of aflatoxin B1 and aflatoxin M1 in urine and liver from affected calves. This report describes a large-scale outbreak of aflatoxicosis and demonstrates the need for careful quality control of feed products susceptible to aflatoxin contamination.

Aflatoxins↗