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At least 19 recordsLinked to original sources
PubMed2004

Outbreak of aflatoxin poisoning--eastern and central provinces, Kenya, January-July 2004.

In May 2004, CDC Kenya, trainees of the CDC-supported Field Epidemiology and Laboratory Training Program (FELTP) in Kenya, the World Health Organization, and CDC were invited by the Kenya Ministry of Health (KMOH) to participate in the investigation of an outbreak of jaundice with a high case-fatality rate (CFR) in the districts of Makueni and Kitui, Eastern Province. Preliminary laboratory testing of food collected from the affected area revealed high levels of aflatoxin, suggesting that the outbreak was caused by aflatoxin poisoning, as was a previous outbreak in the same area in 1981. In the United States, aflatoxin concentrations are limited to 20 parts per billion (ppb), a level also adopted by Kenyan authorities. The 2004 outbreak resulted from widespread aflatoxin contamination of locally grown maize, which occurred during storage of the maize under damp conditions. Urgent replacement of the aflatoxin-contaminated maize with noncontaminated maize proved to be a critical intervention; however, as of July 21, a limited number of new cases continued to be detected. This report summarizes the preliminary results of the outbreak investigation. Aflatoxin poisoning likely will continue to be a public health problem until culturally appropriate storage methods for dry maize are implemented by the local population. In addition, enhanced surveillance for human aflatoxin poisoning and testing of commercially sold maize for aflatoxin levels will lead to long-term improvements in public health.

Adolescent↗
PubMedDate not supplied

[Morphologic and morphometric studies of the liver of the white rat during inadequate feeding and aflatoxin poisoning].

The authors carried out morphological and morphometric studies of the liver of rats under malnutrition and chronic aflatoxin intoxication for 2 and 7 months. Malnourished animals demonstrated atrophic alterations. Animals exposed to aflatoxin B1 manifested severe dystrophic and necrobiotic alterations which did not depend on the nutrition regimen. In rats administered aflatoxin, blastomic processes were identified only at the 7th month. Whatever the diet.

Animals↗
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↗