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Results for “Aflatoxin Poisoning”

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At least 19 recordsLinked to original sources
PubMed1966

Induced tolerance in turkeys to aflatoxin poisoning.

The consumption of moderately poisonous levels of toxic groundnut meal by turkey poults induced a degree of tolerance to aflatoxin Poults thus ;conditioned' gained more than ;unconditioned' birds on successively higher levels of aflatoxin and were enabled to survive and gain on rations which killed mature turkeys. Ingestion of aflatoxin led to marked alterations in the serum electrophoretic patterns followed in a few weeks by a return to nearly normal patterns. Subsequent increases in aflatoxin intake induced only minimal alternations in the serum patterns but the tolerance appeared unrelated to the hepatotoxic effect because extensive pathological changes developed in the liver.

Animal Feed↗
PubMed1991

[Search for lesions caused by aflatoxin B1 poisoning in 3 industrial chicken farms on the Ivory Coast].

A systematic search for feed contamination by aflatoxin-B1 as well as for lesions indicating an acute or chronic aflatoxicosis was made in three groups of industrially raised hens in Côte-d'Ivoire. The contamination rates were low although they were 6 to 10 times higher than the official standards. No lesion due to an acute or chronic intoxication by aflatoxins was observed. However, the repeated intake of small amounts of aflatoxins might eventually have repercussions on the technics-economical performance either by a direct action of the toxin or via the development of an immune depression in the animals.

Aflatoxin B1↗
PubMed1992

Major biological consequences of aflatoxicosis in animal production.

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.

Animal Feed↗
PubMed1992

Perak, Malaysia, mass poisoning. Tale of the Nine Emperor Gods and rat tail noodles.

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.

Boric Acids↗
PubMed1991

Clinical implications of food contaminated by aflatoxins.

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.

Acute Disease↗
PubMed1987

Acute mycotoxicosis in sheep: field cases.

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.

Animals↗
PubMed1991

An outbreak of aflatoxicosis and boric acid poisoning in Malaysia: a clinicopathological study.

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.

Aflatoxins↗