[Light and electron-optic studies on the liver cirrhosis following experimenal poisoning with aflatoxin in ducklings].
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Two episodes of acute aflatoxin poisoning in horses suggest that horses are susceptible to the toxic effects of this mycotoxin. Lesions associated with exposure to aflatoxin included encephalomalacia of cerebral hemispheres, fatty degeneration, necrosis, bile duct hyperplasia, fibrosis of the liver, fatty infiltration of the kidney, hemorrhagic enteritis, and myocardial degeneration. Hypoglycemia, hyperlipidemia, and depletion of lymphocytes accompanied these lesions. The diagnosis was based on gross and histopathologic observations, consistent with observations of other species poisoned with aflatoxin, and isolation of the toxin from feed and animal tissues. Removing contaminated feed prevented further morbidity or mortality.
Aflatoxins, a family of closely related, biologically active mycotoxins, have been known as a prominent cause of animal disease for 30 yr. The toxins occur naturally on several key animal feeds, including corn, cottonseed, and peanuts. Occurrence of aflatoxin on some field crops tends to spike in years when drought and insect damage facilitate invasion by the causative organisms, Aspergillus flavus and A. parasiticus, which abound in the crop's environment. Acute aflatoxicosis causes a distinct overt clinical disease marked by hepatitis, icterus, hemorrhage, and death. More chronic aflatoxin poisoning produces very protean signs that may not be clinically obvious; reduced rate of gain in young animals is a sensitive clinical register of chronic aflatoxicosis. The immune system is also sensitive to aflatoxin, and suppression of cell-mediated immune responsiveness, reduced phagocytosis, and depressed complement and interferon production are produced. Acquired immunity from vaccination programs may be substantially suppressed in some disease models. In such cases the signs of disease observed are those of the infectious process rather than those of the aflatoxin that predisposed the animal to infection. Mixtures of aflatoxin with other mycotoxins can result in greatly augmented biological responses in terms of rate of gain, lethality, and immune reactivity. Because of its great biological activity, its wide-spread potential presence in areas where critical feed crops are grown, and its propensity to spike in problem years, aflatoxin promises to be a continuing problem in animal production.
In October 1988, a series of food poisoning cases occurred in the State of Perak in Malaysia. Most of the victims were children. Ultimately 13 children between the ages of 2.5 and 11 years died. Epidemiological investigations showed that the probable source of the poison was Loh See Fun, a noodles in the shape of a rat's tail. All the deceased ate the noodles from one supplier. Clinical and pathological findings were similar in each case. Postmortem examination was performed in 11 cases. Toxicological examination on organs in 10 cases showed a high concentration of aflatoxin in tissues of the deceased. High levels of boric acid were excreted from most of the victims. Histological examination of the liver in these cases showed necrotic changes found in aflatoxin poisoning. Combination of the epidemiological, clinical, toxicological, and pathological findings pointed to the fact that there was a common toxin or toxins responsible for the deaths. These were thought to be a combination of boric acid and aflatoxin.
Aflatoxins have been incriminated, mainly on circumstantial evidence, in hepatocellular carcinoma, acute hepatic failure and Reye's syndrome, but other possible effects of continuous or intermittent dietary exposure to aflatoxins, which occurs widely in the tropics, have received little study. Over the past 10 years evidence has steadily accumulated that incriminates aflatoxins in the aetiology of kwashiorkor, a widespread and serious disorder of children in the tropics, previously believed to be caused by protein deficiency. Investigation of human breast milk, undertaken initially to elucidate the pathogenesis of kwashiorkor in breastfed infants, has revealed widespread and serious exposure to aflatoxins from this source. Extension of these studies to pregnant women, in turn, revealed widespread and serious prenatal aflatoxin exposure. In laboratory and farm animals, such exposure has serious implications for immune and hepatic functions, and is detrimental to growth and development. Recent analysis of heroin samples show that heroin addicts may also be exposed to these toxins. These findings show that human exposure to aflatoxins may begin prenatally, persist during breastfeeding, and continue into adult life. It is postulated that aflatoxins (i) play a role in the aetiology of kwashiorkor, (ii) increase neonatal susceptibility to infection and jaundice, (iii) increase childhood susceptibility to infections and malignant disease, (iv) compromise immune responses to prophylactic immunisations and (v) may play a role in the pathogenesis of diseases in heroin addicts. There are indications also that acute, fatal aflatoxin poisoning which masquerades as 'hepatitis' may occur more frequently than is currently appreciated.
Using the thrombotest technique blood clotting times were measured in the duck and the chicken after an intraperitoneal (I.P.) administration of aflatoxin B1 (58 microgram/kg body weight). Six hours after injection, the average thrombotest (blood clotting) time of the blood of the young duck was 194.5 +/- 1.3 sec (control time was 101.5 +/- 1.4, P less than .0001) and that of the young chicken averaged 70.2 +/- sec (control time was 51.7 +/- 2 sec, P less than .001). Corresponding times for the aflatoxin-treated adult birds were 249.5 +/- 1.4 sec (control, 118.5 +/- 1.1 sec; P less than .001) and 82.9 +/- .2 sec (control, 66.8 +/- .1 sec; P less than .001) for the duck and chicken respectively. In addition to the relatively low concentration of blood clotting factors in the plasma of the bird the present results suggest that there is a weak interaction of blood clotting factors II, VII, IX, and X in the avian species during aflatoxin poisoning. There is an inter-species difference in the anticoagulant effects of aflatoxin in the avian class.
Aflatoxins are mycotoxins produced by some strains of fungus (Aspergillus) which develop in peanut seeds. Peanut oil and past are very used up in Senegal, then the aflatoxin poisoning risk is very actual. The aim of this study was to determinate the aflatoxin level in artisanal and industrial peanut pastry food from Dakar (Sénégal). High Performance Liquid Chromatography (HPLC) analysis of the different samples showed that the most contaminated by aflatoxins are artisanal pastry sold in different market of Dakar (Sénégal). Indeed, 40% of these samples contained mean values of aflatoxin B1 (the most dangerous) widely over allowable EEC specifications (5ppb). Furthermore, most of industrial and domestic peanut pastry were cleaned and could be consumed without risk.
Aflatoxins are mycotoxins produced by some strains of fungus (Aspergillus) which develops in peanuts seeds. Peanuts oil and past are very used up in Senegal, then the aflatoxins poisoning risk are very actual. This study relates to the determination of contamination levels by aflatoxins from peanut oil food prepared by small scale production in areas of Kaolack and Diourbel. High Performance Liquid Chromatography (HPLC) analysis of the different samples showed that 80% of them were contaminated in the areas of Kaolack and Diourbel. Aflatoxin B1, B2, G1 and G2 has been detected with a profile of contamination almost identical in the both areas. Aflatoxin B1 was prevalent and has been found in over 85% of samples. Mean contents of this mycotoxin (the most dangerous toxin) is about 40 ppb, value widely superior to allowable specifications.
In 2 x 3 factorial experiments, 240 broiler chicks were fed diets containing 0, 0.01, and 0.02% beta-carotene or canthaxanthin with or without 5 ppm aflatoxin to determine the effects of these two carotenoids on the health and well-being of broilers subjected to aflatoxin poisoning. Neither beta-carotene nor canthaxanthin was effective at overcoming the growth-depressing effects of aflatoxin. Relative liver weights were significantly higher in broilers receiving dietary aflatoxin in the presence of beta-carotene but not canthaxanthin. beta-Carotene and canthaxanthin had no effect on antibody production against infectious bursal disease (IBD). Interestingly, secondary antibody production against IBD was enhanced by the presence of aflatoxin in the diet. Canthaxanthin significantly increased the concentrations of cholesterol, total protein, uric acid, and triglyceride, all of which were significantly depressed by aflatoxin. beta-Carotene did not effect any of the measured blood analytes. There was a significant interaction between canthaxanthin and aflatoxin with respect to creatine kinase activity. Creatine kinase activity decreased as dietary canthaxanthin increased in the presence of aflatoxin. The data suggest that beta-carotene is not effective at ameliorating aflatoxicosis in broiler chickens but that canthaxanthin may be somewhat effective with respect to certain clinical blood chemistry indicators.
A study to determine mould incidence and aflatoxin contamination of maize kernels was carried out among dealers (traders) in the three agroecological zones of Uganda. The maize kernels were categorized into those stored for two to six months or for more than six months to one year. Results indicate that the mean moisture content of the kernels was within the recommended safe storage levels of < or =15% but was significantly lower in the Highland maize kernels followed by the Mid-Altitude (dry) kernels while the Mid-Altitude (moist) kernels had the highest levels. Across the agroecological zones, Aspergillus, Fusarium, Penicillium and Rhizopus were the most predominant fungal genera identified and, among their species, A. niger had the highest incidence, followed by A. flavus, F. verticillioides, A. wentii, A. penicillioides and Rhizopus stolonifer. There were more aflatoxin positive samples from the Mid-Altitude (moist) zone (88%) followed by those samples from the Mid-Altitude (dry) zone (78%) while samples from the Highland zone (69%) were least contaminated. Aflatoxin levels increased with storage time such that maize samples from the Mid-Altitude (dry and moist) stored for more than six months had mean levels greater than the 20 ppb FDA/WHO regulatory limits. Aflatoxin B1 was the most predominant type and was found to contaminate maize kernels from all the three agroecological zones. These results indicate that maize consumers in Uganda are exposed to the danger of aflatoxin poisoning. Thus, there is the need for policy makers to establish and enforce maize quality standards and regulations related to moulds and aflatoxins across the agroecological zones to minimize health hazards related to consumption of contaminated kernels.
Inappetence, apathy and neurological signs were seen in a flock of sheep at an out-station of Khartoum, that were fed on groundnut cake meal contaminated with aflatoxins (750 ppb). The gross and microscopic lesions were confined to the liver. The biochemical analysis of the serum was consistent with the presence of liver damage. The presence of aflatoxins in the feeds and tissues of the dead sheep supports that the condition was due to aflatoxin poisoning.
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An outbreak of food poisoning resulting in 13 deaths in children occurred in Malaysia during the Chinese Festival of the Nine-Emperor Gods in 1988. The offending food was a Chinese noodle called 'Loh See Fun' (LSF). The source was traced to a factory where a banned food preservative was added to make the LSF. The food poisoning was attributable to aflatoxins and boric acid. The clinical features included vomiting, pyrexia, diarrhoea, abdominal pain, anorexia, giddiness, seizures, and eventual coma. Initially, many presented with a Reye-like syndrome. Eleven post-mortem examinations were performed. The pathological findings included extensive coagulative necrosis of the liver with proliferative 'ductal/ductular metaplasia of the hepatocytes'. Giant cell formation, central vein sclerosis, bile stasis, and steatosis were also noted. There was presence of acute tubular necrosis, superficial upper gastrointestinal erosions, and ensuing encephalopathy. The eventual cause of death is acute hepatic and renal failure.
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